Young cancer survivors may face faster aging and possible early-onset dementia
Adolescent and young adult cancer survivors exhibit accelerated aging at both cellular and brain function levels, regardless of treatment type, with chemotherapy contributing most to this effect. Increased biological age correlates with cognitive deficits such as impaired memory and attention. Lifestyle changes like exercise and improved nutrition may help reverse some aging effects.
AnnaLynn M. Williams et al, Epigenetic age acceleration, telomere length, and neurocognitive function in long-term survivors of childhood cancer, Nature Communications (2025). DOI: 10.1038/s41467-025-65664-5
Millions of Your Mother's Cells Persist Inside You
Every human born on this planet is not entirely themselves.
A tiny fraction of our cells – around one in a million – is actually not our own, but comes from our mothers. That means each of us has millions of cells that our immune systems would normally recognize as foreign; yet somehow, in most of us, they hang around peacefully without causing any immune problems.
It's called microchimerism, and it goes both ways: every human who has ever been pregnant retains cells from their fetus, and every human retains cells from their mother.
Now, immunologists have figured out why. A small number of maternal immune cells that cross the placenta during pregnancy actively train the fetus's immune system to tolerate the mother's cells for their entire life.
Micro chimerism is increasingly linked with so many health disorders. This study provides an adaptable platform for scientists to investigate whether these rare cells are the cause of disease, or alternatively, found in diseased tissue at increased levels as part of the natural healing process.
The oldest animal keeps its eyes sharp Greenland sharks (Somniosus microcephalus) can live to be up to 400 years old, making them the longest-lived vertebrate. They dwell in the almost-sunless waters of the Arctic deep sea, and are often infested with parasites that attach to their eyes, leading scientists to suppose that the animals might be functionally blind. But researchers who studied the sharks’ eyeball in the lab say that it’s quite the contrary: the sharks appear to maintain their vision over centuries with no signs of retinal degeneration — perhaps thanks to a DNA repair mechanism in the retina — and could offer clues to treating age-related vision loss in people.
Omega-3 supplements fail to improve depressive symptoms in young people
Is fish oil the new snake oil?
Fish oil pills rich in omega-3 fatty acids gained attention as a possible add-on treatment for depression, as a few studies on adults found noticeable improvements in symptoms when combined with antidepressants.
When a similar study was conducted with children and adolescents, omega-3 fatty acids did not do any better than a placebo.
A team of researchers from Switzerland carried out a large clinical trial at five different centers, spanning nine months, to test whether adding omega-3 supplements to standard treatment could help teenagers and young adults with moderate-to-severe depression. The study involved 257 participants aged 8 to 18 who were randomly assigned to receive either 1.5 grams of omega-3 supplements or placebo pills daily.
The results are published inJAMA Network Open.
This study revealed that supplementing depression treatment with fish oil pills didn't prove more effective than placebo at improving quality of life, reducing suicidal ideation, or the need for antidepressants. Both groups showed similar improvements during the study and showed depression scores of 36.5 with omega-3 vs. 36.8 with placebo.
The results indicate that omega-3 supplements provide no additional benefit for depression.
Please note that the trial was conducted during the COVID-19 pandemic, which may have influenced the outcomes.
Tree bark microbes also clean the air by removing greenhouse and toxic gases
Microbes living on tree bark consume significant amounts of climate-active gases such as methane, hydrogen, and carbon monoxide, in addition to CO2 absorbed by trees. This microbial activity occurs on a global scale, enhancing air purification and contributing to both climate regulation and improved air quality. Different tree species host distinct microbial communities with varying gas-removal capacities.
Twin study ties childbearing timing to biological aging
Analysis of Finnish twins indicates that both the number and timing of pregnancies are linked to women's biological aging and lifespan. Women with two to three children and pregnancies between ages 24 and 38 show slower aging and longer life expectancy, while childlessness, early childbearing, or having more than four children are associated with accelerated aging. Epigenetic data support these associations.
A study based on Finnish twins shows that reproductive history is associated, at the population level, with women's lifespan and biological aging. In the study, mothers of large families, women who had no children, or women who had their first child at a very young age appeared to age somewhat faster than other women.
The results suggest that both the number of children and the timing of pregnancies are reflected in women's adult health and life expectancy. The paper is published in the journal Nature Communications.
From an evolutionary biology perspective, organisms have limited resources such as time and energy. When a large amount of energy is invested in reproduction, it is taken away from bodily maintenance and repair mechanisms, which could reduce lifespan.
Somewhat unexpectedly, the study also found that childless women showed faster aging than women with a few children. This result may be explained by other lifestyle or health-related factors whose effects could not be fully controlled for in the analyses.
The research group emphasizes that the findings apply only at the population level. They do not demonstrate cause–effect relationships, nor do they provide a basis for individual recommendations for women of reproductive age. For example, family size has decreased and the age at first birth has increased compared with the period covered by the study.
A novel aspect of this study was that aging was also measured biologically. Epigenetic clocks were determined from blood samples from more than one thousand participants. Epigenetic clocks aim to measure biological aging—that is, the gradual deterioration of cells and tissues. With such methods, aging-related changes can be detected years or even decades before death.
The results supported earlier conclusions based on mortality data. According to the epigenetic clocks, women who had either many children or no children at all were biologically somewhat older than their chronological age. A person who is biologically older than their calendar age is at a higher risk of death. Having a child at a young age was also associated with biological aging. This too may relate to evolutionary theory, as natural selection may favor earlier reproduction that entails shorter overall generation times, even if it entails health-related costs associated with aging.
Mikaela Hukkanen et al, Epigenetic aging and lifespan reflect reproductive history in the Finnish Twin Cohort, Nature Communications (2026). DOI: 10.1038/s41467-025-67798-y
Suppressing postoperative inflammation may prolong pain
Suppressing inflammation after surgery by inhibiting TNF-α can delay recovery and prolong pain, rather than relieve it. Allowing natural inflammation leads to quicker pain resolution and recovery. These findings suggest that inflammation plays a beneficial role in healing, and indiscriminate use of anti-inflammatory drugs post-surgery may increase the risk of chronic pain.
Taking anti-inflammatory drugs after surgery is fairly standard protocol. But a new study by researchers suggests this approach may be backfiring and that blocking inflammation during this critical time may, in fact, delay recovery and prolong pain rather than relieve it.
If you look across all types of surgeries—anything from an extracted tooth to a hip replacement—the pain resolves normally for 90% of patients. But the other 10% develop chronic pain. That persistent pain is very hard to treat; it's very resistant to medication and it can last for years.
In the new study, published recently in the Journal of Pain Research, the researchers report that letting inflammation run its course led to a quicker cessation of pain and an overall quicker recovery after a surgery or injury.
Although this study suggests that blocking TNF-α after surgery is likely unwise, there are other scenarios where it may still make sense, such as improving mobility by reducing arthritic inflammation in the joints for autoimmune diseases like rheumatoid arthritis.
Inflammation is not necessarily a bad thing, the researchers say.
Yes, it hurts, but it's also working on the inside to promote the resolution of that pain. The idea in the medical field that when you have an injury, you should absolutely block the inflammation right away might not always be the best strategy, they conclude.
They think that one day we'll be able to block the pain but allow the healing inflammation.
Sophie Laumet et al, Unexpected Role of TNFα Signaling in the Resolution of Postoperative Pain in Mice, Journal of Pain Research (2025). DOI: 10.2147/jpr.s543971
People with cancer receiving immunotherapy earlier in the day survived longer, suggesting that adjusting treatment timing may improve outcomes.
Mounting evidence suggests that the time of day at which cancer patients receive treatment could impact their outcomes. This effect is likely due to the circadian rhythm-dependent fluctuations in the function of immune cells as well as proteins that regulate their function, also called checkpoints.
In line with this, in a recent meta-analysis, researchers found that patients with various types of advanced cancer who underwent immune checkpoint inhibitor (ICI) infusions earlier in the day survived longer than their counterparts treated in the late afternoons or evenings.
In a new study, researchers discovered that patients with a highly aggressive lung cancer who received treatment before 3PM survived significantly longer than their counterparts who were treated later in the day.
Genetic study uncovers unknown causes of blindness
Researchers have discovered new genetic causes of inherited blindness. Their study, published in Nature Genetics, shows that changes in specific pieces of DNA, which play a role in processing genetic information, can lead to retinitis pigmentosa.
This eye condition affects about one in 5,000 people worldwide, causing "tunnel vision" and often leads to legal blindness. The discovery provides clarity for dozens of families globally and opens new possibilities for diagnostics and counseling in hereditary conditions.
Retinitis pigmentosa (RP) is a disorder in which the rod and cone cells in the retina gradually die. Affected individuals first experience night blindness, followed by tunnel vision. Some eventually lose their sight completely.
Although more than a hundred genes are known to cause RP, in 30 to 50% of patients the genetic cause remains unresolved, even after extensive DNA testing. Researchers have now solved part of this puzzle.
Researchers found a variation in the gene RNU4-2. The change occurs in a special gene, RNU4-2, which does not produce a protein but only RNA. RNA from such genes associate with proteins and other RNAs and the whole resulting complex assists in editing genetic information (splicing), a step required before a cell can make proteins.
Other changes in RNU4-2 were recently linked to developmental disorders.
This breakthrough goes beyond these specific genetic variants causing RP. It shows that we should also look beyond protein-coding genes.
De novo and inherited dominant variants in U4 and U6 snRNA genes cause retinitis pigmentosa, Nature Genetics (2026). DOI: 10.1038/s41588-025-02451-4
Roads can become more dangerous on hot days—especially for pedestrians, cyclists and motorcyclists
Road injury risk increases significantly on very hot days, with pedestrians, cyclists, and motorcyclists facing the greatest danger due to direct heat exposure. The risk rises sharply above 30°C, with pedestrian injuries more than doubling and cyclist and motorcyclist injuries increasing by 80% and 50%, respectively. Heat also elevates crash severity and fatality risk, especially on rural roads and among older drivers. Effects can persist for days due to fatigue and sleep disruption.
During heat waves, everyday life tends to feel more difficult than on an average day. Travel and daily movement are no exception.
But while most of us know rain, fog and storms can make driving conditions challenging, not many people realize heat also changes transport risk. At very high temperatures, overall crash risk is about 15% higher than on cool days.
In particular, research evidence consistently suggests roads, trips and daily commutes can become more dangerous on very hot days compared with an average day. Road injury risk rises much more steeply once temperatures move into the 30°C–40°C range.
Importantly, the increase is even larger for crashes linked to driver fatigue, distraction or illness.
The hidden carbon footprint of wearable health care
Researchers analyzed wearable health care electronics and reported carbon impacts of 1.1–6.1 kg CO2-equivalent per device. With global device consumption projected to rise 42-fold by 2050, approaching 2 billion units annually, their moderate projection adds 3.4 million metric tons of CO2-equivalent emissions alongside ecotoxicity and e-waste.
Wearable electronics—glucose, heart and blood pressure monitors, integrated into patches, chest straps, clothes and smartwatches—are transforming health care through real-time monitoring, device interaction, and therapeutic interventions.
Compared with rigid consumer electronics, wearable health care systems—ranging from biophysical and biochemical sensors to e-textiles and biointegrated therapeutics—offer high compliance and continuous tracking and intervention capabilities.
With wireless integration, wearable health care electronics are evolving into digital infrastructure networks adopted globally by patients, older people, athletes, and health-conscious people.
Reliance on energy-intensive manufacturing, hazardous chemicals, fossil-based plastics, and critical metals can lead to substantial carbon emissions, ecological risks, and e-waste issues. Rising energy demands from artificial-intelligence-driven data processing and advanced digital infrastructures further enlarge the eco-footprint of even the smallest devices.
In the study, "Quantifying the global eco-footprint of wearable health care electronics,"publishedinNature, researchers integrated life-cycle assessment with forecasting adoption growth over time to quantify global eco-footprint hotspots and evaluate mitigation strategies.
Four devices anchored the assessment—a non-invasive continuous glucose monitor, a continuous electrocardiogram monitor, a blood pressure monitor, and a point-of-care ultrasound patch. Selection criteria included clinical relevance, diversity of sensing modalities, and coverage across an expanding technology spectrum.
Cradle-to-grave attributional life-cycle assessment covered raw-material acquisition, manufacturing, transportation, use, and end-of-life disposal. Monte Carlo simulation quantified uncertainty for environmental impacts, and diffusion modeling projected future scale of use.
A single continuous glucose monitor from production to use carried a carbon footprint equivalent to about 2 kg CO2-equivalent, or driving a gas-powered car for around 5 miles. More than 95% of that impact was attributed to printed circuit boards and semiconductors inside the device, tied to energy required to purify raw materials and power manufacturing processes.
Single glucose monitor use lasted 14 days before being discarded and replaced. Repetition of that short cycle has stacked impacts across the scale of users. Wearable glucose monitor sales are estimated to exceed 1.4 billion devices a year by 2050.
Expected greenhouse-gas emissions from these units alone were around 2.7 million metric tons CO2-equivalent annually.
Per-device warming impacts ranged from 1.06 kg CO2-equivalent for a blood pressure monitor to 6.11 kg CO2-equivalent for a point-of-care ultrasound patch. Values of 1.30 kg CO2-equivalent for a continuous electrocardiogram monitor.
