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Meet The Axolotl — The Salamander That Can Regrow Its Own Brain

But over evolutionary time, mammals have obviously lost the vast majority of this regenerative capacity. Instead, evolution opted for faster wound sealing, stronger immune responses and more stable neural systems in mammals. This is likely because surviving injury would have mattered more than perfectly reconstructing tissue months later.

Salamanders, on the other hand, have retained far more of this ancestral regenerative toolkit. Their ecology may have reinforced this retention, since small amphibians are especially vulnerable to predation and environmental injury. Limbs, tails and nervous tissue can be damaged surprisingly easily in aquatic habitats filled with predators, debris, and competition. For an animal living close to the edge of survival, the ability to recover from catastrophic injury could dramatically improve reproductive success.

The axolotl’s strange life history has most probably also enabled this unique ability. Unlike many amphibians, axolotls remain in a juvenile-like aquatic state throughout adulthood, a phenomenon known as “neoteny.” Intriguingly, juvenile tissues in many vertebrates tend to be more regenerative than adult tissues. Thus, by retaining aspects of its developmental state for life, the axolotl may preserve cellular programs that would otherwise be “switched off” after maturation.

New recyclable protein textiles could cut microplastic pollution and lower clothing waste

The textile industry produces a substantial portion of the world’s waste, with only about 12% of fiber materials ending up in recycling. Textiles also account for much of the microplastics in oceans. During every wash cycle, synthetic fibers shed microplastics that are flushed down the drain and eventually enter aquatic environments. Increasing textile recycling alone won’t solve this problem because most petrochemical-based fibers are difficult to recycle and continue to release persistent microplastics throughout their life cycle.

Engineers from Washington University in St. Louis may have a solution, thanks to dedicated synthetic biology work in the lab of Fuzhong Zhang, the Francis F. Ahmann Professor in the Department of Energy, Environmental & Chemical Engineering in the McKelvey School of Engineering and co-director of Synthetic Biology Manufacturing of Advanced Materials Research Center (SMARC).

The results of that work, now published in the journal Advanced Materials, created protein-based materials, which are produced in bioreactors (think giant brewing tanks) using genetically engineered microbes. These materials can be readily recycled after use and remade into the same fibers over multiple cycles. In addition, any microparticles, if released from these fibers during washing, would be biodegradable.

Hidden small RNA in cholera bacterium helps determine whether it can infect humans

Scientists from St. Jude Children’s Research Hospital have uncovered what gives Vibrio cholerae, the bacterium that causes cholera, the ability to colonize the human gut. The researchers found that a small RNA embedded within another gene controls where cholera thrives, a discovery that could improve prediction and prevention strategies. The study is published in the journal Nature Communications.

Infectious diseases remain the leading cause of pediatric mortality worldwide. V. cholerae causes a severe diarrheal disease leading to more than 143,000 deaths and millions of cases each year, primarily affecting young children. While there are many strains of the V. cholerae species, only one can infect humans. The reason for this has been unclear for 50 years, hampering efforts to predict and prevent outbreaks.

“For decades, we’ve been trying to understand what allows cholera to infect humans,” said corresponding author Salvador Almagro-Moreno, Ph.D., St. Jude Department of Host-Microbe Interactions. “The answer was right in front of us the whole time—this small RNA hiding inside another gene is the real culprit.”

Scientists discover tiny gut particles that may drive aging and chronic disease

A new study suggests microscopic particles from the gut may actively drive inflammation and chronic diseases associated with aging. Remarkably, gut particles from young animals appeared to counter some aging-related damage in older animals, hinting at new possibilities for future treatments.

Scientists Build a Living Computing Device Using Real Brain Cells

Princeton researchers have built a 3D device that combines living brain cells with advanced electronics in one system.

The device uses computational methods to recognize electrical patterns and may help researchers study brain function, neurological disease, and low-power computing.

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Scientists restore memory by blocking a single Alzheimer’s protein

Researchers have identified a new potential weapon against Alzheimer’s: blocking a protein called PTP1B. In mice, this approach boosted memory and helped brain immune cells clear harmful plaque buildup. Since PTP1B is also linked to diabetes and obesity—both risk factors for Alzheimer’s—it could offer a broader treatment strategy.

How lungs balance defense and damage by tuning responses to deeper threats

Barrier organs that form boundaries between the body and the outside environment, such as the lungs, skin, and intestines, face a difficult balancing act. They must respond quickly to threats such as infection, but they also need to avoid triggering unnecessary inflammation that can damage the tissue. A new study led by Whitehead Institute member Pulin Li and graduate student in her lab Diep Nguyen reveals one way the lung manages that tradeoff.

Published in Cell Systems, the research found that immune sensitivity is not evenly distributed across the lung. Instead, it arranges in tiers: cells at the outer surface respond cautiously, while cells deeper in the tissue are more likely to sound the alarm when a threat breaks through.

“The central question was how tissues balance the benefits and harmful effects of immune activation when they face different degrees of danger or stress,” says Li, who is also a professor of biology at MIT. “Too little immune activation leaves the tissue unprotected, but too much can create inflammation and damage.”

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