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Comment by Dr. Krishna Kumari Challa 15 hours ago

Duct tape kept out more floodwater than sandbags in laboratory tests
In laboratory tests, exterior duct tape reduced water leakage through household doors by 97%–98%, compared with a maximum reduction of 70% for sandbags with plastic sheeting. Tape offers temporary protection at door gaps but cannot prevent entry through other routes or replace property-specific flood protection.

https://zenodo.org/records/23220942

original article.

Comment by Dr. Krishna Kumari Challa 15 hours ago

As healthy cells divide, they accumulate subtle genetic marks that act like a cellular record of their history. By examining normal tissues from both twins alongside placental samples, researchers can unlock these genetic clues to retrace the earliest cell divisions and uncover how the embryo split to form identical twins.

In this study, the researchers used a genetic method called DNA lineage tracing, which essentially builds an evolutionary family tree for the cells of both twins, their tumors, and the placenta.

The team collected 23 normal tissue samples—six from each twin and 11 from the placenta—and 10 tumor samples from both twins. They then performed high-depth whole-genome sequencing on all samples to map complete DNA sequences, along with RNA sequencing to verify the specific gene fusion driving the sarcoma.

To trace the cancer's evolution, researchers sorted 212 tumour mutations into 13 distinct genetic clusters, revealing the steady pace at which mutations accumulated in the cells.
It spread from A to B
Every tumor sample from both children carried Twin A's distinctive genetic signature, revealing that the soft-tissue sarcoma originated in Twin A before crossing the placenta to Twin B. The genetic evidence pointed to a single transfer of cancer cells, suggesting that this kind of transmission between twins before birth is extremely rare.

In addition, the researchers uncovered evidence of blood-cell exchange during pregnancy, with about 75% of the cells in Twin A's spleen originating from Twin B.

The findings also raised questions about how identical twins begin to form. The traditional view is that twins sharing a placenta develop when an embryo splits around day six after conception, at the blastocyst stage, when it contains roughly 100 cells. The twins, however, shared only one early mutation, while each carried distinct genetic labels. This pointed to a much earlier split, possibly when the embryo contained as few as four cells.

The sequencing also revealed that early embryonic cells contributed unevenly to the placenta and the two twins, with each twin arising almost entirely from a different set of early cell lineages.
The researchers note that this study does more than follow a cancer's path through the womb. It offers a powerful way to reconstruct the earliest moments of life, from a single fertilized egg to the point where two separate twins take shape.

Barbara Walkowiak et al., Embryonic origin of cancer in newborn twins, Nature Communications (2026). DOI: 10.1038/s41467-026-78178-5

Part 2

Comment by Dr. Krishna Kumari Challa 15 hours ago

A rare cancer spread between twins before birth

Two identical sisters came into the world carrying the same rare cancer. They lost their lives to an undifferentiated sarcoma, a soft-tissue cancer driven by a unique gene fusion (MN1::ZNF341). The story began before they were born, when pregnancy imaging picked up a tumor on Twin A's face. Then came the birth, when cancer deposits were found in both Twin A and Twin B. Researchers now had to work out how the cancer reached both girls. Did the cancer start on its own in each sister, or did it begin in one and pass to the other while they were still in the womb?

The researchers sequenced the entire genetic code of healthy and tumor tissues, along with placental samples, to trace the cancer's journey between the twins. All tumor samples from both twins carried a distinctive genetic signature belonging to Twin A.

The cancer likely began as a facial tumor in Twin A at the end of the first trimester, which was visible on scans before birth. The cancer then crossed the placenta to reach Twin B late in the second trimester.

Beyond tracing the cancer's spread, the findings challenged the classical model of how identical twins develop from an early embryo. These findings are published in Nature Communications.

Identical twins share the same starting point, developing from a single fertilized egg, but it is extremely unusual for both to develop the same cancer. This can happen if each twin develops a tumor independently, particularly when both carry an inherited cancer-causing mutation. In rarer cases, cancer cells from one twin can cross the placenta and establish a tumour in the other while they are still in the womb.