Annualized warming impacts, accounting for typical replacement frequencies, were 0.5 kg CO2-equivalent for the blood pressure monitor, 33.8 kg CO2-equivalent for the continuous electrocardiogram monitor, 50.6 kg CO2-equivalent for the non-invasive continuous glucose monitor, and 6.1 kg CO2-equivalent for the point-of-care ultrasound patch.
Greenhouse-gas emissions from all wearables in the model were 3.4 million metric tons CO2-equivalent annually, or about the carbon footprint of the transport sector of Chicago. Component-level analysis placed flexible printed circuit board assemblies at the center of warming impacts across all four devices, with hotspots tied to gold in integrated circuits, silicon wafers, polyimide, and batteries. part 2
Researchers modeled four mitigation approaches that included plastic substitution or recycling, critical-metal substitution, modular designs for reuse and replacement, and a transition to green energy.
Chuanwang Yang et al, Quantifying the global eco-footprint of wearable healthcare electronics, Nature (2025). DOI: 10.1038/s41586-025-09819-w
Fatigue before cancer treatment linked to adverse events
Investigators found that higher patient-reported fatigue before cancer treatment aligned with higher odds of severe, life-threatening, and fatal treatment-related toxic effects.
Cancer-related fatigue harms quality of life and is a persistent tiredness or exhaustion tied to cancer or cancer treatment. It interferes with usual physical and mental functioning and does not match the patient's normal recent activity. Patients report that fatigue is among the most distressing symptoms of cancer and its treatment, yet physicians routinely underreport fatigue.
Some studies have suggested prevalence ranging from 25% to 50%. Separate estimates place moderate fatigue at 25% and severe fatigue at 15% to 20%, levels often associated with poor performance status.
In the study, "Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy," published in JAMA Oncology, researchers pooled baseline fatigue data to evaluate associations between pretreatment fatigue and subsequent adverse events in cancer treatment trials.
Across 17 trials, 103,738 adverse events were recorded. Higher baseline fatigue aligned with higher odds of severe toxic effects. Some or greater baseline fatigue, compared with less than some fatigue, yielded an odds ratio of 2.11 for grade 3 or higher toxic effects and 1.98 for life-threatening toxic effects. Comparison between quite a lot or very much fatigue and no baseline fatigue produced an odds ratio of 4.99 for grade 5 toxic effects. Fatal toxic effects were uncommon, though risk rose with higher fatigue to an odds ratio of 2.35. Severe or worse toxic effects occurred in 34.2% of patients reporting no fatigue, 39.4% reporting a little fatigue, 52.8% reporting some fatigue, and 58.3% reporting quite a lot or very much fatigue. Subset analyses did not show statistically significant differences in the fatigue to adverse event association by age, sex, race, ethnicity, or obesity status. Cancer stage mattered in subgroup patterns. Advanced-disease trials showed clearer monotonic relationships between baseline fatigue and adverse events, while adjuvant or early-stage trials did not show statistically significant associations for grade 3 or higher or grade 4 or higher adverse events.
Patient-reported fatigue before cancer treatment was associated with increased risk of severe, life-threatening, and fatal adverse events during treatment. Pre-treatment fatigue assessments could be seen as an early marker of vulnerability that could inform treatment strategies and symptom monitoring.
Joseph M. Unger et al, Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy, JAMA Oncology (2025). DOI: 10.1001/jamaoncol.2025.5549
Why some people are more resistant to developing blood cancer even when they carry cancer-risk mutations
Blood cancer is an umbrella term for a variety of diseases that affect the blood, bone marrow and lymphatic system. Like most cancers, the cause is usually mutations in the DNA, which are genetic errors that accumulate as we age. However, some people are more resistant to developing blood cancer even when they carry cancer-risk mutations.
In a new study published in the journal Science, researchers discovered why. They identified a rare genetic variant that reduces the risk of several blood cancers, including leukemia, by slowing down a process called clonal hematopoiesis (CH).
CH occurs when a hematopoietic stem cell, which can develop into any type of blood cell, mutates and grows into a large population of identical mutated cells.
In their study, the team performed a large-scale analysis (known as a GWAS meta-analysis) of more than 640,000 individuals. By comparing 43,000 people with CH mutations to 600,000 without them, they pinpointed the genetic variant that protects against CH.
The researchers identified a noncoding regulatory variant, rs17834140-T, on chromosome 17q22.
The experiments revealed that rs17834140-T reduces the amount of a protein called MSI2, which acts as a growth booster in stem cells. In cancer, MSI2 causes mutated cells to multiply rapidly and take over the bone marrow. However, the protective variant results in lower levels of the protein, forcing these mutated cells to grow much more slowly and reducing their chances of progressing to leukemia. According to the study authors, people with the variant have up to a 30% lower risk of developing CH.
The research could lead to new ways to prevent cancer even before it starts. Now that we know that lowering MSI2 is protective, scientists may be able to develop drugs or other therapeutic approaches that mimic or enhance this natural protection.
Gaurav Agarwal et al, Inherited resilience to clonal hematopoiesis by modifying stem cell RNA regulation,Science(2026).DOI: 10.1126/science.adx4174
Tire rubber decays into a potentially dangerous chemical cocktail, research shows
Crumb rubber from recycled tires, commonly used in artificial turf, generates hundreds of transformation chemicals as it decays under sunlight and environmental conditions. Some of these chemicals, such as 6PPD-quinone, are highly toxic to aquatic life, while others are known human health hazards. The long-term effects of most transformation products remain unknown.
The small, spongy black beads used as fill material in most artificial turf fields are called crumb rubber, which has long been touted as a major win for recycling. However, conflicting studies have alternately identified crumb rubber as either safe for people to play atop or dangerous to human health.
New researchout of Northeastern University investigated the decay cycle of crumb rubber, which is fashioned out of old tires. By simulating the conditions in which the rubber decays, like strong sunlight, they discovered that crumb rubber is highly reactive, generating hundreds of previously untracked chemicals as it decays, some of which are hazardous to humans.
The work is published in the journalEnvironmental Science & Technology.
Madison H. McMinn et al, From the Road to the Field: Decoding Chemical Transformation in Aging Tire and Artificial Turf Crumb Rubber, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c08260
Popular large language models (LLMs) often reproduce harmful stereotypes about Indian castes — hereditary groups traditionally associated with specific occupations and social status. Researchers used a custom-designed tool to detect ‘caste bias’ in LLMs and found that every model they tested exhibited some bias. GPT-4o and GPT-3.5, created by OpenAI, had some of the highest bias scores. Information on minority groups might be less likely to appear in prestigious journals or other outlets, and might be written in local languages, which could result in it being filtered out of AI training data who studies cultural biases in LLMs.
Immune stress during pregnancy changes how fetal brain cells communicate
Research has found that immune-related genes vary by location and cell type across the developing mouse brain before birth. Maternal immune activation and maternal microbiome depletion shifted parts of that immune signaling pattern, with differences observed between male and female embryos.
Immune molecules, including cytokines, chemokines, and cognate receptors, are critical regulators of synapse development, cellular communication, and neural precursor cell migration in the developing brain. During development, nerve cells are born in one area, move to their destinations, and settle into stacked layers, especially in the cortex. Those layers line up in an ordered way, with different types of neurons ending up in different layers.
Changes to the maternal immune system and microbiome have been linked to abnormal fetal neurodevelopment, influencing neurogenesis, cell fate, and precursor cell migration. Knowledge of immune signaling networks within the developing brain is needed to understand the mechanisms of how the mother's stressors impart influence.
In the study, "Spatial transcriptomics of the developing mouse brain immune landscape reveals effects of maternal immune activation and microbiome depletion,"publishedinNature Neuroscience, researchers used multiplexed error-robust fluorescence in situ hybridization (MERFISH) to measure immune activity in embryonic mouse brains during mid and late gestation to see how maternal immune activation and maternal microbiome depletion altered those patterns.
Embryonic mouse brain single-cell RNA sequencing data supported identification of spatially restricted cell populations, followed by cell clustering, differential gene expression analyses, and ligand–receptor analyses.
The research connects maternal immune activation and maternal microbiome depletion with sex-specific shifts in immune gene expression, ligand–receptor signaling, and cell spacing within the embryonic brain. Specifically, CXCL12 and CXCR7 signaling stood out as an important mediator of abnormal neural differentiation and migration after maternal immune activation and maternal microbiome depletion.
Bharti Kukreja et al, Spatial transcriptomics of the developing mouse brain immune landscape reveals effects of maternal immune activation and microbiome depletion, Nature Neuroscience (2026). DOI: 10.1038/s41593-025-02162-3
Spaceflight causes astronauts' brains to shift, stretch and compress in microgravity
Spaceflight takes a physical toll on astronauts, causing muscles to atrophy, bones to thin and bodily fluids to shift. According to a new study published in the journal PNAS, we can now add another major change to that list. Being in microgravity causes the brain to change shape.
Here on Earth, gravity helps to keep the brain anchored in place while the cerebrospinal fluid that surrounds it acts as a cushion. Scientists already knew that, without gravity's steady pull, the brain moves upward, but this new research showed that it is also stretched and compressed in several areas.
The study authors found significant differences between the brains of astronauts and those of the volunteers. While both groups experienced a shift, the astronauts' brains moved further upward. And the longer they stayed in space, the more pronounced these changes became. The supplementary motor cortex (which helps to control movement) moved upward by about 2.5 millimeters in astronauts on one-year missions. The brain movement isn't uniform. The team discovered that as the brain moves, it becomes compressed at the top and the back while other areas stretch. This has a noticeable effect on balance and coordination. In tests, astronauts who experienced the largest brain shifts struggled the most to stay steady on their feet after returning to Earth.
While the brain mostly returns to its normal position after several months back on Earth, scientists still need to know more to ensure safer conditions for longer missions, such as those to Mars.
Tianyi Wang et al, Brain displacement and nonlinear deformation following human spaceflight, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2505682122
Tibetan Plateau-Himalayan uplift shaped Asian summer monsoons
The uplift of the Tibetan Plateau, particularly when it exceeded 3.5 km elevation around 27–38 million years ago, was crucial in intensifying and expanding the Asian summer monsoon. This topographic change shifted rainbelts northward and increased rainfall over South and Southeast Asia, with tectonic uplift playing a more dominant role than atmospheric CO2 in shaping monsoon evolution.
S. Abhik et al, A brief history of Asian summer monsoon evolution in the Cenozoic era, npj Climate and Atmospheric Science (2026). DOI: 10.1038/s41612-025-01259-7
The global water cycle and how is it amplifying climate disasters
The global water cycle, involving evaporation, precipitation, and runoff, is intensifying due to rising temperatures. This leads to faster evaporation, increased atmospheric moisture, and more frequent extreme events such as floods, droughts, and heatwaves. These amplified fluctuations, sometimes termed "climate whiplash," are destabilizing ecosystems and societies worldwide.
The aggressive use of antibiotics could fuel mood disorders and anxiety
Antibiotics (ABs) are among the most used pharmaceutical drugs worldwide, as they are currently the most effective medicines for the treatment of bacterial infections. An excessive use of these drugs, however, can damage the gut microbiota, the population of microorganisms living in the intestines that help us to digest food.
Bacteria and other microorganisms in the gut are known to also communicate with the brain via a communication pathway that is referred to as the gut-brain axis. Recent research suggests that some gut bacteria help to reduce inflammation and support the healthy functioning of the brain.
Researchers have carried out a study exploring the possibility that the effects of ABs on gut bacteria could also facilitate the development of mental health disorders, particularly increasing anxiety. Their findings, published in Molecular Psychiatry, suggest that ABs do in fact damage gut bacteria that help regulate mood, linking their excessive use with higher levels of anxiety.
When they analyzed the data they collected, the researchers found that the use of ABs was linked to anxiety-like behaviors in mice and higher levels of anxiety in humans. Moreover, the drugs appeared to reduce the amounts of some helpful gut bacteria, particularly those in the Bacteroides group.
In addition, the team found an association between the intake of ABs and a reduction in the neurotransmitter acetylcholine, a chemical that supports communication between nerve cells. Mice and human patients who had received ABs were found to have lower levels of acetylcholine both in the gut and brain compared to those who had not taken ABs.
"In both AB-treated mice and patients, co-occurrence analysis indicated that the Bacteroides-acetylcholine pair may play an important role in AB-induced anxiety," wrote the researchers in their paper.
Ke Xu et al, Consistent decline of acetylcholine in microbiota-gut-brain axis mediates antibiotic-induced anxiety via regulating hippocampus microglial activation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03431-0.
Your voice gives away valuable personal information!
Human voices carry extensive personal information, including health, background, and emotional state, which can be extracted by advanced speech analysis technologies. This raises privacy risks such as misuse by insurers, employers, or malicious actors. New metrics now quantify how much information a speech recording contains, aiding the development of privacy-preserving tools and user interfaces. You can probably quickly tell from a friend's tone of voice whether they're feeling happy or sad, energetic or exhausted. Computers can already do a similar analysis, and soon they'll be able to extract a lot more information. It's something we should all be concerned about, according to experts in the field. Personal information encoded in your voice could lead to increased insurance premiums or to advertising that exploits your emotional state. Private information could also be used for harassment, stalking or even extortion. When someone talks, a lot of information about their health, cultural background, education level and so on is embedded in the speech signal. That information gets transmitted with the speech, even though people don't realize it. For example, even subtle patterns of intonation or word choice can be a giveaway as to your political preferences, while clues in breathing or voice quality may correlate with certain health conditions. One important risk is that medical information inferred from voice recordings could affect insurance prices or be used to market medication. The fear of monitoring or the loss of dignity if people feel like they're constantly monitored—that's already psychologically damaging. And employers might extract personal information from voice recordings which could be used against employees or to screen candidates, or exes might use such tools for stalking or harassment. So how can engineers tackle these problems? Protecting against abuses means ensuring that only the information that's strictly necessary is transmitted and that this information is securely delivered to the intended recipient. One approach is to separate out the private information and only transmit the information needed to provide a service. Speech can also be processed locally on a phone or computer rather than sent to the cloud, and acoustic technologies can be used to make sure that sounds are only recorded from (or audible in) a specific place.
