Archive for the '–' Category

Classroom Activities Using the Dash & Dot Robots | Technology for Learners

November 21, 2020

https://technologyforlearners.com/classroom-activities-using-dash-dot-robots/

Scientific American article

November 21, 2020

Mysteries of COVID Smell Loss Finally Yield Some Answers

Explanations begin to arise at the molecular level for this vexing but commonplace symptom

https://www.scientificamerican.com/article/mysteries-of-covid-smell-loss-finally-yield-some-answers1/

Message Center (AMZN, where messages from buyers appear)

November 21, 2020

https://www.amazon.com/gp/message#!/inbox

https://www.amazon.com/gp/communication-manager/inbox.html

Suggested Hikes Archives – Guilford Land Conservation Trust

November 20, 2020

https://guilfordlandtrust.org/wordpress/category/suggested-hikes
1st 2 are off 146

The Children Never Had Covid. So Why Did They Have Coronavirus Antibodies? – The New York Times

November 19, 2020

Wonder whether the chronic inflammation in asthmatic patients also has similar effects & if this explains why #COVID19 didn’t hit asthmatics quite as hard as was expected.

https://www.nytimes.com/2020/11/10/health/coronavirus-children.html

QT:{{”
After examining blood taken from 190 people before the pandemic emerged, Dr. Elledge and his colleagues concluded that many already had antibodies, including the one targeting the base of the spike — presumably from infections with related coronaviruses that cause colds.

But while adults might get one or two colds a year, Dr. Elledge said, children may get up to a dozen. As a result, many develop floods of coronavirus antibodies that are present almost continuously; they may lessen cold symptoms, or even leave children with colds that are symptomless but still infectious.
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https://twitter.com/MarkGerstein/status/1329640801668829186

What’s the worst that could happen? – The world should think better about catastrophic and existential ri sks | Briefing | The Economist

November 19, 2020

https://www.economist.com/briefing/2020/06/25/the-world-should-think-better-about-catastrophic-and-existential-risks +
https://en.wikipedia.org/wiki/Carrington_Event

Saliva tests show promise for widespread COVID-19 surveillance at universities and workplaces

November 19, 2020

https://cen.acs.org/analytical-chemistry/diagnostics/Saliva-tests-show-promise-widespread/98/web/2020/08

Immunity to the Coronavirus May Last Years, New Data Hint – The New York Times

November 17, 2020

https://www.nytimes.com/2020/11/17/health/coronavirus-immunity.html

Johnson Farm

November 17, 2020

https://www.essexlandtrust.org/Assets/Trail%20Maps/1-Johnson%20Farm%20map%20021319.pdf +
many more trails in the Essex Area
https://www.essexlandtrust.org/04_trails.html

Making the leap | C&EN Global Enterprise

November 16, 2020

https://pubs.acs.org/doi/10.1021/cen-09833-cover

https://cen.acs.org/content/cen/articles/98/i33/How-do-viruses-leap-from-animals-to-people-and-spark-pandemics.html

QT:{{”
So far, though, efforts to find other mutations that might power the virus’s pandemic prowess have largely fallen short. Starr, Bloom, and their colleagues set out to mutate every position in the
201-amino-acid RBD one by one and then examine how each mutation affects the protein’s folding pattern and capacity to bind ACE2. They found that the region has a high tolerance for mutations. “It can handle a high number of mutations and do its job just fine,” Starr says. The team even found dozens of mutations that boosted the RBD’s ability to bind the ACE2 receptor, but the virus seems to have not adopted any of them (Cell 2020, DOI: 10.1016/j.cell.2020.08.012). That finding suggests that the virus functions effectively with the binding affinity it has, and that there’s no strong selective pressure pushing for mutations that might increase it, Starr says. He wonders if that’s because the virus is tearing through a population that has never encountered it and has no immune defenses against it. “Right now, the virus has basically found a buffet table of susceptible [hosts].”
As the COVID-19 pandemic has progressed, one virus mutation does appear to have become a permanent feature of SARS-CoV-2’s genome. Researchers collecting virus samples from infected patients have been sequencing viral genomes and analyzing the strains spreading in different parts of the world. They have found that one mutation, a change from an aspartic acid (D614) to a glycine (G614), is now present in the majority of SARS-CoV-2 viral sequences. People infected with strains carrying this mutation tend to shed more virus than those infected with strains that don’t, hinting that this mutation may make the virus more infectious (Cell 2020, DOI:
10.1016/j.cell.2020.06.043). Farzan’s team has conducted cell studies with the lab-made viruses carrying SARS-CoV-2 spike proteins and found that the mutation causes the virus to more readily infect human cells, perhaps because there are more spike proteins on the virus’s surface (bioRxiv 2020, DOI: 10.1101/2020.06.12.148726v1). The data from those studies have not yet been peer reviewed.
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