Part 1

Comment by Dr. Krishna Kumari Challa 15 hours ago

AI designs working molecular scissors that recognize and cut selected protein targets
Proteases are naturally occurring enzymes that break down proteins into peptides and even single amino acids. They are useful in medicine and industrial processes, where they clean tissue, digest waste and help in the manufacture of everyday products. Now scientists have used artificial intelligence to design new versions from scratch.
AI tools have already successfully generated new protein shapes and structures, but using AI to create functional proteases is a significant leap forward. That's because the resulting enzyme has to both recognize a chosen protein sequence and cut it efficiently.

To see if it could be done, researchers combined several advanced artificial intelligence tools to create both cysteine and zinc proteases.

First, they used a version of RFdiffusion2 called RFD2-MI to design the 3D shape and core backbones of the proteins. Next, they applied ProteinMPNN and a related program called EnhancedMPNN to select the amino acid sequences needed to build the enzymes and their targets, helping them fit together correctly.

To find options that actually worked, the researchers repeated this process dozens of times for both types of protease. They then used AlphaFold 3 to predict the final shape of these digital versions of proteins and check how closely they matched the intended designs.

With that done, it was time to test the designs. That involved using bacteria to produce a single, long protein chain that linked the candidate enzyme to its intended target sequence and a glowing marker protein.

The team tested 69 versions of the cysteine protease and 135 of the zinc protease. An enzyme design would be deemed workable if it chopped the target sequence and set the marker free.

So how well did they do?

Their findings on cysteine proteases and zinc proteases are detailed in two papers published in Nature.

Out of the 69 cysteine protease candidates, 13 successfully cut their targets. The zinc protease designs performed even better, with 36% of the 135 candidates cutting their matching peptide targets.

The scientists then used AI to refine the most promising options further. This boosted the cutting speed of the top zinc protease by 30 times. It also led to the design of a cysteine protease that cut its target at precisely the intended site.
As well as demonstrating proof of concept, some of the engineered enzymes showed therapeutic promise. For example, one of the AI-designed proteases successfully cut full-length TDP-43, a protein that builds up abnormally in ALS, the most common type of motor neuron disease, and some types of dementia.

Other customized versions chopped targeted fragments of amyloid-beta, which is linked to Alzheimer's disease, and serum amyloid A, which is associated with severe organ damage in systemic amyloidosis conditions.

Although the enzymes have not yet been tested in human clinical trials, the study authors think using AI to design proteases could open up new possibilities in medicine, biotechnology and industrial chemistry.

Anqi Chen et al., Computational design of metalloproteases, Nature (2026). DOI: 10.1038/s41586-026-11167-2

Hojae Choi et al., De novo design of cysteine proteases, Nature (2026). DOI: 10.1038/s41586-026-11143-w

Comment by Dr. Krishna Kumari Challa yesterday

Skin has a gender: Females and males do not renew their skin in the same way

Researchers have discovered that in females skin cells renew the skin in a more coordinated way than in males. This difference, controlled by sex hormones, goes hand in hand with faster wound healing in female mice. This research could eventually pave the way for personalized treatments taking into account patients' sex.

For a long time, differences between females and males were mainly associated with the reproductive organs. Yet organs that have nothing to do with reproduction, such as the skin, can also be shaped by sex. This question, essential for better preventing and treating inflammatory diseases and cancer, has long been underestimated by some in the scientific community.
The researchers also observed that a wound on the skin of the back closes markedly faster in female mice, especially during the first few days. This head start is partly explained by an earlier activation of stem cells, which also work in a more coordinated way. The gap then narrows as the wound closes.
In mice, female skin stem cells showed greater coordination and earlier activation during wound healing, accompanying faster wound closure than in males. Estrogens promoted stem cell proliferation and coordination, while androgens accelerated differentiation. Testosterone also accelerated differentiation in laboratory-reconstructed human skin.

