John, thank you so much for joining us. Pleasure. Sure. And Laney, there are only two more minutes to go. One more. Okay. Actually, I can start now since I'm spending the early part introducing the panelists and no one really cares about who we are. They really. I'm going to start off by talking about John Barry. So I think I'm just going to start. Welcome everyone to this exciting zoom lecture as part of our series on COVID-19. Today we're going to be interviewing and having a conversation with John Barry, the author of the great influenza, the epic story of the deadliest pandemic in history. Before I introduce John, I thought I would introduce our panel so that he would know who's speaking. John Barry is a professor of medicine, and he has written several books on pediatric ethics and transplantation ethics. One of the other co-directors of this series is Brian calendar, who's an adult hospitalist. And on faculty at the McLean center for clinical medical ethics, he's interested in the health humanities with a focus on the phenomenology of illness, the visual culture of medicine and the role of comics and healthcare. We also have Bob Richards, theory and the impact of German romanticism on the development of science in the 19th century. Next we have Mindy Schwartz, a clinician, historian, and medical educator. She has produced educational resources for use in undergraduate and graduate medical education. We also have Michael Rossi, a historian of medicine and science at the University of Chicago. His most recent book, The Republic of Color, is a history of color theory and perception in America. And of course we have our director of the Bucksbaum Institute in the McLean Center for Clinical Medical Ethics, Dr. Mark Siegler. So now to introduce John Barry. So John was born and raised in Providence, Rhode Island. He graduated from Brown University in 1968, started with a master's in history in 1969 from the University of Rochester, but then withdrew from the PhD program. He then coached high school and college football and his first published article appeared in a professional journal for coaches, called Scholastic Coach. So I have to ask John, did you play football? I sat on the bench, that's why I... That's why you wrote the article. Twenty years later, John published his first book, The Ambition and the Power, a true story of Washington, published in 1989, which examined the rise and fall of Jim Wright, who succeeded Tipo Neela, speaker of the House. His next three books had a science medical term. First in 1993, he published The Transform Cell, Unlocking the Mysteries of Cancer, which he wrote with Stephen Rosenberg, Chief of Surgery at the NCI. Next in 1997, he wrote Rising Tide, The Great Mississippi Flood of 1927 and How It Changed America, which was recognized by the National Academies of Science, which invited him to give the 2006 Able-Walman Distinguished Lecture on Water Resources. He's the only non-scientist who have given that lecture. And finally, in 2004, he published The Great Influenza, The Epic Story of the Greatest Plague in History, which won the 2005 Keck Communication Award from the National Academies of Science, Engineering and Medicine. He served on Federal Government Infectious Disease Board of Experts on the Advisory Board of MIT Center for Engineering Fundamentals and on the Advisory Committee at Hopkins School of Public Health for its Center for Refugee and Disaster Response. The twists in terms of his career don't end there, although I'm going to stop here because we want to talk about that book. But just to note that in 2012, John wrote a book about Roger Williams and the creation of the American Soul, Church, State and the Birth of Liberty. But as I said, today we're going to focus on The Great Influenza. So John, while this panel has spent the past month reading your book, just for those who have not read it, who are in the audience and there's over a hundred who have already arrived, can you just summarize the book's main findings? That's too big a question. One of the two take home points. How's that? Well, first, the pandemic probably killed between 1500 million people. I think the lowest modern estimate, although there is one outlier, is probably 40 million people. So if you adjust for population, that would be roughly between 225 to 450 million people today. The main lessons, I think, from the pandemic are two. Number one, public health leaders and all leaders need to tell the truth if they expect to have a good result. And number two, non-pharmaceutical interventions can have some impact on the outcome. So that is in brief. You know, the book itself focused a lot on the scientists who confronted the pandemic. So talking about the non-pharmacological interventions, how much was known about that in 1918 and when? And did they understand masks and if so, did they use it or what was it? Well, actually the masks, that's a very interesting question. They were running lab tests and some pretty good experiments on masks in 1917 during the measles epidemic in army camps, which killed quite a few soldiers. And they concluded then, in fact, they aborted the experiments because they were effective and they transferred the information to pretty much everybody else, that masks, when put on somebody who was ill, were effective in protecting people who were well. And a lot of cities that, you know, that information spread through the medical community and a lot of cities mandated masks in 1918. However, most of the studies, in fact, all the studies after the pandemic and there were quite a few of them, concluded that masks for the general public were not useful. Now, whether that was because most of the masks, most were using simple gauze or some other material, other people were sloppy and how they wore them. I don't know, but that was the conclusion pretty much universally held in studies, comprehensive reviews of epidemiological data in the 20s. And based on that information, like pretty much everybody else, when this pandemic started, I was saying, I don't think masks for the public were useful. But of course, you know, you do get presymptomatic transmission and influenza, but nothing like the asymptomatic or presymptomatic transmission in COVID-19. You know, there's still some controversy about masks here, but I think most of the observational data is pretty compelling. And based on that, I know I changed my position on masks as has pretty much everybody else. I wish I had everybody else. You know, we're talking now with COVID-19 that we're hitting our third spike here. How much was understood that the influenza 1918 was going to return and whether it was expected to mutate and become either more severe or less severe? And how does that compare with today's Vikings? Well, of course, in 1918, they didn't even know what a virus was. They did know there were very small organisms that passed through filters, which I refer to as filterable viruses. But the pathogen that supposedly caused influenza, identified by a disciple of Robert Koch, obviously very well respected is named Richard Pfeiffer. And that bacteria still bears the name influenza, homophilus influenza. Obviously, that was not the pathogen. There was a very mild spring wave and it didn't get that much attention because of the mildness. In fact, you could see, read medical journal articles saying this looks and smells like influenza, but it can't be because it's not killing enough people. In my view, and I think the view of most virologists whose view matters more than nine, I guess, the virus mutated. There is a minority view that thinks the spring and fall waves were so different in terms of virulence that they were actually different viruses. I think the evidence is compelling that they were the same virus. I could go into detail if anybody cares. At any rate, in the fall, you got a very, very virulent strain spread around the world. There was no expectation of it. And then a few months later, late winter, very early spring in 1919, you got a third wave. I would say probably about two thirds of the deaths occurred in a period of about 14 or 15 weeks between late September and December 1918. In any given city, the virus moved much more rapidly through a particular location. So it would have been probably six to 10 weeks at most that any particular city was suffering with the second wave. The third wave was shorter by any standard except the second wave. The third wave was lethal, but it was still nothing like the second wave. So I've read that the book took seven years to research and write. And so my question is, why were you interested in influenza in 1997? Well, it's a good... When I was a kid, there were only two things I wanted to do. One was be a writer, and the other was do biomedical research. And I guess I had always had some interest in the pandemic. I actually was planning to write a book about the home front during World War I, not, in fact, the influenza pandemic at all. The way I viewed that book, it was going to take me at least seven years to write. As a... I live on the advance. It wasn't going to get an advance for that book on the home front in World War I that could keep me paying the mortgage for seven years. So I thought I would bite off this chunk of the book on influenza that would subsidize a larger book. I was very confident I could write the influenza book in probably two years, no more than two and a half years. And didn't work out that way. During the first five and a half years, I was working on the book. I wish I had never agreed to write it. I wanted to throw the whole thing out the window. And there's a one scientist in the book named Oswald Avery, brilliant scientist, probably the single person most deserving in the Nobel Prize who never got it. And maybe a lot of people can make that claim, but Avery's number one on the list, I think. At any rate, his frustrations over his research career, which I tracked, sort of kept me going. And in fact, speaking of football, Lloyd Carr, the former Michigan football coach, is a friend of mine. When he was still coaching at Michigan, they had a couple of down times for Michigan. And he actually told his team the story of Oswald Avery, what Avery went through, not publishing for like 11 years, which as you know, for scientists