Where are we with COVID-19? — Notes from my discussion with ACE-Naperville
When I came back from New York City in May, I felt a new motivation to take what I experienced, and work to better understand COVID-19. I started designing research trials in my head, and put ideas on paper. I continued to read. However, I got a bit off track for awhile due to the challenges of our non-COVID pulmonary clinic picking back up again (a good problem), and various battles that fall under the umbrella of my regular job. That is why I am grateful to ACE-Naperville for asking me to participate as a panelist in their latest Zoom Meeting. The topic: COVID-19: The State of the Current Pandemic?
ACE stands for Act-Connect-Engage, and I’m so grateful to have had the chance to do this with my family and friends back home in Illinois. Because this war against COVID-19 is a fight we must continue to pursue, as we continue to literally learning about a new disease as we treat it in realtime.
I had the honor of leading off the discussion, and worked to set up a basic framework to address some questions the audience had sent me in advance. As I mentioned in my talk, the opinions in that talk and in this blog are mine and not those of my employer.
We discussed first what is SARS-CoV-2, and how it is one of three highly pathogenic coronaviruses known to infect humans. There are actually 7 species of coronaviruses that infect humans, and the other 4 are responsible for 10–30% of upper respiratory infections (a.k.a. colds) worldwide (Paules, Marston, Fauci. JAMA 2020; 323: 707–8).
We walked through the timeline of SARS-CoV-2 to bring us through where we’ve traveled and where we currently stand, using as a framework the excellent recent review article by Dr. Wiersinga and colleagues: Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19) (Wiersinga et al, JAMA 2020; 324: 782–93). Please see the figure.
We discussed how the virus was first a novel coronavirus 2019-nCoV and then was renamed to SARS-CoV-2 (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses. Nature Microbiology 2020; 5: 536–544). We reviewed how the virus binds to ACE2 on a patient’s cells, and then enters the cell via endocytosis and replicates as well as causes damage. ACE2 protein is expressed in the upper airway, lower respiratory tract in airway epithelial cells and pulmonary vascular cells, as well as in many tissues throughout the body (Gheblawi M et al. Circ Res 2020; 126: 1456–1474).
We walked through transmission and presentation, and what I did not mention, but have been reading is that the percentage of asymptomatic transmission may actually be increasing. There are two recent interesting articles by Dr. Monica Gandhi about the topic of how face masks may also reduce spread, not only by protecting an asymptomatic wearer by lowering the respiratory droplets they emit through talking, but by reducing the effective dose a wearer may be exposed to, making it more likely they’ll mount an immune response to a limited exposure to the virus rather than a full dose of exposure. It has been shown throughout the pandemic that those with repeated, direct contact are most at risk of infection. One can think of respiratory therapists, nurses, and other healthcare workers, for example. Therefore the authors propose that limiting that exposure dose through cloth masks logically would allow for fewer viral particles and a less potent inoculum, thereby giving the infected patient a chance to fight it off perhaps without even feeling the effects of the illness or having more limited disease. (Gandhi M, Rutherford GW. Facial Masking for Covid-19 — Potential for “Variolation” as We Await a Vaccine. NEJM 2020: DOI: 10.1056/NEJMp2026913 and Ghandhi M, Beyrer C, Goosby E. Masks Do More Than Protect Others During COVID-19: Reducing the Inoculum of SARS-CoV-2 to Protect the Wearer. J Gen Intern Medicine 2020; 382: DOI: 10.1007/s11606–020–06067–8). We discussed both modifiable (diseases like obesity and hypertension and type 2 diabetes) and non-modifiable (age) risk factors for infection and hospitalization, and shared data from the CDC.gov website. Finally we talked about the different ways this disease presents, what is ARDS, and current treatments. I shared the concepts of how trials so far have shown that certain treatments are indicated in particular levels of disease (e.g., use of steroids in patients who require supplemental oxygen, for example, but not in patients that don’t require supplemental oxygen). For more information on the various treatments, see the living document from the NIH here: COVID-19 Treatment Guidelines Panel. Coronavirus Disease 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Available at https://www.covid19treatmentguidelines.nih.gov/. This is updated as new information is reviewed by NIH Treatment Guidelines panel of experts.
