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Category: biotech/medical – Page 87

Pathophysiology of irritable bowel syndrome

Despite the continued absence of a definitive biomarker for irritable bowel syndrome (IBS), research over the last three decades has identified a wide range of underlying pathophysiological abnormalities. Peripheral mechanisms include gastrointestinal infection, changes in the gut microbiome, visceral hypersensitivity, increased intestinal permeability, low-grade mucosal inflammation and altered immune function, abnormal gastrointestinal motility, and the role of serotonin, bile acid metabolism, and carbohydrate metabolism.

Scientists identify new mitochondrial pathway linked to harmful inflammation in aging

ROCHESTER, Minn. — Researchers have uncovered a previously unknown mechanism that helps aging cells drive the chronic inflammation linked to many age-related diseases. The findings reveal how dysfunctional mitochondria — the cell’s energy-producing structures — work with the cell’s epigenetic machinery to switch on inflammatory genes, opening the door to a new therapeutic approach for

JCI: Centre for Immuno-Oncology, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom

2 Chinese Academy of Medical Sciences Oxford Institute, Oxford, United Kingdom.

3State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, NHC Key Laboratory of AIDS Prevention and Treatment, National Clinical Research Center for Laboratory Medicine, The First Hospital of China Medical University, China Medical University, Shenyang, China.

Scientists find a simple way to stop cavities without drilling

A liquid brushed onto cavities in seconds may spare many young children from pain, infection, and surgery. A major U.S. trial found that silver diamine fluoride stopped decay in more than half of treated baby teeth. The treatment requires no drilling, shots, or sedation, although it does permanently darken the decayed area.

Cell junction proteins regulate stem cell signaling and tissue homeostasis

In many animal tissues, stem cells continually divide to create new cells that replace old or damaged ones. However, this capacity requires strict regulation, as uncontrolled stem cell proliferation can disrupt tissue homeostasis and contribute to tumorigenesis.

Researchers at the National Institute for Physiological Sciences have identified a previously unknown mechanism that controls stem cell proliferation in the Drosophila intestine. The study reveals that smooth septate junction (sSJ) proteins, known for their role in cell-cell adhesion, also regulate signaling in differentiating intestinal progenitor cells to prevent excessive stem cell growth.

Spray-on coating traps particles more tightly and nearly doubles air filter lifespan

Breathing clean air is essential for human health, making air filters indispensable in homes, hospitals, workplaces and industrial settings. However, despite decades of advances in filter materials and design, a major challenge remains. Capturing airborne particles is only half the battle; keeping them securely trapped is equally important.

Conventional air filters rely on weak adhesive forces, allowing some captured particles to detach and re-enter the air. This reduces filtration efficiency, shortens filter lifespan and highlights the need for smarter, more durable air filtration technologies.

Cellular and signalling mechanisms that regulate the bloodbrain barrier Reviews Molecular Cell Biology

This Review summarizes the latest advances in blood–brain barrier (BBB) research, highlighting how emerging findings on the modulation of BBB function and heterogeneity by cellular interactions and signalling pathways might shape BBB-targeted therapeutics.

Inflammation may drive Dravet syndrome, offering a potential new treatment target

An overactive immune response in the brain may play a role in Dravet syndrome, a rare and severe genetic epilepsy that typically begins in infancy, according to Weill Cornell Medicine researchers. Children with the condition experience frequent seizures that are often difficult to control with medication and may also face developmental, cognitive and behavioral challenges. Until now, most research has focused on how a mutation in the SCN1A gene disrupts electrical signaling in the brain.

“Rather than being a disorder only involving abnormal electrical signaling, the disease may also involve a self-sustaining immune response triggered by DNA released from stressed neurons,” said study senior author Dr. Li Gan, the Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases and director of the Helen and Robert Appel Alzheimer’s Disease Research Institute at Weill Cornell. “As a result, inflammation may help drive and sustain the disease. This finding links seizures to the brain’s immune system in a way that had not been fully appreciated before.”

The new preclinical study, published July 29 in Nature Neuroscience, identified an inflammatory pathway called cGAS-STING-interferon (IFN-I) signaling as a major contributor to disease progression. Blocking this molecular pathway could lead to new therapeutic strategies for epilepsy disorders.

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