Fathers Using Cocaine Can Put Their Sons at Risk of Memory Loss

Singapore, May 25: COVID-19 patients are no longer infectious after 11 days of getting sick even though some may still test positive, according to a new study by infectious disease experts in Singapore.

A positive test "does not equate to infectiousness or viable virus," a joint research paper by Singapore's National Centre for Infectious Diseases and the Academy of Medicine, Singapore said. The virus "could not be isolated or cultured after day 11 of illness."

The paper was based on a study of 73 patents in the city-state.

The latest findings may have implications on the country's patient discharge policy. The discharge criteria is currently based on negative test results rather than infectiousness.

Singapore's strategy on managing COVID-19 patients is guided by the latest local and international clinical scientific evidence, and the Ministry of Health will evaluate if the latest evidence can be incorporated into its patient clinical management plan, according to a report by the Straits Times.

So far, 13,882, or about 45% of the total 31,068 Covid-19 patients in Singapore have been discharged from hospitals and community facilities. Singapore reported 642 new Covid-19 cases as of noon on Saturday.

The government has been actively screening pre-school staff as it prepares to reopen pre-schools from June 2. On Friday, two pre-school employees tested positive for the novel coronavirus, bringing the total number of confirmed cases among pre-school staff to seven, according to the Ministry of Health.

Washington D.C, Feb 10: Children's vulnerability towards depression, anxiety, impulsive behaviour, and poor cognitive performance could be determined by considering the hours of sleep they manage to get.

Sleep states are active processes that support the reorganisation of brain circuitry. This makes sleep especially important for children, whose brains are developing and reorganising rapidly.

In a study by researchers from the University of Warwick -- recently published in the journal Molecular Psychiatry -- cases of 11,000 children aged between 9 and 11 years from the Adolescent Brain Cognitive Development dataset were analyzed to find out the relationship between sleep duration and brain structure.

The study was carried out by researchers Professor Jianfeng Feng, Professor Edmund Rolls, Dr. Wei Cheng and colleagues from the University of Warwick's Department of Computer Science and Fudan University.

Measures of depression, anxiety, impulsive behaviour and poor cognitive performance in the children were associated with shorter sleep duration. Moreover, the depressive problems were associated with short sleep duration one year later.

The reduced brain volume of areas such as orbitofrontal cortex, prefrontal, and temporal cortex, precuneus, and supramarginal gyrus was found to be associated with the shorter sleep duration.

Professor Jianfeng Feng, from the University of Warwick's Department of Computer Science, comments: "The recommended amount of sleep for children 6 to 12 years of age is 9-12 hours. However, sleep disturbances are common among children and adolescents around the world due to the increasing demand on their time from school, increased screen time use, and sports and social activities."

A previous study showed that about 60 per cent of adolescents in the United States receive less than eight hours of sleep on school nights.

Professor Jianfeng Feng further added: "Our findings showed that the total score for behavior problems in children with less than 7 hours sleep was 53 per cent higher on average and the cognitive total score was 7.8 per cent lower on average than for children with 9-11 hours of sleep. It highlights the importance of enough sleep in both cognition and mental health in children."

Professor Edmund Rolls from the University of Warwick's Department of Computer Science also commented: "These are important associations that have been identified between sleep duration in children, brain structure, and cognitive and mental health measures, but further research is needed to discover the underlying reasons for these relationships."

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.