Chapter 05: Medical School Leads to a Research Focus on Cytokines
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Description
Dr. Tweardy begins this chapter by noting that he was always a physician-scientist, and he explains why he did several post-doctoral fellowships after medical school [MD, 1978, Harvard Medical School, Medicine] instead of doing a PhD program.
He explains that he approached medical school through the sciences and particularly enjoyed the coursework in the first two years, when he refined his interest in chemical structures and macromolecules: he began to focus exclusively on proteins and their interactions with small molecules. He was doing this work in the early days of cloning, which led to his work on cytokines.
Next, Dr. Tweardy reflects on a “wrenching experience” at Case Western Reserve [1980 Case Western Reserve, Intern/Resident], when a patient with AML died of sepsis. Dr. Tweardy then became interested in how to treat infection and have an impact on the underlying problem of chemotherapy-induced neutropenia by working with molecular mechanisms that “jumpstart the marrow.”
Dr. Tweardy then speaks about his discovery of the complexity of immunology [1982] during his fellowship in infectious diseases at the same institution. He explains mechanisms for influencing macrophage activation to address the immune system. Through his work with Jerry Ellner, he was able to conduct a study where he isolated monocytes from patients and show that they didn’t have as much HLAD on their surfaces. After incubating them, they grew and they believed they were producing macrophage activating factor. They wrote a letter to Genentech requesting [WHAT?], which enabled him to show a positive result on all the immunological XXX that would affect the white cells.
Identifier
TweardyDJ_01_20190122_C05
Publication Date
1-22-2019
City
Houston, Texas
Interview Session
David J. Tweardy, MD, Oral History Interview, January 22, 2019
Topics Covered
The Interview Subject's Story - The Researcher; The Researcher; Character, Values, Beliefs, Talents; Personal Background; Professional Path; Evolution of Career; Inspirations to Practice Science/Medicine; Influences from People and Life Experiences; Patients, Treatment, Survivors; Mentoring; On Mentoring; Definitions, Explanations, Translations; Overview; Discovery and Success
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.
Disciplines
History of Science, Technology, and Medicine | Oncology | Oral History
Transcript
Tacey. A. Rosolowski, PhD:
Yeah. What about the decision to go to medical school? When did that come in?
David Tweardy, MD:
Yes. That’s a really good question. So here I was, I started as an aerospace engineer, and who knows: if the market were doing better—I should say the aerospace market were better—in 1970, I could’ve been happily ensconced at Boeing and designing airplanes or whatever. But then what happened is in the course of my freshman year I had to take two engineering-level basic sciences: one was physics for engineers, and chemistry for engineers. And while I really, really enjoyed the second semester of physics—I still think Maxwell’s equations are one of the greatest collective inventions of mankind; I think they rank up in the top five—I really enjoyed chemistry more. And so I said, okay, I’m not going to do aerospace engineering; let’s go with the chemical engineering. So I moved into chemical engineering for my second year. And then I came into the harsh realization that, as a chemical engineer, I had to take partial differential equations. (laughter) And so my fall semester I took linear algebra, and that was my—I had two really amazing academic—well, not amazing but embarrassing academic experiences at Princeton. One was linear algebra. It’s the smallest book. It’s literally no more than maybe 50 pages. It’s orange. And you basically—(laughs) it was like I was loaded up so much in that semester I essentially went to no classes. And so, of course, midterm, I studied as hard as I could, and I got a C on my midterm, and I went, oh, no. I said, this is not looking good. (laughs) But I didn’t change my ways. I didn’t go to classes again. I never did homework. And then I just put this incredible sprint on so that I took the final, I got a B, high B, and I ended up getting a B-minus for the final grade.
