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COVID-19: The President’s Infection (Part 1 of 4)

COVID-19: The President’s Infection (Part 1 of 4)

by

Columbia University Professor Emeritus, Dr. David Figurski

presented by

Donna O’Donnell Figurski

(Disclaimer: The World Health Organization <WHO> has officially named the new coronavirus as SARS-CoV-2 and the disease it causes as COVID-19. Because the majority of people, including much of the press, commonly refer to the virus as “COVID-19,” to avoid confusion I use COVID-19 as the name of the virus in this post.)

This is an unusually long post, so I’ve divided it into four parts. It is easy to read, even though it’s filled with much information.

David H. Figurski, Ph.D & Survivor of Brain Injury

The complete story of the President’s COVID-19 infection and treatment is not known by the public. Virologist, Dr. Vincent Racaniello, interviewed Dr. Daniel Griffin, a New York City physician who has been treating hospitalized COVID-19 patients since the beginning of the pandemic. Vincent has been releasing podcasts about COVID-19 every couple of days. His TWiV podcast (This Week in Virology) of October 5, 2020, is a special podcast in which he and Dr. Griffin have a conversation about COVID-19 infection and treatments, as they relate to the President’s infection.

Vincent Racaniello is a professor and virologist and my former colleague in the Department of Microbiology & Immunology at Columbia University. His guest, Daniel Griffin, is a physician in the Infectious Disease Department of Columbia. Because Dr. Griffin has both an M.D. and a Ph.D., he is a physician-scientist and so has an additional appointment as Professor of Biochemistry & Molecular Biophysics. Dr. Griffin is also the Chief of the Division of Infectious Disease for ProHEALTH Care Associates. ProHEALTH Care is the largest physician-owned multi-specialty practice in the nation. He is also on the COVID-19 response team for the tri-state area.

Dr. Griffin has applied his clinical and molecular knowledge of COVID-19 to the few details we know about President Trump’s infection. In doing so, we now have a better idea of the President’s case. I urge you to listen to the complete 34-minute TWiV podcast of October 5th. I have defined some terms and explained some concepts that may be unfamiliar to you.

President Trump announced at 1:00 am on Friday, October 2, 2020, that he and the First Lady tested positive for COVID-19. Later that day, the President was admitted to Walter Reed National Military Medical Center. He returned to the White House at 6:30 pm the next Monday. Many of the details of the infection and the President’s condition have remained unknown.

When the President’s COVID-19 infection began is unclear. The President first reported a positive test in the early morning of October 2nd. The President said he is not tested for COVID-19 every day, and the White House will not say when the President’s last negative test occurred. In his Town Hall on October 15th, the President said he didn’t know for sure that he had taken a test before the debate three days before he was admitted.

(To Be Continued)

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(Photos compliments of contributor.)

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COVID-19 — It’s Everywhere . . . Drug Breakthrough Significantly Prevents COVID-19 Deaths

Drug Breakthrough Significantly Prevents COVID-19 Deaths

by

Columbia University Professor Emeritus, Dr. David Figurski

presented by

Donna O’Donnell Figurski

 

(Disclaimer: The World Health Organization <WHO> has officially named the new coronavirus as SARS-CoV-2 and the disease it causes as COVID-19. Because the majority of people, including much of the press, commonly refer to the virus as “COVID-19,” to avoid confusion I use COVID-19 as the name of the virus in these posts.)

COVID-19

David H. Figurski, Ph.D & Survivor of Brain Injury

Research at the University of Oxford in England showed for the first time that a drug prevented a major fraction of deaths in severely sick patients with COVID-19.

Dexamethasone was found in a large clinical trial to cause a significant reduction in deaths. It can be prescribed as pills, and it is a common, readily available, and relatively inexpensive drug

A major problem after infection by COVID-19 is that the immune response of some individuals is too aggressive (often causing what’s called a “cytokine storm”) and can lead to death. Because dexamethasone is a steroid that dampens the immune response, the prediction was that it might help to prevent deaths by COVID-19.

The research showed that it does.

There are about 3 deaths for every 8 patients on ventilators.  Dexamethasone treatment reduced those deaths by one-third.  So, 1 death would be prevented for every 8 patients on ventilators.  About 5 deaths occur in every 25 patients on oxygen only. Dexamethasone treatment reduced those deaths by one-fifth, or about 1 less death for every 25 patients on oxygen only. Dexamethasone treatment had no effect on patients not on ventilators or receiving oxygen only.

