09-05-2020, 03:12 AM
I am interested in comments from those of you with medical backgrounds.
https://elemental.medium.com/a-supercomp...cb8eba9d63
https://elemental.medium.com/a-supercomp...cb8eba9d63
Bradykinin Storms Theory Article
I am interested in comments from those of you with medical backgrounds.
https://elemental.medium.com/a-supercomp...cb8eba9d63
https://elemental.medium.com/a-supercomp...cb8eba9d63
09-05-2020, 07:44 AM
Wow. I don't have a medical background so I don't have anything to add but what a fabulous read. I'm following to see what the medical folks have to say.
Wow. I don't have a medical background so I don't have anything to add but what a fabulous read. I'm following to see what the medical folks have to say.
The research described in the medium.com article was submitted or published on July 2 in the online journal eLife.
Another, more readable description is in this article from TheScientist.
From the medium.com article:
"By acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs."
The research paper suggests seven potential therapeutic interventions targeting (1) reducing Bradykinin production, (2) reducing Bradykinin signaling, (3) reducing Renin production, (4) reducing hyaluronan, or (5) increasing fibrinolysis.
For those of us (like me) that are trying to absorb & filter what is being said about COVID-19, be aware that ACE and ACE2 are physically similar enzymes that act differently.
I found a 2005 medical journal editorial "ACE and ACE2: a tale of two enzymes". Among the very technical material:
"This editorial refers to ‘Myocardial infarction increases ACE2 expression in rat and humans’"
"ACE2, the recently described homologue of ACE" [Reference 1 is to a 2000 paper that apparently describes ACE2 for the first time.]
"ACE2 contains a single HEXXH zinc-binding domain which is homologous to one of the active sites of ACE and has 40% overall identity to ACE."
"The initial description of ACE2 suggested that it was expressed solely in endothelial cells in the human heart. However, in the setting of myocardial infarction, it now appears that ACE2 protein is found in multiple cell types including macrophages, smooth muscle cells, and cardiac myocytes in addition to endothelial cells."
"If ACE is the worst of enzymes, is ACE2 the best of enzymes?"
"In addition, ACE2 has recently been shown to be a ‘receptor’ for the SARS virus (not a good thing)." [referencing a 2003 paper]
It sometimes is amazing to reflect upon how much medical & biological science knowledge is gained in just 20 years.
Another, more readable description is in this article from TheScientist.
From the medium.com article:
"By acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs."
The research paper suggests seven potential therapeutic interventions targeting (1) reducing Bradykinin production, (2) reducing Bradykinin signaling, (3) reducing Renin production, (4) reducing hyaluronan, or (5) increasing fibrinolysis.
For those of us (like me) that are trying to absorb & filter what is being said about COVID-19, be aware that ACE and ACE2 are physically similar enzymes that act differently.
I found a 2005 medical journal editorial "ACE and ACE2: a tale of two enzymes". Among the very technical material:
"This editorial refers to ‘Myocardial infarction increases ACE2 expression in rat and humans’"
"ACE2, the recently described homologue of ACE" [Reference 1 is to a 2000 paper that apparently describes ACE2 for the first time.]
"ACE2 contains a single HEXXH zinc-binding domain which is homologous to one of the active sites of ACE and has 40% overall identity to ACE."
"The initial description of ACE2 suggested that it was expressed solely in endothelial cells in the human heart. However, in the setting of myocardial infarction, it now appears that ACE2 protein is found in multiple cell types including macrophages, smooth muscle cells, and cardiac myocytes in addition to endothelial cells."
"If ACE is the worst of enzymes, is ACE2 the best of enzymes?"
"In addition, ACE2 has recently been shown to be a ‘receptor’ for the SARS virus (not a good thing)." [referencing a 2003 paper]
It sometimes is amazing to reflect upon how much medical & biological science knowledge is gained in just 20 years.
The research described in the medium.com article was submitted or published on July 2 in the online journal eLife.
Another, more readable description is in this article from TheScientist.
From the medium.com article:
"By acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs."
The research paper suggests seven potential therapeutic interventions targeting (1) reducing Bradykinin production, (2) reducing Bradykinin signaling, (3) reducing Renin production, (4) reducing hyaluronan, or (5) increasing fibrinolysis.
For those of us (like me) that are trying to absorb & filter what is being said about COVID-19, be aware that ACE and ACE2 are physically similar enzymes that act differently.
I found a 2005 medical journal editorial "ACE and ACE2: a tale of two enzymes". Among the very technical material:
"This editorial refers to ‘Myocardial infarction increases ACE2 expression in rat and humans’"
"ACE2, the recently described homologue of ACE" [Reference 1 is to a 2000 paper that apparently describes ACE2 for the first time.]
"ACE2 contains a single HEXXH zinc-binding domain which is homologous to one of the active sites of ACE and has 40% overall identity to ACE."
"The initial description of ACE2 suggested that it was expressed solely in endothelial cells in the human heart. However, in the setting of myocardial infarction, it now appears that ACE2 protein is found in multiple cell types including macrophages, smooth muscle cells, and cardiac myocytes in addition to endothelial cells."
"If ACE is the worst of enzymes, is ACE2 the best of enzymes?"
"In addition, ACE2 has recently been shown to be a ‘receptor’ for the SARS virus (not a good thing)." [referencing a 2003 paper]
It sometimes is amazing to reflect upon how much medical & biological science knowledge is gained in just 20 years.
Another, more readable description is in this article from TheScientist.
From the medium.com article:
"By acting like a natural ACE inhibitor, Covid-19 may be causing the same effects that hypertensive patients sometimes get when they take blood pressure–lowering drugs."
The research paper suggests seven potential therapeutic interventions targeting (1) reducing Bradykinin production, (2) reducing Bradykinin signaling, (3) reducing Renin production, (4) reducing hyaluronan, or (5) increasing fibrinolysis.
For those of us (like me) that are trying to absorb & filter what is being said about COVID-19, be aware that ACE and ACE2 are physically similar enzymes that act differently.
I found a 2005 medical journal editorial "ACE and ACE2: a tale of two enzymes". Among the very technical material:
"This editorial refers to ‘Myocardial infarction increases ACE2 expression in rat and humans’"
"ACE2, the recently described homologue of ACE" [Reference 1 is to a 2000 paper that apparently describes ACE2 for the first time.]
"ACE2 contains a single HEXXH zinc-binding domain which is homologous to one of the active sites of ACE and has 40% overall identity to ACE."
"The initial description of ACE2 suggested that it was expressed solely in endothelial cells in the human heart. However, in the setting of myocardial infarction, it now appears that ACE2 protein is found in multiple cell types including macrophages, smooth muscle cells, and cardiac myocytes in addition to endothelial cells."
"If ACE is the worst of enzymes, is ACE2 the best of enzymes?"
"In addition, ACE2 has recently been shown to be a ‘receptor’ for the SARS virus (not a good thing)." [referencing a 2003 paper]
It sometimes is amazing to reflect upon how much medical & biological science knowledge is gained in just 20 years.
09-08-2020, 01:14 PM
It seems to fit nicely within the context of observations. Need to see some more data/research. Computational genetics can point you in the right directly (it can vastly reduce your possible solution space), but it is never going to give you the smoking gun for which actual bench and clinical data are needed.
It seems to fit nicely within the context of observations. Need to see some more data/research. Computational genetics can point you in the right directly (it can vastly reduce your possible solution space), but it is never going to give you the smoking gun for which actual bench and clinical data are needed.
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