not to publish for an 11-year period is that's like losing 35, 40 football games in a row. But anyway, we'll get on to the next question. So I want to waste your time talking about that. Good that you sat on the bench. You didn't get concussions. Do you believe? I did have a concussion, as a matter of fact. Well, I didn't sit on the bench in high schools, only college. Do you believe that the war exacerbated or didn't exacerbate the spread of influenza? And how does that external factor? So 1918, we have the war. Today we have college campuses, more widespread air travel, how do those compare and contrast? Okay. First, as far as the war, you know, the war may have accelerated the spread, but I don't think at any impact beyond that. You know, there are some evolutionary biologists who argue that the proximity of people in the trenches allowed a very own strain to emerge. I don't think that, you know, what is Thomas Huxley said, the great tragedy of science is a beautiful theory slain by an ugly fact. I don't think any facts support that theory, including the fact that the first widespread lethal form of the disease occurred in Switzerland, which was not a war. Also, even in the virulent form, you still got 98% of people who have ordinary attack of influenza. So I don't know how much evolutionary pressure that puts on the virus. So it may have accelerated the spread. You may not have even done that, but and remember of the 50 to 100 million people who died, the vast majority of them were not in Western Europe. So I don't think the war had a lot of impact. And then you asked another part of the question. The other part was just now that we have air travel, we have, you know, lots of yeah, certainly that accelerates things and gives you less time to react. But we need to remember that not only in 1918, did a pandemic spread around the world without air travel, but in 1889. And going back to 1698, we had an influenza pandemic make it from Europe to North America when it took weeks to cross the ocean. And it was quite effective in killing Native Americans in North America. So, you know, air travel is certainly something of importance because spread is a couple of, you know, four or five, six hours or long flight, 12 hours, as opposed to a matter of days. But I think a virus, once it's out there in a population, like well, obviously, it's going to get around the world inevitably, almost no matter what you do. So I'm a pediatrician. And here in Chicago, we have bars that are now reopened, but our schools are closed. And so what was done about schooling back in 1918 and sort of how did they just address that at all levels? Almost every city in the country with the Chicago noted exception closed schools. New York didn't close schools either. And in fact, both New York and Chicago had relatively benign experiences, at least compared to the really hard hit cities. And, you know, I think there's strong evidence as far as I'm concerned, both of them had spring outbreaks, which bypassed a lot of cities in the United States didn't have any spring, like Los Angeles didn't have a single influenza or pneumonia death in the spring in 1918, at least not one that was recorded. At any rate, I think the exposure to the first wave in Chicago and New York led to that relatively benign experience. That's one of the reasons why I think there's compelling evidence that the first and second waves were the same virus. But almost every place closed schools. We do remember, though, that influenza and COVID-19 are different viruses.  We know kids are vulnerable. We also know kids are super spreaders. So there's a pretty good reason to close schools for influenza in a pandemic. And COVID-19, they may or may not spread like everybody else, but they're not super spreaders. And they're certainly not particularly vulnerable. So the whole issue of the schools closing is much different for COVID-19 than for influenza, I think. So you suggested that by the second and third wave, there was enough sort of immunity in the community. I read your piece in the New York Times yesterday where you don't think that's a good strategy for COVID-19. Well, I mean, in 1918, you had nothing but herd immunity. You know, they developed a lot of vaccines, but they were all aimed at one bacterial pathogen or another. They didn't know, as I said, what a virus was, much less how to grow one. So the vaccines didn't work. If you were fortunate enough to be attacked by bacteria that the vaccine was carrying against them, they could be effective. Incidentally, Avery, whom I mentioned earlier, developed an antinomacoccal vaccine, which if you get a shot today, it's a straight line descendant of what he developed back then. You know, the disease would arrive. It would move through the community and move on. Generally, probably about somewhere between, well, the highest morbidity occurred in San Antonio. There's some very good work done in San Antonio. 53% of the population was infected. 98% of every household had at least one person in the household infected. But that was a bit of an outlier. Generally speaking, I think it's estimated about 28% of the US population was infected, about a third of the world. COVID-19, as we all know, probably everybody on this Zoom call knows, is actually more transmissible than influenza. I think most of the estimates, you know, there's one sort of low ball estimate that 40% of the population would achieve herd immunity. I think most of the models really suggest that it would be considerably higher than that. And I think the real world data from prisons, and I mentioned Latin America, the op-ed that ran in the times yesterday, the real world data suggests it would be over 60% needed for herd immunity. I think the death toll for that would be unacceptable. Plus, I mean, if you want me to get into this, I could go more as to why I don't think that's a good policy, but I'll leave that to you. No, I'm not going to take you up on that offer, because I have to share this panel, but maybe for another time. From your book, it seemed that there was actually broad collaboration, the sharing of samples and methods between this cadre of, a small cadre of men, all of whom trained in the same place and seemed to all know each other, even if they didn't get along. And my question is, how would you compare the willingness of the scientists to work together then versus the competition of today? Well, I think there certainly is tremendous competition today, in general. However, I think maybe the only piece of good news out of COVID-19 is that the collaboration from what I understand is just really incredible and not what has been normal way to proceed over the, not just the last couple of years, but pretty much in science. It's a very competitive field, but people really do seem to be sharing information. There's also much more interdisciplinary work that's going on. Sylo's broken down. I don't really like that word, but you don't know what it means. I think people are being much more creative and open to ideas and willing to try anything and following proper procedures and so forth. You know, that was back in 1918 as a much smaller group of people. They were great scientists. You know, one minor character in the book won the Nobel Prize in 1966 for work he did in 1911. So he was 55 years ahead of the curve. It's pretty good work. They did, most of them know each other. It was a much smaller community. You know, they had egos then, but I think there was maybe more sharing than is normally the case today, but we're not in a normal situation now. So I think there is a tremendous amount of collaboration and sharing going on now. So I've read that Woodrow Wilson experienced neurological complications from flu that he got. And how common of a problem was that with the great influenza and how does it compare with the long-term health sequelae that we're seeing today with COVID-19? It was extremely common in 1918. Edward Jordan, who was from Chicago and edited the Journal of Infectious Disease at the time was asked by the AMA to write a comprehensive review of the pandemic, which came out in 1927. And he said it was second only to the long in terms of the 1918 virus like COVID-19 or SARS-CoV-2 infected pretty much every organ. When you looked at pathology reports from H5N1 in the early 2000s, I remember reading one that said none of these findings have ever been reported in influenza before. Well, they never read the reports from 1918. Everything from 1918, you know, from literally from the testes to the brain, you know, kidneys, heart, all of that, everything separate. But neurological complications were extremely common. They'd been widely reported with COVID-19, probably not quite as common with COVID-19. You know, obviously impressionistic. I do follow it very closely and in fact, I'm writing a book on it. So I'm, you know, reasonably familiar with the literature. Very common today, but probably not quite as common as in 1918. Obviously, in looking to the future, we just don't know. All right. I'm getting close to the end. So I want to just raise two last questions. The first is in your book, you talked about the disease quoting you from chapter 33. The disease was too universal, too obviously not tied to race or class. And so I just want to push you on that, given that those living in crowded conditions were most at risk, such that the poor died in larger numbers than the rich. Can we really say with 2020 hindsight that influenza was a true equalizer? Or is it similar today that the excess deaths of COVID-19 in black and brown communities? Well, the part that you read, I was speaking in terms of blaming somebody, not that it was necessarily equally, that the burden was equally shared. You know, there is a tendency in the past with disease outbreaks to blame someone for it. And if you were really looking for that advice, you could see in Denver, for example, they were blaming Hispanics in Denver. And, you know, there is some evidence, some other place, some immigrants in New England, maybe. But by and large, you know, again, if you're really looking for the evidence, you can find some. But by and large, that was not the case. And that was fairly unusual. I was not trying to say that the burden was shared equally. Interestingly, African