We discussed briefly the longterm effects of COVID-19, and the “long haulers” as described in the media recently. The short answer is that we are still learning as we treat patients what are the mid-term and long-term effects. There is a fascinating story in The Atlantic that describes how patients are finding each other and working to describe this post-COVID phenomenon.
Finally, I shared our experience in Colorado, and the impact of the mask mandate on lowering our cases. We talked about the concept of a second wave, and the history of the second wave in the 1918 Influenza, and how that might inform us of what may come this fall and winter. There is great information on the 1918 influenza pandemic on the CDC website, and I recommend the book, The Great Influenza by John Barry.
At the end of my talk I shared a little of my personal experience as a doctor taking care of patients with COVID-19, how it changed how I view medicine and my calling to try to make a difference, not only at the bedside, but in the longterm as we strive to figure this out. I talked about my experience in New York City, and my admiration for the New York physicians who worked there for months when the system was truly overrun and system overwhelmed at the peak of the pandemic. I have so much respect for my colleagues who were on the early front lines of this pandemic.
After the talk, one question came across asking about the bradykinin hypothesis, which I find quite interesting. They basically describe how increased bradykinin, which can happen when the renin-angiotensin system (RAS) becomes dysregulated by the virus infecting and downregulating ACE2 expression, which then skews the system toward exacerbating the effects of bradykinin, leading to elevated bradykinin activity in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. I’ll dive more into hypotheses about COVID-19 pathogenesis in a future blog post, but in the meantime check out this blog post by Thomas Smith. Here is the original article describing the research into the bradykinin hypothesis by Garvin et al from eLife: (eLife 2020;9:e59177 DOI: 10.7554/eLife.59177).
Where are we with COVID-19? — Notes from my discussion with ACE-Naperville
When I came back from New York City in May, I felt a new motivation to take what I experienced, and work to better understand COVID-19. I started designing research trials in my head, and put ideas on paper. I continued to read. However, I got a bit off track for awhile due to the challenges of our non-COVID pulmonary clinic picking back up again (a good problem), and various battles that fall under the umbrella of my regular job. That is why I am grateful to ACE-Naperville for asking me to participate as a panelist in their latest Zoom Meeting. The topic: COVID-19: The State of the Current Pandemic?
[ACE stands for Act-Connect-Engage](https://actconnectengage.com), and I’m so grateful to have had the chance to do this with my family and friends back home in Illinois. Because this war against COVID-19 is a fight we must continue to pursue, as we continue to literally learning about a new disease as we treat it in realtime.
I had the honor of leading off the discussion, and worked to set up a basic framework to address some questions the audience had sent me in advance. As I mentioned in my talk, the opinions in that talk and in this blog are mine and not those of my employer.
We discussed first what is SARS-CoV-2, and how it is one of three highly pathogenic coronaviruses known to infect humans. There are actually 7 species of coronaviruses that infect humans, and the other 4 are responsible for 10–30% of upper respiratory infections (a.k.a. colds) worldwide ([Paules, Marston, Fauci. JAMA 2020; 323: 707–8](https://jamanetwork.com/journals/jama/fullarticle/2759815)).
We walked through the timeline of SARS-CoV-2 to bring us through where we’ve traveled and where we currently stand, using as a framework the excellent recent review article by Dr. Wiersinga and colleagues: Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19) ([Wiersinga et al, JAMA 2020; 324: 782–93](https://jamanetwork.com/journals/jama/fullarticle/2768391)). Please see the figure. We discussed how the virus was first a novel coronavirus 2019-nCoV and then was renamed to SARS-CoV-2 (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses. Nature Microbiology 2020; 5: 536–544). We reviewed how the virus binds to ACE2 on a patient’s cells, and then enters the cell via endocytosis and replicates as well as causes damage. ACE2 protein is expressed in the upper airway, lower respiratory tract in airway epithelial cells and pulmonary vascular cells, as well as in many tissues throughout the body ([Gheblawi M et al. Circ Res 2020; 126: 1456–1474](https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.317015)).
