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Electric stimulation may be able to help blood vessels carry white blood cells and oxygen to wounds, speeding healing, a new study suggests.

The study, published in the Royal Society of Chemistry journal Lab on a Chip, found that steady generates increased permeability across vessels, providing new insight into the ways might grow.

The electrical stimulation provided a constant voltage with an accompanying electric current in the presence of fluid flow. The findings indicate that stimulation increases permeability of the blood vessel—an important characteristic that can help wound-healing substances in the blood reach injuries more efficiently.

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As the world fights the SARS-CoV-2 virus causing the COVID-19 pandemic, another group of dangerous pathogens looms in the background. The threat of antibiotic-resistant bacteria has been growing for years and appears to be getting worse. If COVID-19 taught us one thing, it’s that governments should be prepared for more global public health crises, and that includes finding new ways to combat rogue bacteria that are becoming resistant to commonly used drugs.

In contrast to the current pandemic, viruses may be be the heroes of the next epidemic rather than the villains. Scientists have shown that viruses could be great weapons against bacteria that are resistant to antibiotics.

I am a biotechnology and policy expert focused on understanding how personal genetic and biological information can improve human health. Every person interacts intimately with a unique assortment of viruses and bacteria, and by deciphering these complex relationships we can better treat infectious diseases caused by antibiotic-resistant bacteria.

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The hematopoietic (blood-forming) stem cells (HSCs) residing in our bone marrow produce all of our blood cells, including key immune cells that protect us from bacteria and viruses. As we age, our HSCs become less efficient and less able to make healthy new blood cells. In a study published online today in Nature, researchers at Albert Einstein College of Medicine have found that this reduction in HSC efficiency is caused in part by the deterioration of chaperone-mediated autophagy (CMA), the housekeeping process that removes damaged proteins and other waste materials that interfere with cells’ ability to function.

“While the aging of HSCs in our bone marrow is inevitable, the good news is that it may be reversible,” said co-study leader Ana Maria Cuervo, M.D., Ph.D., professor of developmental and , of anatomy and structural biology, and of medicine, and the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases at Einstein. “Our studies in mice suggest that drugs we’ve developed at Einstein can activate CMA and potentially restore the vitality of HSCs in older people.”

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Circa 2010

About 48 kilometers off the eastern coast of the United States, scientists from Rutgers, the State University of New Jersey, peered over the side of a small research vessel, the Arabella. They had just launched RU27, a 2-meter-long oceanographic probe shaped like a torpedo with wings. Although it sported a bright yellow paint job for good visibility, it was unclear whether anyone would ever see this underwater robot again. Its mission, simply put, was to cross the Atlantic before its batteries gave out.

Unlike other underwater drones, RU27 and its kin are able to travel without the aid of a propeller. Instead, they move up and down through the top 100 to 200 meters of seawater by adjusting their buoyancy while gliding forward using their swept-back wings. With this strategy, they can go a remarkably long way on a remarkably small amount of energy.

When submerged and thus out of radio contact, RU27 steered itself with the aid of sensors that registered depth, heading, and angle from the horizontal. From those inputs, it could dead reckon about where it had glided since its last GPS navigational fix: Every 8 hours the probe broke the surface and briefly stuck its tail in the air, which exposed its GPS antenna as well as the antenna of an Iridium satellite modem. This allowed the vehicle to contact its operators, who were located in New Brunswick, N.J., in the Rutgers Coastal Ocean Observation Lab, or COOL Room.

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The South Pole neutrino detector saw a Glashow resonance event, a phenomenon predicted by Nobel laureate physicist Sheldon Glashow in 1960 where an electron antineutrino and an electron interact to produce a W-boson.

On December 62016, a high-energy particle called an electron antineutrino hurtled to Earth from outer space at close to the speed of light carrying 6.3 petaelectronvolts (PeV) of energy. Deep inside the ice sheet at the South Pole, it smashed into an electron and produced a particle that quickly decayed into a shower of secondary particles. The interaction was captured by a massive telescope buried in the Antarctic glacier, the IceCube Neutrino Observatory.

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In the new study, researchers instead aimed to reduce the amount of Nav1.7 that cells make in the first place. Bioengineer Ana Moreno and her colleagues at the University of California, San Diego, modified the “molecular scissors” of the gene editor CRISPR. Changes to the cutting enzyme Cas9 caused it to bind to DNA that makes Nav1.7 without slicing it, effectively preventing the Nav1.7 protein from being made. The researchers enhanced this silencing effect by hitching Cas9 to a repressor, another protein that inhibits gene expression.

The researchers tested the Cas9 approach—and a similar approach using another gene-editing protein known as a zinc finger—in mice given the chemotherapy drug paclitaxel, which can cause chronic nerve pain in cancer patients. The team measured pain by poking the animals’ paws with a thin nylon filament. Paclitaxel prompted mice to withdraw from gentler pokes, indicating that a normally nonpainful stimulus had become painful. But 1 month after an injection of the gene-silencing treatment into their spinal fluid, rodents responded much like mice that had never gotten paclitaxel, whereas untreated rodents remained hypersensitive, the team reports today in.

The approach could also prevent pain when given before paw injections of either the inflammation-causing compound carrageenan or a molecule called BzATP that increases pain sensitivity. And treated mice behaved no differently from untreated ones when their opposite paw—not inflamed by carrageenan—was exposed to a hot surface. That’s an encouraging initial sign that the injection didn’t silence Nav1.7 so completely that it creates a dangerous numbness to all pain, Moreno says. Behavioral tests so far haven’t turned up evidence of potentially concerning side effects; the injections didn’t appear to alter the animals’ movement, cognition, or anxiety levels.

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Geoscientists at Sandia National Laboratories used 3D-printed rocks and an advanced, large-scale computer model of past earthquakes to understand and prevent earthquakes triggered by energy exploration.

Injecting water underground after unconventional oil and gas extraction, commonly known as fracking, geothermal energy stimulation and carbon dioxide sequestration all can trigger earthquakes. Of course, energy companies do their due diligence to check for faults—breaks in the earth’s upper crust that are prone to earthquakes—but sometimes earthquakes, even swarms of earthquakes, strike unexpectedly.

Sandia geoscientists studied how pressure and from injecting water can transfer through pores in rocks down to fault lines, including previously hidden ones. They also crushed rocks with specially engineered weak points to hear the sound of different types of fault failures, which will aid in early detection of an induced .

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