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Comment by Dr. Krishna Kumari Challa 2 minutes ago

At the frontier between two lives—the evolutionary origins of pregnancy

An international research team  has uncovered new insights into how specialized cell types and communication networks at the interface between mother and fetus evolved over millions of years. These discoveries shed light on one of nature's most remarkable innovations—the ability to sustain a successful pregnancy. The findings have just been published in Nature Ecology & Evolution.

Pregnancy that lasts long enough to support full fetal development is a hallmark evolutionary breakthrough of placental mammals—a group that includes humans. At the center of this is the fetal-maternal interface: the site in the womb where a baby's placenta meets the mother's uterus, and where two genetically distinct organisms—mother and fetus—are in intimate contact and constant interaction.

This interface has to strike a delicate balance: intimate enough to exchange nutrients and signals, but protected enough to prevent the maternal immune system from rejecting the genetically "foreign" fetus.

To uncover the origins and mechanisms behind this intricate structure, the team analyzed single-cell transcriptomes—snapshots of active genes in individual cells—from six mammalian species representing key branches of the mammalian evolutionary tree. These included mice and guinea pigs (rodents), macaques and humans (primates), and two more unusual mammals: the tenrec (an early placental mammal) and the opossum (a marsupial that split off from placental mammals before they evolved complex placentas).

By analyzing cells at the fetal-maternal interface, the researchers were able to trace the evolutionary origin and diversification of the key cell types involved. Their focus was on two main players: placenta cells, which originate from the fetus and invade maternal tissue, and uterine stromal cells, which are of maternal origin and respond to this invasion.

Using molecular biology tools, the team identified distinct genetic signatures—patterns of gene activity unique to specific cell types and their specialized functions. Notably, they discovered a genetic signature associated with the invasive behavior of fetal placenta cells that has been conserved in mammals for more than 100 million years.

Part 1

Comment by Dr. Krishna Kumari Challa 15 hours ago

Food contact articles as source of micro- and nanoplastics

Comment by Dr. Krishna Kumari Challa 20 hours ago

Unlocking the mystery behind Barrett's esophagus

A research team has shed light on the process that drives Barrett's esophagus formation. This condition affects the lining of the esophagus—the tube that carries food from the mouth to the stomach—and increases the risk of developing esophageal adenocarcinoma, a serious and often deadly cancer.

The study, published in the Journal of Clinical Investigation, reveals that two important genes involved in guiding and maintaining the identity of the esophagus and intestine, SOX2 and CDX2, are altered in Barrett's esophagus. The findings not only deepen our understanding of how the disease develops but also open the door to new ways of identifying people at risk and potentially preventing the condition from progressing to cancer.

It is known that Barrett's esophagus usually develops after long-term exposure to acid and bile reflux, which transforms the cells of the lining of the esophagus into cells that look more like those in the stomach and the intestine.

The esophagus, which is not normally exposed to acid, adapts to acid reflux by becoming more like the stomach or the intestine, organs that are used to an acidic or bile-rich environment.

Eliminating acid reflux with medication does not heal Barrett's esophagus; the cells do not revert to their typical esophagus characteristics.

Under the microscope, Barrett's lesions show increased cell proliferation and a disorganized tissue with stomach-like and intestine-like cells where only esophageal cells should be.

To gain insight into what drives the transformation of esophageal cells into stomach and intestinal cells, the team investigated transcription factors SOX2 and CDX2, which are proteins that regulate the identity of esophageal and intestinal cells, respectively.

The findings support the idea that Barrett's esophagus may arise from the acid- and bile-triggered reprogramming of normal esophageal cells by altering the balance of SOX2 and CDX2. This new understanding could help scientists find strategies to intervene earlier in the disease process as well as develop new ways to provide an early diagnosis.

Ramon U. Jin et al, SOX2 regulates foregut squamous epithelial homeostasis and is lost during Barrett's esophagus development, Journal of Clinical Investigation (2025). DOI: 10.1172/JCI190374

Comment by Dr. Krishna Kumari Challa 21 hours ago

Air pollution is linked to adverse birth outcomes in India

Prenatal exposure to ambient fine particulate matter and climatic factors, such as temperature and rainfall, are associated with adverse birth outcomes in India, according to a study published in PLOS Global Public Health 

Ambient air pollution poses a global threat to human health, with a disproportionate burden of its detrimental effects falling on those residing in low and middle-income countries. Referred to as the silent killer, ambient air pollution is among the top five risk factors for mortality in both males and females.

With a diameter of less than 2.5 microns, ambient fine particulate matter 2.5 (PM2.5), which primarily originates from the burning of fossil fuels and biomass, is considered the most harmful air pollutant. In the 2023 World Air Quality Report, India was ranked as the third-most polluted country out of 134 nations based on its average yearly PM2.5 levels.