We walked through transmission and presentation, and what I did not mention, but have been reading is that the percentage of asymptomatic transmission may actually be increasing. There are two recent interesting articles by Dr. Monica Gandhi about the topic of how face masks may also reduce spread, not only by protecting an asymptomatic wearer by lowering the respiratory droplets they emit through talking, but by reducing the effective dose a wearer may be exposed to, making it more likely they’ll mount an immune response to a limited exposure to the virus rather than a full dose of exposure. It has been shown throughout the pandemic that those with repeated, direct contact are most at risk of infection. One can think of respiratory therapists, nurses, and other healthcare workers, for example. Therefore the authors propose that limiting that exposure dose through cloth masks logically would allow for fewer viral particles and a less potent inoculum, thereby giving the infected patient a chance to fight it off perhaps without even feeling the effects of the illness or having more limited disease. ([Gandhi M, Rutherford GW. Facial Masking for Covid-19 — Potential for “Variolation” as We Await a Vaccine. NEJM 2020: DOI: 10.1056/NEJMp2026913](https://www.nejm.org/doi/full/10.1056/NEJMp2026913) and G[andhi M, Beyrer C, Goosby E. Masks Do More Than Protect Others During COVID-19: Reducing the Inoculum of SARS-CoV-2 to Protect the Wearer. J Gen Intern Medicine 2020; 382: DOI: 10.1007/s11606–020–06067–8](https://link.springer.com/article/10.1007/s11606-020-06067-8)). We discussed both modifiable (diseases like obesity and hypertension and type 2 diabetes) and non-modifiable (age) risk factors for infection and hospitalization, and shared data from the CDC.gov website. Finally we talked about the different ways this disease presents, what is ARDS, and current treatments. I shared the concepts of how trials so far have shown that certain treatments are indicated in particular levels of disease (e.g., use of steroids in patients who require supplemental oxygen, for example, but not in patients that don’t require supplemental oxygen). For more information on the various treatments, see the living document from the NIH here: COVID-19 Treatment Guidelines Panel. Coronavirus Disease 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Available at https://www.covid19treatmentguidelines.nih.gov/. This is updated as new information is reviewed by NIH Treatment Guidelines panel of experts.
We discussed briefly the longterm effects of COVID-19, and the “long haulers” as described in the media recently. The short answer is that we are still learning as we treat patients what are the mid-term and long-term effects. There is a fascinating story in The Atlantic that describes how patients are finding each other and working to describe this post-COVID phenomenon.
Finally, I shared our experience in Colorado, and the impact of the mask mandate on lowering our cases. We talked about the concept of a second wave, and the history of the second wave in the 1918 Influenza, and how that might inform us of what may come this fall and winter.
At the end of my talk I shared a little of my personal experience as a doctor taking care of patients with COVID-19, how it changed how I view medicine and my calling to try to make a difference, not only at the bedside, but in the longterm as we strive to figure this out. I talked about my experience in New York City, and my admiration for the New York physicians who worked there for months when the system was truly overrun and system overwhelmed at the peak of the pandemic. I have so much respect for my colleagues who were on the early front lines of this pandemic.
After the talk, one question came across asking about the bradykinin hypothesis, which I find quite interesting. They basically describe how increased bradykinin, which can happen when the renin-angiotensin system (RAS) becomes dysregulated by the virus infecting and downregulating ACE2 expression, which then skews the system toward exacerbating the effects of bradykinin, leading to elevated bradykinin activity in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. I’ll dive more into hypotheses about COVID-19 pathogenesis in a future blog post, but in the meantime check out this [blog post by Thomas Smith. ](https://elemental.medium.com/a-supercomputer-analyzed-covid-19-and-an-interesting-new-theory-has-emerged-31cb8eba9d63)Here is the original article describing the research into the bradykinin hypothesis by Garvin et al from eLife: ([eLife 2020;9:e59177 DOI: 10.7554/eLife.59177](https://elifesciences.org/articles/59177)).
To see my slides, feel free to download the pdf.