Americans for whatever reason seem to have less morbidity than the white community, although they had higher case mortality. And, you know, why that would be, I don't know, you could say, well, medical care. But I mean, there was nothing but supportive care. And there wasn't very supportive. There's no ICUs. So I'm not sure why that would have been the case, either for the less morbidity or for the somewhat higher case mortality. Wow. And so my last question is, tell us about what you didn't cover in your book about post-pandemic grade influenza. So what happened in 1920 and beyond in the sense, how long did it take for life to sort of, quote, normalize? And was it coordinated at any government level? Or did things just return without? No, it's very hard to separate because the war had was ongoing, of course. You know, there was a recession, fairly steep, not as bad as what we're going through right now, but pretty quick recovery in terms of the economics. There was someone, I can't think of off hand or I'd cite the actual work, someone maybe 10 or 15 years ago started looking at the impact of World War I on suicide and discovered he didn't see a link between the war and suicide, but he saw a link between the pandemic and suicide. And I wasn't even looking for that. So that, you know, was kind of significant, I think. On the other hand, there was a lot of forgetfulness and an amazing lack of literature on the disease, not scientific literature, plenty of that. I mean, fiction, for example, you know, John Dust Pasos got influenza on a troop ship going to Europe, one of the worst places he could have it. And in his body of work, he wrote about two lines about influenza. You know, there's some fiction about it, but not what you would expect from an event like that. So it's hard to buy the same token. So I said, you got the suicides. And the book I quoted Christopher Isherwood wrote Berlin stories from which a great movie cat, you know, what's, I don't know. Cabaret, right, right, right. Great movie came from that. And I recommend it highly to anybody who hasn't seen it. But when the Nazis entered Berlin, he said you could feel it like influenza in the bones. So he expected his audience to understand the dread and the physical symptoms. And they probably did. I think he was he was correct there. So there was a sense that was still out there, but still very, very little written about it. Okay. Thank you very much. I'm going to pass the baton to Brian calendar. But first, I'm just going to Michael, are there any pressing questions related to any of this? Or can we just Well, we have one question about about bioethics, but maybe we could hold that until after Brian after Brian's questions about ethics. So take it away, Brian. Great. Thanks, Laney. And it's a pleasure to get to talking about Professor Barry. So since this is a ethics series, let's focus a little bit of attention on on ethics. So you spend the opening chapters of the book describing the sorry state of medical education and research in the United States leading up to the 1918 pandemic, followed by how these these institutions were transformed into sort of respectable entities. So in 1918, the only country with research ethics code was Germany and sort of setting aside the fact that that didn't safeguard anyone given the atrocities 20 years later. So what was the state of medical and or research ethics in 1918 in the United States? And during the rise of American medical education and research, are you aware of any discussions or initiatives that existed around developing formal or codified clinical or research ethics, especially since many of the key figures in your book studied in Germany or know about sort of German German research methodology. So a bit there to unpack. Yeah, but I can give you a very short answer. I don't know. I didn't come across that. That doesn't mean that it didn't exist. It wasn't an area that I was investigating. On the other hand, I did look pretty deeply into the state of education and one would expect certainly if that was anything that was being widely discussed that I would have come across it. There were ethics questions, not addressed directly as that. Well, I guess they were ethical questions, just the very nature of the education itself. The overwhelming majority of medical schools, the faculty's entire income came from student salaries. So student fees rather not salaries, their salaries came from the fees. So they had no motivation to reject people or flunk people out. You could get into a medical school without a high school diploma. Most of them had essentially no requirements of any kind. At Harvard in the 1870s, you could fail four out of nine courses and get a degree that changed after a recent graduate killed half a dozen patients in a row because they didn't know the lethal dose of opium or morphine, I guess, rather not opium. So certainly those are ethical issues. That began to change with the founding of Hopkins. The med school was 1891. I guess the school itself was 1876. And Hopkins did impose standards. They had some real concerns whether or not anybody would apply. But in fact, most people went to med school really wanted to do the right thing. And they ended up attracting all the best students and Harvard and Columbia and Penn and so forth. A few other schools had to raise their standards to compete with Hopkins. Then in 1910, you got the Flexner report, which in an incredibly short time revolutionized American medical education. So now there are no bad medical schools or some that are a little bit better, but they're all good. But that's in terms of patients and experimentation and things like that, which you normally think of today when you raise a question about ethics. I do not recall ever coming across discussions. And I pretty thoroughly went through William Welsh's papers in the archives at Hopkins. I probably would have seen it if it was there. And he was, you know, William Welsh was the founding dean at Hopkins, and he was easily the most important person in the history of American medicine, arguably the most important in the history of American science. So if he's not referring to it some way, then it's probably not there. It's possible I missed it. I'd say maybe the closest thing in terms of experimentation that would be an ethical issue was there was, when they founded Rockefeller University Hospital, it was then Rockefeller Institute of Medical Research. And there was a question over who was going to control the scientific investigations, whether it would be simply a lab rat, or whether it would be the clinician who was treating the patient.  And, you know, that model remains in foresets, NIH and so forth, and probably pretty much everywhere, I guess. So that would be an ethical consideration, but I think that was done more as a, not out of the ethics of the situation, but simply a power move over who is going to be in charge. Great. Since you're talking about research ethics, I'll sort of come back to that and sort of thinking about informed consent. You know, so informed consent is an important part of the research process, you know. Now, what is your sense of what that was like in terms of who was enrolling in these trials, if they were even sort of considered trials back then, and what was the informed consent process? I really don't have any information on that. So I probably better off not commenting. I can say that there was a different view towards science than at least at the patients that would, for example, go to the Rockefeller Institute Hospital. You know, for millennia, medicine had been able to do very, very little for its patients beyond surgery. You know, maybe there were a few drugs that were developed that at least could relieve pain, but not much more than that. And all of a sudden, at the last part of the 19th century and early in the 20th century, with the germ theory and other things, suddenly medicine was able to do some good. So this is speculation entirely. But my guess is that a patient who went to the Rockefeller Institute Hospital was very happy to be there and submit to anything that they were going to try because it was much more likely to save a life. It would be kind of like someone going to NCI. And I mean, they're there because they want to try everything experimental and they're going to largely agree to pretty much any informed consent that you put in front of them. But I don't know of any systematic effort to inform patients when they were being experimented on.  That's why you're there. Somewhere else, some other hospital, I don't know. In terms of the 1918, you know, people were willing to try everything. I mean, the doctors certainly were, including injecting hydrogen peroxide IV, interestingly. And indeed, the doctor who tried that and wrote it up in JAM, I think half of his patients died. He claimed success.  