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Comment by Dr. Krishna Kumari Challa 10 hours ago

Burns and fireworks injuries: What to do when seconds count

This is what experts advice....

From a barbecue explosion to a severe firework injury, a lot can go wrong when celebrating.

When it does, minutes—even seconds—can significantly impact the extent of the injury. Although prevention is key,  response is also essential.

Alcohol impairs your reaction time. 

If a firework or sparkler injures an eye, immediately protect it from pressure or further trauma by placing a cup or makeshift device over it. Don't try to cover it with a towel or anything that touches the eye.

More than a third of firework burns are to the hands and fingers. Should a firework go off in your hand, wrap it in a clean towel and keep it covered until you get to the hospital.

If you catch on fire, from a firework, bonfire, barbecue or cooking incident,  immediately stop, drop and roll.

A lot of people like to run and jump in the water. That's not always the best thing. Unless you're standing on a dock or on the edge of a pool, those few seconds it's going to take you to run to the water, you're burning that whole time. It's much more effective to stop, drop, and roll.

Experts also advise against icing a burn, which can cause further damage.

You can run normal temperature water over it, and then if it's very serious, of course, call emergency ambulance or seek medical care.

If running water isn't accessible, a cool, wet cloth can be used as an alternative. However, once the initial pain subsides, you should replace the damp towel with a clean, dry cloth to prevent the burn from becoming infected.

Comment by Dr. Krishna Kumari Challa 11 hours ago

A single genetic mutation may have made humans more vulnerable to cancer than chimpanzees

New research has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This insight could lead to more powerful cancer treatments.

The study was published in Nature Communications. It revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates.

This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumor-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

The evolutionary mutation in FasL may have contributed to the larger brain size in humans. But in the context of cancer, it was an unfavorable trade-off because the mutation gives certain tumors a way to disarm parts of our immune system.

FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient's immune system, use apoptosis to kill cancer cells.
The UC Davis team discovered that in human genes, a single evolutionary amino acid change—serine instead of proline at position 153—makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons—FasL—can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

Brice E. N. Wamba et al, Evolutionary regulation of human Fas ligand (CD95L) by plasmin in solid cancer immunotherapy, Nature Communications (2025). DOI: 10.1038/s41467-025-60990-0

Comment by Dr. Krishna Kumari Challa 11 hours ago

New neurons continue to form in the adult human hippocampus: Study

A study in the journal Science presents compelling new evidence that neurons in the brain's memory center, the hippocampus, continue to form well into late adulthood. The research from Karolinska Institutet in Sweden provides answers to a fundamental and long-debated question about the human brain's adaptability.

The hippocampus is a brain region that is essential for learning and memory and involved in emotion regulation. Back in 2013, a research group showed in a high-profile study that new neurons can form in the hippocampus of adult humans. The researchers then measured carbon-14 levels in DNA from brain tissue, which made it possible to determine when the cells were formed.

In the new study, the researchers combined several advanced methods to examine brain tissue from people aged 0 to 78 years from several international biobanks. They used a method called single-nucleus RNA sequencing, which analyzes gene activity in individual cell nuclei, and flow cytometry to study cell properties. By combining this with machine learning, they were able to identify different stages of neuronal development, from stem cells to immature neurons, many of which were in the division phase.

To localize these cells, the researchers used two techniques that show where in the tissue different genes are active: RNAscope and Xenium. These methods confirmed that the newly formed cells were located in a specific area of the hippocampus called the dentate gyrus. This area is important for memory formation, learning and cognitive flexibility.

The results show that the progenitors of adult neurons are similar to those of mice, pigs and monkeys, but that there are some differences in which genes are active. There were also large variations between individuals—some adult humans had many neural progenitor cells, others hardly any at all.

This gives us an important piece of the puzzle in understanding how the human brain works and changes during life.

 Ionut Dumitru et al, Identification of proliferating neural progenitors in the adult human hippocampus, Science (2025). DOI: 10.1126/science.adu9575.

Comment by Dr. Krishna Kumari Challa 13 hours ago

This material emits infrared light better than it absorbs it, without violating the laws of physics

New results published in the journal Physical Review Letters detail how a specially designed metamaterial was able to tip the normally equal balance between thermal absorption and emission, enabling the material to better emit infrared light than absorb it.