Tacey. A. Rosolowski, PhD:
Yeah. Yeah, you were lucky you did that. That’s testimony to you. (laughs)
David Tweardy, MD:
Well, it’s panic. But then, after that was partial differential equations, and I went, I don’t know, this is not fun. I’m not having fun here. So I said, let me move out of chemistry, chemical engineering. And I had done organic chemistry that fall, and I just nailed organic. I just was—I could think like an electron, at one point, so I knew exactly where electrons wanted to go. (laughter) And organic chemistry—I told my son this, I said, “Organic chemistry is just thinking like an electron. Where would you like to hang out? What’s the lowest energy state that you can achieve? And then you just work through all of those energy states, and that’s how organic chemistry works.” And so I have to say, if you ask anybody of my generation that went to Princeton and took organic chemistry—Lamar Jones-- there was … Sorry, Maitland, Maitland Jones is the teacher who taught organic chemistry first and second semester, and Maitland—Welsh, I think, name—was just the most gifted teacher I’ve ever seen. I mean, he could go up there with multiple colored chalk, and this is back when they used the chalkboards. He would give these lectures, and it was, like, magical. So Maitland just turned me into a chemist. After that, I said bye to chemical engineer, bye to engineering; I just love the chemistry. So I moved into chemistry. And then this is the beginning of biochemistry at Princeton. And I loved the chemistry, but I really loved the organic. I didn’t like the—I didn’t really care for inorganic, so I never took inorganic, and so I moved into biochemistry and biology, cell biology. And then I had a very influential friend, a very good friend of mine, who we did the thesis together in Biochemistry Department. There was a remarkable biochemistry department at Princeton, it turns out. It was a sub—it was not a depart—I should say it’s a section of the Chemistry Department. They didn’t name it a separate department at that point, but the chief, if you will, of that section was Bruce Alberts, and Bruce Alberts probably is one of the most gifted biochemistry teachers on the planet. He became so noted for—he did research, very solid research. Went from Princeton to UCSF, and ended up being the President of the American Association for the Advancement of Science, was the editor of Science for five years. But amazingly enabling. Again, from the point of view of—Maitland was incredible in a lecture hall, but in small groups this guy was unbelievable, and gathered around him some amazing luminaries in the Department of Biochemistry—in chemistry. I mean, my actual thesis advisor was Mark Kirschner. Mark was just recruited from his—he’d just done a postdoc, and he had nobody as a thesis advisor, so I latched onto him and he was a phenomenal mentor. But then there was Art Pardee. I mean, the names of people there— Uli Laemmli. People have forgotten this, but Uli Laemmli, L-A-E-M-L-I [sic], Uli developed this methodology of separating proteins so that you can determine their molecular weight, and a mixture of proteins. He developed a Laemmle gel, SDS-PAGE gel system. And during this early ’80s, mid-’80s, he was the—his article in Nature was the number one most cited article in the universe. And he was actually at Princeton, and the second apparatus was ever made on the planet was made for me to do my senior thesis project. (laughter) So, I mean, here I was, again, kismet. And I would run these gels day and night. And then there are a couple other—there were a couple—Arnold Levine, a very well-known guy around p53 was in that department. I mean, just incredible people. Each one of them went on to become a member of the American Association of Advancement of Science, and several of them became members of the National Academy of Science. I mean, it was just amazing how good—and they were small, it was a small department. It was like six or eight people.
Tacey. A. Rosolowski, PhD:
But these are all people who were really, really focused on the research—
David Tweardy, MD:
Right.
Tacey. A. Rosolowski, PhD:
—(inaudible) research side, so—
David Tweardy, MD:
Right. That’s right. So how did I get into medicine? So here I am. I stayed at Princeton during the summer to work on my thesis, because between junior and senior year I worked in Mark’s lab. I was going to apply in the fall to PhD programs in biochemistry. Then I met a really cool person. Actually, her name was Judy Wasserheit, who was very well—very successful in medicine. And I got to know her well, and she kind of talked me—she told me or made me think about medicine as an alternative. Her mother—
Tacey. A. Rosolowski, PhD:
Now, was she an MD?
David Tweardy, MD:
No. No, she’s not. Yes, yes, yes.
Tacey. A. Rosolowski, PhD:
Okay, but then—
David Tweardy, MD:
At that time she was a classmate.
Tacey. A. Rosolowski, PhD:
Oh, a classmate, okay.
David Tweardy, MD:
Yeah, she was one of these Manhattan whizzes who skipped at least one grade in high school, came into college, skipped actually a grade in college, as well, and moved up, actually, to our year, my class of ’74. And her mother was a podiatrist, Elizabeth Roberts. And she, I think, really inculcated strongly the value of education, but also a thought about becoming a physician. And I was just the fortunate (laughs) recipient of her discussions around medicine, why she wanted to do it. And so I wouldn’t say reluctantly, but I said, yeah, I think—I had a physician, I actually had a—I have a bicuspid aortic valve, that obviously I’ve had, since it’s congenital, and my doctor … It’s just one of these—again, you think about it, as a child I was very healthy, but I remember my doctor telling me, “Hey, you have a heart sound,” when I was like … And then he said something (laughs) which endeared me to him forever—endeared him to me, I should say, forever—which is he said, “You have an athletic heart.” And that was because I had a low heart rate, and below 60 is athletic, and then below 40 is elite. And so I said, “Yeah, yeah, thanks, doc! I have an athletic heart! Yay!” (laughs) And so I always had a good relationship with doctors. Of course, I didn’t have much of a relationship with doctors, but that was enough. And so when she started talking about medicine, and I started thinking about what I was going to do with my life, I had a—so I said, “Yeah, I think I’ll apply to med school instead of graduate school.” And I think my mentor, Mark Kirschner, never forgave me for that.