Where are we with COVID-19? — Notes from my discussion with ACE-Naperville
When I came back from New York City in May, I felt a new motivation to take what I experienced, and work to better understand COVID-19. I started designing research trials in my head, and put ideas on paper. I continued to read. However, I got a bit off track for awhile due to the challenges of our non-COVID pulmonary clinic picking back up again (a good problem), and various battles that fall under the umbrella of my regular job. That is why I am grateful to ACE-Naperville for asking me to participate as a panelist in their latest Zoom Meeting. The topic: COVID-19: The State of the Current Pandemic?
[ACE stands for Act-Connect-Engage](https://actconnectengage.com), and I’m so grateful to have had the chance to do this with my family and friends back home in Illinois. Because this war against COVID-19 is a fight we must continue to pursue, as we continue to literally learning about a new disease as we treat it in realtime.
I had the honor of leading off the discussion, and worked to set up a basic framework to address some questions the audience had sent me in advance. As I mentioned in my talk, the opinions in that talk and in this blog are mine and not those of my employer.
We discussed first what is SARS-CoV-2, and how it is one of three highly pathogenic coronaviruses known to infect humans. There are actually 7 species of coronaviruses that infect humans, and the other 4 are responsible for 10–30% of upper respiratory infections (a.k.a. colds) worldwide ([Paules, Marston, Fauci. JAMA 2020; 323: 707–8](https://jamanetwork.com/journals/jama/fullarticle/2759815)).
We walked through the timeline of SARS-CoV-2 to bring us through where we’ve traveled and where we currently stand, using as a framework the excellent recent review article by Dr. Wiersinga and colleagues: Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19) ([Wiersinga et al, JAMA 2020; 324: 782–93](https://jamanetwork.com/journals/jama/fullarticle/2768391)). Please see the figure. We discussed how the virus was first a novel coronavirus 2019-nCoV and then was renamed to SARS-CoV-2 (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses. Nature Microbiology 2020; 5: 536–544). We reviewed how the virus binds to ACE2 on a patient’s cells, and then enters the cell via endocytosis and replicates as well as causes damage. ACE2 protein is expressed in the upper airway, lower respiratory tract in airway epithelial cells and pulmonary vascular cells, as well as in many tissues throughout the body ([Gheblawi M et al. Circ Res 2020; 126: 1456–1474](https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.317015)).
We walked through transmission and presentation, and what I did not mention, but have been reading is that the percentage of asymptomatic transmission may actually be increasing. There are two recent interesting articles by Dr. Monica Gandhi about the topic of how face masks may also reduce spread, not only by protecting an asymptomatic wearer by lowering the respiratory droplets they emit through talking, but by reducing the effective dose a wearer may be exposed to, making it more likely they’ll mount an immune response to a limited exposure to the virus rather than a full dose of exposure. It has been shown throughout the pandemic that those with repeated, direct contact are most at risk of infection. One can think of respiratory therapists, nurses, and other healthcare workers, for example. Therefore the authors propose that limiting that exposure dose through cloth masks logically would allow for fewer viral particles and a less potent inoculum, thereby giving the infected patient a chance to fight it off perhaps without even feeling the effects of the illness or having more limited disease. ([Gandhi M, Rutherford GW. Facial Masking for Covid-19 — Potential for “Variolation” as We Await a Vaccine. NEJM 2020: DOI: 10.1056/NEJMp2026913](https://www.nejm.org/doi/full/10.1056/NEJMp2026913) and G[andhi M, Beyrer C, Goosby E. Masks Do More Than Protect Others During COVID-19: Reducing the Inoculum of SARS-CoV-2 to Protect the Wearer. J Gen Intern Medicine 2020; 382: DOI: 10.1007/s11606–020–06067–8](https://link.springer.com/article/10.1007/s11606-020-06067-8)). We discussed both modifiable (diseases like obesity and hypertension and type 2 diabetes) and non-modifiable (age) risk factors for infection and hospitalization, and shared data from the CDC.gov website. Finally we talked about the different ways this disease presents, what is ARDS, and current treatments. I shared the concepts of how trials so far have shown that certain treatments are indicated in particular levels of disease (e.g., use of steroids in patients who require supplemental oxygen, for example, but not in patients that don’t require supplemental oxygen). For more information on the various treatments, see the living document from the NIH here: COVID-19 Treatment Guidelines Panel. Coronavirus Disease 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Available at https://www.covid19treatmentguidelines.nih.gov/. This is updated as new information is reviewed by NIH Treatment Guidelines panel of experts.