Dan Engelman et al., Sexual dimorphism in epidermal stem cell dynamics, Nature (2026). DOI: 10.1038/s41586-026-11159-2

Comment by Dr. Krishna Kumari Challa yesterday

A new Fingerprint authentication uses ultrasound without storing biometric information as digital data

A research team has developed a new biometric authentication technology that can identify users without storing their fingerprint information as digital data. The study is published in Nature Sensors.
Fingerprint recognition is widely used in everyday applications, from unlocking smartphones to financial transactions and access control. Unlike passwords, however, fingerprints cannot easily be changed once compromised.

Conventional biometric authentication systems first convert a fingerprint into digital data and then compare it with previously stored fingerprint information. Even when the stored information is encrypted, the authentication process still requires access to biometric data, leaving potential security vulnerabilities.
Instead of sending fingerprint data to a computer for analysis, the system completes the required computation through the physical interaction between ultrasound and the fingerprint.

To achieve this, the team proposed a metasurface-driven loop-diffractive neural network, or loop-DNN. A metasurface is an artificial structure capable of precisely controlling the direction, intensity and phase of ultrasound and, in this study, functions similarly to elements in an artificial neural network.

The researchers designed the system so that ultrasound passing through the metasurface is directed to different locations depending on the fingerprint.

When a registered fingerprint is presented, the acoustic energy is concentrated in a "registered" region, whereas an unregistered fingerprint directs the energy toward a "non-registered" region. Authentication can therefore be determined simply by comparing the signal intensities in the two regions, without reconstructing a fingerprint image or extracting fingerprint features through separate digital computation.
The researchers further controlled the phase, amplitude and switch states of the ultrasound, allowing a single metasurface to process fingerprint information with expanded degrees of freedom for wave manipulation.

An ultrasound metasurface authenticated fingerprints through physical wave processing without storing digital fingerprint data. Accuracy was 97.92% across 192 samples from four people; numerical analysis reached 99.75% for one registered user. Practical use requires miniaturization to MHz frequencies and support for multiple registered users.

Seokho Lee et al., All-wave computational ultrasonic fingerprint identification with metasurface-driven loop-diffractive neural network, Nature Sensors (2026). DOI: 10.1038/s44460-026-00102-7

Comment by Dr. Krishna Kumari Challa yesterday

Fine particles from aircraft exhaust become more harmful over time, lab tests suggest

Fine particulate matter consists of tiny particles with diameters in the nanometer range. They are produced, for example, by fuel combustion, remain suspended in the air and can penetrate deep into the respiratory tract. There, they can trigger oxidative stress, a process that promotes inflammation and, over the long term, can lead to serious health problems such as respiratory or cardiovascular diseases. Scientists call this harmful property the particles' oxidative potential.
However, fine particles usually remain in the atmosphere for hours or even several days before people inhale them. Little is known about how these particles' harmful properties change over time. A research team investigated how the oxidative potential, and thus the toxicity, of fine particles emitted by a small aircraft jet engine and a marine diesel engine develops over time.
Simulated atmospheric aging over 1–12 days significantly increased the oxidative potential of aircraft exhaust particles, while marine diesel particles remained largely unchanged. Chemical changes during aging indicate that fresh emissions alone may not capture particles’ potential health hazards.
The World Health Organization estimates that more than 7 million premature deaths occur annually due to exposure to high concentrations of air pollution particles—more than twice the number of global deaths from AIDS, malaria and tuberculosis combined.

Alexandre Barth et al., Online characterisation of oxidative potential and reactive oxygen species of fresh and aged aircraft turbine and ship engine particulate emissions, Environmental Science: Atmospheres (2026). DOI: 10.1039/d5ea00174a

Comment by Dr. Krishna Kumari Challa yesterday

Intensive blood pressure control protects the heart—with no added kidney failure risk detected

High blood pressure forces the heart to work harder to pump blood. Over time, this extra strain can thicken the heart muscle and narrow the arteries, further complicating cardiovascular health. Even in people with no other health conditions, a 20 mmHg rise in blood pressure doubles the risk of dying from heart disease.
Lowering high blood pressure protects the heart and blood vessels, but how low should it go? Doctors have long debated whether more aggressive targets, such as a systolic blood pressure below 120 or 130 mmHg, offer additional protection or cause harm, particularly in people with chronic kidney disease (CKD).

