Humans can now pilot drones with their brains, scientists are making an end run around the bug that causes tuberculosis, and bacteria in the belly have been found to produce a charge. We’ve got a gut feeling there’s something that might electrify you, too, in this week’s premier scientific discoveries.
What is it? Because it is not enough to pilot just one plane telepathically, the Defense Advanced Research Projects Agency announced technology that enables pilots to use an implanted brain chip to steer up to three drones — or fighter jets — at a time.
Why does it matter? “In essence,” reports the website Defense One, “it’s the difference between having a brain joystick and having a real telepathic conversation with multiple jets or drones about what’s going on, what threats might be flying over the horizon, and what to do about them.” Building on previous research concerning brain-computer interfaces, this chip allows for better communication between pilots and their remote planes than was previously possible. While steering multiple crafts simultaneously, pilots receive necessary data coming back from each craft in order to do things right. Not just applicable to flying, the tech could also lead to more responsive prosthetic limbs and better bodily control following paralysis.
How does it work? In 2015, DARPA announced it had developed a chip that allowed a paralyzed woman to fly a fighter jet in a flight simulator. As Wired reported back then, this was accomplished through a sensor embedded in her brain with 96 microelectrodes, which recorded signals from the motor cortex; the DARPA team reprogrammed those signals so they’d control a simulated fighter jet instead of, say, a prosthetic arm. The new chip builds on that technology, but expands the range of what users can control.
What is it? At the University of Manchester, scientists have developed a new drug to treat tuberculosis — and for the first time, it’s not an antibiotic.
Why does it matter? It potentially sidesteps the growing problem of antibiotics resistance, for one. And — so far in animal trials — it offers an easier path to health than the usual course of treatment, which typically requires six to eight months of strong antibiotics, with their occasionally unhappy side effects. (And for all that, there’s a 20 percent chance of the disease recurring.) As Manchester notes, too, 1.7 million people across the globe die from TB every year, with 7.3 million receiving diagnoses in 2018.
How does it work? Rather than directly targeting the bacterium that causes tuberculosis, the new drug goes after its defense systems. The TB-causing bacterium, called Mycobacterium tuberculosis, secretes molecules known as virulence factors that have been referred to as the disease’s “secret weapon”; they block the immune system from properly responding to infection. The Manchester team developed a drug that blocks a particular virulence factor — after which the body’s white blood cells have a much easier time getting at the tuberculosis bacterium. They hope to get trials in humans going in three or four years.
What is it? The bacteria Listeria monocytogenes, which leads to listeriosis, doesn’t just cause stomach discomfort — it also produces stomach electricity, according to researchers at the University of California, Berkeley, who’ve identified it as one strain among a whole host of electrogenic gut bacteria.
Why does it matter? Electricity-producing bacteria aren’t themselves a new discovery, but previously they were thought to live in specific, mineral-rich environments, like mines. The Berkeley team, reporting its results in Nature, found they also live rather closer at hand, down in our viscera. Specifically, researchers learned that various disease-causing bacteria and bacteria involved in the fermenting processes, such as the Lactobacilli, are particularly adept at producing electricity. The finding raises the possibility of, for instance, harvesting electricity from waste-treatment plants. (And also raises certain questions about the relationship between electricity and, say, the taste of fermented favorites like cheese and sauerkraut.)
How does it work? As Berkeley explains, “bacteria generate electricity for the same reason we breathe oxygen: to remove electrons produced during metabolism and support energy production.” They can’t transfer their electrons to oxygen when there isn’t any, though, which is why in low-oxygen environments — like mines — they transfer it to minerals outside the cell like iron or manganese, generating a tiny current. Bacteria in the low-oxygen gut environment, scientists found, rely on an electron acceptor called flavin to create their current — yielding about as much juice as known electrogenic bacteria.
What is it? Researchers at the University of California, San Francisco, recently announced they have figured out how to use the gene-editing tool CRISPR to flip the “immortality switch” that enables some 50 types of cancer cells to endlessly reproduce.
Why does it matter? The focus of the research here is a mutation in the TERT promoter, which regulates gene activity — it’s “the third most common mutation among all human cancers,” according to UCSF, and the most common mutation in glioblastoma, the deadly brain cancer. Once a certain protein activates the TERT promoter mutation, cancer cells achieve a kind of immortality — they divide endlessly, without the kind of preprogrammed cell death that restricts the lives of most cells. UCSF neuro-oncologist Joseph Costello oversaw a team of researchers who studied the TERT promoter, publishing their findings in the journal Cancer Cell.
How does it work? Working on cells from glioblastoma, researchers zeroed in on a subunit of a protein called GABP that activates the TERT promoter mutations. The particular subunit isn’t otherwise necessary for cell function, they found, and disabling it using CRISPR proved promising: It “dramatically slowed the growth” of human cancer cells both in the lab and in mice they’d been transplanted into. Costello called the subunit “a promising new drug target for aggressive glioblastoma and potentially the many other cancers with TERT promoter mutations.”
What is it? A team of researchers from Georgia State University found that a molecule produced during fasting, or periods of restricted calorie intake, can have anti-aging effects on the human vascular system. Their study is just out in the journal Molecular Cell.
Why does it matter? “The most important part of aging is vascular aging,” said Ming-Hui Zou, director of Georgia State’s Center for Molecular and Translational Medicine and the senior author of the study. As people age, the blood vessels that supply their organs degrade, leading to things like cardiovascular disease, cancer and Alzheimer’s. One understudied part of the process is the link between reduced food intake and aging — which is what Zou’s team focused on.
How does it work? Specifically, they looked at a water-soluble molecule that’s produced in the liver “during periods of low food intake, carbohydrate restrictive diets, starvation or prolonged intensive exercise,” according to Georgia State. Zou said, “This compound can delay vascular aging through endothelial cells, which line the interior surface of blood vessels and lymphatic vessels. It can prevent one type of cell aging called senescence, or cellular aging” — senescent cells being those that can no longer divide and multiply. Conversely, the molecule might be suppressed when people overeat, possibly hastening the aging process. While it might be difficult to convince people to fast in order to live longer, Zou’s lab is looking for a “new chemical” that could mimic the properties of the molecule.