We discussed briefly the longterm effects of COVID-19, and the “long haulers” as described in the media recently. The short answer is that we are still learning as we treat patients what are the mid-term and long-term effects. There is a fascinating story in The Atlantic that describes how patients are finding each other and working to describe this post-COVID phenomenon.
Finally, I shared our experience in Colorado, and the impact of the mask mandate on lowering our cases. We talked about the concept of a second wave, and the history of the second wave in the 1918 Influenza, and how that might inform us of what may come this fall and winter.
At the end of my talk I shared a little of my personal experience as a doctor taking care of patients with COVID-19, how it changed how I view medicine and my calling to try to make a difference, not only at the bedside, but in the longterm as we strive to figure this out. I talked about my experience in New York City, and my admiration for the New York physicians who worked there for months when the system was truly overrun and system overwhelmed at the peak of the pandemic. I have so much respect for my colleagues who were on the early front lines of this pandemic.
After the talk, one question came across asking about the bradykinin hypothesis, which I find quite interesting. They basically describe how increased bradykinin, which can happen when the renin-angiotensin system (RAS) becomes dysregulated by the virus infecting and downregulating ACE2 expression, which then skews the system toward exacerbating the effects of bradykinin, leading to elevated bradykinin activity in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. I’ll dive more into hypotheses about COVID-19 pathogenesis in a future blog post, but in the meantime check out this [blog post by Thomas Smith. ](https://elemental.medium.com/a-supercomputer-analyzed-covid-19-and-an-interesting-new-theory-has-emerged-31cb8eba9d63)Here is the original article describing the research into the bradykinin hypothesis by Garvin et al from eLife: ([eLife 2020;9:e59177 DOI: 10.7554/eLife.59177](https://elifesciences.org/articles/59177)).
To see my slides, feel free to download the pdf.
Where are we with COVID-19? — Notes from my discussion with ACE-Naperville
When I came back from New York City in May, I felt a new motivation to take what I experienced, and work to better understand COVID-19. I started designing research trials in my head, and put ideas on paper. I continued to read. However, I got a bit off track for awhile due to the challenges of our non-COVID pulmonary clinic picking back up again (a good problem), and various battles that fall under the umbrella of my regular job. That is why I am grateful to ACE-Naperville for asking me to participate as a panelist in their latest Zoom Meeting. The topic: COVID-19: The State of the Current Pandemic?
[ACE stands for Act-Connect-Engage](https://actconnectengage.com), and I’m so grateful to have had the chance to do this with my family and friends back home in Illinois. Because this war against COVID-19 is a fight we must continue to pursue, as we continue to literally learning about a new disease as we treat it in realtime.
I had the honor of leading off the discussion, and worked to set up a basic framework to address some questions the audience had sent me in advance. As I mentioned in my talk, the opinions in that talk and in this blog are mine and not those of my employer.
We discussed first what is SARS-CoV-2, and how it is one of three highly pathogenic coronaviruses known to infect humans. There are actually 7 species of coronaviruses that infect humans, and the other 4 are responsible for 10–30% of upper respiratory infections (a.k.a. colds) worldwide ([Paules, Marston, Fauci. JAMA 2020; 323: 707–8](https://jamanetwork.com/journals/jama/fullarticle/2759815)).
We walked through the timeline of SARS-CoV-2 to bring us through where we’ve traveled and where we currently stand, using as a framework the excellent recent review article by Dr. Wiersinga and colleagues: Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19) ([Wiersinga et al, JAMA 2020; 324: 782–93](https://jamanetwork.com/journals/jama/fullarticle/2768391)). Please see the figure. We discussed how the virus was first a novel coronavirus 2019-nCoV and then was renamed to SARS-CoV-2 (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses. Nature Microbiology 2020; 5: 536–544). We reviewed how the virus binds to ACE2 on a patient’s cells, and then enters the cell via endocytosis and replicates as well as causes damage. ACE2 protein is expressed in the upper airway, lower respiratory tract in airway epithelial cells and pulmonary vascular cells, as well as in many tissues throughout the body ([Gheblawi M et al. Circ Res 2020; 126: 1456–1474](https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.317015)).
