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In a classic physics experiment, scientists set up quantum entanglement between sunlight and light generated here on Earth.

The researchers in China, the United States, Germany, and the United Kingdom wondered whether any two particles of light, called photons, could show the spooky interactions governed by the rules of quantum mechanics, even if they originated from vastly distant sources. The experiment was mainly curiosity-driven, but it demonstrates that in the future, researchers might be able to use the Sun as a source of light for quantum mechanics-related purposes.

Last month, Elon Musk’s Neuralink, a neurotechnology company, revealed its plans to develop brain-reading technology over the next few years. One of the goals for Musk’s firm is to eventually implant microchip-devices into the brains of paralyzed people, allowing them to control smartphones and computers.

Although this Black Mirror-esque technology could hold potentially life-changing powers for those living with disabilities, according to Cognitive Psychologist Susan Schneider, it’s not such a great idea, and I can’t help but feel relieved, I’m with Schneider on this.

For a core of longevity true believers, the time to intervene is now.


“How old are you?” James Clement wanted to know.

I turn 50 this year. There’s a new creaking in my bones; my skin doesn’t snap back the way it used to. It’s developed a dull thickness—you can’t tickle me at all. My gums are packing it in and retreating toward my jaw. These changes have been gradual or inexplicably sudden, like the day when I could no longer see the typed words that are my profession. Presbyopia, the ophthalmologist told me. Totally normal. You’re middle-aged.

To Clement, though, my age was great news. “Yep, you are going to live forever,” he said. “I think anybody under 50 who does not have a genetic liability will make it to longevity escape velocity.”

The Food and Drug Administration on Wednesday approved a new antibiotic that, when combined with two existing antibiotics, can tackle the most formidable and deadly forms of tuberculosis. The trio of drugs treats extensively drug-resistant tuberculosis (XDR-TB), along with cases of multidrug-resistant tuberculosis (MDR-TB) that have proven unresponsive to other treatments.

Tuberculosis is the single leading infectious killer in the world, infecting an estimated 10 million people in 2017 and killing 1.6 million of them. XDR-TB and MDR-TB are even more savage forms of the disease, which is caused by the bacterium Mycobacterium tuberculosis. The drug-resistant strains of TB kill an estimated 60% and 40% of their victims, respectively.

MDR-TB strains can resist at least the two most powerful anti-TB drugs, isoniazid and rifampin. A strain gets into XDR-territory when they also become resistant to any fluoroquinolone drug, such as ciprofloxacin or levofloxacin, plus at least one of three injectable second-line drugs, which are amikacin, kanamycin, and capreomycin. Drug-resistant strains of tuberculosis infected an estimated 558,000 people in 2017.

A team of scientists at UC San Francisco and the National Institutes of Health have achieved another CRISPR first, one which may fundamentally alter the way scientists study brain diseases.

In a paper published August 15 in the journal Neuron, the researchers describe a technique that uses a special version of CRISPR developed at UCSF to systematically alter the activity of in human neurons generated from , the first successful merger of stem cell-derived cell types and CRISPR screening technologies.

Though mutations and other genetic variants are known to be associated with an increased risk for many , technological bottlenecks have thwarted the efforts of scientists working to understand exactly how these genes cause .

A new study outlines multiple ways in which epiblast stem cells can be reprogrammed back into a fully pluripotent state, paving the way for a better understanding of epigenetics.

The role of epigenetics

Epigenetics are why our cells, which all have the same DNA, differ in function. A bone cell has the same genetics as a nerve cell, but its epigenetic switches instruct it to perform the functions of a bone cell and not a nerve cell. Epigenetic alterations, however, are one of the primary hallmarks of aging. As we age, harmful epigenetic switches are activated and beneficial ones are deactivated, causing age-related dysfunction. This may even lead to inflammation, which causes further epigenetic damage, leading to a dangerous feedback loop.