Inflammation in the lungs combined with high viral loads of the novel coronavirus create a perfect storm for obese patients with COVID-19, UTSW scientists say
Conditions related to obesity, including inflammation and leaky gut, leave the lungs of obese patients more susceptible to COVID-19 and may explain why they are more likely to die from the disease, UTSW scientists say in a new article published online in eLife. They suggest that drugs used to lower inflammation in the lungs could prove beneficial to obese patients with the disease.
What do vapers, smokers, and non-smokers with chronic conditions such as high blood pressure or diabetes have in common? They all are at higher risk for COVID-19.
The scientific explanation behind this is complex and not yet certain — but it may boil down to an enzyme known as ACE2, that lives on the surface of many cells in the lungs and serves as the entry point for the coronavirus.
Macrophages are white blood cells that, depending on the signals they get from the immune system, become specialized in either increasing or decreasing inflammation. When macrophages are programmed to be pro-inflammatory, they help to increase inflammation, which is beneficial for fighting infections; when they are programmed to be anti-inflammatory, they help to decrease inflammation.
The research described in this article has been published as a working paper but has not yet been peer-reviewed by experts in the field.
Masks reduce the spread of Covid-19. But just how much of an effect do they have? A study co-authored by an MIT professor finds that if the U.S. had introduced a uniform national mask mandate for employees of public-facing businesses on April 1, the number of deaths in the U.S. would likely have been 40 percent lower on June 1.
Changes in blood platelets triggered by COVID-19 could contribute to the onset of heart attacks, strokes, and other serious complications in some patients who have the disease, according to University of Utah Health scientists. The researchers found that inflammatory proteins produced during infection significantly alter the function of platelets, making them “hyperactive” and more prone to form dangerous and potentially deadly blood clots.
An overactive defense response may lead to increased blood clotting, disease severity, and death from COVID-19. A phenomenon called NETosis—in which infection-fighting cells emit a web-like substance to trap invading viruses—is part of an immune response that becomes increasingly hyperactive in people on ventilators and people who die from the disease.
Employers across the country can advance reopening efforts with technology developed by the University of Rochester to check employees for potential COVID-19 symptoms before they report to work each day.
A new study shows that residents of long-term care facilities with lower nurse staffing levels, poorer quality scores, and higher concentrations of disadvantaged residents suffer from higher rates of confirmed COVID-19 cases and deaths.
Three drugs that are already approved by the Food and Drug Administration (FDA) or other international agencies can block the production of the novel coronavirus that causes COVID-19 in human cells, according to computational and pharmaceutical studies performed by UT Southwestern scientists.