But there was nothing that he had to do, no consent that he, you probably know much more about the state of things back then than I do because it's your field. But there's nothing I know of that required that physician to inform his patients of that really anything. Great. Since you brought up sort of the sort of JAM and publications, one of the things that sort of is happening now is sort of this rush to get out information and data and trials. And there have been some significant retractions from both the Lancet and the New England Journal of Medicine. And you wrote that back then sort of, they were publishing anything that at least seemed to make sense. There was no time for peer review, no time for careful analysis. So the question is sort of how concerned were journals back then about the quality of the studies they were publishing? And were there any notable retractions that you came across? I can't think of a single retraction. And, you know, I read several years of JAMA, you know, and including the study I just mentioned where a physician had claimed success when literally half of the patients died. And, you know, there were some pretty outlandish treatments tried. People were desperate. Incidentally, convalescent serum was tried and was not found by a very, very good scientist and Boston guy named Milt Rosenau, sort of quite a large figure in the history of public health. And he found it surprisingly ineffective. And there were some other places. But, you know, I don't think the journals went around retracting stuff. And I'm not sure what the peer review process was in terms of getting into a journal back then. You know, there were a couple of journals that were probably higher quality than others, you know, edited by a Welsh or his protegees. But I'm not really sure what the standards were for acceptance. Just to sort of turn some attention to sort of resource allocation. And justice and equitable allocation of resources are important tenants of contemporary bioethics. And so since you were talking about sort of certain interventions like convalescent plasma, vaccine development, when these treatments were developed, it seems to have in the book that they've gone to the military first. So was there any discussion about who first received these resources? And whether or not it was publicly decided or what was the process by which resources were allocated? Well, most of the, you know, first in a very significant proportion of the medical community, particularly the better educated physicians, was in the military. The entire Rockefeller Institute of Medical Research was incorporated into the army. Everybody there became an army officer, except for Avery, whom I mentioned earlier, because Avery was a Canadian. He only became a carpal. William Welsh was a colonel. You know, Victor Vaughn, the dean of the University of Michigan Medical School became a colonel. A lot of the laboratories were army laboratories where these things were developed. So those things sort of naturally went to the military. But there were also a lot of vaccines that were developed in the civilian community, usually locally, and they were usually distributed locally. There was some effort saying, you know, they took a while for the virus to move across the country, look a few weeks. And so the East Coast got hit first. The West Coast got hit several weeks later. There was a highly publicized train ride in which a lot of vaccine developed on the East Coast was being shipped to San Francisco. And got a lot of publicity. Of course, it didn't do any good because it wasn't aimed at the right pathogen. But that was an instance where something was shipped across countries. But again, most of the, certainly in the larger cities, the local medical community, everybody knew how to make a vaccine. You know, it was a well-known technology. Many places developed that the best labs intended to go to the military, but those were military labs. And, you know, so I guess I answered your question. I'm closing up on sort of my time, but one thing I want to sort of ask about is sort of just public health ethics. And particularly around sort of super spreader events. So it seemed like troop movements and the war bond parade played an important role in sort of the spread and explosion of the pandemic as described in the book. But they are certainly contextualized as being central to the war effort, which didn't take priority back then. So the question I have in terms of sort of contemporizing those events with today is what do you make of the contemporary arguments that either the economy and or our liberty and freedom in the form of not wearing masks or holding super spreader events like political rallies or say the Sturgis motorcycle rally are more important than fully controlling the COVID-19 pandemic? Yeah, well, of course, I think that position is ridiculous. You know, as I say, it's not the economy or public health, you know, which is unfortunately the way the Trump administration sees it. You know, as I said, in an op ed in August, they're not antagonistic, they're dance partners and public health is in the lead. If you want the economy to come back, I think the data is very good that the way to do that is to control the virus in places where they have controlled the virus. The economies are doing fairly well. You know, in Germany, for example, restaurants are doing more business today than they did at this time last year. In the United States, even where the restaurants are fully open without restrictions, there are a few places where that's the case, the restaurants are still not doing very well because people are afraid. And there was a Federal Reserve, one of the Federal Reserve banks earlier this year was comparing two states where the communities were right on the border. One state had much stricter regulation than the other state, and they found almost no difference whatsoever in the economy in one state versus the other.  Again, it was fear, it was keeping people out. Nobody's going to go to the movie theaters, whether they're open or not, if they're afraid they're going to get sick and possibly die. So this idea of, and of course the idea of, well, I'm imposing on my liberty by making me wear a mask, that's absurd.  I think that's a reasonable analogy for a fairly decent one, not a stretch at all. So I'm going to pass it along then to Bob Richards to continue the questioning at this time. But Michael, I don't know if you want to check to see in the Q&A if there are any sort of ethics related questions to chat about. There is one question that I think follows from the conversation about freedom. This one comes from, and maybe it's the flip side of freedom perhaps. So this one comes from Tiffany Vaughn and Tiffany asks, how would you compare the public response to the pandemic in 1918 versus today? And the question is specifically focused around fear. So do the people of 1918 exhibit the same type of fear as we see today? Or I suppose, you know, the flip side could be, were they as nonchalant as some people are today? Well, 1918 is very different because the virus was a lot more very long. It also moved a lot faster. You know, if I mean, there are quite a few deaths reported 24 hours after the first symptom, plus two thirds of the deaths were probably people between 18 and 45 years old. P-gates for death was 28. So you have some horrific symptoms. Cyanosis is so intense, you have physicians saying you couldn't tell African American soldiers from white soldiers.  Nosebleed and 15% of the cases in a military camp where the date is good, and you have a significantly smaller percentage, but still it happened, where people were bleeding from their eyes and ears. Pretty horrific symptom. So nobody took this disease lightly in 1918. The government lied about it, literally said this is ordinary influenza by another name was referred to as Spanish influenza, although it didn't start in Spain. But the only thing that didn't reassure anybody, all it did was alienate them because they knew they were being lied to. So you can't really compare 1918 to today in that context. I mean, there was real fear out there, and in some cases terror. At its worst, well, I mentioned Victor Vaughn earlier, dean of the University of Michigan Medical School, major figure in the history of American medicine, had a communicable diseases in the army during the war. So at the peak, he wrote that if this disease continues its current rate of acceleration for a few more weeks, civilization could easily disappear from the face of the era. So that's a pretty extreme statement. And this is, you know, not some guy who goes out there exaggerating everything. This is a private comment he's making written in his own hand, not for public distribution. So, you know, the context was different. You know, there was some resistance from the business community of closing orders. But I didn't really sense any from the general public. There was an anti-masking league that was organized in San Francisco. It's gotten a lot of publicity in the last few months. But that's really an outlier. Also, that came about after the city imposed masks, then lifted the order because it seemed that the pandemic had disappeared. They had to re-close the city and re-impose an asking order. Then they got some resistance. But even that resistance I think has been overblown. And so on that level, it's not really comparable today to today. Excellent. Thank you. Much more to ask. But let me turn it over to Professor Richards.  And I'm interested in the strategies that you have employed in writing your book. You weave your tail around four or five major characters. William Welsh, Paul Lewis, Rufus Cole, Oswald Avery, William Gorgas. Did you antecedently know that you were going to focus on these major characters or did they come out in just the writing of the narrative? They emerged. In fact, one of the reasons actually that I said earlier, I guess one of the first questions was how I came to write the book and so forth. I'd actually drafted a proposal and then abandoned the idea. And if I and my agent had the draft and an editor asked him what I was doing now and against my wishes actually handed the editor the draft and ended up writing the book. Had I fully fleshed out the proposal, which I would normally have done, I would normally have done a lot more research. Maybe those characters would have surfaced. But at the time I drafted the proposal, I knew relatively little. Well, knew hardly anything. It was a long time ago. You're talking about more than 20 years. So I don't remember exactly what that proposal said, but certainly I didn't have all those characters clearly. I think I did know that American medicine had been pretty unimpressive in the 19th century and in an incredibly short time became equal to the best in the world, at least the best part of American medicine did. And I guess I knew that that was going to be part of the story. The other thing that, you know, I'm probably the only person who thinks this, but if you ask me what I write about, I'll tell you I write about power. And in the case of a pandemic, the people with power are going to be the scientific community who confronts that. So I knew that I was going to look for people within the scientific community to help carry the story. But who those people were, I didn't really know. So antecedently you had a notion that you were going to deal with some of the major characters, as it were those who had power and were going to operate as were top down instead of bottom up. As you may know in the current historical community, there is a tendency to avoid histories of great men. This is indeed a history of great men with a lot of subsidiary characters. And it makes it a compelling read, I think, because of that. But going into it, I presume that you recognize that you were going against the grain of the historical community. Yeah. I did plan when I left college to become an academic historian. I did drop out of a school or took a leave of absence. I think the University of Rochester informed me about 15 years later that I was no longer a matriculated student. So I was familiar with historiography. On the other hand, as a political journalist, as someone who's in my first book, I was in the room during some pretty important things that happened. And people at the top have a lot of leverage over what's happening. And anybody who doubts that and need only look around us right now, what would have happened if in 2016, Hillary Clinton had won the world in the United States would be a very, very different place. So I'm more with Aristotle than with the idea of fighting about just people at the bottom, which is not by the same token, some of my favorite, like John Steinbeck and so forth. And obviously there is a great literature written about people from the bottom and some very good history. But my own focus, I think history doesn't happen, people make it.  