Tacey. A. Rosolowski, PhD:
I was going to ask how they responded.
David Tweardy, MD:
I actually think he never forgave me for that, in a way, at a certain level. And I—it is what it is. And, frankly, I have sort of done one of those things that are not that common anymore but the physician-scientist track, where I actually practice medicine but also maintain a very active—
Tacey. A. Rosolowski, PhD:
But that was a very new idea.
David Tweardy, MD:
You know, it is new in some—you’re right. Lewis Thomas, it turns out, The Lives of a Cell, he probably guided me in that regard. I still quote him in the lectures I give. I still give a couple lectures (overlapping dialogue; inaudible)—
Tacey. A. Rosolowski, PhD:
I taught his essays.
David Tweardy, MD:
Did you?
Tacey. A. Rosolowski, PhD:
Yeah. Yeah.
David Tweardy, MD:
I mean, he is a brilliant guy.
Tacey. A. Rosolowski, PhD:
He’s a brilliant, brilliant writer.
David Tweardy, MD:
Yes, extraordinarily good writer. In fact, his phrase that I use in my lecture is: “And the body reads gram-negative bacteremia as the very worst of bad news.” (laughter) It’s just brilliant. I mean, I love that turn of phrase. And so when I talk about sepsis … I give lectures in sepsis, and I still use this, 1974 Lives of a Cell. Anyway, but I think you’re right, it was not that common a path. What most people, MDs have done is they get the MD training. It gives them a real perspective around human biology and disease, and then they, like Ron [DePinho; oral history interview], basically just kill it on the science side, never practice. Two of my classmates at Princeton did exactly that. In fact, the second thesis advisee that Mark had was a guy by the name of Dan Littman, and he did just that: he got an MD/PhD in immunology, and then just stayed in the research, and became a Howard Hughes. Bob Siliciano, he stayed as a chemistry major. (laughs) He was a really nice guy. He went on, went to—got his medical degree at Hopkins. I don’t think he actually got a true PhD, though. And then worked in AIDS, and became a Howard Hughes. So, very successful track. I, like I say, I just love—I ended up loving medicine, but I love research. So I did the dual MD/PhD. I never—oh, I’m sorry, the physician-scientist. I never got a PhD, because, in a way, as you can tell, I was tracking towards that PhD. I didn’t get it, but I kind of felt, because of my senior thesis at Princeton, and I did a couple postdocs. I did a postdoc in infectious disease with Jerry Ellner and Ed Case, and then I did a second postdoc in molecular hematology, in particular cytokine, hematopoietic cytokine biology and molecular biology, especially, with Giovanni Rovera. I kind of—and I thought, what am I going to get a PhD for? I’m ready to start my career. And so I didn’t get the PhD. But it was Judy, and good experience with my doc when I was growing up, Judy who really made me realize that medicine can be done, as well as research, or research can be done in the context of medicine.
Tacey. A. Rosolowski, PhD:
So was it mostly—? Were you thinking about it in terms of a research environment? I mean, what about the patient care? How were you factoring that part?
David Tweardy, MD:
Yeah.
Tacey. A. Rosolowski, PhD:
Or was that not really something you were thinking about at that time?
David Tweardy, MD:
No, it turns out—at that time—so I think I approached my medical school career more as a guy who loved the science. So I was one of those rare medical students who loved the first two years (laughs) of medical school. I did. But, again, I just …Because of the patient-orientedness, and the human-orientedness of medicine, I—who knows? I could’ve done just what Bob Siliciano did, what Dan Littman did, which is get my MD and then use that as a great base of knowledge around human biology to then really attack a problem full-bore, as a PhD would, and go deep and do the deep dive. But when I started doing my clinical rotations, I just loved that. I just loved the medicine part.
