Exosomes, a subset of extracellular vesicles (EVs), can be visualized as messages and packages that cells send to one another. Along with lifespan studies, EVs have been investigated for their ability to treat liver fibrosis, and they have been identified as potential biomarkers of disease [1].
Cirrhosis, hepatitis infection and other causes can trigger liver fibrosis—a potentially lethal stiffening of tissue that, once begun, is irreversible. For many patients, a liver transplant is their only hope. However, research at Cedars-Sinai in Los Angeles may offer patients a glimmer of hope. Scientists there say they’ve successfully reversed liver fibrosis in mice.
Reporting in the journal Nature Communications, the team say they’ve discovered a genetic pathway that, if blocked, might bring fibrosis to a halt.
The three genes involved in this fibrotic process are called FOXM1, MAT2A and MAT2B.
Discovery advances development of new therapeutic options for cancer and other diseases. A research team led by the University of California, Irvine has engineered an efficient new enzyme that can produce a synthetic genetic material called threose nucleic acid. The ability to synthesize artificial chains of TNA, which is inherently more stable than DNA, advances the discovery of potentially more powerful, precise therapeutic options to treat cancer and autoimmune, metabolic and infectious diseases.
A paper recently published in Nature Catalysis describes how the team created an enzyme called 10–92 that achieves faithful and fast TNA synthesis, overcoming key challenges in previous enzyme design strategies.
Inching ever closer to the capability of natural DNA synthesis, the 10–92 TNA polymerase facilitates the development of future TNA drugs.
A new method developed by Penn State biologists allows them to turn stripped-down plant cells into other types of cells, similar to the way stem cells differentiate into different cell types. Using this method, the research team explored the banding patterns that increase the stability of plant cell walls—much like the corrugated patterns in cardboard—and how they are created. Additionally, the researchers revealed how the assembly of these structures can go astray in different mutant plant cells, which they said could ultimately inform methods to break down plant cells for biofuels.
EngineAI’s SE01 humanoid robot redefines robotics with its smooth, human-like movement powered by advanced AI neural networks, showcasing a new level of realism in robotic technology. Clone Robotics pushes the boundaries further, creating a lifelike torso with synthetic muscles and joints that replicate the human musculoskeletal system, setting a new standard in AI-driven, realistic robotics. These innovations from EngineAI and Clone Robotics are transforming the future of humanoid robots, bringing AI and robotics closer to lifelike androids capable of human-like behavior, movement, and dexterity.
🔍 Key Topics Covered: EngineAI’s groundbreaking humanoid robot, SE01, with AI-driven natural movement that mimics human gait. Clone Robotics’ advanced torso robot, featuring synthetic muscles and joints for lifelike movement. Real-world applications and implications for humanoid robots in industries, education, and daily life.
🎥 What You’ll Learn: How EngineAI achieved smooth, human-like movement in SE01 through a unique neural network approach. Clone Robotics’ development of a lifelike torso that mirrors the human musculoskeletal structure. The future of humanoid robots as they move beyond warehouses, with potential roles in schools, hospitals, and even homes.
“This research marks the first time that we have been able to identify a specific chemical change that is unique to the development of Huntington’s disease, which opens the possibility of developing new tests to study the early changes of the disease before irreversible damage occurs.”
U.K. and German researchers are hopeful that their discovery of a key biochemical change involved in the development of Huntington’s disease could lead to its early detection and treatment.
Alzheimer’s disease, fronto temporal dementia and progressive supra nuclear palsy. Using this study design, the investigators found four genes that marked vulnerable neurons across all three disorders, highlighting pathways that could be used to develop new therapeutic approaches.
The discovery of genes that marked vulnerable neurons could open options for therapeutic approaches.
At some point in your life, you must’ve experienced a lightbulb moment when an amazing idea just popped into your head out of nowhere. But what is your brain doing during these brief periods of creativity?
Researchers from the University of Utah Health and Baylor College of Medicine looked into the origin of creative thinking in the brain. They found that different parts of the brain work together to produce creative ideas, not just one particular area.
“Unlike motor function or vision, they’re not dependent on one specific location in the brain,” Ben Shofty, the senior author of the study and an assistant professor of neurosurgery at the Spencer Fox Eccles School of Medicine, said. “There’s not a creativity cortex.”