How small mammals shrink their brains to survive the cold
An international team of researchers has conducted a study that explains the evolutionary origins of the Dehnel phenomenon, a unique seasonal adaptation in small mammals that involves the ability to reduce and recover brain volume and function. The study is published in Molecular Biology and Evolution.
The Dehnel phenomenon is a case of extreme plasticity through which some mammals reduce and regenerate their brains according to the season. This mechanism allows species such as the common shrew to reduce the size of their brain, skull and other organs by up to 30% during the winter to save energy in conditions of extreme cold and food scarcity.
In the spring, these tissues regenerate, making this phenomenon an exceptional example of physiological plasticity. Furthermore, comparative studies show that it is not exclusive to shrews: European moles and mustelids (such as weasels) also exhibit seasonal brain reductions, which extends the evolutionary framework of this strategy to mammals with high metabolisms.
Through comparative genomics and gene expression analysis in key tissues, such as the hypothalamus, the team identified genes associated with several fundamental processes, such as energy homeostasis and calcium signaling, essential for adjusting energy balance in demanding environments; the integrity of the blood-brain barrier, which ensures efficient control of molecules accessing the brain during the seasonal cycle; and water regulation, involved in reversible brain volume loss without cell death, a key finding for understanding how this adaptation is achieved.
The plasticity reflected by the Dehnel phenomenon influences survival, reproduction, and resilience to climate variability. According to the research team, even though these species are not human, understanding the mechanisms that allow reversible reductions in brain volume without permanent damage could inspire new lines of research in neurology and metabolism.
The role of genes related to energy homeostasis and the blood-brain barrier points to possible biomarkers and therapeutic targets for neurodegenerative diseases, always with the necessary caution when extrapolating to humans.
William R Thomas et al, Genomic comparisons shed light on the adaptive basis of brain size plasticity and chromosomal instability in the Eurasian common shrew, Molecular Biology and Evolution (2026). DOI: 10.1093/molbev/msag006
Gut bacteria cause rare alcohol syndrome Researchers have found more evidence that ethanol-producing gut bacteria are the main drivers of auto-brewery syndrome (ABS) — a rare and poorly understood condition in which people become drunk when they haven’t consumed alcohol. A team found that strains of Klebsiella bacteria and Escherichia coli that produce ethanol were much more prevalent in the gut microbiomes of people with ABS than in those of people who didn’t have the condition. One person with ABS was successfully treated with a faecal microbiota transplant, but the authors say a targeted intervention, such as disrupting the metabolic pathways the bacteria use to produce ethanol, might be more effective.
Vaccines create a halo of benefits Growing evidence suggests that vaccines have benefits in older adults beyond protecting against infectious diseases. These ‘off-target effects’ include a reduced risk of dementia and cardiovascular events. Exactly why vaccines have these protective effects is unclear, but researchers suggest that in protecting against infection, vaccines also protect against the inflammation that comes with them. Many experts now worry that opposition to childhood vaccinations could dissuade some adults from getting vaccinated, which would leave them vulnerable to the diseases that vaccines can protect against, both infectious and not.
Antibiotic and immunosuppressant treatment administered before, during and after a solid-organ or haematopoietic-stem-cell transplant can dysregulate the gut microbiome. On the flipside, the gut microbiome can also influence the long-term success of such procedures by, for example, metabolizing immunosuppressants into less active forms. A better understanding of these interactions could yield targeted interventions that improve outcomes in transplant recipients, write five internal-medicine specialists in their review.
Hijacking the energy-producing organelles from immune cells seems to help tumours in mice to infiltrate lymph nodes. Cancer cells use mitochondria stolen from immune cells to escape detection and spread. Researchers found that when cancer cells take on these mitochondria in mice, it both weakens the immune cells and triggers a molecular pathway in the cancer cells that help them fly under the immune system’s radar and invade lymph nodes. This beneficial molecular pathway was activated even when researchers disrupted the mitochondria’s ability to produce the energy-carrying molecule ATP. The findings could explain how cancer cells survive in lymph nodes, which are packed with immune cells that should be able to kill them.
Scientists discover natural 'brake' that could stop harmful inflammation
Researchers have uncovered a key mechanism that helps the body switch off inflammation—a breakthrough that could lead to new treatments for chronic diseases affecting millions worldwide.
Inflammation is the body's frontline defense against infection and injury, but when it doesn't switch off properly, it can drive serious health conditions such as arthritis, heart disease, and diabetes. Until now, scientists didn't fully understand how the body decides to stop the immune "fight" response and start healing.
Published inNature Communications,the study reveals that tiny fat-derived molecules called epoxy-oxylipins act as natural brakes on the immune system. These molecules prevent the overgrowth of certain immune cells, known as intermediate monocytes, that can cause chronic inflammation—linked to tissue damage, illness and disease progression.
Tests revealed that one epoxy-oxylipin, 12,13-EpOME, works by shutting down a protein signal called p38 MAPK, which drives monocyte transformation. This was confirmed in lab experiments and in volunteers given a p38-blocking drug.
Targeting this mechanism could lead to safer treatments that restore immune balance without suppressing overall immunity.
Epoxy-Oxylipins Direct Monocyte Fate in Inflammatory Resolution in Humans, Nature Communications (2026). DOI: 10.1038/s41467-025-67961-5
Super agers tend to have at least two key genetic advantages
The gene variant posing the greatest genetic risk of late-onset Alzheimer's disease (AD) is called APOE-ε4. A different variant of the same gene, APOE-ε2, is thought to confer protection against AD.
A comparatively large study reported in Alzheimer's & Dementia by researchers measures the frequency of APOE-ε4 and APOE-ε2 in so-called super agers—people ages 80 or older whose cognitive function is comparable to people 20 or 30 years younger.
Super agers were 68% less likely to harbor the gene nobody wants, APOE-ε4, compared to individuals with AD dementia in the same 80+ age group.
Most notably, super agers were 19% less likely to harbor APOE-ε4 than were cognitively normal participants in the same age group.
Super agers were also found for the first time to have higher frequency of the variant you'd want, APOE-ε2: They were 28% more likely to carry APOE-ε2 than were cognitively normal controls ages 80+, and 103% more likely to carry the variant than were participants with AD dementia aged 80 or older.
Focusing on variety and balance is the best way to reduce exposure to heavy metals in food while keeping your plate full of nutritious choices.
Mix it up. Eat a variety of grains, proteins, fruits, and vegetables—and even vary the brands you buy. Relying too heavily on one food type, source, or growing location can risk repeated exposure to an element that happens to be particularly high in that food or region. Low levels of heavy metals make their way into foods. A varied, healthy diet can limit exposure and absorption.
Choose safer seafood. Fish is one of the healthiest foods you can eat. Opt for smaller fish, which are lower on the food chain, such as salmon, canned light and skipjack tuna, sardines, pollock, or tilapia. Shellfish like scallops, clams, crab, and shrimp are good choices as well. Limit large predatory fish, like swordfish, orange roughy, and king mackerel.
Cook rice smartly. Cook rice with extra water (like pasta) that you drain off. This simple step can reduce arsenic levels (but it also lowers nutritional value). Try other grains like oats, quinoa, bulgur, or barley for variety.
Check your home. If you have older pipes, test your tap water for lead and consider a certified filter if needed. Paint in houses built before 1978 should be tested for lead. (Test kits can be purchased at home improvement stores and may be available for free through local health departments and/or water utilities.)
Refer to trusted sources. The U.S. Food and Drug Administration and Environmental Protection Agency are tasked with helping to ensure your food and water meet safety standards. If unusually high levels of any heavy metals are discovered in a particular food, the media will be alerted, and recalls will be put in place. Heavy metals are part of our environment, and small amounts do make their way into foods. But research shows that the benefits of a varied, nutrient-rich diet far outweigh the minimal risks from trace exposure.
As they roll across shadowed regions of the moon's surface, future lunar rovers could develop hazardous buildups of electric charge on their wheels.
With an interest in lunar exploration now reigniting worldwide, several space agencies are considering how the moon's surface could be explored in unprecedented detail using wheeled rovers. One challenge these vehicles will face is the buildup of 'triboelectric charge' as their wheels move across the regolith: a dry, granular, and highly insulating layer of dust and rock that blankets the moon. If allowed to accumulate, this charge could trigger discharges that threaten a rover's sensitive electronics and instruments.
Under many circumstances, charge buildup is naturally limited by the solar wind—a continuous stream of charged particles that emanate from the sun. Because this plasma is far more conductive than the regolith, it provides a pathway for excess charge to dissipate into the surrounding environment. However, this helpful effect can't always be guaranteed.
As the moon travels through the solar wind, it creates a long plasma "wake" on its night-time side, where particle densities drop dramatically. "If the plasma flux levels are reduced, charge dissipation will slow. In essence, it will become increasingly difficult to remediate charge buildups in these plasma-starved regions.
These conditions are also found inside the moon's permanently shadowed polar craters—potential harbors of frozen water and carbon dioxide that could be prime targets for upcoming missions. For rovers operating in these environments, engineers must take steps to prevent triboelectric charging from reaching problematic levels.
Using advanced simulations, researchers modeled the balance between triboelectric charging and plasma-based charge dissipation under realistic lunar conditions. Their results show that keeping a rover's speed extremely low—below about 0.2 cm per second—can prevent charge from accumulating.
If a rover moves faster than this speed limit in the given plasma environment, then the wheel tribocharging currents will exceed plasma dissipation currents and the wheel will build up charge. If the rover moves slower than this speed limit, then the plasma currents will dissipate the charge before it builds up to large levels
Part 1
The researchers also found that a rover's approach path into a crater can strongly influence its charging environment. If it enters a crater on the downwind side—facing the sun and solar wind—it can remain in a relatively dense plasma flow. If the rover enters the leeward edge of the crater—moving with the sun at its back—the rover enters a region where the local mini-wake first forms Finally, they examined how a rover's wheels should be electrically connected to its body. While isolating the wheels might seem like a way to protect onboard electronics, the simulations showed that this isolation actually limits the dissipation of charge—only worsening the problem. Instead they recommend that the rover wheel is tested to ensure it is electrically connected to the larger rover structure, ensuring that the wheel has a conductive path to the larger structure. The rover body can then be used to increase the plasma current collection to more quickly dissipate the wheel tribocharge buildup. Together, these findings highlight how space-weather effects on the moon can pose subtle but serious risks to surface operations.
W.M. Farrell et al, Rover wheel tribocharging in lunar shadowed regions: deriving a speed limit for charge accumulation, Advances in Space Research (2026). DOI: 10.1016/j.asr.2025.10.102
Scientists design artificial pain receptor that senses pain intensity and self-heals
All over the body are tiny sensors called nociceptors whose job is to spot potentially harmful stimuli and send warning signals to the brain and spinal cord, helping protect us from injury or tissue damage.
In a recent study, scientists designed a jelly-like artificial nociceptive nerve pathway built using a memristor—a tiny electronic component that controls current flow and retains the memory of how much electricity has flowed through it.
The quantized conductance (QC) phenomenon in memristors, where electricity flows through a material in discrete steps rather than a smooth stream, allowed the pain receptor to go beyond simply turning on and off in response to a stimulus. Instead, it exhibited four distinct levels that correspond to the human pain scale: no pain, mild, moderate, and severe.
The bio-inspired receptor also showed signs of self-healing in terms of repairing physical damage and fading of pain signals.
Xuanyu Shan et al, Bioinspired Artificial Nociceptor Based on Quantized Conductance Memristor With Pain Rating, Self‐Healing, and Neuromodulation Capabilities, Advanced Functional Materials (2025). DOI: 10.1002/adfm.202528900
Tumor cells steal immune mitochondria to aid lymph node spread
Researchers report that tumor cells hijack mitochondria from immune cells, reducing anti-tumor immune function and activating cGAS-STING and type I interferon signaling that promotes lymph node metastasis.
Mitochondrial transfer, the movement of mitochondria between cells, is a mode of intercellular communication that reshapes metabolism, stress responses, and cellular function across diverse physiological and pathological settings. Recruiting outside mitochondria into cancer cells can enhance oxidative phosphorylation, promote survival under metabolic stress, and influence therapy resistance.
Lymph node metastasis is a critical early step in cancer progression that can create a systemic impairment of tumor control.
Previous reports have found that T cells and macrophages can transfer mitochondria to cancer cells. The extent of mitochondrial transfer by other immune cells remains unclear, along with any connections to lymph node colonization.