And I think from a historian's point of view, it's more fun writing about major characters who are interesting in themselves. And I think you cast a net that captured those kinds of characters. Let me just ask maybe a nitty gritty question about plotting. When I have dissertation students coming to me and talking about the development of a dissertation, the advice that I give them is don't do all the research and then start writing, but do a little bit of the research and then start writing and let the narrative develop out of a continuing line of research as opposed to trying to accomplish it all at once, set it aside and then start writing. What is your strategy in approaching the manuscript? Is it do all the research first or is it like a good novelist? One line leads to another and leads you on? Well, I think that probably varies from writer to writer. And I think either method works. I tend to do the research. I won't say that's always the case. I haven't written 20 books, but I've written six. In most cases, I'd say I'd pretty much finish the research before I started writing. I would say that. Or at least I'd done enough research to really feel that I had a very, very good handle on events and character. Historians face, I think, many problems, but there are two major problems, how to begin a book and how to end a book. You end the book in an interesting way. You don't stop with the end of the virus because the virus, as it were, as Mr. Trump has suggested, sort of miraculously melts away. And the figures that you depict were working along the wrong lines. They were working on Pfeiffer's bacterium and trying to nail that down as the culprit in the virus, in the disease. And now as you point out, we know it's a virus. But you didn't end it at 1920. You continue on with two stories, one of Oswald Avery and one with Paul Lewis and contrast them at the end. Why did you choose to do that? Why didn't you just end the story with the end of the virus and the unsuccessful efforts to find a vaccine for the bacillus? Well, I mean, I was writing about the characters. And I think both of them are compelling characters. Lewis, a great tragic hero, or maybe comic hero, depending on how you view him, a man with enormous potential. And the children, people who are prominent scientists today, whose fathers were also prominent scientists in two completely different geographic areas. Their fathers had both worked with Lewis, and they said he was the smartest guy they had ever known. And these are people who work with multiple Nobel laureates, one at Rockefeller University and other somewhere else. But Lewis just did not have the magic touch. His lab work just in turnout. He was advised by Flexner, the head of the Rockefeller Institute. Lewis was offered some great jobs. And Flexner told him, look, you are not going to become a fellow here. We're going to terminate your contract. Take this job. He could have been a great impresario, almost a Welsh-like figure, maybe, but he wanted to be in the lab. And in my view, Lewis committed suicide by giving himself yellow fever. There was a scene in Sinclair Lewis's book, Arrow Smith, where somebody died from a lab accident. And that led to, I mean, Lewis, I think, wanted to go out that way. And a Japanese scientist, Naguchi, died also from a lab accident and had essentially a Viking funeral. And I think Lewis wanted that. It's possible it was just an accident, but I laid out as to why I think it was probably suicide. His wife thought it was suicide. You know, Avery was different. Avery struggled with this tremendous problem that made absolutely no sense and tracked it down. He said, failure is my daily bread. I thrive on it, but he didn't thrive on it. He basically had a nervous breakdown. He didn't publish for more than a decade. He said, whenever you fall down, pick up something, he did do that on one. And he ended up with one of the most important findings of the 20th century that DNA carries the genetic code, which was an extremely controversial finding at the time. Although Jim Watson and Samuel de Allurea and other Nobel laureates immediately picked up on it, but it was very much a minority view. And in fact, he was being considered for the Nobel prize for a lifelong contribution to immunology. When he published this paper and the committee decided, well, they better not give him the prize because this is too controversial. So he never did get the prize. Obviously, he was right. And in the book I quoted half a dozen Nobel laureates giving him credit for launching the entire field of molecular biology. It's why I said earlier it was probably the single person most deserving of the prize who never got it. So I guess he was sort of a happy ending, a question of persistence and so forth and so on. And also, as I said earlier, he kind of kept me going for the first five and a half years where I wanted to throw the book out every day. It just wasn't coming together. It finally did. And the last year and a half, I was, you know, quite happy. I wasn't coasting. I was trying to finish the book, but I liked going to work every day, like sitting down at my desk every day the last year and a half out of seven. Well, the contrasts that I drew are the message that I took from your book in relationship to these two characters is that while you can be a brilliant scientist or at least a brilliant individual, that's not enough. Avery had a kind of doggedness as you portray it and unwilling to give up on an issue. And he succeeded and made the kinds of discoveries that we all admire, where as Lewis, a very bright guy by everyone's estimation, didn't do it. So is it character or just simply brilliance that carries the day in science? Or anything? Is it talent or, you know, football players, you know, as a former football coach who sat on the bench? No, obviously it's both. You know, there was nothing wrong with Lewis's character. He was in some ways as dogged as Lewis, but he started going down the wrong path. And there comes a time when you have to look carefully at where you're going in science as to whether or not you've made the wrong path to go down. And he couldn't get his experiments to yield what he was looking for. He kept trying. You know, it wasn't there. And he should have chosen another field. That led to his failure.  Every failed experiment, Avery gleaned something from that, which did keep him going and moved him a little bit further along. Okay. Thank you. And I'm going to turn it over to Mitt. Well, thank you very much so far. This has been a really enlightening conversation. I just want to end up with a couple of thoughts about media and truth. Okay. So one of the questions that we had as we were reading your book and thought the audience would like is, can you elaborate on the role that Wilson had in suppressing the media and kind of contrast it a little bit to the culture today of how the role of the media in, you know, the information dissemination or disinformation. I just think that's a fruitful category. Well, I mean, there was plenty of fake news in 1918. All of it came from the government. You know, Wilson was entirely focused on the war and the pandemic arrived in a context. And you have to understand that context. Wilson, you know, may have had some reasons for legitimate concern about what the American war effort would be like. The single largest demographic group in the United States was German descent. So are they going to fight against Germany? Another very large demographic group were Irish Americans. Ireland in 1916, rebelled against Britain. Are they going to fight on the side of Britain? And when the US entered the war, he created something called the Committee for Public Information. And the architect of that committee said, nothing in experience teaches us that truth is superior to falsehood. And went on to say the only thing that mattered was the impact of what you say. So this committee had 100,000 volunteers around the United States. And before every public meeting, every vaudeville show, every school board meeting, they would get up, they were referred to as four-minute men. They would give a very brief talk to generate, you know, keep morale up and so forth. At the same time, Congress passed at Wilson's urging something called the Sedition Act, which made it punishable by 20 years in the can to quote, utter, write, print or publish any disloyal, profane, scarless or abusive language by the former government in the United States. A congressman was sentenced to 10 years under this law. It was vigorously prosecuted. So on the one hand, you had the stick of this law. On the other hand, you had the carrot of these lies being disseminated. And that was all because of the war. And Wilson never made a public statement about the pandemic ever, hardly ever mentioned it privately either, at least in writing. And so the pandemic arrives in this context. And there was concern that any bad news about anything would hurt the war effort, not just influenza, but the song, for example, the song I wonder who's kissing her now was banned from military camps because it was bad for morale. So influenza comes along and you have a national public health leader saying this is ordinary influenza by another name. You have another national public health leader saying you have nothing to worry about, proper precautions are taken.  