Intel unveils its first AI-driven neural network chip

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.

Scientists have designed a “catch and kill” air filter which they say can trap the novel coronavirus and neutralise it instantly, an invention that may reduce the spread of COVID-19 in closed spaces such as schools, hospitals and health care facilities, as well as public transit environments like airplanes.

According to the study, published in the journal Materials Today Physics, the device killed 99.8 per cent of the novel coronavirus, SARS-CoV-2, in a single pass through its filter. It said the device, made from commercially available nickel foam heated to 200 degrees Celsius, also killed 99.9 per cent of the spores of the deadly bacterium Bacillus anthracis which causes the anthrax disease.

“This filter could be useful in airports and in airplanes, in office buildings, schools, and cruise ships to stop the spread of COVID-19,” said Zhifeng Ren, a co-author of the study from the University of Houston (UH) in the US.

“Its ability to help control the spread of the virus could be very useful for society,” Ren added.

The researchers said they are also developing a desk-top model for the device which is capable of purifying the air in an office worker’s immediate surroundings. According to the scientists, since the virus can remain in the air for about three hours, a filter that could remove it quickly was a viable plan, and with businesses reopening across the world, they believe controlling the spread in air conditioned spaces was urgent.

The study noted that the novel coronavirus cannot survive temperatures above 70 degrees Celsius, so by making the filter temperature far hotter — about 200 degree Celsius, the researchers said they were able to kill the virus almost instantly.

Ren said the nickel foam met several key requirements. “It is porous, allowing the flow of air, and electrically conductive, which allowed it to be heated. It is also flexible,” the researchers noted in a statement.But they added that nickel foam also had low resistivity, making it difficult to raise the temperature high enough to quickly kill the virus.

The researchers said they solved this problem by folding the foam, connecting multiple compartments with electrical wires to increase the resistance high enough to raise the temperature as high as 250 degrees Celsius. By making the filter electrically heated, rather than heating it from an external source, they said the the amount of heat that escaped from the filter is minimised, allowing air conditioning to function with very low strain.

When the scientists built and tested a prototype for the relationship between voltage/current and temperature, they said it satisfies the requirements for conventional heating, ventilation, and air conditioning (HVAC) systems, and could kill the coronavirus.

“This novel biodefense indoor air protection technology offers the first-in-line prevention against environmentally mediated transmission of airborne SARS-CoV-2, and will be on the forefront of technologies available to combat the current pandemic and any future airborne biothreats in indoor environments,” said Faisal Cheema, another co-author of the study from UH.

The researchers have called for a phased roll-out of the device, “beginning with high-priority venues, where essential workers are at elevated risk of exposure.” They believe the novel device will both improve safety for frontline workers in essential industries and allow nonessential workers to return to public work spaces.

Washington, Feb 21: The fat around arteries may play an important role in keeping the blood vessels healthy, according to a study in rats that may affect how researchers test for treatments related to plaque buildup, as seen in conditions leading to heart attack.

The study, published in the journal Scientific Reports, noted that the fat, known as perivascular adipose tissue, or PVAT, helps arteries let go of muscular tension while under constant strain.

According to the researchers, including Stephanie W. Watts from the Michigan State University in the US, this feature is similar to how the bladder expands to accommodate more liquid, while at the same time keeping it from spilling out.

"In our study, PVAT reduced the tension that blood vessels experience when stretched," Watts said.

"And that's a good thing, because the vessel then expends less energy. It's not under as much stress," she added.

According to Watts and her team, PVAT has largely been ignored by researchers believing its main job was to store lipids and do little more.

Until now, she said, scientists only divided blood vessels into three parts, the innermost layer called the tunica intima, the middle layer called the tunica media, and the outermost layer called the tunica adventitia.

Watts believes PVAT is the fourth layer, which others have called tunica adiposa.

Tunica, she said, meant a membranous sheath enveloping or lining an organ, and adiposa is a synonym for fat.

"For years, we ignored this layer -- in the lab it was thrown out. In the clinic it wasn't imaged. But now we're discovering it may be integral to our blood vessels," Watts said.

"Our finding redefines what the functional blood vessels are, and is part of what can be dysfunctional in diseases that afflict us, including hypertension. We need to pay attention to this layer of a blood vessel because it does far more than we originally thought," she added.

Earlier studies, Watts said, had shown that PVAT plays a role in the functioning of blood vessels, finding that it secretes substances that can cause blood vessels to relax as well as substances that can cause it to contract.

In the current study, the researchers decided to test whether PVAT provides a structural benefit to arteries by assisting the function of stress relaxation.

They tested the thoracic aorta in rats, and found those with intact PVAT had more stress relaxation than those without.

The study revealed that the pieces of artery with surrounding fat had measurably relaxed more than those without.

Watts and her colleagues then tested other arteries, and were able to duplicate the same response.

"It's not something you see only in this particular vessel or this particular species or this particular strain. But that maybe it's a general phenomenon," she said.