In the experiments, Tumor cells acquired mitochondria from host cells across colon, breast, and melanoma models. Immune cells were identified as a donor source in bone marrow chimera experiments that restricted the reporter signal to hematopoietic cells. Draining lymph nodes carried a higher fraction of tumor cells with immune-derived mitochondria than primary tumors.
Direct physical contact supported transfer, with higher transfer under hypoxic stress and inflammatory cues. Disruption of transfer structures and knockdown of a transfer-related factor reduced transfer, paired with reduced lymph node metastasis incidence in reported mouse experiments. mtDNA polymorphism tracing added a second line of evidence that donor mitochondrial DNA could be detected in tumor material.
Immune cells that lost mitochondria showed reduced antigen-presentation and co-stimulatory machinery, with reduced activation and cytotoxic capacity reported for natural killer and CD8 T cells. Changes aligned with impaired immune surveillance in the co-culture systems described.
Researchers identify immune-to-tumor cell mitochondrial transfer as a central mechanism that facilitates lymph node colonization through two coordinated effects. Loss of mitochondria disables anti-tumor immunity by diminishing antigen presentation and impairing cytotoxic function across multiple immune lineages, while immune-derived mitochondria activate the cGAS-STING pathway in tumor cells and induce a type I interferon program that promotes immune evasion and lymph node colonization.
Targeting mitochondrial transfer or the resulting cGAS-STING signaling represents a promising strategy to restrict lymph node metastasis, a critical early step in systemic cancer progression.
Azusa Terasaki et al, Mitochondrial transfer from immune to tumor cells enables lymph node metastasis, Cell Metabolism (2026). DOI: 10.1016/j.cmet.2025.12.014
A new anti-biofilm strategy Nanopatterned surfaces with nanoscale protrusions physically disrupt bacterial cells, preventing biofilm formation through mechanical means rather than chemical agents. These surfaces, inspired by insect wings, can kill a broad range of microbes, including bacteria and fungi. Scalability challenges are being addressed with adaptable materials like metal-organic frameworks, enabling more practical applications.
Combining mechanical killing mechanisms with chemical agents or near-infrared light irradiation could enhance efficacy against diverse organisms.
Zhejian Cao et al, Mechano‐Bactericidal Surfaces Achieved by Epitaxial Growth of Metal–Organic Frameworks, Advanced Science (2025). DOI: 10.1002/advs.202505976
Human heart regrows muscle cells after heart attack, researchers discover
Until now we've thought that, because heart cells die after a heart attack, those areas of the heart were irreparably damaged, leaving the heart less able to pump blood to the body's organs.
But Pioneering research by experts has shown that heart muscle cells regrow after a heart attack, opening up the possibility of new regenerative treatments for cardiovascular disease.
This new work shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
Though increased mitosis(a process in which cells divide and reproduce) after a heart attack has been observed in the heart muscles of mice, this is the first time the phenomenon has been demonstrated in humans.
Although this new discovery of regrowing muscle cells is exciting, it isn't enough to prevent the devastating effects of a heart attack. Therefore, in time, the researchers hope to develop therapies that can amplify the heart's natural ability to produce new cells and regenerate the heart after an attack.
Robert D. Hume et al, Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction, Circulation Research (2026). DOI: 10.1161/circresaha.125.327486
Why adapting to the environment is more difficult as people age
Age-related structural changes in specific brain regions reduce adaptability to environmental changes. Older adults rely more on brain structures involved in task switching and updating information, but these structures deteriorate over time, correlating with decreased adaptive behaviour in later adulthood. Researchers characterized changes in the brain across two periods of adulthood that may correspond to changes in adaptive behaviour.
Identifying these changes may help track adaptability decline.
No clear evidence that cannabis-based medicines relieve chronic nerve pain, updated review finds
Current evidence does not support that cannabis-based medicines, including THC, CBD, or balanced THC/CBD products, provide clinically meaningful relief for chronic neuropathic pain compared to placebo. Adverse event data are uncertain, with THC products linked to increased dizziness and drowsiness. Higher-quality, longer-term studies are needed.
Cannabis-based medicines for chronic neuropathic pain in adults, Cochrane Database of Systematic Reviews (2026). DOI: 10.1002/14651858.CD012182.pub3
Scientists discover a hidden RNA 'aging clock' in human sperm
Increasing paternal age has been linked to elevated health risks for the next generation, including higher risks of obesity and stillbirth. So, what drives this increased risk?
Most research into this link focuses on how the DNA inside sperm changes with age. But sperm carries other molecules as well, including a diverse array of molecules called RNAs.
Now, new research has shown that the RNA contents of sperm go through similar shifts over time in both mice and humans, which may lead to a rapid, dramatic shift at midlife. What's more, "old RNA" seems to change cells' metabolism—potentially contributing to the health risks of having kids later in life.
It's like finding a molecular clock that ticks with age in both mice and humans, suggesting a fundamental, conserved molecular signature of sperm aging.
The researchers were only able to detect some of these changes when they looked at RNA from the sperm head alone—the part of the sperm that delivers its contents to the egg. The long tail of the sperm contains other RNA that obscured the pattern until now.
If we can understand the enzymes driving this shift, they could become actionable targets for interventions to potentially improve sperm quality in aging males.
Conserved shifts in sperm small non-coding RNA profiles during mouse and human aging, The EMBO Journal (2026). DOI: 10.1038/s44318-025-00687-8
Exposure to wildfire smoke late in pregnancy may raise autism risk in children
Analysis of over 200,000 births in Southern California indicates that exposure to wildfire smoke during the third trimester of pregnancy is associated with a 23% higher risk of autism diagnosis by age 5. The association is strongest with exposure exceeding 10 days. These findings support concerns about air pollution's impact on fetal neurological development.
Prenatal Exposure to Wildfire and Autism in Children, Environmental Science & Technology (2026). DOI: 10.1021/acs.est.5c08256
Scientists have discovered an answer to the longstanding mystery of why more than half of patients with chronic kidney disease ultimately die of cardiovascular problems: Their kidneys produce a substance that poisons the heart.
Chronic kidney disease leads to the production of circulating extracellular vesicles in the kidneys, which carry toxic miRNA that harm the heart. Blocking these vesicles in animal models improved heart function. This mechanism may enable earlier identification and targeted treatment of heart failure risk in CKD patients.
The researchers say the discovery could let doctors identify people at risk and develop new treatments to help prevent and treat heart failure for these patients.
Xisheng Li et al, Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease, Circulation (2026). DOI: 10.1161/circulationaha.125.075579
Certain antibiotics may may boost immune system Fluoroquinolone antibiotics can directly alter macrophage metabolism by stressing their mitochondria, leading to increased production of nitric oxide and enhanced bacterial clearance. This effect is specific to certain younger macrophage subsets in the lung and gut. While these antibiotics may boost immune cell function, they also carry risks such as microbiome disruption and potential tissue damage from excessive inflammation.
Alexander W Hardgrave et al, Fluoroquinolones directly drive mitochondrial hyperpolarization and modulate iNOS expression in monocyte-derived macrophage populations, Discovery Immunology (2025). DOI: 10.1093/discim/kyaf018
Cancer patients warned popular supplement may interfere with treatment
Biotin supplements, commonly used by cancer patients to address hair loss, lack strong evidence for promoting hair or nail regrowth and can interfere with lab tests, potentially leading to inaccurate results and delayed or altered treatment. Biotin may cause false readings in tests for prostate, thyroid, ovarian, and breast cancers. Minoxidil is a safer, effective alternative for hair loss.
Layna Mager et al, Biotin Supplements for Hair and Nail Regrowth: A Caution for Oncologists, JCO Oncology Practice (2025). DOI: 10.1200/op-25-00693
What the brain's shape and complexity say about a newborn's development
The neonatal period, which is defined as the first 28 days after birth, is known to be a crucial stage in the development of the human brain. During this stage, the brain is known to grow significantly in size, with billions of new connections forming between neurons and supporting basic physiological functions.
Researchers recently carried out a study aimed at further exploring how the human brain's overall shape and size as well as the dimensions of distinct regions are linked to a newborn's development and maturity. Their findings, published in Nature Neuroscience, suggest that the brain's shape is a key marker of development during the neonatal period.
They analyzed publicly available magnetic resonance imaging (MRI) data collected from almost 800 human newborns as part of the developing Human Connectome Project (dHCP). Employing a mathematical method called fractal analysis, they tried to delineate the shape of the newborns' brains.
This approach yields a geometric measure called fractal dimensionality (FD) that describes the shape of a brain region in terms of its structural complexity.
Brain shape predicted the infants' ages significantly better than brain size, say teh researchers. Moreover, brain shape captured signatures of premature birth that were not detected with brain size.
They found that the brains of infants who were related to each other, such as twins, were more similar in shape than those of unrelated infants. The shape of the brains of identical twins, who share almost 100% of genes, was found to be more similar than those of fraternal twins, who share approximately 50% of genes.
Based on this relationship, the researchers were able to predict which babies are twin siblings from their brain shapes with high accuracy (~77% overall, ~97% in identical twins), again outperforming all other studied brain measures.
These results suggest that the early-life formation of brain shape represents a fundamental maturational process in human brain development.
Stephan Krohn et al, Fractal analysis of brain shape formation predicts age and genetic similarity in human newborns, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02107-w
Maternal genetic factors may reveal why pregnancy loss is so common
Pregnancy loss in humans is common, with about 15% of recognized pregnancies resulting in miscarriage and many more conceptions being lost at early stages without people realizing it. Analysis of genetic data from nearly 140,000 IVF embryos demonstrates that common maternal genetic variants, particularly in genes involved in chromosome cohesion and recombination, contribute to individual differences in the risk of pregnancy loss due to chromosomal errors. These findings clarify molecular pathways underlying aneuploidy and suggest potential targets for future therapies.
By studying genetic data from nearly 140,000 IVF embryos, scientists have with unprecedented detail revealed why fewer than half of human conceptions survive to birth. The research uncovered the strongest evidence yet for how common genetic differences leave some individuals more vulnerable to pregnancy loss.
The vast dataset allowed the team to demonstrate robust connections between specific variations in a mother's DNA and their risk of miscarriage.
The findings shed new light on human reproduction and suggest pathways for developing treatments to lower the risk of pregnancy loss.
Most chromosome errors originate in the egg and increase in frequency with a mother's age. More mysterious is how factors beyond age, such as genetic differences, may predispose a person to produce eggs with abnormal numbers of chromosomes in the first place.
Figuring that out requires analyzing genetic data from large numbers of embryos before pregnancy loss, as well as their biological parents.
The strongest associations appear in genes that govern how chromosomes pair, recombine, and are held together during egg formation, including a gene (SMC1B) that encodes part of the ring-shaped structure that encircles and binds chromosomes, the team found. These rings are essential for accurate chromosome segregation and tend to break down as women age.
Dr. Krishna Kumari Challa
Young cancer survivors may face faster aging and possible early-onset dementia
Adolescent and young adult cancer survivors exhibit accelerated aging at both cellular and brain function levels, regardless of treatment type, with chemotherapy contributing most to this effect. Increased biological age correlates with cognitive deficits such as impaired memory and attention. Lifestyle changes like exercise and improved nutrition may help reverse some aging effects.
AnnaLynn M. Williams et al, Epigenetic age acceleration, telomere length, and neurocognitive function in long-term survivors of childhood cancer, Nature Communications (2025). DOI: 10.1038/s41467-025-65664-5
Jan 8
Dr. Krishna Kumari Challa
Millions of Your Mother's Cells Persist Inside You
Every human born on this planet is not entirely themselves.
A tiny fraction of our cells – around one in a million – is actually not our own, but comes from our mothers. That means each of us has millions of cells that our immune systems would normally recognize as foreign; yet somehow, in most of us, they hang around peacefully without causing any immune problems.
Now, immunologists have figured out why. A small number of maternal immune cells that cross the placenta during pregnancy actively train the fetus's immune system to tolerate the mother's cells for their entire life.
Micro chimerism is increasingly linked with so many health disorders. This study provides an adaptable platform for scientists to investigate whether these rare cells are the cause of disease, or alternatively, found in diseased tissue at increased levels as part of the natural healing process.
Tolerance to non-inherited maternal antigen is sustained by LysM+ C...
Jan 8
Dr. Krishna Kumari Challa
The oldest animal keeps its eyes sharp
Greenland sharks (Somniosus microcephalus) can live to be up to 400 years old, making them the longest-lived vertebrate. They dwell in the almost-sunless waters of the Arctic deep sea, and are often infested with parasites that attach to their eyes, leading scientists to suppose that the animals might be functionally blind. But researchers who studied the sharks’ eyeball in the lab say that it’s quite the contrary: the sharks appear to maintain their vision over centuries with no signs of retinal degeneration — perhaps thanks to a DNA repair mechanism in the retina — and could offer clues to treating age-related vision loss in people.
The visual system of the longest-living vertebrate, the Greenland s...
Jan 8
Dr. Krishna Kumari Challa
Omega-3 supplements fail to improve depressive symptoms in young people
Is fish oil the new snake oil?
Fish oil pills rich in omega-3 fatty acids gained attention as a possible add-on treatment for depression, as a few studies on adults found noticeable improvements in symptoms when combined with antidepressants.
When a similar study was conducted with children and adolescents, omega-3 fatty acids did not do any better than a placebo.