In fact, in one Wisconsin newspaper that tried to tell the truth initially, the army started proceedings to prosecute them under the Sedition Act, send the editors to jail for telling the truth. They dropped that as a pandemic proceeded, but nonetheless. So all that context is important. And the result is that to take an extreme example in Philadelphia, when they're using steam shovels to miss big mass graves, and finally when they finally close belatedly the schools, saloons, and so forth. One of the newspapers says this is not a public health measure. You have no cause for alarm.  Of course, it's a public health measure and the people knew that. And earlier, I referred to the fact that these untruths and lies and exaggerations on the downside, all they did was lead to alienation, because people knew this was a deadly disease. You know, the case mortality in the U.S. was probably only two to two and a half percent. It was a lot worse than that in the developing world where probably they had never seen influenza virus, so they were virgin populations. But in different demographic communities, it was much worse than that. For example, according to MetLife, not case mortality, mortality, 3.2 percent of all industrial workers in between 18 and 45 died. Not case mortality, mortality. Over 6 percent of all the minors in that group died. Not case mortality, mortality. Pregnant women, there are a dozen studies that had case mortality between 21 percent and 71 percent. So, when you look at those kinds of realities, because they're reality, not a statistic. And you put them up against the message that's coming out. And it's not a surprise that Victor Vaughn, as I quoted earlier, said civilization could easily disappear from the face of the earth. Because when you're being lied, I think the society ultimately is based on truth. When truth disappears, you can trust no one. Society begins to disintegrate because it's everyone for himself or herself or every family for itself. And that happened. You have reports of people starving to death in 1918 because nobody had the courage to bring them food. And you have that's occurring both in rural communities and in big cities. And that's unlike other disasters where people tend to come together. You know, that's not to say they weren't heroes in 1918. They were. But there was a tremendous amount of fear that was unnecessary and was generated by, I mean, there was plenty of fear that was legitimate. You were facing a deadly threat.  Okay, I want to end my with one last question before we open up to the question and answer period. Is there anybody in the 1918 epidemic who was like Anthony Fauci or any were there any like signs of their leadership or moral leadership or kind of comforting factors in a terrible crisis? Not nationally. You know, there are a couple of local leaders. I think somebody I've seen some stories that came out in the last couple of months about exactly about what you're saying. I think there was somebody in Seattle and so forth and so on who played that role. And there may have been one or two other places and where that was the case. But certainly not on a national level. They would have been prosecuted. Yeah. And you know, none that I didn't write really much. I didn't do actually I did do a little bit of research in Seattle, but apparently I missed this character. My research, Seattle was not a main focus for my work. As I say that I remember seeing that story, but nobody nationally. I'm going to turn it over to Michael who's going to, you know, see what other questions we have as we round out the hour here. Before I give it back to Michael, I'm going to just hand it over to Mark Siegler who wanted to ask one specific question. Two. Two of it's all right. The first question, John, is that you said earlier that it was called the Spanish flu and did not originate in Spain by any matter. As I remember reading your book, it seemed to originate in among seven military men in rural Kansas in the U.S. Is that your idea? I wrote that in the book and even published a, you know, journal article on it, which got a reasonable amount of attention. And I thought the evidence was, I won't say it was compelling. I think it was better than any other hypothesis. As I said in the journal article, but, you know, that was 16 years ago. There's been a lot of research since then. I think the Kansas hypothesis is still alive as a possibility. But personally, I think it's much more likely that it started in China. And, you know, I think the best evidence for that is not so much some disease outbreaks which were known at the time and were rejected by people saying, you know, that was actually mnemonic plague. It wasn't influenza. And obviously, people understood what mnemonic plague was in 1918. You know, they could culture the pathogen. And there were some other disease outbreaks. But the epidemiological research evidence, you know, pretty much suggests that, I mean, for example, Hong Kong was barely touched by the 1918 pandemic. So what would be an explanation for that? It's prior exposure. So that's why I think China was the most likely source. But, you know, there's a very good virologist in China Oxford who's convinced it. I don't know if he's convinced, but he makes the most likely sources France in 1915, I think.  I don't think that one makes any sense. There's been, it was clearly an outbreak of influenza in New York City, which I did not know about at the time I did the book. But no later than the middle of February, that it began to show up statistically. And it could have surfaced considerably earlier. So, you know, New York's possibility. You know, some virologists argue that the virus was around for a couple years. You know, who knows. My second question is based upon what you said earlier on the second wave of the influenza epidemic of 2018 between September and December of 2018, which killed the vast majority of the 50 to 150 million people. And my question for you is whether the third wave of the coronavirus vaccine, which is following similar months, may itself be not comparable to what happened in 2018, but maybe a dangerous period. Well, first, I'm probably the least able to answer that question intelligent thing than anybody on the Zoom call, because I'm, you know, not a virologist, not an epidemiologist, and not a clinician.  Different viruses, mutation rate is radically different, as, you know, influenza mutates much more rapidly, moves through a population much more rapidly. That's one of the biggest differences between the viruses is the speed of influenza. You know, as a community in six to 10 weeks, even if we had not intervened with NPIs to slow transmission, it still would take much, much longer than influenza to COVID-19 to move through a community. But, you know, this virus hasn't shown the slightest evidence anywhere in the world of an increase in virulence. You know, there is the mutation, the argument that it is made it more transmissible. But, and that mutation seems to have taken hold, certainly in the United States. I think, not sure if it's quite worldwide, but in Europe as well, I think. You know, but there's no, and that may or may not be the case, but there's no evidence that that mutation has any impact on, you know, what people see in the clinic or virulence or anything like that. Michael, thank you very much. Thanks for that. I'll ask one question, then I'll turn it back over to Laney. So we have a question from one of our bioethicists, Martin Chan, who's asked, asked you to comment on the principle of accountability. And so the question is the bioethical principle of justice suggests that we should hold responsible parties accountable throughout the history of pandemics. Has this been the case? Well, I really only, I mean, who's the, who's the responsible person? We don't have a responsible person in 1918, unless you want to say Woodrow Wilson for not doing more. You know, there's the idea of blaming someone, which we talked about earlier. I, you know, that in many disease outbreaks, there's, there's always been a bad guy, usually somebody in lower, in fact, always somebody either racially different or social economic lower status has been blamed. As I said earlier, I don't think that really occurred in 1918. If you want to talk about blaming people in COVID-19, you know, personally, I would say, yeah, Trump's incompetence and incompetence of the administration has killed a lot of people who otherwise would be alive. You know, and we will see in a couple of weeks whether he's held accountable or not. Well, that's a good way to end. Anybody from the panel want to ask a final question or should we just all say thank you very much to John Barry for a really interesting and informative session. Thank you very much. Okay. Thank you. It was fun. Okay. Bye-bye now. Okay. Thank you. Yep. Bye. Thank you, Lanny.


