Comment

Comment by Dr. Krishna Kumari Challa 13 hours ago

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 15 hours ago

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 15 hours ago

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 15 hours ago

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 16 hours ago

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 16 hours ago

 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.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Partial Vision Restored in Some Blind Patients With New Experimental Treatment
Night vision often fades first, followed by a narrowing of peripheral vision. In retinitis pigmentosa, this progressive loss can eventually lead to blindness.

An experimental treatment has now helped some patients recover limited visual abilities.

The approach combines a gene injection with special goggles. In a small trial involving 10 people with profound vision loss in both eyes, some participants became better able to detect objects, locate them, and reach toward them while using the device.
--
Retinitis pigmentosa is a group of inherited disorders in which genetic changes damage the retina's photoreceptors, the cells that normally detect light.

Symptoms can begin in childhood or later, and progression varies. People without known affected relatives can also develop the disease.

Variants in more than 100 genes can cause it, complicating efforts to develop treatments for each genetic cause. This approach, called optogenetic therapy, gives nerve cells that survive the disease a new way to respond to light.

Each participant received one injection into their worse-seeing eye. A modified virus delivered instructions for producing a light-sensitive protein called ChrimsonR into retinal ganglion cells, the nerve cells that transmit visual signals toward the brain.

The gene therapy delivers a light sensor to the blind retina, making it light-sensitive again. The goggles provide light stimulation at the wavelength to which this sensor responds.
A camera in the goggles captures changes in brightness. A processor turns those changes into patterns of amber light, which a projector directs onto the retina to activate the protein.
In addition, the goggles adapt to outside light conditions and modify the signal to ensure optimal stimulation of the retina.
Participants practiced using the goggles. During visual tests, their untreated eye was covered.

The trial primarily assessed safety, but researchers also examined light sensitivity and object detection.

They measured the dimmest light participants could detect through the goggles before and after treatment. Seven showed increased sensitivity, ranging from about twofold to 62-fold. Six reached roughly a fourfold increase or more, which the team considered clinically meaningful.
Differences between patients in the increase in sensitivity may reflect how well the gene therapy vector reaches the retinal cells, or how many retinal cells remain, or other variables such as training to wear the goggles.
Brain recordings from five selected participants supported the possibility that visual signals reached the brain. Four had already responded in behavioural tests. For some estimates, the confidence interval included zero.

https://www.nejm.org/doi/10.1056/NEJMoa2602215

**

Comment by Dr. Krishna Kumari Challa yesterday

Why butterflies are so hard to catch

Butterflies are incredibly evasive insects, with no predators that specialize in hunting them as they fly. Why this is has been a bit of a mystery, but now new research suggests that the patterns on their wings create optical illusions to mislead predators. This finding not only explains butterflies nimble dodging, but may also help researchers understand why many animals have stripes and patterns.

Comment by Dr. Krishna Kumari Challa yesterday

Introduced species aren't good or bad—they are labeled according to human interests
Animal classifications in Australia reflect human interests as well as ecological impacts. Introduced species can harm biodiversity, but valued livestock also cause damage, and native species can become invasive outside their bioregions. Context-specific management is proposed as an alternative to treating species as inherently good or bad.

original article.

Comment by Dr. Krishna Kumari Challa yesterday

Sustained pressure halts cancer cell migration and triggers death in 3D lab models

In 3D models, sustained mechanical confinement halted migration and induced death in cancer cells undergoing the mesenchymal-to-amoeboid transition. Physical pressure activated MLKL-mediated necroptosis, linking mechanical stress to programmed cell death.

Long-term confinement triggers RIPK3-independent necroptosis in amoeboid cancer cells to shape tumor evolution, Developmental Cell (2026). DOI: 10.1016/j.devcel.2026.09.003

• ‹ Previous
• 1
• 2
• 3
• …
• 1306
• Next ›
• Page