A team of researchers from Switzerland carried out a large clinical trial at five different centers, spanning nine months, to test whether adding omega-3 supplements to standard treatment could help teenagers and young adults with moderate-to-severe depression. The study involved 257 participants aged 8 to 18 who were randomly assigned to receive either 1.5 grams of omega-3 supplements or placebo pills daily.
The results are published in JAMA Network Open.
This study revealed that supplementing depression treatment with fish oil pills didn't prove more effective than placebo at improving quality of life, reducing suicidal ideation, or the need for antidepressants. Both groups showed similar improvements during the study and showed depression scores of 36.5 with omega-3 vs. 36.8 with placebo.
The results indicate that omega-3 supplements provide no additional benefit for depression.
Please note that the trial was conducted during the COVID-19 pandemic, which may have influenced the outcomes.
Gregor Berger et al, ω-3 Fatty Acids in Pediatric Major Depressive Disorder, JAMA Network Open (2026). DOI: 10.1001/jamanetworkopen.2025.48703
Jan 9
Dr. Krishna Kumari Challa
Tree bark microbes also clean the air by removing greenhouse and toxic gases
Microbes living on tree bark consume significant amounts of climate-active gases such as methane, hydrogen, and carbon monoxide, in addition to CO2 absorbed by trees. This microbial activity occurs on a global scale, enhancing air purification and contributing to both climate regulation and improved air quality. Different tree species host distinct microbial communities with varying gas-removal capacities.
Pok Man Leung et al, Bark microbiota modulate climate-active gas fluxes in Australian forests, Science (2026). DOI: 10.1126/science.adu2182. www.science.org/doi/10.1126/science.adu2182
Jan 9
Dr. Krishna Kumari Challa
Twin study ties childbearing timing to biological aging
Analysis of Finnish twins indicates that both the number and timing of pregnancies are linked to women's biological aging and lifespan. Women with two to three children and pregnancies between ages 24 and 38 show slower aging and longer life expectancy, while childlessness, early childbearing, or having more than four children are associated with accelerated aging. Epigenetic data support these associations.
A study based on Finnish twins shows that reproductive history is associated, at the population level, with women's lifespan and biological aging. In the study, mothers of large families, women who had no children, or women who had their first child at a very young age appeared to age somewhat faster than other women.
The results suggest that both the number of children and the timing of pregnancies are reflected in women's adult health and life expectancy. The paper is published in the journal Nature Communications.
From an evolutionary biology perspective, organisms have limited resources such as time and energy. When a large amount of energy is invested in reproduction, it is taken away from bodily maintenance and repair mechanisms, which could reduce lifespan.
Somewhat unexpectedly, the study also found that childless women showed faster aging than women with a few children. This result may be explained by other lifestyle or health-related factors whose effects could not be fully controlled for in the analyses.
The research group emphasizes that the findings apply only at the population level. They do not demonstrate cause–effect relationships, nor do they provide a basis for individual recommendations for women of reproductive age. For example, family size has decreased and the age at first birth has increased compared with the period covered by the study.
Part 1
Jan 9
Dr. Krishna Kumari Challa
A novel aspect of this study was that aging was also measured biologically. Epigenetic clocks were determined from blood samples from more than one thousand participants. Epigenetic clocks aim to measure biological aging—that is, the gradual deterioration of cells and tissues. With such methods, aging-related changes can be detected years or even decades before death.
The results supported earlier conclusions based on mortality data. According to the epigenetic clocks, women who had either many children or no children at all were biologically somewhat older than their chronological age.
A person who is biologically older than their calendar age is at a higher risk of death.
Having a child at a young age was also associated with biological aging. This too may relate to evolutionary theory, as natural selection may favor earlier reproduction that entails shorter overall generation times, even if it entails health-related costs associated with aging.
Mikaela Hukkanen et al, Epigenetic aging and lifespan reflect reproductive history in the Finnish Twin Cohort, Nature Communications (2026). DOI: 10.1038/s41467-025-67798-y
Part 2
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Jan 9
Dr. Krishna Kumari Challa
Suppressing postoperative inflammation may prolong pain
Suppressing inflammation after surgery by inhibiting TNF-α can delay recovery and prolong pain, rather than relieve it. Allowing natural inflammation leads to quicker pain resolution and recovery. These findings suggest that inflammation plays a beneficial role in healing, and indiscriminate use of anti-inflammatory drugs post-surgery may increase the risk of chronic pain.
Taking anti-inflammatory drugs after surgery is fairly standard protocol. But a new study by researchers suggests this approach may be backfiring and that blocking inflammation during this critical time may, in fact, delay recovery and prolong pain rather than relieve it.
If you look across all types of surgeries—anything from an extracted tooth to a hip replacement—the pain resolves normally for 90% of patients. But the other 10% develop chronic pain. That persistent pain is very hard to treat; it's very resistant to medication and it can last for years.
In the new study, published recently in the Journal of Pain Research, the researchers report that letting inflammation run its course led to a quicker cessation of pain and an overall quicker recovery after a surgery or injury.
Although this study suggests that blocking TNF-α after surgery is likely unwise, there are other scenarios where it may still make sense, such as improving mobility by reducing arthritic inflammation in the joints for autoimmune diseases like rheumatoid arthritis.
Inflammation is not necessarily a bad thing, the researchers say.
Yes, it hurts, but it's also working on the inside to promote the resolution of that pain. The idea in the medical field that when you have an injury, you should absolutely block the inflammation right away might not always be the best strategy, they conclude.
They think that one day we'll be able to block the pain but allow the healing inflammation.
Sophie Laumet et al, Unexpected Role of TNFα Signaling in the Resolution of Postoperative Pain in Mice, Journal of Pain Research (2025). DOI: 10.2147/jpr.s543971
Jan 9
Dr. Krishna Kumari Challa
Cancer Immunotherapy May Work Better Before 3PM
People with cancer receiving immunotherapy earlier in the day survived longer, suggesting that adjusting treatment timing may improve outcomes.
Mounting evidence suggests that the time of day at which cancer patients receive treatment could impact their outcomes. This effect is likely due to the circadian rhythm-dependent fluctuations in the function of immune cells as well as proteins that regulate their function, also called checkpoints.
In line with this, in a recent meta-analysis, researchers found that patients with various types of advanced cancer who underwent immune checkpoint inhibitor (ICI) infusions earlier in the day survived longer than their counterparts treated in the late afternoons or evenings.
In a new study, researchers discovered that patients with a highly aggressive lung cancer who received treatment before 3PM survived significantly longer than their counterparts who were treated later in the day.
Landré T, et al. Effect of immunotherapy-infusion time of day on survival of patient.... ESMO Open. 2024;9(2):102220.
Huang Z, et al. Overall survival according to time-of-day of immunochemotherapy for.... Cancer. 2025.
Jan 9
Dr. Krishna Kumari Challa
Jan 10
Dr. Krishna Kumari Challa
Genetic study uncovers unknown causes of blindness
Researchers have discovered new genetic causes of inherited blindness. Their study, published in Nature Genetics, shows that changes in specific pieces of DNA, which play a role in processing genetic information, can lead to retinitis pigmentosa.
This eye condition affects about one in 5,000 people worldwide, causing "tunnel vision" and often leads to legal blindness. The discovery provides clarity for dozens of families globally and opens new possibilities for diagnostics and counseling in hereditary conditions.
Retinitis pigmentosa (RP) is a disorder in which the rod and cone cells in the retina gradually die. Affected individuals first experience night blindness, followed by tunnel vision. Some eventually lose their sight completely.
Although more than a hundred genes are known to cause RP, in 30 to 50% of patients the genetic cause remains unresolved, even after extensive DNA testing. Researchers have now solved part of this puzzle.
Researchers found a variation in the gene RNU4-2. The change occurs in a special gene, RNU4-2, which does not produce a protein but only RNA. RNA from such genes associate with proteins and other RNAs and the whole resulting complex assists in editing genetic information (splicing), a step required before a cell can make proteins.
Other changes in RNU4-2 were recently linked to developmental disorders.
This breakthrough goes beyond these specific genetic variants causing RP. It shows that we should also look beyond protein-coding genes.
De novo and inherited dominant variants in U4 and U6 snRNA genes cause retinitis pigmentosa, Nature Genetics (2026). DOI: 10.1038/s41588-025-02451-4
Jan 10
Dr. Krishna Kumari Challa
Roads can become more dangerous on hot days—especially for pedestrians, cyclists and motorcyclists
Road injury risk increases significantly on very hot days, with pedestrians, cyclists, and motorcyclists facing the greatest danger due to direct heat exposure. The risk rises sharply above 30°C, with pedestrian injuries more than doubling and cyclist and motorcyclist injuries increasing by 80% and 50%, respectively. Heat also elevates crash severity and fatality risk, especially on rural roads and among older drivers. Effects can persist for days due to fatigue and sleep disruption.
During heat waves, everyday life tends to feel more difficult than on an average day. Travel and daily movement are no exception.
But while most of us know rain, fog and storms can make driving conditions challenging, not many people realize heat also changes transport risk. At very high temperatures, overall crash risk is about 15% higher than on cool days.
In particular, research evidence consistently suggests roads, trips and daily commutes can become more dangerous on very hot days compared with an average day. Road injury risk rises much more steeply once temperatures move into the 30°C–40°C range.
Importantly, the increase is even larger for crashes linked to driver fatigue, distraction or illness.
Ambient temperature and risk of motor vehicle crashes: A countrywid...
Heat waves and fatal traffic crashes in the continental United Stat...
Jan 10
Dr. Krishna Kumari Challa
The hidden carbon footprint of wearable health care
Researchers analyzed wearable health care electronics and reported carbon impacts of 1.1–6.1 kg CO2-equivalent per device. With global device consumption projected to rise 42-fold by 2050, approaching 2 billion units annually, their moderate projection adds 3.4 million metric tons of CO2-equivalent emissions alongside ecotoxicity and e-waste.
Wearable electronics—glucose, heart and blood pressure monitors, integrated into patches, chest straps, clothes and smartwatches—are transforming health care through real-time monitoring, device interaction, and therapeutic interventions.
Compared with rigid consumer electronics, wearable health care systems—ranging from biophysical and biochemical sensors to e-textiles and biointegrated therapeutics—offer high compliance and continuous tracking and intervention capabilities.
With wireless integration, wearable health care electronics are evolving into digital infrastructure networks adopted globally by patients, older people, athletes, and health-conscious people.
Reliance on energy-intensive manufacturing, hazardous chemicals, fossil-based plastics, and critical metals can lead to substantial carbon emissions, ecological risks, and e-waste issues. Rising energy demands from artificial-intelligence-driven data processing and advanced digital infrastructures further enlarge the eco-footprint of even the smallest devices.
In the study, "Quantifying the global eco-footprint of wearable health care electronics," published in Nature, researchers integrated life-cycle assessment with forecasting adoption growth over time to quantify global eco-footprint hotspots and evaluate mitigation strategies.
Four devices anchored the assessment—a non-invasive continuous glucose monitor, a continuous electrocardiogram monitor, a blood pressure monitor, and a point-of-care ultrasound patch. Selection criteria included clinical relevance, diversity of sensing modalities, and coverage across an expanding technology spectrum.
Cradle-to-grave attributional life-cycle assessment covered raw-material acquisition, manufacturing, transportation, use, and end-of-life disposal. Monte Carlo simulation quantified uncertainty for environmental impacts, and diffusion modeling projected future scale of use.
Part 1
Jan 11
Dr. Krishna Kumari Challa
A single continuous glucose monitor from production to use carried a carbon footprint equivalent to about 2 kg CO2-equivalent, or driving a gas-powered car for around 5 miles. More than 95% of that impact was attributed to printed circuit boards and semiconductors inside the device, tied to energy required to purify raw materials and power manufacturing processes.
Single glucose monitor use lasted 14 days before being discarded and replaced. Repetition of that short cycle has stacked impacts across the scale of users. Wearable glucose monitor sales are estimated to exceed 1.4 billion devices a year by 2050.
Expected greenhouse-gas emissions from these units alone were around 2.7 million metric tons CO2-equivalent annually.
Per-device warming impacts ranged from 1.06 kg CO2-equivalent for a blood pressure monitor to 6.11 kg CO2-equivalent for a point-of-care ultrasound patch. Values of 1.30 kg CO2-equivalent for a continuous electrocardiogram monitor.
Annualized warming impacts, accounting for typical replacement frequencies, were 0.5 kg CO2-equivalent for the blood pressure monitor, 33.8 kg CO2-equivalent for the continuous electrocardiogram monitor, 50.6 kg CO2-equivalent for the non-invasive continuous glucose monitor, and 6.1 kg CO2-equivalent for the point-of-care ultrasound patch.
Greenhouse-gas emissions from all wearables in the model were 3.4 million metric tons CO2-equivalent annually, or about the carbon footprint of the transport sector of Chicago. Component-level analysis placed flexible printed circuit board assemblies at the center of warming impacts across all four devices, with hotspots tied to gold in integrated circuits, silicon wafers, polyimide, and batteries.
part 2
Jan 11
Dr. Krishna Kumari Challa
Researchers modeled four mitigation approaches that included plastic substitution or recycling, critical-metal substitution, modular designs for reuse and replacement, and a transition to green energy.
Chuanwang Yang et al, Quantifying the global eco-footprint of wearable healthcare electronics, Nature (2025). DOI: 10.1038/s41586-025-09819-w
Part3
Jan 11
Dr. Krishna Kumari Challa
Fatigue before cancer treatment linked to adverse events
Investigators found that higher patient-reported fatigue before cancer treatment aligned with higher odds of severe, life-threatening, and fatal treatment-related toxic effects.