This meeting is being recorded. Okay, so Professor Abirbakh will resume his talks on Brionskan Skoda Theorem. All right, well, thank you very much, Professor Trivedi. Hello, everybody. I said good morning earlier, but I think I'm one of the few people for whom it's morning. All right, so last time we discussed the Brionskan Skoda Theorem in character from holds up to type closure. And we ended the talk by noting that this reduction J if it's L generated, then a key observation was that J to the LQ is contained in the Q's bracket power. And then we said, well, what about the kind of remaining powers of J can we get any more information? So, let's suppose that we don't have the type closure here so that we're in say a regular ring, then if we look at I to the L in a real closure that's contained in J and say that's generated by A1 through Al. So, then an element X in I to the L bar implies that X is equal to R1 A1 plus R2 A2 plus RL Al. And the question then becomes what can we say about the R? So what can we say about R1 through RL? So, for instance, can we say something really nice like are the R's in I to the L minus 1? Well, that's probably unlikely. But it turns out we can make some statements. And one has to be careful. It's difficult to do the computations here because of course the any information you get is up to say causal relations on the R's with respect to the A's. And it's not necessarily that easy a computation. So that's the beginning of today's lecture is to talk about Branson-Skoda theorems with coefficients. In other words, we're looking to say ask to get some information on those R's. Let's start with some, a couple of definitions. If I is contained in R, and here I just want to assume that we're in a netherian ring, then let's let I un-mixed be the intersection of the minimal component of the ideal I. So this just removes the embedded components. Okay. And the second definition we need is something related to the height, what we call the big height of I. So this is equal to the maximum of the height of P such that P is a minimal prime of I. So this is exactly the height if this ideal has minimal primes of all of the same height, but in general, we can have heights, different heights. And so the big height might be strictly larger than the height. So here is the first theorem. I'm using again, I'm using the numbering from the write-up. So this was proved in 1993 by myself and Craig Hewneke. And what it says is the following. Let's let our M be a regular local ring that contains a field containing a field. Say we have I is an ideal of R. Let's let L equal the analytic spread of I. And let's let H be the big height. I've usually used H for the height, but here it is the big height. So and J contained in I a reduction. So then for all W greater than or equal to zero, if we look at I to L plus W integral closure, this is contained in J to the W plus one. This is a regular ring. So that, that by itself is the Branson-Skoda theorem. But what we can say then is that this is in J to the L minus H unmixed. So in other words, we can take the Rs on the left-hand page to be in this ideal that is related to I itself. And we were interested in this in part because it. Hewneke that he had proved about the connection between Cohen Macaulay graded rings and re-sranks over Cohen Macaulay rings. I think maybe there are some people who could mute who that might be helpful. So I want to do the proof of this. Let me make some observations. And so what are my observations? I'm already forgetting. Okay, so in, in this setting. So if, if we have J contained in I a reduction, then the minimal primes these two are these two ideals are the same up to radicals so the minimum of ideals, primes of J are the same as the minimum primes of I. We have that the big heights are the same. So that's one thing we'll need. And the second is that in a regular local ring, well in a regular ring of characteristic P. So for any ideal a contained in are the associated primes of our mod a to the bracket Q are these are equal to the associated primes of our mod a that again that's the flatness of Frobenius. So, most of the work is in the following lemma. Let's prove this lemma. So we're really working on this serum so let's let R I J L. Maybe H should show up here too. As in the statement of the serum. And what is our lemma say, it says, yeah, let's throw in H. It says. This is an F. Not equal to zero such that for all Q sufficiently large. If we multiply J to the L minus one cube by F. Then we are in the following ideal J to the L minus H. Unmixed all taken to the Q bracket power. Okay, so what this is saying here is, you look back at our question. Over here, this extra information. If we have, we'd like to get something from it. And so this is saying there's a uniform multiplier. That takes that quantity and puts it in a Q's bracket power and sure enough, right. It's the Q's bracket power of the coefficients and so that's how we're going to prove our theorem. Okay, so. Let's look at the proof of this. All right, so let's, let's let P be a minimal prime of J, which is also a minimal prime of I. So, then, if we localize, so J localized to P. This has a minimal reduction. That is generated by the, the analytics spread of J RP. But that's less than or equal to the dimension of RP. And that is less than or equal to the big height because we took a minimal prime of J here.  And right. And of course, the number of generators of L sub P is less. So, we can choose.  This is not a localization now this is an index to P. As in exercise to, and that's this LP contained in J RP. Okay, and without loss of generality, we can assume that F P is actually an R we can clear denominators. So, then, what do we get. So we do the computation. As in the proof of theorem 1.8. Okay, and now using the work that you guys are going to do so in exercise three. Here is the what the computation gives us, we have that F sub P times J RP to the L minus one Q. Where does that sit. Well, you see the L in when to localize the analytics spread is dropped so what's what the now L has become a W that's bigger than or bigger than zero. Okay, so this is contained in. We're putting things in a power of the reduction. And so where, what power do we get. Well, once we finish the computation we're in a cute bracket power, but the power is, we've got L minus one minus H plus one. We're taking that whole thing to the cute power. So again this is just a right this is this is a W in the in the argument. And then this is where subtracting off something that's at least as big as the analytics spread, and then the plus one. Okay. So where is this. Well now we can make our. So this is, once we simplify. I guess it's we're just doing a simplification. This is LP to the L minus H to the bracket Q. And that's contained in J are P to the L minus H to the bracket Q. So, the thing is now that we apply observation to. By observation to, and take the product of all the FPs to get our result. Okay, so perhaps I haven't been as clear as I could be but I'll let you think about it or go back to the notes where it's maybe written up a little bit more can clearly. And so this is the key to the whole thing. So I think I gave myself an extra page, meaning I was going to say more. Now we can go to the proof of the actual theorem. And again I'll do the W equals zero case. So, let's prove that I to the L integral closure is contained in J times I to the L minus H quantity and mix so we again remember when we when we take powers of an ideal even if we started with an ideal without any embedded primes were likely to get embedded prime so we have to remove them in in this argument. Or in this theorem. Okay, so let's let J contained in I be our minimal reduction I guess that's actually stated in the theorem. And what do we want to do take C. Not equal to zero as in exercise to. And that's for the ideal I to the L are F not equal to zero as in the lemma. So we start with some x in I to the L bar in the integral closure, and then for all q sufficiently large. We have the following we look at C times F x to the q. And so where is that well, using the C that's in J to the L Q, which is now contained in J to the bracket q J to the L minus one q times let's put back that F. Okay, and now by the lemma. This is contained in J to the q bracket q times J to the L minus H on mixed to the bracket q. Bracket cues are nice in the sense of multiplication so that's J times J L minus H on mixed all to the q. That's exactly the criteria for being in tight closure. So, X is in J times J to the L minus H on mixed closure, and that is equal to J times J L minus H on next, because we're in a regular local ring and so all ideals are tightly close. And one of the early kind of revelations to me was the idea that you know in a regular ring or in weekly F regular rings in general ideals are tightly closed. And so you might think well, you can't really use tight closure to prove theorems in such a ring all that easily. But it turns out that using the tight closure is incredibly powerful even in rings, or especially in rings, where every ideal is tightly closed. So, I did include in the notes a some information about how we use this stated graded rings and column calling us but I decided that in this talk, I wouldn't be able to squeeze that all in so I'll refer you to the notes for that. Okay. And so I want to turn my attention to F rational rings and go back to trying to understand the Branson-Skoda theorem in F rational rings and if you remember, even in the regular case, sorry, not in the regular, even in the pseudo rational case or rational singularities case, the full Branson-Skoda theorem was not known. And so let's talk about that. And so we want to switch our attention now to the case of F rational rings. And so as I said, this result of Lippmann and Tessier is only partial. There wasn't quite the full Branson-Skoda theorem. So that leaves the question, is this full Branson-Skoda theorem true? And the answer at least to some extent is yes. So, Uniki and I were able to prove the following theorem in 2001. And so let me state the theorem. Let's let RM be an F rational local ring. And in this case, by F rational, that means it's characteristic P. Suppose I contained in R is an ideal. J contained in I is a reduction and say L equals the analytic spread of I. Then as usual for all W greater than or equal to zero, we do get the full Branson-Skoda theorem. So the L plus W bar, the interval closure, is contained in J to the W plus one. That then in characteristic zero, this gives the same result for algebras of finite type over, finite type over a field of characteristic zero rational singularities. So again, that's that's a reduction to characteristic P result, which I'm not going to discuss in these lectures. I want to try to go over the proof of this. There's some technical information that we'll have to deal with. So we'll get to that in a minute. So remember that F rational says that parameter ideals are tightly closed. Since we're only dealing, we're only going to deal here with local rings. It's a little nicer. So it's basically kind of any, any ideal generated by part of a system of parameters is probably the best way to think about that. So, but not all ideals. Okay. And so the thing is that if the analytics spread of I is strictly bigger than the height of I, and J is a minimal reduction. J