Ambient air pollution has been associated with a range of pediatric morbidities, including adverse birth outcomes, asthma, cancer, and an increased risk of chronic diseases.

To address the knowledge gap, the researchers investigated the impact of ambient air pollution on adverse birth outcomes at the national level, focusing on  low birth weight and preterm birth, and used different geospatial models to highlight vulnerable areas. The analysis provided evidence of the association between in-utero exposure to PM2.5 and adverse birth outcomes by leveraging satellite data and large-scale survey data.

The individual-level analysis revealed that an increase in ambient PM2.5 is associated with a greater likelihood of low birth weight and preterm birth. Climatic factors such as rainfall and temperature were also linked to adverse birth outcomes. Children residing in the Northern districts of India appeared to be more susceptible to the adverse effects of ambient air pollution.

PLOS Global Public Health (2025). DOI: 10.1371/journal.pgph.0003798

Comment by Dr. Krishna Kumari Challa 21 hours ago

Engineered bacterial vesicles created to combat antimicrobial resistance

Bacteria are ubiquitous microscopic organisms capable of rapid growth. While beneficial strains like lactic acid bacteria (LAB) promote gut health and food preservation, pathogenic bacteria such as Escherichia coli and Staphylococcus aureus can cause severe infections. These harmful microbes produce toxins and enzymes that compromise health and, increasingly, show resistance to conventional antibiotics.

In recent years, scientists have explored alternative approaches to tackle pathogenic bacteria. Among them, endolysins—enzymes that degrade bacterial cell walls—have emerged as potent tools. These proteins, often derived from bacteriophages or engineered microbes, offer specificity in targeting pathogens. However, their widespread use is limited by challenges such as high production costs, instability during storage or circulation, and susceptibility to enzymatic degradation.

To address this research gap, researchers have turned their attention to extracellular vesicles (EVs)—membrane-bound nanoparticles released by cells that transport biologically active molecules like proteins or nucleic acids. They engineered EVs derived from LAB to carry pathogen-specific endolysins on their surface.

Their findings were published in the Chemical Engineering Journal on 15 May, 2025. The research outlines the discovery and application of a novel surface-displaying protein found on EVs from Lacticaseibacillus paracasei.

Jeongmin Lee et al, Surface-displaying protein from Lacticaseibacillus paracasei–derived extracellular vesicles: Identification and utilization in the fabrication of an endolysin-displaying platform against Staphylococcus aureus, Chemical Engineering Journal (2025). DOI: 10.1016/j.cej.2025.162196

Comment by Dr. Krishna Kumari Challa yesterday

Psilocybin rewires brain circuits to boost fear extinction and behavioural flexibility in mice

Psilocybin, a psychedelic compound contained in some varieties of mushrooms, has recently been found to be promising for the treatment of some neuropsychiatric disorders, including depression, some anxiety disorders and post-traumatic stress disorder(PTSD). Some studies suggest that the consumption of this compound may be particularly advantageous for individuals who struggle to adapt their behavior in helpful ways when facing unexpected events or changes in their environment.

While a growing pool of research has been assessing the therapeutic benefits of psilocybin  the neural mechanisms through which it promotes long-lasting psychological changes remain poorly understood. If it does prompt greater behavioral flexibility in individuals diagnosed with some psychiatric disorders, the processes through which it does so are not yet clear.

Researchers  recently carried out a new study on mice, which was aimed at better understanding how psilocybin could increase adaptability and potentially ease symptoms of anxiety disorders or PTSD. Their findings, published in Nature Neuroscience, suggest that the compound prompts the reorganization of neural circuits in the retrosplenial cortex , a part of the brain located in the posterior region of the cerebral cortex (i.e., the outermost layer of the mammalian brain).

Researchers, in their experiments,   found that a single dose of psilocybin altered cortical ensemble turnover and oppositely modulated fear- and extinction-active neurons. Suppression of fear-active neurons and recruitment of extinction-active neurons predicted psilocybin-enhanced fear extinction.

These results suggested that psilocybin enhances behavioral flexibility by recruiting new neuronal populations and suppressing fear-active populations in the retrosplenial cortex.

Sophie A. Rogers et al, Psilocybin-enhanced fear extinction linked to bidirectional modulation of cortical ensembles, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-01964-9.

Comment by Dr. Krishna Kumari Challa yesterday

Next, to test mitochondrial transfer from neurons to cancer cells, the team engineered neurons to express mitochondria tagged with fluorescent markers with a novel tracking system called MitoTRACER. The system allowed researchers to monitor cancer cells after mitochondrial transfer, enabling detailed tracing of their fate during disease progression.

Direct mitochondrial transfer was observed via tunneling nanotubes, initiated by neurons towards the cancer cells. Rho-zero cancer cells regained oxidative phosphorylation and uridine-independent growth after acquiring neuronal mitochondria, confirming functional rescue.