Cancer-related fatigue harms quality of life and is a persistent tiredness or exhaustion tied to cancer or cancer treatment. It interferes with usual physical and mental functioning and does not match the patient's normal recent activity. Patients report that fatigue is among the most distressing symptoms of cancer and its treatment, yet physicians routinely underreport fatigue.
Some studies have suggested prevalence ranging from 25% to 50%. Separate estimates place moderate fatigue at 25% and severe fatigue at 15% to 20%, levels often associated with poor performance status.
In the study, "Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy," published in JAMA Oncology, researchers pooled baseline fatigue data to evaluate associations between pretreatment fatigue and subsequent adverse events in cancer treatment trials.
Across 17 trials, 103,738 adverse events were recorded. Higher baseline fatigue aligned with higher odds of severe toxic effects. Some or greater baseline fatigue, compared with less than some fatigue, yielded an odds ratio of 2.11 for grade 3 or higher toxic effects and 1.98 for life-threatening toxic effects.
Comparison between quite a lot or very much fatigue and no baseline fatigue produced an odds ratio of 4.99 for grade 5 toxic effects.
Fatal toxic effects were uncommon, though risk rose with higher fatigue to an odds ratio of 2.35.
Severe or worse toxic effects occurred in 34.2% of patients reporting no fatigue, 39.4% reporting a little fatigue, 52.8% reporting some fatigue, and 58.3% reporting quite a lot or very much fatigue.
Subset analyses did not show statistically significant differences in the fatigue to adverse event association by age, sex, race, ethnicity, or obesity status.
Cancer stage mattered in subgroup patterns. Advanced-disease trials showed clearer monotonic relationships between baseline fatigue and adverse events, while adjuvant or early-stage trials did not show statistically significant associations for grade 3 or higher or grade 4 or higher adverse events.
Part 1
Jan 11
Dr. Krishna Kumari Challa
Patient-reported fatigue before cancer treatment was associated with increased risk of severe, life-threatening, and fatal adverse events during treatment.
Pre-treatment fatigue assessments could be seen as an early marker of vulnerability that could inform treatment strategies and symptom monitoring.
Joseph M. Unger et al, Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy, JAMA Oncology (2025). DOI: 10.1001/jamaoncol.2025.5549
Part 2
Jan 11
Dr. Krishna Kumari Challa
Why some people are more resistant to developing blood cancer even when they carry cancer-risk mutations
Blood cancer is an umbrella term for a variety of diseases that affect the blood, bone marrow and lymphatic system. Like most cancers, the cause is usually mutations in the DNA, which are genetic errors that accumulate as we age. However, some people are more resistant to developing blood cancer even when they carry cancer-risk mutations.
In a new study published in the journal Science, researchers discovered why. They identified a rare genetic variant that reduces the risk of several blood cancers, including leukemia, by slowing down a process called clonal hematopoiesis (CH).
CH occurs when a hematopoietic stem cell, which can develop into any type of blood cell, mutates and grows into a large population of identical mutated cells.
In their study, the team performed a large-scale analysis (known as a GWAS meta-analysis) of more than 640,000 individuals. By comparing 43,000 people with CH mutations to 600,000 without them, they pinpointed the genetic variant that protects against CH.
The researchers identified a noncoding regulatory variant, rs17834140-T, on chromosome 17q22.
The experiments revealed that rs17834140-T reduces the amount of a protein called MSI2, which acts as a growth booster in stem cells. In cancer, MSI2 causes mutated cells to multiply rapidly and take over the bone marrow. However, the protective variant results in lower levels of the protein, forcing these mutated cells to grow much more slowly and reducing their chances of progressing to leukemia. According to the study authors, people with the variant have up to a 30% lower risk of developing CH.
The research could lead to new ways to prevent cancer even before it starts. Now that we know that lowering MSI2 is protective, scientists may be able to develop drugs or other therapeutic approaches that mimic or enhance this natural protection.
Gaurav Agarwal et al, Inherited resilience to clonal hematopoiesis by modifying stem cell RNA regulation, Science (2026). DOI: 10.1126/science.adx4174
Francisco Caiado et al, Genetic resistance to leukemia, Science (2026). DOI: 10.1126/science.aed5244
Jan 11
Dr. Krishna Kumari Challa
Tire rubber decays into a potentially dangerous chemical cocktail, research shows
Crumb rubber from recycled tires, commonly used in artificial turf, generates hundreds of transformation chemicals as it decays under sunlight and environmental conditions. Some of these chemicals, such as 6PPD-quinone, are highly toxic to aquatic life, while others are known human health hazards. The long-term effects of most transformation products remain unknown.
The small, spongy black beads used as fill material in most artificial turf fields are called crumb rubber, which has long been touted as a major win for recycling. However, conflicting studies have alternately identified crumb rubber as either safe for people to play atop or dangerous to human health.
New research out of Northeastern University investigated the decay cycle of crumb rubber, which is fashioned out of old tires. By simulating the conditions in which the rubber decays, like strong sunlight, they discovered that crumb rubber is highly reactive, generating hundreds of previously untracked chemicals as it decays, some of which are hazardous to humans.
The work is published in the journal Environmental Science & Technology.
Madison H. McMinn et al, From the Road to the Field: Decoding Chemical Transformation in Aging Tire and Artificial Turf Crumb Rubber, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c08260
Jan 13
Dr. Krishna Kumari Challa
AI shows bias against some Indian castes
Popular large language models (LLMs) often reproduce harmful stereotypes about Indian castes — hereditary groups traditionally associated with specific occupations and social status. Researchers used a custom-designed tool to detect ‘caste bias’ in LLMs and found that every model they tested exhibited some bias. GPT-4o and GPT-3.5, created by OpenAI, had some of the highest bias scores. Information on minority groups might be less likely to appear in prestigious journals or other outlets, and might be written in local languages, which could result in it being filtered out of AI training data who studies cultural biases in LLMs.
[2508.03712] How Deep Is Representational Bias in LLMs? The Cases o...
[2510.02742] IndiCASA: A Dataset and Bias Evaluation Framework in L...
[2505.14971] DECASTE: Unveiling Caste Stereotypes in Large Language...
AIs are biased toward some Indian castes — how can researchers fix ...
Jan 13
Dr. Krishna Kumari Challa
Immune stress during pregnancy changes how fetal brain cells communicate
Research has found that immune-related genes vary by location and cell type across the developing mouse brain before birth. Maternal immune activation and maternal microbiome depletion shifted parts of that immune signaling pattern, with differences observed between male and female embryos.
Immune molecules, including cytokines, chemokines, and cognate receptors, are critical regulators of synapse development, cellular communication, and neural precursor cell migration in the developing brain. During development, nerve cells are born in one area, move to their destinations, and settle into stacked layers, especially in the cortex. Those layers line up in an ordered way, with different types of neurons ending up in different layers.
Changes to the maternal immune system and microbiome have been linked to abnormal fetal neurodevelopment, influencing neurogenesis, cell fate, and precursor cell migration. Knowledge of immune signaling networks within the developing brain is needed to understand the mechanisms of how the mother's stressors impart influence.
In the study, "Spatial transcriptomics of the developing mouse brain immune landscape reveals effects of maternal immune activation and microbiome depletion," published in Nature Neuroscience, researchers used multiplexed error-robust fluorescence in situ hybridization (MERFISH) to measure immune activity in embryonic mouse brains during mid and late gestation to see how maternal immune activation and maternal microbiome depletion altered those patterns.
Embryonic mouse brain single-cell RNA sequencing data supported identification of spatially restricted cell populations, followed by cell clustering, differential gene expression analyses, and ligand–receptor analyses.
The research connects maternal immune activation and maternal microbiome depletion with sex-specific shifts in immune gene expression, ligand–receptor signaling, and cell spacing within the embryonic brain. Specifically, CXCL12 and CXCR7 signaling stood out as an important mediator of abnormal neural differentiation and migration after maternal immune activation and maternal microbiome depletion.
Bharti Kukreja et al, Spatial transcriptomics of the developing mouse brain immune landscape reveals effects of maternal immune activation and microbiome depletion, Nature Neuroscience (2026). DOI: 10.1038/s41593-025-02162-3
Jan 14
Dr. Krishna Kumari Challa
Spaceflight causes astronauts' brains to shift, stretch and compress in microgravity
Spaceflight takes a physical toll on astronauts, causing muscles to atrophy, bones to thin and bodily fluids to shift. According to a new study published in the journal PNAS, we can now add another major change to that list. Being in microgravity causes the brain to change shape.
Here on Earth, gravity helps to keep the brain anchored in place while the cerebrospinal fluid that surrounds it acts as a cushion. Scientists already knew that, without gravity's steady pull, the brain moves upward, but this new research showed that it is also stretched and compressed in several areas.
The study authors found significant differences between the brains of astronauts and those of the volunteers. While both groups experienced a shift, the astronauts' brains moved further upward. And the longer they stayed in space, the more pronounced these changes became. The supplementary motor cortex (which helps to control movement) moved upward by about 2.5 millimeters in astronauts on one-year missions.
The brain movement isn't uniform. The team discovered that as the brain moves, it becomes compressed at the top and the back while other areas stretch. This has a noticeable effect on balance and coordination. In tests, astronauts who experienced the largest brain shifts struggled the most to stay steady on their feet after returning to Earth.
While the brain mostly returns to its normal position after several months back on Earth, scientists still need to know more to ensure safer conditions for longer missions, such as those to Mars.
Tianyi Wang et al, Brain displacement and nonlinear deformation following human spaceflight, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2505682122
Jan 14
Dr. Krishna Kumari Challa
Tibetan Plateau-Himalayan uplift shaped Asian summer monsoons
The uplift of the Tibetan Plateau, particularly when it exceeded 3.5 km elevation around 27–38 million years ago, was crucial in intensifying and expanding the Asian summer monsoon. This topographic change shifted rainbelts northward and increased rainfall over South and Southeast Asia, with tectonic uplift playing a more dominant role than atmospheric CO2 in shaping monsoon evolution.
S. Abhik et al, A brief history of Asian summer monsoon evolution in the Cenozoic era, npj Climate and Atmospheric Science (2026). DOI: 10.1038/s41612-025-01259-7
Jan 14
Dr. Krishna Kumari Challa
The global water cycle and how is it amplifying climate disasters
The global water cycle, involving evaporation, precipitation, and runoff, is intensifying due to rising temperatures. This leads to faster evaporation, increased atmospheric moisture, and more frequent extreme events such as floods, droughts, and heatwaves. These amplified fluctuations, sometimes termed "climate whiplash," are destabilizing ecosystems and societies worldwide.
original article.
Jan 14
Dr. Krishna Kumari Challa
The aggressive use of antibiotics could fuel mood disorders and anxiety
Antibiotics (ABs) are among the most used pharmaceutical drugs worldwide, as they are currently the most effective medicines for the treatment of bacterial infections. An excessive use of these drugs, however, can damage the gut microbiota, the population of microorganisms living in the intestines that help us to digest food.
Bacteria and other microorganisms in the gut are known to also communicate with the brain via a communication pathway that is referred to as the gut-brain axis. Recent research suggests that some gut bacteria help to reduce inflammation and support the healthy functioning of the brain.
Researchers have carried out a study exploring the possibility that the effects of ABs on gut bacteria could also facilitate the development of mental health disorders, particularly increasing anxiety. Their findings, published in Molecular Psychiatry, suggest that ABs do in fact damage gut bacteria that help regulate mood, linking their excessive use with higher levels of anxiety.
When they analyzed the data they collected, the researchers found that the use of ABs was linked to anxiety-like behaviors in mice and higher levels of anxiety in humans. Moreover, the drugs appeared to reduce the amounts of some helpful gut bacteria, particularly those in the Bacteroides group.
In addition, the team found an association between the intake of ABs and a reduction in the neurotransmitter acetylcholine, a chemical that supports communication between nerve cells. Mice and human patients who had received ABs were found to have lower levels of acetylcholine both in the gut and brain compared to those who had not taken ABs.
"In both AB-treated mice and patients, co-occurrence analysis indicated that the Bacteroides-acetylcholine pair may play an important role in AB-induced anxiety," wrote the researchers in their paper.
Ke Xu et al, Consistent decline of acetylcholine in microbiota-gut-brain axis mediates antibiotic-induced anxiety via regulating hippocampus microglial activation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03431-0.
Jan 15
Dr. Krishna Kumari Challa
Your voice gives away valuable personal information!
Human voices carry extensive personal information, including health, background, and emotional state, which can be extracted by advanced speech analysis technologies. This raises privacy risks such as misuse by insurers, employers, or malicious actors. New metrics now quantify how much information a speech recording contains, aiding the development of privacy-preserving tools and user interfaces.
You can probably quickly tell from a friend's tone of voice whether they're feeling happy or sad, energetic or exhausted. Computers can already do a similar analysis, and soon they'll be able to extract a lot more information. It's something we should all be concerned about, according to experts in the field.
Personal information encoded in your voice could lead to increased insurance premiums or to advertising that exploits your emotional state. Private information could also be used for harassment, stalking or even extortion.
When someone talks, a lot of information about their health, cultural background, education level and so on is embedded in the speech signal. That information gets transmitted with the speech, even though people don't realize it.