At first glance, these findings appear to violate Kirchhoff's law of thermal radiation, which states that—under specific conditions—an object will absorb infrared light (absorptivity) in one direction and emit it (emissivity) with equal intensity in another, a phenomenon known as reciprocity.

Over the past decade, however, scientists have begun exploring theoretical designs that, under the right conditions, could allow materials to break reciprocity. Understanding how a material absorbs and emits infrared light (heat) is central to many fields of science and engineering. Controlling how a material absorbs and emits infrared light could pave the way for advances in solar energy harvesting, thermal cloaking devices, and other technologies.

Pioneering experiments conducted by a team of researchers in 2023 yielded tantalizing results. By using a single layer of the magneto-optical material indium arsenide (InAs) and subjecting it to a powerful magnetic field of about one tesla (slightly less powerful than an MRI machine but about 100,000 times more powerful than Earth's magnetic field), the team successfully achieved nonreciprocity. Though this confirmed theoretical predictions, the effect was weak and only operated under a very narrow set of conditions.

The newly reported design succeeded in doubling the effect seen previously, making it the first reported observation of "strong" nonreciprocal thermal emission.

To achieve this record-breaking result, researchers created a metamaterial made of five, 440-nanometer-thick layers of electron-doped indium gallium arsenide (InGaAs). The doping concentration increased as the depth increased. The InGaAs layers were then transferred to a silicon substrate.

The sample was then studied with a custom-designed angle-resolved magnetic thermal emission spectroscopy (ARMTES) set up, which heated the sample to 540 Kelvin (512 Fahrenheit) and subjected it to a 5 tesla magnetic field.

The researchers then measured the nonreciprocity of the material, demonstrating that it exhibited twice the effect previously reported. This effect persisted over a wide range of angles and a broad range of infrared wavelengths (from 13 to 23 microns).

This experiment for the first time realizes strong nonreciprocal emission, with nonreciprocity as high as 0.43, which is much higher than nonreciprocity in literature.

Zhenong Zhang et al, Observation of Strong Nonreciprocal Thermal Emission, Physical Review Letters (2025). DOI: 10.1103/PhysRevLett.135.016901

Comment by Dr. Krishna Kumari Challa 14 hours ago

This finding challenges the traditional view that invasive placenta cells are unique to humans, and reveals instead that they are a deeply conserved feature of mammalian evolution. During this time, the maternal cells weren't static, either. Placental mammals, but not marsupials, were found to have acquired new forms of hormone production, a pivotal step toward prolonged pregnancies and complex gestation, and a sign that the fetus and the mother could be driving each other's evolution.
To better understand how the fetal-maternal interface functions, the study tested two influential theories about the evolution of cellular communication between mother and fetus.

The first, the "Disambiguation Hypothesis," predicts that over evolutionary time, hormonal signals became clearly assigned to either the fetus or the mother—a possible safeguard to ensure clarity and prevent manipulation. The results confirmed this idea: certain signals, including WNT proteins, immune modulators, and steroid hormones, could be clearly traced back to one source tissue.
The second, the "Escalation Hypothesis" (or "genomic conflict"), suggests an evolutionary arms race between maternal and fetal genes—with, for example, the fetus boosting growth signals while the maternal side tries to dampen them. This pattern was observed in a small number of genes, notably IGF2, which regulates growth. On the whole, evidence pointed to fine-tuned cooperative signaling.

These findings suggest that evolution may have favored more coordination between mother and fetus than previously assumed.
The so-called mother-fetus power struggle appears to be limited to specific genetic regions and there absolutely isn't any conflict.

Daniel J. Stadtmauer et al, Cell type and cell signalling innovations underlying mammalian pregnancy, Nature Ecology & Evolution (2025). DOI: 10.1038/s41559-025-02748-x

Part 2

Comment by Dr. Krishna Kumari Challa 14 hours 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 yesterday

Food contact articles as source of micro- and nanoplastics

Comment by Dr. Krishna Kumari Challa yesterday

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 yesterday

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 yesterday

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

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