We walked through transmission and presentation, and what I did not mention, but have been reading is that the percentage of asymptomatic transmission may actually be increasing. There are two recent interesting articles by Dr. Monica Gandhi about the topic of how face masks may also reduce spread, not only by protecting an asymptomatic wearer by lowering the respiratory droplets they emit through talking, but by reducing the effective dose a wearer may be exposed to, making it more likely they’ll mount an immune response to a limited exposure to the virus rather than a full dose of exposure. It has been shown throughout the pandemic that those with repeated, direct contact are most at risk of infection. One can think of respiratory therapists, nurses, and other healthcare workers, for example. Therefore the authors propose that limiting that exposure dose through cloth masks logically would allow for fewer viral particles and a less potent inoculum, thereby giving the infected patient a chance to fight it off perhaps without even feeling the effects of the illness or having more limited disease. (Gandhi M, Rutherford GW. Facial Masking for Covid-19 — Potential for “Variolation” as We Await a Vaccine. NEJM 2020: DOI: 10.1056/NEJMp2026913 and Ghandhi M, Beyrer C, Goosby E. Masks Do More Than Protect Others During COVID-19: Reducing the Inoculum of SARS-CoV-2 to Protect the Wearer. J Gen Intern Medicine 2020; 382: DOI: 10.1007/s11606–020–06067–8). We discussed both modifiable (diseases like obesity and hypertension and type 2 diabetes) and non-modifiable (age) risk factors for infection and hospitalization, and shared data from the CDC.gov website. Finally we talked about the different ways this disease presents, what is ARDS, and current treatments. I shared the concepts of how trials so far have shown that certain treatments are indicated in particular levels of disease (e.g., use of steroids in patients who require supplemental oxygen, for example, but not in patients that don’t require supplemental oxygen). For more information on the various treatments, see the living document from the NIH here: COVID-19 Treatment Guidelines Panel. Coronavirus Disease 2019 (COVID-19) Treatment Guidelines. National Institutes of Health. Available at https://www.covid19treatmentguidelines.nih.gov/. This is updated as new information is reviewed by NIH Treatment Guidelines panel of experts.
We discussed briefly the longterm effects of COVID-19, and the “long haulers” as described in the media recently. The short answer is that we are still learning as we treat patients what are the mid-term and long-term effects. There is a fascinating story in The Atlantic that describes how patients are finding each other and working to describe this post-COVID phenomenon.
Finally, I shared our experience in Colorado, and the impact of the mask mandate on lowering our cases. We talked about the concept of a second wave, and the history of the second wave in the 1918 Influenza, and how that might inform us of what may come this fall and winter.
At the end of my talk I shared a little of my personal experience as a doctor taking care of patients with COVID-19, how it changed how I view medicine and my calling to try to make a difference, not only at the bedside, but in the longterm as we strive to figure this out. I talked about my experience in New York City, and my admiration for the New York physicians who worked there for months when the system was truly overrun and system overwhelmed at the peak of the pandemic. I have so much respect for my colleagues who were on the early front lines of this pandemic.
After the talk, one question came across asking about the bradykinin hypothesis, which I find quite interesting. They basically describe how increased bradykinin, which can happen when the renin-angiotensin system (RAS) becomes dysregulated by the virus infecting and downregulating ACE2 expression, which then skews the system toward exacerbating the effects of bradykinin, leading to elevated bradykinin activity in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. I’ll dive more into hypotheses about COVID-19 pathogenesis in a future blog post, but in the meantime check out this [blog post by Thomas Smith. Here is the original article describing the research into the bradykinin hypothesis by Garvin et al from eLife: (eLife 2020;9:e59177 DOI: 10.7554/eLife.59177).
To see my slides, feel free to download the pdf.
Thank you again to ACE-Naperville, for letting me participate in the panel. To see my slides, feel free to download the pdf from Slideshare.