Given that a major fraction of the over 118,000 deaths in the US so far (at 6:00 pm ET on June 18, 2020) were on ventilators or oxygen only, dexamethasone treatment is predicted to prevent many deaths.

The UK’s Chief Scientific Adviser, Sir Patrick Vallance, said: “This is a ground-breaking development in our fight against the disease, and the speed at which researchers have progressed finding an effective treatment is truly remarkable.”

 

Stay Safe and Healthy!

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(Photos compliments of contributor.)

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Please leave a comment by clicking the blue words “Leave a Comment” below this post.

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SPEAK OUT! NewsBit . . . . . . . . Changing a Negative Feeling About a Memory

Changing a Negative Feeling About a Memory

newsboy-thThis is exciting, but complicated, basic research. Here I simplify the main experiments. Neuroscientists at the Massachusetts Institute of Technology (MIT) have identified a neuronal circuit in mice that associates a positive or negative feeling with a memory. In a tour de force of molecular studies of the brain, the researchers conducted experiments that provide considerable hope for future therapy in humans with syndromes like PTSD (post-traumatic stress disorder), anxiety, and depression. The scientists were able to turn a memory associated with a negative feeling into a memory that has a more positive feeling and vice versa.

(How relevant are studies done in mice? The mouse is an accepted animal model for humans. You might not expect it, but mice and humans are very similar genetically. The DNA sequences of the mouse and human chromosomes are known. Many mouse genes have sequences similar to human genes. They both code for proteins that have similar structures and do the same things. Because mouse and human genes are so similar, much of the underlying biology of mice and humans is also similar. Still there are differences. So until something has been shown to be true in humans, a scientist’s conclusions must be conservative. Most of the time, however, much is learned about humans from the mouse. It has become a convenient initial model for humans.)

The researchers at MIT engineered a virus that infects the mouse brain. They specifically infected either the hippocampus, the part of the brain that contains neurons that store contextual information about a memory (for example, the place), or the amygdala, the part of the brain that contains neurons that put a positive or negative emotional tag onto the memory. The engineered virus is essentially a dead-end. It doesn’t reproduce or harm the cell, but it does have an ability to cause infected neurons to make a light-sensitive protein – but only when the neuron is actively making a new memory. In this way, the researchers were able to make neurons involved in making a new memory sensitive to light. By implanting an optical fiber in the part of the brain that contained the light-sensitive neurons (i.e., in the hippocampus or in the amygdala), the scientists could use light to turn on these memory-making neurons at will. The general technique of using a light-sensitive protein to activate a cell is called “optogenetics.” When the light-sensitive neurons are activated by the researcher, the mice recall that memory with its associated positive or negative feeling. To make a memory with a positive feeling, male mice were allowed to mix with female mice. To make a memory having an associated negative feeling, mice were put into a special cage and given a mild electrical shock. For both kinds of memories, the neurons involved could be turned on by light.

The researchers then took the mice and put them into a cage with two compartments. When a mouse with a negative memory explored a particular compartment, the researchers turned on its bad-memory neurons by shining a laser into the optical fiber to activate those neurons. The mice “remembered” the bad feeling and avoided that compartment. When the experiment was done with the mice having a good memory, the mice preferred that compartment. These results were seen only when neurons of the hippocampus were activated. No change in mouse behavior was seen when amygdala neurons were activated. Whereas the amygdala is needed to add the positive or negative feeling to a memory, the researchers concluded that a memory with its associated feeling is stored in the hippocampus.

The researchers then asked if they could change a negative memory into a positive memory and vice versa. They took the male mice with the negative memory and mixed them with females to make a positive memory. When they used light to activate the bad-memory neurons, the positive feeling from mixing them with females dominated. Unexpectedly, those mice did not suddenly avoid the females when the researchers activated the bad-memory neurons. When the mice were put back into the cage with two compartments, they went randomly into both compartments, even when the researchers activated the bad-memory neurons with light. The bad memory was no longer causing them to avoid one of the compartments. The negative tag had been supplanted by the positive feeling. What happened to the first (negative) tag? Was it removed? Was it changed? This question is being investigated. When the experiment was reversed, the scientists found that the positive feeling became more negative.

This new research gives a molecular explanation for why emotion associated with a memory can be changed – the basis of current therapy. Dr. Susumu Tonegawa, who directed the research, believes that the amygdala has two kinds of neurons: neurons that can tag a memory with a positive feeling and other neurons that can tag a memory with a negative feeling. He wants to identify those two populations of cells and understand how they work at the molecular level. Such information will be valuable for the development of new therapies and drugs. (Full story)

(Clip Art compliments of Bing.)

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