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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.

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.

New York, Feb 26:  A new wearable sensor that works in conjunction with artificial intelligence (AI) technology could help doctors remotely detect critical changes in heart failure patients days before a health crisis occurs, says a study.

The researchers said the system could eventually help avert up to one in three heart failure readmissions in the weeks following initial discharge from the hospital and help patients sustain a better quality of life.

"This study shows that we can accurately predict the likelihood of hospitalisation for heart failure deterioration well before doctors and patients know that something is wrong," says the study's lead author Josef Stehlik from University of Utah in the US.

"Being able to readily detect changes in the heart sufficiently early will allow physicians to initiate prompt interventions that could prevent rehospitalisation and stave off worsening heart failure," Stehlik added.

According to the researchers, even if patients survive, they have poor functional capacity, poor exercise tolerance and low quality of life after hospitalisations.

"This patch, this new diagnostic tool, could potentially help us prevent hospitalizations and decline in patient status," Stehlik said.

For the findings, published in the journal Circulation: Heart Failure, the researchers followed 100 heart failure patients, average age 68, who were diagnosed and treated at four veterans administration (VA) hospitals in Utah, Texas, California, and Florida.

After discharge, participants wore an adhesive sensor patch on their chests 24 hours a day for up to three months.

The sensor monitored continuous electrocardiogram (ECG) and motion of each subject.

This information was transmitted from the sensor via Bluetooth to a smartphone and then passed on to an analytics platform, developed by PhysIQ, on a secure server, which derived heart rate, heart rhythm, respiratory rate, walking, sleep, body posture and other normal activities.

Using artificial intelligence, the analytics established a normal baseline for each patient. When the data deviated from normal, the platform generated an indication that the patient's heart failure was getting worse.

Overall, the system accurately predicted the impending need for hospitalization more than 80 per cent of the time.

On average, this prediction occurred 10.4 days before a readmission took place (median 6.5 days), the study said.