Toggle light / dark theme

Tesla seems to be making some serious headway with its Full Self-Driving (FSD) suite with the release of V12.3. But while FSD is currently the company’s flagship advanced driver-assist system, basic Autopilot still plays a huge role in Tesla’s electric cars. With this in mind, Tesla seems to be doubling down on educating drivers about the proper use of basic Autopilot, as well as the system’s limitations.

As could be seen in the company’s Tesla Tutorials channel on YouTube, the company has released a thorough tutorial focused on basic Autopilot’s features and proper use. The video is over four minutes long, and all throughout its duration, Tesla highlighted that the features of basic Autopilot does not make vehicles autonomous. The company also emphasized that basic Autopilot is designed to work with a fully attentive driver.

The video fully discussed the capabilities and limitations of basic Autopilot’s two main features, Traffic-Aware Cruise Control (TACC) and Autosteer (Beta). The Tesla Tutorial video discussed how to engage both features, how to set their specific parameters, and how they are disengaged. Overall, it is quite encouraging to see Tesla publishing a tutorial that’s purely focused on basic Autopilot.

Two progressively degenerative diseases, amyotrophic lateral sclerosis (ALS, commonly known as Lou Gehrig’s disease) and frontotemporal dementia (FTD, recently in the news with the diagnoses of actor Bruce Willis and talk show host Wendy Williams), are linked by more than the fact that they both damage nerve cells critical to normal functioning—the former affecting nerves in the brain and spinal cord leading to loss of movement, the latter eroding the brain regions controlling personality, behavior and language.

Research studies have repeatedly shown that in patients with ALS or FTD, the function of TAR DNA-binding protein 43, more commonly called TDP-43, becomes corrupted. When this happens, pieces of the genetic material called ribonucleic acid (RNA) can no longer be properly spliced together to form the coded instructions needed to direct the manufacture of other proteins required for healthy nerve growth and function.

The RNA strands become riddled with erroneous code sequences called “cryptic exons” that instead affect proteins believed to be associated with increased risk for ALS and FTD development.

Utilizing data from NASA’s James Webb Space Telescope, scientists have unveiled the earliest starlight spectra, revealing low-mass galaxies’ central role in the universe’s dawn. Credit: SciTechDaily.com.

Groundbreaking JWST observations reveal the pivotal role of low-mass galaxies in the early universe’s reionization, challenging existing cosmic evolution theories.

Scientists working with data from NASA’s James Webb Space Telescope (JWST) have obtained the first full spectra of some of the earliest starlight in the universe. The images provide the clearest picture yet of very low-mass, newborn galaxies, created less than a billion years after the Big Bang, and suggest the tiny galaxies are central to the cosmic origin story.

A recently tenured faculty member in MIT’s departments of Mechanical Engineering and Materials Science and Engineering, Kim has made numerous discoveries about the nanostructure of materials and is funneling them directly into the advancement of next-generation electronics.

His research aims to push electronics past the inherent limits of silicon — a material that has reliably powered transistors and most other electronic elements but is reaching a performance limit as more computing power is packed into ever smaller devices.

Today, Kim and his students at MIT are exploring materials, devices, and systems that could take over where silicon leaves off. Kim is applying his insights to design next-generation devices, including low-power, high-performance transistors and memory devices, artificial intelligence chips, ultra-high-definition micro-LED displays, and flexible electronic “skin.” Ultimately, he envisions such beyond-silicon devices could be built into supercomputers small enough to fit in your pocket.

When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows. The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last.

It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City.