MitoTRACER revealed that recipient cancer cells displayed enhanced respiration, higher ATP, improved redox balance, and greater resistance to oxidative and mechanical stress.

In animal models, these labeled recipient cells were significantly enriched in metastases, especially in the brain and liver, indicating that neuronal mitochondria confer a selective advantage during dissemination.

Together, these two experimental arms show that nerves both sustain tumor energetics broadly and act as direct donors of functional mitochondria, a dual mechanism that promotes cancer survival and spread.
Denervation experiments established that disrupting nerve input deprives cancer cells of essential bioenergetic capacity, reducing their invasiveness. Cancer cells that had received neuronal mitochondria more readily survived metastatic stressors such as oxidative damage and mechanical shear forces, common hurdles faced during cancer dissemination.

Gregory Hoover et al, Nerve-to-cancer transfer of mitochondria during cancer metastasis, Nature (2025). DOI: 10.1038/s41586-025-09176-8

Part 2

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Comment by Dr. Krishna Kumari Challa yesterday

Neurons duped into delivering mitochondria to cancer cells found fueling tumor spread

Researchers report that neurons can transfer mitochondria directly to cancer cells, enhancing their metastatic potential.

Oncologists have long suspected that tumors thrive partly by enlisting help from surrounding nerves. Pathologists studying cancer tissues have observed that tumors nestled among dense networks of nerves often grow faster and spread farther. Previous rodent and human studies demonstrated that cutting off this neural input slowed cancer growth.

Intercellular mitochondrial transfer is a recognized cellular rescue attempt where healthy donor cells revive compromised recipients by donating functional mitochondria. 

In the study, "Nerve-to-cancer transfer of mitochondria during cancer metastasis," published in Nature, researchers employed murine breast cancer models and advanced lineage-tracing reporters to test whether neurons confer metabolic assets to tumor cells via mitochondrial transfer.

Researchers performed chemical denervation by injecting botulinum neurotoxin A (BoNT/A) around breast tumors in mice. Denervation refers to the deliberate interruption of nerve supply to a tumor to chemically disable local nerve function.

The team then compared these denervated tumors to saline-injected controls using transcriptomic profiling, histopathology, and measurements of mitochondrial content.

Denervated tumors showed a marked reduction in mitochondrial load, downregulation of metabolic gene pathways (notably the tricarboxylic acid cycle), and significantly lower incidence of invasive lesions (from 55% in controls to 12% in denervated mice). These findings demonstrate that nerve inputs actively sustain tumor bioenergetics and promote progression.

part 1

Comment by Dr. Krishna Kumari Challa yesterday

This research provides a novel twist on prior studies of the effects of high-altitude living. Prior studies have mostly focused on adaptation by gaining new functions or traits to cope with harsh environments, while this study shows that animals can also lose certain abilities. These understudied mechanisms of maladaptation and trait loss may have future implications for evolutionary biology and medicine.

 Allie M. Graham et al, Convergent reduction of olfactory genes and olfactory bulb size in mammalian species at altitude, Current Biology (2025). DOI: 10.1016/j.cub.2025.05.061

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Animals living at higher elevations found to have decreased sense of smell

A recent study published in Current Biology has found that animals living at elevations of 1,000 meters and higher have a reduction in genes related to smell and a smaller olfactory bulb than similar low-altitude species.

The researchers screened the genomes of 27 different species of animals living in high-altitude environments, as well as their low-altitude relatives. A wide range of mammal types was studied, including monkeys, goats, llamas and guinea pigs. Both domesticated and wild mammals were included.

Scientists found a 23% reduction in genes related to smell and an average of an 18% size reduction of the olfactory bulb, a kind of smell processing center located in the brain. These evolutionary changes appear to be specific to smell. No changes were found in the genes related to pheromone and taste detection.

Environmental differences at high altitudes include thinner, drier and colder air, which can lead to difficulties in breathing, increased nasal congestion and hypoxia—low levels of oxygen in the body. These conditions also make it harder for scent molecules to travel—meaning there are fewer available scents for animals to detect in the air.

Although the exact mechanism is still unclear, the reduced sense of smell may be related to the reduction of available scents and to nasal inflammation, which causes additional difficulties in picking up scents. Over time, these issues may have led to mountain-dwelling animals evolving a worse sense of smell, but possibly compensating with better  other senses.

The study also compared the genomes of human communities at high and low altitudes. Researchers studied the genomes of Tibetans, who were estimated to have established their mountain-dwelling communities at altitudes above 3,000 meters sometime between 9,000 and 30,000 years ago. These were compared with the genomes of the low-altitude Han Chinese populations.

Interestingly, no olfactory changes were found in human populations. Researchers posit that this may be due to the continued mixing of lowland and highland populations, or because there may not have been enough generations for the genetic changes to occur yet.

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