is not contained in a parameter ideal. Okay, so there's, there's, you can't get at this directly. That's, that's the problem. So here is the idea. So given our J contained in I, that's a reduction. And find a parameter ideal. I'll call V sub n such that. Well, you can't get J to be inside V sub n, but you can get them to be ematically close so that J is congruent to be and at least once we mod out the maximum ideal to the end power. Okay. And then, then if our is F rational. That implies B sub n is tightly closed. Right. And now, let N go to infinity and use the parole intersection theorem to conclude that we get our result. I'll say, I guess I'll say that again as when we do the proof. Okay, so in order to do this, we'll need to technical results are both rather long. And so what I've done is I've already written them out, because I figured I would just mess up writing them. But let me try to go over them and tell you what's going on. And I'm going to suggest for those of you if you're taking notes, you may not want, you may want to not try to write all of this down. But it is all in the notes that are online. So, let me start with lemma 2.8. So suppose we have our local ring. And I will be assuming here that we have infinite residue field. And as usual, we have our minimal reduction J contained in I and L is the analytics spread. So it turns out that the key is to pick a very nice generating set for the ideal J. And so what qualities does that have. That's these one, two and three, which I'll go over. So suppose, whoops. So it turns out, there exists a generating set a one through a L for J. And in the next few arguments, let me use J sub I to mean the partial ideal generated by a one up to a I. So the properties that this has is suppose we take a prime containing I. Okay, and that prime has height up to the analytics spread. Okay, so we've got this height, H ideal, the analytics spread is larger. And we've got a prime kind of somewhere in that range containing I, then, then J sub I, let's, even though I wrote it ahead of time, I still manage to mess up. So suppose I is the height of that prime. So then if we take the first I elements, we do get a reduction of the ideal locally at that prime. Okay, now it's not necessarily minimal, but it is a reduction. Okay, so that turns out to be very powerful. All right, so second for if we take n large enough. If we look at the following ideal we look at J sub I, I to the end colon I to the n plus one. If we look at that ideal, and then we also add I, then the height of that is at least I plus one so that says that there's no primes too small containing both I, and this colon ideal. Okay, and notice, this is very much related to thinking about reduction numbers that colon is related to reduction numbers. And the third property is that if we take the ai's and we change them by elements of the square of the ideal. So to get ci's, then both of these properties still hold. Okay, so once we've got this nice generating set, you can use elements of I squared to modify them at no cost. So that is the limit 2.8. And then proposition 2.9. Right, so we need a little bit more information on our so suppose our local ring are is equidimensional and catenary. So just, I think, complete domain. That's as nice as we can get. And again with infinite residue field. So suppose again we have J is our minimal reduction of an height, each ideal analytics brand L suppose we've written J as in limit 2.8 but I'll use primes on to start with. But this is a little bit more technical. So let's fix an n greater than zero that n is like in our B and where I'm going to want to think about m to the end and a w that comes from the brands and scota theorem. So we can change the a primes to to a to a is in J. So, again, just modifying by elements of I squared, that's the first condition, we can also pick teas. So th plus one through TL in the maximal ideal. And for the lower ones, th through T one, I'm just going to set those equal to zero. Those T is we can pick an M to the end. Alright, so we're going to do this for a sequence of ends going to infinity. Then, if we take the A is and we add the teas. So be we get B one through B one BL these will be part of the system of parameters. If we take the ideal of bees and we're in an F rational ring, that ideal will be tightly closed. I don't know that we're going to use it very much in our argument but these teas are actually part of the system of parameters in our mod I. The last one that is a little hard to gauge what it really means but we will use this is that we for for some M, some exponent large enough in the range of eyes between H and L minus one. So what happens to T I plus one so this is, in other words, this is th plus one through TL. It is in this nice colon that multiplies high powers of I back into powers of J sub I to notice, in other words, so here, we are using the index here, right from I plus one to I, right. And this happens in a certain range that that we need. Okay, so again, reminding you J sub I is the ideal generated by the first I elements. I'm going to. So now what I want to do is I want to go through the argument in the simplest case, which is when L is h plus one. And show you how this works. Let's keep 2.9 available. Let's do the proof of theorem 2.6 when L is h plus one and W is equal to zero. Okay. Let me catch up on my notes to where I am. All right, so first off, let's fix fix and bigger than zero and let's let's choose. A equals a one through a h a h plus one. All right, and T h plus one in M to the end, as in proposition 2.9. So, I think I'm running maybe a little sift. I think I have time. So I won't try to condense the argument too much. So, then, let's make the following observation. Well, let's let's also choose M large enough, such that we have T h plus one. T h to the M plus K. This is a bad notation. My, my little K here is an index. It's not the residue field. So where is this this is in J h to the K. I to the M. Okay. So where J h is just the first each of the days. All right. So, then, we can check. I'll let you guys do the work that for all, let me call it N prime greater than zero. I to the H plus one to the N prime. I to the M plus K and prime. Well, we just repeatedly use the inclusion above. And this over and over again and where does that land that lands in J h to the K and prime. I to the M. Okay, so that's the key observation. All right. So now, let's pick X. I to the L bar. And C as in exercise two. Okay. And C prime in I to the M. Not in our not in this case in our F rational ring or not is just everything but zero. Sorry, not minus or not. That should be. Let me just say the, this just needs to not be zero needs to be in our not. Sorry, not, not out of work. Okay. So, now we want to compute. So, so what do we get, we get that, let's look at C times C prime X to the Q. Okay. So, where is this well, we're not going to use the C prime yet. C times X to the Q is in J to the QL. Right. And so, where is this. So this is in C prime. This is the bracket Q times J to the L minus one. Q. So let's say that the CC prime X to the Q is equal to, we still got the C prime. We've got our one. A one to the Q. Plus R H. A H to the Q plus R H plus one. A H plus one to the Q. And these, the R's, the R survives are in J to the L minus one. That's what we have. Okay. All right. So, let's think about what happens when we multiply this last coefficient. We really only care about that coefficient. So this coefficient, we can multiply by T H plus one. So, so then let's look at T H plus one to the Q. Times C prime. R H plus one. That's what we want to look at. And where does that land. Well, this is in T H plus one. The C prime R H plus one is in I to the H Q plus M. That's where the C the C prime gets us that plus M. And that is contained in J sub H. To the H Q. Over here by that observation. All right. But this ideal is H generated. And we've got the H Q power. And so this is contained in J H to the bracket Q. Right. So what we're going to do is in the sum above. In this sum. We're going to add and subtract that value. So that's, that's adding zero. And we're going to use the fact that when we. That the result lives back in the earlier part. So. So. Add and subtract. T H plus one Q. C prime. R H plus one. Okay. To get that. C C prime X to the Q. So that's what we're going to do. Is in a little short on time. So, so we're going to get in a one to the Q. A H to the Q. Plus. Well, we've added in subtracted. So we have. A coefficient of a H plus one Q and a coefficient. So this is going to be in that. This ideal plus the ideal generated by. A H plus one to the Q. Plus T H plus one to the Q. And so this. Is a one through a H. B H plus one. This guy is a parameter ideal. And so what we've now shown is that we have. I to the L plus one bar. Is contained in. A one. Through a H. B H plus one. Star. Which is equal to the ideal. A one. Through a H. Oops. B H plus one. Because we're in a national ring. And so. So now we let. And go to infinity. And we've got. I to the L bar. Is contained in. J plus M to the N. So maybe over here. This is contained in. J plus. M to the N. For all N. And so. What we get is that. I to the L bar. Is contained in J. B H plus one bar. And that's the proof. So. Looks like I'm out of time. So let me, let me take one more minute if I may. Just to say the, what is the general strategy? You know, what if, what if the analytics spread were H plus two. What we'd have is. We'd have a T plus one bar. And we'd have a T plus one bar. And we'd have a T plus one bar. On the, over here in this sum, there'd be one more piece of the sum. Right. And we'd also have a second T. And so we just work backwards. We'd start with T H plus two. And we would multiply by the Q's power of it. And that would push. We would be able to push. With some information about the coefficients on a H plus one. That's good enough to then. Multiply by T H plus one and push stuff back into here. And that's the general argument. It works. Nicely, but it's, it's a little technical. So. So there you have. The Reansons go to theorem now in F rational. And it's full. Beauty. I don't know in mixed characteristic that anybody has actually proved this. I'm not sure about that. No, thank you. So. Are there any questions or comments?