Injectable tissue patch may help repair damaged heart

Agencies
August 15, 2017

Toronto, Aug 15: Scientists have developed an injectable tissue bandage smaller than a postage stamp that can repair damaged hearts.

Repairing heart tissue destroyed by a heart attack or medical condition with regenerative cells or tissues usually requires invasive open-heart surgery.

Researchers at the University of Toronto in Canada have developed a technique that lets them use a small needle to inject a repair patch, without the need to open up the chest cavity.

The AngioChip is a tiny patch of heart tissue with its own blood vessels and heart cells beating with a regular rhythm.

"If an implant requires open-heart surgery, it's not going to be widely available to patients," said Milica Radisic from University of Toronto.

She said that after a heart attack, the heart's function is reduced so much that invasive procedures like open-heart surgery usually pose more risks than potential benefits.

Miles Montgomery, a PhD candidate in Radisic's lab, has spent nearly three years developing a patch that could be injected, rather than implanted.

Researchers found a design that matched the mechanical properties of the target tissue, and had the required shape- memory behaviour: as it emerges from the needle, the patch unfolds itself into a bandage-like shape.

"The shape-memory effect is based on physical properties, not chemical ones," said Radisic.

This means that the unfolding process does not require additional injections and would not be affected by the local conditions within the body.

The next step was to seed the patch with real heart cells. After letting them grow for a few days, they injected the patch into rats and pigs.

Not only does the injected patch unfold to nearly the same size as a patch implanted by more invasive methods, the heart cells survive the procedure well.

Over time, the scaffold will naturally break down, leaving behind the new tissue.

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Agencies
May 19,2020

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.

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Agencies
April 14,2020

There is no evidence that the Bacille Calmette-Guerin (BCG) vaccine, which is primarily used against tuberculosis, protects people against infection with the novel coronavirus, the World Health Organization (WHO) said.

The WHO therefore didn't recommend BCG vaccination for the prevention of COVID-19 in the absence of evidence, according to its daily situation report on Monday, Xinhua news agency reported.

"There is experimental evidence from both animal and human studies that the BCG vaccine has non-specific effects on the immune system. These effects have not been well characterized and their clinical relevance remains unknown," WHO stated.

Two clinical trials addressing the question are underway, and WHO will evaluate the evidence when it is available, it noted.

BCG vaccination prevents severe forms of tuberculosis in children and diversion of local supplies may result in an increase of disease and deaths from the tuberculosis, it warned.

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