A recent meta-analysis screened multiple prior clinical trials to assess the effects of intensive blood pressure lowering (below 120 or 130 mmHg) versus standard blood pressure targets (below 140 mmHg).

Across the trials, intensive treatment reduced major cardiovascular events by 15% for each 10 mmHg reduction in systolic pressure in adults with or without chronic kidney disease. While the treatment did not increase the risk of kidney failure compared with standard treatment, it did make temporary or mild declines in eGFR more likely. This measure, based on a blood test, indicates how well the kidneys filter waste from the blood.

Fotini Iatridi et al., Intensive vs Standard Blood Pressure Lowering in People With and Without Chronic Kidney Disease, JAMA Cardiology (2026). DOI: 10.1001/jamacardio.2026.4445

Comment by Dr. Krishna Kumari Challa yesterday

Female rats, however, proved more resilient. Despite gut inflammation, their neurons retained their structure, membrane integrity and normal electrical signaling. They adapted at a molecular level by selectively increasing calcium ion channel levels, which protected against damage.

In rats given daily oral creatine, hippocampal creatine concentrations increased by 20%–30%, reaching normal levels in both sexes. In males, creatine prevented structural neuron loss, stopped electrical membrane leaks and normalized the neuron firing threshold.

Creatine selectively repaired colitis-altered parameters without disrupting normal, healthy brain functions. Before creatine can be recommended as a brain supplement.

Alejandro Ruiz-Calero et al., Modulating effects of creatine prevent sex-dependent hippocampal neuroinflammation, neuronal damage, and electrophysiological dysfunction induced by chronic colitis, Brain, Behavior, and Immunity (2026). DOI: 10.1016/j.bbi.2026.106929

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

 Creatine may help shield the brain from damage linked to gut inflammation

The gut-brain axis is a two-way biochemical hotline, with messages zipping back and forth all day long. When the gut is chronically inflamed, inflammatory signals travel through the body to the brain and trigger neuroinflammation. The hippocampus, which governs memory, learning and mood, is especially vulnerable, so its disruption can affect how you think, remember and feel.

A recent study published in Brain, Behaviour, and Immunity investigated how chronic ulcerative colitis, a type of inflammatory bowel disease, impacts the brain and whether oral intake of creatine, a popular supplement in sports nutrition, can protect against brain damage. The researchers chemically induced chronic colitis in rats and observed their recovery with or without creatine. The creatine group received the supplement in drinking water, starting 10 days before colitis induction and continuing throughout the experiment.

Chronic colitis fueled inflammation in the hippocampus and activated immune cells in the brain in both sexes, but males took a harder hit. They showed greater hippocampal inflammation, along with clear neuronal damage and impaired neuronal activation. Daily oral creatine supplementation brought energy stores back to normal control levels. It also prevented the rise in inflammatory cytokines and stopped activation of brain immune cells in both sexes.

Inflammatory bowel disease such as ulcerative colitis is primarily a gastrointestinal disorder, but many patients living with this condition also experience neurological problems like mood disorders, cognitive difficulties and memory issues. Due to the gut-brain axis, inflammatory molecules such as cytokines released in the gut enter the bloodstream and cross into the brain. These chemicals then activate brain immune cells (microglia), triggering neuroinflammation.

Brain cells need huge amounts of energy in the form of ATP to survive and function, but chronic gut inflammation can leave the hippocampus struggling to meet those energy demands. Creatine, an organic compound the body naturally makes from amino acids, acts like a rapid-recharging battery, creating an energy buffer that quickly restores cellular ATP and helps brain cells survive inflammatory stress.

The experiments revealed a clear sex difference in how hippocampal nerve cells, known as CA1 pyramidal neurons, responded to gut inflammation. Male rats suffered structural damage and neuronal loss, reflected in reduced levels of proteins that help maintain neurons. Their surviving nerve cells also became electrically leaky and harder to activate, requiring stronger currents to fire electrical signals.

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