Lifeboat Foundation

It occurred naturally, and scientists know this for certain.

Regardless of size, all black holes experience similar accretion cycles, a new study finds.

On September 9, 2018, astronomers spotted a flash from a galaxy 860 million light years away. The source was a supermassive black hole about 50 million times the mass of the sun. Normally quiet, the gravitational giant suddenly awoke to devour a passing star in a rare instance known as a tidal disruption event. As the stellar debris fell toward the black hole, it released an enormous amount of energy in the form of light.

Researchers at MIT, the European Southern Observatory, and elsewhere used multiple telescopes to keep watch on the event, labeled AT2018fyk. To their surprise, they observed that as the supermassive black hole consumed the star, it exhibited properties that were similar to that of much smaller, stellar-mass black holes.

Pediatrician, Medical Innovator, Educator — Dr. Jamie Wells, MD, FAAP — Director, Research Science Institute (RSI), Center for Excellence in Education, Massachusetts Institute of Technology (MIT) — Professor, Drexel University School of Biomedical Engineering, Science and Health Systems.

Dr. Jamie L. Wells, MD, FAAP, is an Adjunct Professor at Drexel University’s School of Biomedical Engineering, Science and Health Systems, where she has been involved in helping to spearhead the nation’s first-degree program focused on pediatric engineering, innovation, and medical advancement.

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Archaea are more than just oddball lifeforms that thrive in unusual places — they turn out to be quite widespread. Moreover, they might hold the key to understanding how complex life evolved on Earth. Many scientists suspect that an ancient archaeon gave rise to the group of organisms known as eukaryotes, which include amoebae, mushrooms, plants and people — although it’s also possible that both eukaryotes and archaea arose from some more distant common ancestor.

As scientists learn more about enigmatic archaea, they’re finding clues about the evolution of the complex cells that make up people, plants and more.

“Clearly AI is going to win[against human intelligence]. It’s not even close,” Kahneman told the paper. “How people are going to adjust to this is a fascinating problem.”

Of course, and the reaction, right up to the last minute will be: “No way Man!!! there will be new jobs these crazy Ai’s cant do!”

Artificial intelligence will be beating humans — outworking if not entirely outmoding them — in plenty of functions as the future approaches. Here’s why.

There goes the Coder Camps.

IBM has announced Project CodeNet, a large dataset that aims to help teach AI how to understand and even write code.

Project CodeNet was announced at IBM’s Think conference this week and claims to be the largest open-source dataset for code (approximately 10 times the size of the closest.)

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In a major breakthrough, researchers at Massachusetts General Hospital (MGH) have discovered how amyloid beta—the neurotoxin believed to be at the root of Alzheimer’s disease (AD)—forms in axons and related structures that connect neurons in the brain, where it causes the most damage. Their findings, published in Cell Reports, could serve as a guidepost for developing new therapies to prevent the onset of this devastating neurological disease.

Among his many contributions to research on AD, Rudolph Tanzi, Ph.D., vice chair of Neurology and co-director of the McCance Center for Brain Health at MGH, led a team in 1986 that discovered the first Alzheimer’s disease gene, known as APP, which provides instructions for making amyloid protein precursor (APP). When this protein is cut (or cleaved) by enzymes—first, beta secretase, followed by gamma secretase—the byproduct is amyloid beta (sometimes shortened to Abeta). Large deposits of amyloid beta are believed to cause neurological destruction that results in AD. Amyloid beta formed in the brain’s axons and nerve endings causes the worst damage in AD by impairing communication between nerve cells (or neurons) in the brain. Researchers around the world have worked intensely to find ways to block the formation of amyloid beta by preventing cleavage by beta secretase and gamma secretase. However, these approaches have been hampered by safety issues.

Despite years of research, a major mystery has remained. “We knew that Abeta is made in the axons of the brain’s nerve cells, but we didn’t know how,” says Tanzi. He and his colleagues probed the question by studying the brains of mice, as well as with a research tool known as Alzheimer’s in a dish, a three-dimensional cell culture model of the disease created in 2014 by Tanzi and a colleague, Doo Yeon Kim, Ph.D. Earlier, in 2013, several other MGH researchers, including neurobiologist Dora Kovacs, Ph.D. (who is married to Tanzi), and Raja Bhattacharyya, Ph.D., a member of Tanzi’s lab, showed that a form of APP that has undergone a process called palmitoylation (palAPP) gives rise to amyloid beta. That study indicated that, within the neuron, palAPP is transported in a fatty vesicle (or sac) known as a lipid raft. But there are many forms of lipid rafts.

And there’s an important lesson to be learned about how it achieved this impressive return.

The chemical reaction 2KRb → K2 + Rb2 is studied under ultralow temperatures at the quantum state-to-state level, allowing unprecedented details of the reaction dynamics to be observed.