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Stopping fatal blood loss with clay

Traumatic injury is the third leading cause of death in the state of Texas, surpassing strokes, Alzheimer’s disease and diabetes, according to the Centers for Disease Control and Prevention. A massive number of these deaths are the result of uncontrolled bleeding. “Severe blood loss can rapidly lead to hemorrhagic shock,” said Dr. Akhilesh Gaharwar, a biomedical engineering professor at Texas A&M University. “Many patients die within one to two hours of injury. This critical period is often referred to as the ‘golden hour.’”

Gaharwar and his fellow researchers in the biomedical engineering department have found a way to extend this golden hour—using clay.

Gaharwar, Dr. Duncan Maitland and Dr. Taylor Ware are developing a suite of injectable hemostatic bandages —biomedical materials that stop bleeding and promote blood to clot faster. Their research is specifically targeting deep internal bleeding where traditional methods like compression are not possible.

Immunoglobulin A-producing cells mediate the clinical benefits of metformin via interleukin-10

Guo et al. show that metformin enhances intestinal IgA immunity via gut microbiota and increases gut antigen-specific IgA-producing IL-10+ cells in the liver and VAT. IL-10 from these cells mediates the clinical benefits of metformin.

Scientists find a mechanism showing how exercise protects the brain

Researchers at UC San Francisco have discovered a mechanism that could explain how exercise improves cognition by shoring up the brain’s protective barrier. With age, the network of blood vessels—called the blood–brain barrier—gets leaky, letting harmful compounds enter the brain. This causes inflammation, which is associated with cognitive decline and is seen in conditions like Alzheimer’s disease. The research is published in the journal Cell.

Six years ago, the team identified a brain-rejuvenating enzyme called GPLD1 that mice produced in their livers when they exercised. But they couldn’t understand how it worked, because it cannot get into the brain.

The new study answers that question. Researchers discovered that GPLD1 was working through another protein called TNAP. As the mice age, the cells that form the blood-brain barrier accumulate TNAP, which makes it leaky. But when mice exercise, their livers produce GPLD1. It travels to the vessels that surround the brain and trims TNAP off the cells.

Pop-up-style 3D electrode array captures organoid-wide brain rhythms in real time

A team led by Northwestern University and Shirley Ryan AbilityLab scientists have developed a new technology that can eavesdrop on the hidden electrical dialogues unfolding inside miniature, lab-grown human brain-like tissues. Known as human neural organoids—and sometimes called “mini brains”—these millimeter-sized structures are powerful models of brain development and disease. But until now, scientists could only record and stimulate activity from a small fraction of their neurons—missing network-wide dynamics that give rise to coordinated rhythms, information processing and the complex patterns of activity that define brain function.

For the first time, the new technology overcomes that stubborn limitation. The soft, three-dimensional (3D) electronic framework wraps around an organoid like a breathable, high-tech mesh. Rather than sampling select regions, it delivers near-complete, shape-conforming coverage with hundreds of miniaturized electrodes. That dense, three-dimensional interfacing enables scientists to map and manipulate neural activity across almost the entire organoid.

By moving from localized probing to true whole-network mapping, the work brings organoid research closer to capturing how real human brains develop, function and even fail.

Senescent cells after pregnancy may fuel postpartum breast cancer spread

Postpartum breast cancer is diagnosed five to ten years after giving birth. It is associated with a higher risk of metastasis and a lower survival rate compared with women who have not been pregnant or those diagnosed during pregnancy. A team from the Institut Pasteur set out to understand the mammary gland mechanisms involved in tumor formation during involution, a major tissue remodeling process that occurs after pregnancy.

In a preclinical study, the scientists revealed how senescence, a cellular response inducing stable cell cycle arrest, plays an ambivalent role during mammary gland involution. While it is crucial for the normal tissue remodeling process in the mammary gland, senescence can also be hijacked by tumor cells to help them spread. This discovery, published in Nature Aging on February 18, 2026, suggests that targeting senescent cells during mammary gland involution could reduce the risk of postpartum breast cancer.

How ADHD Stimulants

In a large US-based brain imaging study, researchers found that these drugs do not primarily affect attention networks, but instead act on systems linked to arousal, sleep, and motivation.

The puzzle of ADHD stimulants

Prescription stimulants such as methylphenidate and amphetamines are among the most used psychoactive drugs in children and adolescents with ADHD, where they remain a first-line treatment. Estimates for receiving a prescription for ADHD medication among diagnosed children vary from 38–81%. Despite their widespread use, there is still disagreement about how these drugs work in the brain.

Sjögren Syndrome Candidate Autoantigen AQP5 Triggers AQP4 CNS Autoimmunity Through Self-Antigen Mimicry

Tumor-immune-neural circuit in cancer cachexia.

The mechanisms involved in cancer-mediated cachexia and anorexia are not well understood.

The researchers in this study delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia.

The authors show thay loss of GDF15 protects against appetite loss, muscle wasting, and fat loss in pancreatic, lung, and skin cancers.

Disrupting this feedforward loop with GDF15-neutralizing antibody, anti-CSF1R antibody, or Rearranged during Transfection (RET) inhibitor alleviates cachexia and anorexia across cancer models. sciencenewshighlights ScienceMission https://sciencemission.com/Tumor-immune-neural-circuit


Shi et al. delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia. Specifically, tumor-derived CSF1 induces macrophage GDF15, which signals through the GFRAL-RET neural axis to enhance β-adrenergic activity and systemic wasting. Disrupting this feedforward loop alleviates cachexia across cancer models.

Did Life Begin in the Cold? New Experiments Point to an Icy Origin

Experiments reveal that unsaturated lipid membranes promote vesicle fusion and DNA retention during freeze–thaw cycles, highlighting icy environments as potential drivers of protocell evolution. Today’s cells are extraordinarily intricate. They contain internal scaffolding known as cytoskeletons.

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