For example, even subtle patterns of intonation or word choice can be a giveaway as to your political preferences, while clues in breathing or voice quality may correlate with certain health conditions.
One important risk is that medical information inferred from voice recordings could affect insurance prices or be used to market medication.
The fear of monitoring or the loss of dignity if people feel like they're constantly monitored—that's already psychologically damaging.
And employers might extract personal information from voice recordings which could be used against employees or to screen candidates, or exes might use such tools for stalking or harassment.
So how can engineers tackle these problems?
Protecting against abuses means ensuring that only the information that's strictly necessary is transmitted and that this information is securely delivered to the intended recipient. One approach is to separate out the private information and only transmit the information needed to provide a service. Speech can also be processed locally on a phone or computer rather than sent to the cloud, and acoustic technologies can be used to make sure that sounds are only recorded from (or audible in) a specific place.
Tom Bäckström, Privacy in Speech Technology, Proceedings of the IEEE (2025). DOI: 10.1109/jproc.2025.3632102
Jan 15
Dr. Krishna Kumari Challa
How small mammals shrink their brains to survive the cold
An international team of researchers has conducted a study that explains the evolutionary origins of the Dehnel phenomenon, a unique seasonal adaptation in small mammals that involves the ability to reduce and recover brain volume and function. The study is published in Molecular Biology and Evolution.
The Dehnel phenomenon is a case of extreme plasticity through which some mammals reduce and regenerate their brains according to the season. This mechanism allows species such as the common shrew to reduce the size of their brain, skull and other organs by up to 30% during the winter to save energy in conditions of extreme cold and food scarcity.
In the spring, these tissues regenerate, making this phenomenon an exceptional example of physiological plasticity. Furthermore, comparative studies show that it is not exclusive to shrews: European moles and mustelids (such as weasels) also exhibit seasonal brain reductions, which extends the evolutionary framework of this strategy to mammals with high metabolisms.
Through comparative genomics and gene expression analysis in key tissues, such as the hypothalamus, the team identified genes associated with several fundamental processes, such as energy homeostasis and calcium signaling, essential for adjusting energy balance in demanding environments; the integrity of the blood-brain barrier, which ensures efficient control of molecules accessing the brain during the seasonal cycle; and water regulation, involved in reversible brain volume loss without cell death, a key finding for understanding how this adaptation is achieved.
The plasticity reflected by the Dehnel phenomenon influences survival, reproduction, and resilience to climate variability. According to the research team, even though these species are not human, understanding the mechanisms that allow reversible reductions in brain volume without permanent damage could inspire new lines of research in neurology and metabolism.
The role of genes related to energy homeostasis and the blood-brain barrier points to possible biomarkers and therapeutic targets for neurodegenerative diseases, always with the necessary caution when extrapolating to humans.
William R Thomas et al, Genomic comparisons shed light on the adaptive basis of brain size plasticity and chromosomal instability in the Eurasian common shrew, Molecular Biology and Evolution (2026). DOI: 10.1093/molbev/msag006
Jan 16
Dr. Krishna Kumari Challa
Gut bacteria cause rare alcohol syndrome
Researchers have found more evidence that ethanol-producing gut bacteria are the main drivers of auto-brewery syndrome (ABS) — a rare and poorly understood condition in which people become drunk when they haven’t consumed alcohol. A team found that strains of Klebsiella bacteria and Escherichia coli that produce ethanol were much more prevalent in the gut microbiomes of people with ABS than in those of people who didn’t have the condition. One person with ABS was successfully treated with a faecal microbiota transplant, but the authors say a targeted intervention, such as disrupting the metabolic pathways the bacteria use to produce ethanol, might be more effective.
Gut microbial ethanol metabolism contributes to auto-brewery syndro...
Jan 16
Dr. Krishna Kumari Challa
Vaccines create a halo of benefits
Growing evidence suggests that vaccines have benefits in older adults beyond protecting against infectious diseases. These ‘off-target effects’ include a reduced risk of dementia and cardiovascular events. Exactly why vaccines have these protective effects is unclear, but researchers suggest that in protecting against infection, vaccines also protect against the inflammation that comes with them. Many experts now worry that opposition to childhood vaccinations could dissuade some adults from getting vaccinated, which would leave them vulnerable to the diseases that vaccines can protect against, both infectious and not.
Vaccines Are Helping Older People More Than We Knew - The New York ...
Jan 16
Dr. Krishna Kumari Challa
How the gut microbiome affects transplants
Antibiotic and immunosuppressant treatment administered before, during and after a solid-organ or haematopoietic-stem-cell transplant can dysregulate the gut microbiome. On the flipside, the gut microbiome can also influence the long-term success of such procedures by, for example, metabolizing immunosuppressants into less active forms. A better understanding of these interactions could yield targeted interventions that improve outcomes in transplant recipients, write five internal-medicine specialists in their review.
The gut microbiome in solid-organ and haematopoietic-stem-cell tran...
Jan 16
Dr. Krishna Kumari Challa
Cancer cells use stolen goods to stay hidden
Hijacking the energy-producing organelles from immune cells seems to help tumours in mice to infiltrate lymph nodes.
Cancer cells use mitochondria stolen from immune cells to escape detection and spread. Researchers found that when cancer cells take on these mitochondria in mice, it both weakens the immune cells and triggers a molecular pathway in the cancer cells that help them fly under the immune system’s radar and invade lymph nodes. This beneficial molecular pathway was activated even when researchers disrupted the mitochondria’s ability to produce the energy-carrying molecule ATP. The findings could explain how cancer cells survive in lymph nodes, which are packed with immune cells that should be able to kill them.
Mitochondrial transfer from immune to tumor cells enables lymph nod...
Cancer might evade immune defences by stealing mitochondria
Jan 16
Dr. Krishna Kumari Challa
Scientists discover natural 'brake' that could stop harmful inflammation
Researchers have uncovered a key mechanism that helps the body switch off inflammation—a breakthrough that could lead to new treatments for chronic diseases affecting millions worldwide.
Inflammation is the body's frontline defense against infection and injury, but when it doesn't switch off properly, it can drive serious health conditions such as arthritis, heart disease, and diabetes. Until now, scientists didn't fully understand how the body decides to stop the immune "fight" response and start healing.
Published in Nature Communications, the study reveals that tiny fat-derived molecules called epoxy-oxylipins act as natural brakes on the immune system. These molecules prevent the overgrowth of certain immune cells, known as intermediate monocytes, that can cause chronic inflammation—linked to tissue damage, illness and disease progression.
Tests revealed that one epoxy-oxylipin, 12,13-EpOME, works by shutting down a protein signal called p38 MAPK, which drives monocyte transformation. This was confirmed in lab experiments and in volunteers given a p38-blocking drug.
Targeting this mechanism could lead to safer treatments that restore immune balance without suppressing overall immunity.
Epoxy-Oxylipins Direct Monocyte Fate in Inflammatory Resolution in Humans, Nature Communications (2026). DOI: 10.1038/s41467-025-67961-5
Jan 17
Dr. Krishna Kumari Challa
Super agers tend to have at least two key genetic advantages
The gene variant posing the greatest genetic risk of late-onset Alzheimer's disease (AD) is called APOE-ε4. A different variant of the same gene, APOE-ε2, is thought to confer protection against AD.
A comparatively large study reported in Alzheimer's & Dementia by researchers measures the frequency of APOE-ε4 and APOE-ε2 in so-called super agers—people ages 80 or older whose cognitive function is comparable to people 20 or 30 years younger.
Super agers were 68% less likely to harbor the gene nobody wants, APOE-ε4, compared to individuals with AD dementia in the same 80+ age group.
Most notably, super agers were 19% less likely to harbor APOE-ε4 than were cognitively normal participants in the same age group.
Super agers were also found for the first time to have higher frequency of the variant you'd want, APOE-ε2: They were 28% more likely to carry APOE-ε2 than were cognitively normal controls ages 80+, and 103% more likely to carry the variant than were participants with AD dementia aged 80 or older.
Evaluating the association of APOE genotype and cognitive resilience in SuperAgers, Alzheimer's & Dementia (2026). DOI: 10.1002/alz.71024. alz-journals.onlinelibrary.wil … oi/10.1002/alz.71024
Jan 17
Dr. Krishna Kumari Challa
Focusing on variety and balance is the best way to reduce exposure to heavy metals in food while keeping your plate full of nutritious choices.
Mix it up. Eat a variety of grains, proteins, fruits, and vegetables—and even vary the brands you buy. Relying too heavily on one food type, source, or growing location can risk repeated exposure to an element that happens to be particularly high in that food or region. Low levels of heavy metals make their way into foods. A varied, healthy diet can limit exposure and absorption.
Choose safer seafood. Fish is one of the healthiest foods you can eat. Opt for smaller fish, which are lower on the food chain, such as salmon, canned light and skipjack tuna, sardines, pollock, or tilapia. Shellfish like scallops, clams, crab, and shrimp are good choices as well. Limit large predatory fish, like swordfish, orange roughy, and king mackerel.
Cook rice smartly. Cook rice with extra water (like pasta) that you drain off. This simple step can reduce arsenic levels (but it also lowers nutritional value). Try other grains like oats, quinoa, bulgur, or barley for variety.
Check your home. If you have older pipes, test your tap water for lead and consider a certified filter if needed. Paint in houses built before 1978 should be tested for lead. (Test kits can be purchased at home improvement stores and may be available for free through local health departments and/or water utilities.)
Refer to trusted sources. The U.S. Food and Drug Administration and Environmental Protection Agency are tasked with helping to ensure your food and water meet safety standards. If unusually high levels of any heavy metals are discovered in a particular food, the media will be alerted, and recalls will be put in place.
Heavy metals are part of our environment, and small amounts do make their way into foods. But research shows that the benefits of a varied, nutrient-rich diet far outweigh the minimal risks from trace exposure.
What to Know About Heavy Metals in Food | Tufts Now
Jan 17
Dr. Krishna Kumari Challa
This a the first cow ever documented using a tool
on Tuesday
Dr. Krishna Kumari Challa
Charge buildup in a lunar rover
As they roll across shadowed regions of the moon's surface, future lunar rovers could develop hazardous buildups of electric charge on their wheels.
With an interest in lunar exploration now reigniting worldwide, several space agencies are considering how the moon's surface could be explored in unprecedented detail using wheeled rovers. One challenge these vehicles will face is the buildup of 'triboelectric charge' as their wheels move across the regolith: a dry, granular, and highly insulating layer of dust and rock that blankets the moon. If allowed to accumulate, this charge could trigger discharges that threaten a rover's sensitive electronics and instruments.
As the moon travels through the solar wind, it creates a long plasma "wake" on its night-time side, where particle densities drop dramatically. "If the plasma flux levels are reduced, charge dissipation will slow. In essence, it will become increasingly difficult to remediate charge buildups in these plasma-starved regions.Under many circumstances, charge buildup is naturally limited by the solar wind—a continuous stream of charged particles that emanate from the sun. Because this plasma is far more conductive than the regolith, it provides a pathway for excess charge to dissipate into the surrounding environment. However, this helpful effect can't always be guaranteed.
These conditions are also found inside the moon's permanently shadowed polar craters—potential harbors of frozen water and carbon dioxide that could be prime targets for upcoming missions. For rovers operating in these environments, engineers must take steps to prevent triboelectric charging from reaching problematic levels.
Using advanced simulations, researchers modeled the balance between triboelectric charging and plasma-based charge dissipation under realistic lunar conditions. Their results show that keeping a rover's speed extremely low—below about 0.2 cm per second—can prevent charge from accumulating.
If a rover moves faster than this speed limit in the given plasma environment, then the wheel tribocharging currents will exceed plasma dissipation currents and the wheel will build up charge. If the rover moves slower than this speed limit, then the plasma currents will dissipate the charge before it builds up to large levels
Part 1
on Tuesday
Dr. Krishna Kumari Challa
The researchers also found that a rover's approach path into a crater can strongly influence its charging environment. If it enters a crater on the downwind side—facing the sun and solar wind—it can remain in a relatively dense plasma flow.
If the rover enters the leeward edge of the crater—moving with the sun at its back—the rover enters a region where the local mini-wake first forms
Finally, they examined how a rover's wheels should be electrically connected to its body. While isolating the wheels might seem like a way to protect onboard electronics, the simulations showed that this isolation actually limits the dissipation of charge—only worsening the problem.
Instead they recommend that the rover wheel is tested to ensure it is electrically connected to the larger rover structure, ensuring that the wheel has a conductive path to the larger structure. The rover body can then be used to increase the plasma current collection to more quickly dissipate the wheel tribocharge buildup.
Together, these findings highlight how space-weather effects on the moon can pose subtle but serious risks to surface operations.
W.M. Farrell et al, Rover wheel tribocharging in lunar shadowed regions: deriving a speed limit for charge accumulation, Advances in Space Research (2026). DOI: 10.1016/j.asr.2025.10.102
Part 2**
on Tuesday
Dr. Krishna Kumari Challa
Scientists design artificial pain receptor that senses pain intensity and self-heals
All over the body are tiny sensors called nociceptors whose job is to spot potentially harmful stimuli and send warning signals to the brain and spinal cord, helping protect us from injury or tissue damage.
