Study questions if violent video games lead to acts of violence

The World Health Organisation on Wednesday said that anti-malarial drug hydroxychloroquine (HCQ) will return to the solidarity trial for the potential treatment of coronavirus disease.

At a press conference in the WHO headquarters in Geneva, Director General Tedros Adhanom Ghebreyesus said: "On the basis of the available mortality data, the members of the committee recommended that there are no reasons to modify the trial protocol. The Executive Group received this recommendation and endorsed continuation of all arms of the solidarity trial, including hydroxychloroquine."

The world health body had temporarily suspended the usage of HCQ from the solidarity trial for coronavirus treatment on May 25 soon after a study published in one of the most reliable medical journals, which had suggested that the drug could cause more fatalities among COVID-19 patients.

However, the WHO chief said that the decision was taken as a precaution while the safety data was reviewed.

Ghebreyesus also said that the Data Safety and Monitoring Committee will continue to closely monitor the safety of all therapeutics being tested in the solidarity trial.

"So far, more than 3,500 patients have been recruited in 35 countries. WHO is committed to accelerating the development of effective therapeutics, vaccines and diagnostics as part of our commitment to serving the world with science, solutions and solidarity," he said.

Soon after HCQ was suspended from the trial, the Indian government had said that the antimalarial drug has been known for its benefits for a long time and its usage will be continued on the frontline workers, including police and healthcare professionals, as prophylaxis. The government had also said that studies were being conducted and the drug would be included in the clinical trial also for the treatment of coronavirus disease.

US President Donald Trump also had strongly advocated the use of HCQ and called it a "game-changer". He went to the extent of saying that he had taken the medicine.

Launched by WHO and partners, solidarity trial is an international clinical trial to find an effective treatment for COVID-19, including drugs to slow the progression of the disease or improve survival. The trial, which enrols patients from different countries, "will compare four treatment options against standard of care to assess their relative effectiveness against COVID-19", said WHO. 

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.