Tacey. A. Rosolowski, PhD:
Now, let me just say, for the record, you were at Harvard Med, and it says you have an MA and an MD. How did that—?
David Tweardy, MD:
No, I didn’t get (overlapping dialogue; inaudible)—
Tacey. A. Rosolowski, PhD:
Oh, no, that’s like— [So I?] probably didn’t—
David Tweardy, MD:
Yeah. No, I never got another deg—well, I did not get a degree in addition beyond—
Tacey. A. Rosolowski, PhD:
You know what? I bet I didn’t erase all of the Boston, and it’s probably the acronym for Massachusetts.
David Tweardy, MD:
Massachusetts, yeah, yeah.
Tacey. A. Rosolowski, PhD:
That’s it. So, MD in medicine, and you got your MD in ’78?
David Tweardy, MD:
Yes, that’s correct.
Tacey. A. Rosolowski, PhD:
Okay. Okay, cool. So you went right from Princeton to Harvard Medical School and then did all that. So tell me about—you have the study-study-dissect-things first two years, and then you have your clinical rotation. So tell me about the kind of feel of those two parts of med school for you.
David Tweardy, MD:
Well, I love the first two years. I just—that was kind of a continuation of what I was doing at Princeton, learning the sciences, and I really—
Tacey. A. Rosolowski, PhD:
What about getting into the anatomy lab, though, and doing all that get your hands in the body thing?
David Tweardy, MD:
Well, it was not—
Tacey. A. Rosolowski, PhD:
It’s tactile. It’s visual.
David Tweardy, MD:
It’s tactile, yeah. I guess—
Tacey. A. Rosolowski, PhD:
But not—
David Tweardy, MD:
Yeah, it didn’t—it didn’t turn me—it didn’t sort of appeal to me as much as the process of biochem. I already came into medical school with a process-oriented and a chemical orientation, so anatomy was something I had to get through. It was not something I found especially stimulating. So it just didn’t work for me like the biochemistry did, and understanding how—and the chemistry in biochemistry. So, in a way, what I’m doing with the company Tvardi is really a direct connection to that. I always was interested in chemicals and structures and chemical space, and how they interacted with macro molecules, and proteins are just by far the most interesting macro molecules. They just—we’re all sitting—we’re all a collection of proteins that are carrying out a series of incredibly important functions --I just—in a cellular context. So, in fact, when I had to figure out where I really was excited about science, I loved cell biology but I really in the end think the cell is a little too complex. I like just the proteins, how they interact, and how they interact with the small molecules, perhaps. I wasn’t—that wasn’t my forte when I started in science. I was in the real truly serious part of my career. Cytokines is where I started. So the notion of a protein circulating, binding to its receptor, and telling a cell, signaling the cell to do something different, or even do what it was doing even better, that just appealed to me. So, again, it was the biochemistry of it, and I think it was from Mark. I did really—Mark had a huge impact on what I—in terms of what I thought were really interesting questions. In fact, the entire Biochemistry Department at Princeton had a deep and long-lasting effect on what I thought was cool with science, ’cause really in the end it’s got to be cool. Otherwise, what’s the point? You can do other things. I mean, that’s one of the things: I’ve been very, very fortunate around my career. And a lot of it is serendipity and kismet, but I, frankly, have been able to survive with a mentality that if it’s not fun or cool, do something else. And that’s not—I don’t know if a lot of people can necessarily say that. Maybe they can. I hope they can. But it’s just one of the things I’ve been able to do. But that issue of proteins interacting with proteins to change what happens to a cell is what absolutely became a real focus of my work. And even that was serendipity, because the thing that really got me interested in that particular issue of cytokines was kind of a funny story, which is—not a funny story, but an interesting scientific story-- which is this is the very beginning of the molecular cloning revolution, where people—scientists—Maniatis, I think, probably deserves more credit for being the kind of—the person whose book—it was Maniatis’s book—it was Maniatis’s Molecular Biology, or Handbook—that’s it—it was the Handbook of Molecular Biology. He basically took this—all of molecular biology and made it accessible for you to do it in the laboratory, and it was very practical. It was almost recipes for buffers. And so I happened to be—and after my first postdoc, I got ahold of a cytokine that was molecularly cloned, using Maniatis’s—well, using the techniques that are in his book. I was—it turned out it was—the cytokine was interferon gamma, and it was earlier called macrophage activating factor. And so this is where the medicine part that you’re probably not hearing yet much of intersected with this protein interaction part. When I was an intern, my first month, actually, I admitted a patient to Division 40 at University Hospitals in Cleveland with—a 19-year-old fellow with acute myelogenous leukemia. He was induced with the usual therapy at the time, and