In a recent study, scientists designed a jelly-like artificial nociceptive nerve pathway built using a memristor—a tiny electronic component that controls current flow and retains the memory of how much electricity has flowed through it.
The quantized conductance (QC) phenomenon in memristors, where electricity flows through a material in discrete steps rather than a smooth stream, allowed the pain receptor to go beyond simply turning on and off in response to a stimulus. Instead, it exhibited four distinct levels that correspond to the human pain scale: no pain, mild, moderate, and severe.
The bio-inspired receptor also showed signs of self-healing in terms of repairing physical damage and fading of pain signals.
Xuanyu Shan et al, Bioinspired Artificial Nociceptor Based on Quantized Conductance Memristor With Pain Rating, Self‐Healing, and Neuromodulation Capabilities, Advanced Functional Materials (2025). DOI: 10.1002/adfm.202528900
on Tuesday
Dr. Krishna Kumari Challa
Tumor cells steal immune mitochondria to aid lymph node spread
Researchers report that tumor cells hijack mitochondria from immune cells, reducing anti-tumor immune function and activating cGAS-STING and type I interferon signaling that promotes lymph node metastasis.
Mitochondrial transfer, the movement of mitochondria between cells, is a mode of intercellular communication that reshapes metabolism, stress responses, and cellular function across diverse physiological and pathological settings. Recruiting outside mitochondria into cancer cells can enhance oxidative phosphorylation, promote survival under metabolic stress, and influence therapy resistance.
Lymph node metastasis is a critical early step in cancer progression that can create a systemic impairment of tumor control.
Previous reports have found that T cells and macrophages can transfer mitochondria to cancer cells. The extent of mitochondrial transfer by other immune cells remains unclear, along with any connections to lymph node colonization.
In the experiments, Tumor cells acquired mitochondria from host cells across colon, breast, and melanoma models. Immune cells were identified as a donor source in bone marrow chimera experiments that restricted the reporter signal to hematopoietic cells. Draining lymph nodes carried a higher fraction of tumor cells with immune-derived mitochondria than primary tumors.
Direct physical contact supported transfer, with higher transfer under hypoxic stress and inflammatory cues. Disruption of transfer structures and knockdown of a transfer-related factor reduced transfer, paired with reduced lymph node metastasis incidence in reported mouse experiments. mtDNA polymorphism tracing added a second line of evidence that donor mitochondrial DNA could be detected in tumor material.
Immune cells that lost mitochondria showed reduced antigen-presentation and co-stimulatory machinery, with reduced activation and cytotoxic capacity reported for natural killer and CD8 T cells. Changes aligned with impaired immune surveillance in the co-culture systems described.
Researchers identify immune-to-tumor cell mitochondrial transfer as a central mechanism that facilitates lymph node colonization through two coordinated effects. Loss of mitochondria disables anti-tumor immunity by diminishing antigen presentation and impairing cytotoxic function across multiple immune lineages, while immune-derived mitochondria activate the cGAS-STING pathway in tumor cells and induce a type I interferon program that promotes immune evasion and lymph node colonization.
Targeting mitochondrial transfer or the resulting cGAS-STING signaling represents a promising strategy to restrict lymph node metastasis, a critical early step in systemic cancer progression.
Azusa Terasaki et al, Mitochondrial transfer from immune to tumor cells enables lymph node metastasis, Cell Metabolism (2026). DOI: 10.1016/j.cmet.2025.12.014
on Tuesday
Dr. Krishna Kumari Challa
A new anti-biofilm strategy
Combining mechanical killing mechanisms with chemical agents or near-infrared light irradiation could enhance efficacy against diverse organisms.Nanopatterned surfaces with nanoscale protrusions physically disrupt bacterial cells, preventing biofilm formation through mechanical means rather than chemical agents. These surfaces, inspired by insect wings, can kill a broad range of microbes, including bacteria and fungi. Scalability challenges are being addressed with adaptable materials like metal-organic frameworks, enabling more practical applications.
https://pubmed.ncbi.nlm.nih.gov/22674670/
Zhejian Cao et al, Mechano‐Bactericidal Surfaces Achieved by Epitaxial Growth of Metal–Organic Frameworks, Advanced Science (2025). DOI: 10.1002/advs.202505976
on Tuesday
Dr. Krishna Kumari Challa
Human heart regrows muscle cells after heart attack, researchers discover
Until now we've thought that, because heart cells die after a heart attack, those areas of the heart were irreparably damaged, leaving the heart less able to pump blood to the body's organs.
But Pioneering research by experts has shown that heart muscle cells regrow after a heart attack, opening up the possibility of new regenerative treatments for cardiovascular disease.
This new work shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
Though increased mitosis(a process in which cells divide and reproduce) after a heart attack has been observed in the heart muscles of mice, this is the first time the phenomenon has been demonstrated in humans.
Although this new discovery of regrowing muscle cells is exciting, it isn't enough to prevent the devastating effects of a heart attack. Therefore, in time, the researchers hope to develop therapies that can amplify the heart's natural ability to produce new cells and regenerate the heart after an attack.
Robert D. Hume et al, Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction, Circulation Research (2026). DOI: 10.1161/circresaha.125.327486
on Tuesday
Dr. Krishna Kumari Challa
Why adapting to the environment is more difficult as people age
Age-related structural changes in specific brain regions reduce adaptability to environmental changes. Older adults rely more on brain structures involved in task switching and updating information, but these structures deteriorate over time, correlating with decreased adaptive behaviour in later adulthood.
Researchers characterized changes in the brain across two periods of adulthood that may correspond to changes in adaptive behaviour.
Identifying these changes may help track adaptability decline.
eNeuro (2026). DOI: 10.1523/ENEURO.0179-25.2025
on Tuesday
Dr. Krishna Kumari Challa
No clear evidence that cannabis-based medicines relieve chronic nerve pain, updated review finds
Current evidence does not support that cannabis-based medicines, including THC, CBD, or balanced THC/CBD products, provide clinically meaningful relief for chronic neuropathic pain compared to placebo. Adverse event data are uncertain, with THC products linked to increased dizziness and drowsiness. Higher-quality, longer-term studies are needed.
Cannabis-based medicines for chronic neuropathic pain in adults, Cochrane Database of Systematic Reviews (2026). DOI: 10.1002/14651858.CD012182.pub3
on Tuesday
Dr. Krishna Kumari Challa
Scientists discover a hidden RNA 'aging clock' in human sperm
Increasing paternal age has been linked to elevated health risks for the next generation, including higher risks of obesity and stillbirth. So, what drives this increased risk?
Most research into this link focuses on how the DNA inside sperm changes with age. But sperm carries other molecules as well, including a diverse array of molecules called RNAs.
Now, new research has shown that the RNA contents of sperm go through similar shifts over time in both mice and humans, which may lead to a rapid, dramatic shift at midlife. What's more, "old RNA" seems to change cells' metabolism—potentially contributing to the health risks of having kids later in life.
It's like finding a molecular clock that ticks with age in both mice and humans, suggesting a fundamental, conserved molecular signature of sperm aging.
The researchers were only able to detect some of these changes when they looked at RNA from the sperm head alone—the part of the sperm that delivers its contents to the egg. The long tail of the sperm contains other RNA that obscured the pattern until now.
If we can understand the enzymes driving this shift, they could become actionable targets for interventions to potentially improve sperm quality in aging males.
Conserved shifts in sperm small non-coding RNA profiles during mouse and human aging, The EMBO Journal (2026). DOI: 10.1038/s44318-025-00687-8
on Wednesday
Dr. Krishna Kumari Challa
Exposure to wildfire smoke late in pregnancy may raise autism risk in children
Analysis of over 200,000 births in Southern California indicates that exposure to wildfire smoke during the third trimester of pregnancy is associated with a 23% higher risk of autism diagnosis by age 5. The association is strongest with exposure exceeding 10 days. These findings support concerns about air pollution's impact on fetal neurological development.
Prenatal Exposure to Wildfire and Autism in Children, Environmental Science & Technology (2026). DOI: 10.1021/acs.est.5c08256
on Wednesday
Dr. Krishna Kumari Challa
Chronic kidney disease poisons patients' hearts, scientists discover
Scientists have discovered an answer to the longstanding mystery of why more than half of patients with chronic kidney disease ultimately die of cardiovascular problems: Their kidneys produce a substance that poisons the heart.
Chronic kidney disease leads to the production of circulating extracellular vesicles in the kidneys, which carry toxic miRNA that harm the heart. Blocking these vesicles in animal models improved heart function. This mechanism may enable earlier identification and targeted treatment of heart failure risk in CKD patients.
The researchers say the discovery could let doctors identify people at risk and develop new treatments to help prevent and treat heart failure for these patients.
Xisheng Li et al, Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease, Circulation (2026). DOI: 10.1161/circulationaha.125.075579
on Wednesday
Dr. Krishna Kumari Challa
Certain antibiotics may may boost immune system
Fluoroquinolone antibiotics can directly alter macrophage metabolism by stressing their mitochondria, leading to increased production of nitric oxide and enhanced bacterial clearance. This effect is specific to certain younger macrophage subsets in the lung and gut. While these antibiotics may boost immune cell function, they also carry risks such as microbiome disruption and potential tissue damage from excessive inflammation.
Alexander W Hardgrave et al, Fluoroquinolones directly drive mitochondrial hyperpolarization and modulate iNOS expression in monocyte-derived macrophage populations, Discovery Immunology (2025). DOI: 10.1093/discim/kyaf018
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on Wednesday
Dr. Krishna Kumari Challa
Cancer patients warned popular supplement may interfere with treatment
Biotin supplements, commonly used by cancer patients to address hair loss, lack strong evidence for promoting hair or nail regrowth and can interfere with lab tests, potentially leading to inaccurate results and delayed or altered treatment. Biotin may cause false readings in tests for prostate, thyroid, ovarian, and breast cancers. Minoxidil is a safer, effective alternative for hair loss.
Layna Mager et al, Biotin Supplements for Hair and Nail Regrowth: A Caution for Oncologists, JCO Oncology Practice (2025). DOI: 10.1200/op-25-00693
Cancer patients warned popular supplement may interfere with treatment
on Wednesday
Dr. Krishna Kumari Challa
What the brain's shape and complexity say about a newborn's development
The neonatal period, which is defined as the first 28 days after birth, is known to be a crucial stage in the development of the human brain. During this stage, the brain is known to grow significantly in size, with billions of new connections forming between neurons and supporting basic physiological functions.
Researchers recently carried out a study aimed at further exploring how the human brain's overall shape and size as well as the dimensions of distinct regions are linked to a newborn's development and maturity. Their findings, published in Nature Neuroscience, suggest that the brain's shape is a key marker of development during the neonatal period.
They analyzed publicly available magnetic resonance imaging (MRI) data collected from almost 800 human newborns as part of the developing Human Connectome Project (dHCP). Employing a mathematical method called fractal analysis, they tried to delineate the shape of the newborns' brains.
This approach yields a geometric measure called fractal dimensionality (FD) that describes the shape of a brain region in terms of its structural complexity.
Brain shape predicted the infants' ages significantly better than brain size, say teh researchers. Moreover, brain shape captured signatures of premature birth that were not detected with brain size.
They found that the brains of infants who were related to each other, such as twins, were more similar in shape than those of unrelated infants. The shape of the brains of identical twins, who share almost 100% of genes, was found to be more similar than those of fraternal twins, who share approximately 50% of genes.
Based on this relationship, the researchers were able to predict which babies are twin siblings from their brain shapes with high accuracy (~77% overall, ~97% in identical twins), again outperforming all other studied brain measures.
These results suggest that the early-life formation of brain shape represents a fundamental maturational process in human brain development.
Stephan Krohn et al, Fractal analysis of brain shape formation predicts age and genetic similarity in human newborns, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02107-w
yesterday
Dr. Krishna Kumari Challa
Maternal genetic factors may reveal why pregnancy loss is so common
Pregnancy loss in humans is common, with about 15% of recognized pregnancies resulting in miscarriage and many more conceptions being lost at early stages without people realizing it.
Analysis of genetic data from nearly 140,000 IVF embryos demonstrates that common maternal genetic variants, particularly in genes involved in chromosome cohesion and recombination, contribute to individual differences in the risk of pregnancy loss due to chromosomal errors. These findings clarify molecular pathways underlying aneuploidy and suggest potential targets for future therapies.
By studying genetic data from nearly 140,000 IVF embryos, scientists have with unprecedented detail revealed why fewer than half of human conceptions survive to birth. The research uncovered the strongest evidence yet for how common genetic differences leave some individuals more vulnerable to pregnancy loss.
The vast dataset allowed the team to demonstrate robust connections between specific variations in a mother's DNA and their risk of miscarriage.
The findings shed new light on human reproduction and suggest pathways for developing treatments to lower the risk of pregnancy loss.
Most chromosome errors originate in the egg and increase in frequency with a mother's age. More mysterious is how factors beyond age, such as genetic differences, may predispose a person to produce eggs with abnormal numbers of chromosomes in the first place.
Figuring that out requires analyzing genetic data from large numbers of embryos before pregnancy loss, as well as their biological parents.
The strongest associations appear in genes that govern how chromosomes pair, recombine, and are held together during egg formation, including a gene (SMC1B) that encodes part of the ring-shaped structure that encircles and binds chromosomes, the team found. These rings are essential for accurate chromosome segregation and tend to break down as women age.
Part 1
yesterday