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Vision is one of the most important human senses, yet more than 300 million people around the world are at risk of losing it due to various retinal diseases. Although recent treatments have helped slow the progression of these conditions, no effective therapy has been able to restore vision that has already been lost, until now. Researchers at KAIST have developed a new drug that successfully restores vision.

On March 30, KAIST announced that a research team headed by Professor Jin Woo Kim from the Department of Biological Sciences has created a treatment that regenerates retinal nerves to restore vision.

Tuberculosis (TB) is an infectious disease that kills more than a million people worldwide every year. The pathogen that causes the disease, Mycobacterium tuberculosis, is deadly in part because of its complex outer envelope, which helps it evade immune responses of infected hosts.

In an ACS Infectious Diseases paper, researchers developed a chemical probe to study a key component of this envelope. Their results provide a step toward finding new ways of inactivating the bacterium.

Because curing TB requires taking drugs for months, which can result in TB resistance to some antibiotics, scientists are working to develop new treatments. One possible target is the bacterium’s outermost layer, called the mycomembrane, which protects the bacteria from stressors. When M. is attacked by a host’s macrophage , the mycomembrane produces compounds that suppress the infected host’s immune response.

People who suffer from the autoimmune disease myasthenia gravis experience muscle weakness that can affect any of the muscles we use to blink, smile or even move our body around.

Researchers have known that the disease is caused by miscommunication between nerves and muscles. The body’s immune system mistakenly produces “autoantibodies,” or antibodies that attack its own tissues and proteins. In the case of myasthenia gravis, the body produces autoantibodies that target acetylcholine receptors (AChRs), which are essential triggers for normal muscle contraction functions.

Medications prescribed to boost acetylcholine and suppress the immune system have varying levels of success, leading researchers to believe that myasthenia gravis may be caused by varying underlying mechanisms for different people.

Questions to inspire discussion.

🚕 Q: What’s the expected price range for Tesla’s upcoming Robo Taxi? A: Tesla’s Robo Taxi will enter a new price tier under $30,000, significantly increasing sales and profitability due to its lower hardware cost structure.

Tesla’s Expansion in China.

🇨🇳 Q: How is Tesla expanding its Full Self-Driving (FSD) in China? A: Tesla is offering a 30-day free trial of FSD in China, with new software version 13.2.8 for both Hardware 3 and 4, likely rolling out between end of April and early May.

🤝 Q: Why is Tesla’s relationship with China important? A: Tesla’s good relationship with China, established 5 years ago without a joint venture, is crucial for success as China benefits from learning Tesla’s FSD perspective and benchmarking against their own vehicles.

💰 Q: How will tariffs affect low-priced vehicles in the US? A: 25% tariffs on imported vehicles will apply to nearly 80% of vehicles priced under $30,000, impacting popular models like Civic and Corolla.

When Demis Hassabis won the Nobel Prize last year, he celebrated by playing poker with a world champion of chess. Hassabis loves a game, which is how he became a pioneer of artificial intelligence. The 48-year-old British scientist is co-founder and CEO of Google’s AI powerhouse, called DeepMind. We met two years ago when chatbots announced a new age. Now, Hassabis and others are chasing what’s called artificial general intelligence—a silicon intellect as versatile as a human but with superhuman speed and knowledge. After his Nobel and a knighthood from King Charles, we hurried back to London to see what’s next from a genius who may hold the cards of our future.

Demis Hassabis: What’s always guided me and— the passion I’ve always had is understanding the world around us. I’ve always been— since I was a kid, fascinated by the biggest questions. You know, the— meaning of— of life, the— nature of consciousness, the nature of reality itself. I’ve loved reading about all the great scientists who worked on these problems and the philosophers, and I wanted to see if we could advance human knowledge. And for me, my expression of doing that was to build what I think is the ultimate tool for advancing human knowledge, which is— which is AI.

Scott Pelley: We sat down in this room two years ago. And I wonder if AI is moving faster today than you imagined.

There are several physiological reasons why biological organisms sleep. One key one concerns brain metabolism. In our article we discuss the role of metabolism in myelin, based on the recent discovery that myelin contains mitochondrial components that enable the production of adenosine triphosphate (ATP) via oxidative phosphorylation (OXPHOS). These mitochondrial components in myelin probably originate from vesiculation of the mitochondrial membranes in form from mitochondrial derived vesicles (MDVs). We hypothesize that myelin acts as a proton capacitor, accumulating energy in the form of protons during sleep and converting it to ATP via OXPHOS during wakefulness. Empirical evidence supporting our hypothesis is discussed, including data on myelin metabolic activity, MDVs, and allometric scaling between white matter volume and sleep duration in mammals.

Capitalizing on the flexibility of tiny cells inside the body’s smallest blood vessels may be a powerful spinal cord repair strategy, new research suggests.

In mouse experiments, scientists introduced a specific type of recombinant protein to the site of a spinal cord injury where these cells, called pericytes, had flooded the lesion zone. Once exposed to this protein, results showed, pericytes change shape and inhibit the production of some molecules while secreting others, creating “cellular bridges” that support regeneration of axons—the long, slender extensions of nerve cell bodies that transmit messages.

Researchers observed axon regrowth in injured mice that received a single treatment injection of the growth-factor protein, and the animals also regained movement in their hind limbs. An experiment involving suggests the results are not restricted to mice.

A team of researchers from the University of Chicago, in collaboration with researchers from the University of Pittsburgh, has identified a novel oncometabolite that accumulates in tumors and impairs immune cells’ ability to fight cancer.

The study, published in Nature Cell Biology, highlights how the metabolic environment of tumors influences the function of T cells, which are critical immune cells responsible for eliminating cancer. The finding opens new possibilities for improving cancer immunotherapy by targeting .

A new way to deliver disease-fighting proteins throughout the brain may improve the treatment of Alzheimer’s disease and other neurological disorders, according to University of California, Irvine scientists. By engineering human immune cells called microglia, the researchers have created living cellular “couriers” capable of responding to brain pathology and releasing therapeutic agents exactly where needed.

The study, published in Cell Stem Cell, demonstrates for the first time that derived from induced pluripotent stem cells can be genetically programmed to detect disease-specific brain changes—like in Alzheimer’s disease—and then release enzymes that help break down those toxic proteins. As a result, the cells were able to reduce inflammation, preserve neurons and synaptic connections, and reverse multiple other hallmarks of neurodegeneration in mice.

For patients and families grappling with Alzheimer’s and related diseases, the findings offer a hopeful glimpse at a future in which microglial-based cell therapies could precisely and safely counteract the ravages of neurodegeneration.

Results of a randomized, controlled clinical trial in Japan among more than 170 children aged 1 to 6 who underwent surgery show that by using EEG readings of brain waves to monitor unconsciousness, an anesthesiologist can significantly reduce the amount of the anesthesia administered to safely induce and sustain each patient’s anesthetized state.

On average, the patients experienced significant improvements in several post-operative outcomes, including quicker recovery and reduced incidence of delirium.

“I think the main takeaway is that in kids, using the EEG, we can reduce the amount of anesthesia we give them and maintain the same level of unconsciousness,” said study co-author Emery N. Brown, Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience at MIT and an anesthesiologist at Massachusetts General Hospital. The study appears in JAMA Pediatrics.