developed profound neutropenia, which is a drop in their Y count to zero. And so I managed him for the first few days of his admission, until he became septic. And, of course, once you have sepsis you then get transferred to the unit which is around the hall, the corner of the hall. My next rotation was in the ICU, where he was my patient there, and so I cared for him for the entire month until his death. And he was the first patient—yeah, I would say he probably was even the first or second—I think he was the first patient that I had as an intern that died. And it was not a—it was an awful death. Sepsis, acute lung injury that he had, he was on a respirator for most of the rest—the last three weeks of his life. And so I—you keep asking—well, I kept asking myself, what can we do for him? What can we—? And I actually—it was a wrenching experience. But the thing that I—became apparent to me is—and this particular hospital wrote, in many ways, the book on febrile neutropenia—is that he needed white cells. The guy was—in fact, he even got tran—this is back in the first wave of interest in transfusing white cells, and the guy—Roger Herzig was the hematologist who was taking care of him, and he wrote the first paper back in 1979, I think, on white cell transfusions out of Case Western, New England Journal. And so we gave him white cells; it didn’t work. And so that issue of the cells as—and I got into infections. At this point I was just an intern. So I was very interested in—I became interested, because of that experience, in figuring out how to treat infection, the major cause of sepsis, and how to impact that underlying problem that patient had, which is the neutropenia that was chemotherapy-induced. We used to have this Latin phrase, and back then it was more of it because there was little we could interfere with. It’s called iatrogenicus medicus profunda. (laughter) It’s kind of a—there are only a certain number of people I can tell that to. My wife is one], because she and I trained together, it turns. And you would say iatrogenicus medica profunda, medicus or [churgia?]. (laughs) It was either—essentially, iatrogenicus is physician-caused, right? And profunda means seriously bad thing you did to this patient. And, of course, it was medical. You add that additional “medical” on. And here we were, trying to cure this disease, and what we were doing is essentially killing him, because we rendered his defenses essentially ineffective. So I learned relatively early in my medical career that all that we do is not good, and are there ways we can mitigate. And so the infectious piece was—I learned to love infectious diseases, not because—actually, I didn’t like microbiology so much. So it’s interesting: I liked making diagnosis, and getting patients better. And, of course, that’s my attraction to infectious diseases. I learned microbiology, but I was taught how to make it more manageable, because microbiology is quite—it’s a lot of memorization of—can be viewed as memorization of a lot of bacteria, viruses, and fungi, and that doesn’t necessarily appeal to me. I like to know how things work. I’m process-oriented. And when I was able to take microbiology and reduce it to more processes…And that’s why I teach the lecture on sepsis—that’s where my strength is. So this guy died of severe sepsis, and I wanted to know how we could prevent that. And also, I was really interested in knowing—and this is almost not even conscious, is how can we prevent the neutropenia? We can’t give them—it seems the white cell transfusions weren’t going to work, but how could we prevent the neutropenia or reverse it? How can we kick—jumpstart the marrow in the patient like this? So when I—I kind of sidestepped into immunology. Immunology—one thing about infectious diseases is, one, I think infectious disease physicians fall into two categories, two camps: one is those that are really interested in the bacteria/virus/fungal element, or fungi; and the other is interested in how the host are reacting to that invasion. And I clearly fell down on the right side. I was really very interested in seeing if I could understand this and mitigate it in a better—and so the patients would not die. And so I, in my infectious disease fellowship, I trained with Jerry Ellner. Jerry was very interested in how the host responded to the infection with tuberculosis, and he was interested in the cell that was probably the ultimate effector cell in tuberculosis, which are called macrophages. And therefore we’re kind of circling back to macrophage-activating factor. Turns out that T-cells make a protein called interferon gamma, or macrophage-activating factor, that takes—tells the macrophage to activate and kill the TB organism [in its phagocytosis?], get rid of it. And so Jerry was really interested in how those cells didn’t get the signal, and didn’t do their job. And so I started working in his lab, and there are a lot of aspects of that process, but one of them that… It’s kind of an intricate … If you talk to immunologists, I—when I was an undergraduate in Princeton I thought the smartest people at Princeton were the mathematicians and then the physicists and then the chemists, (laughs) and then the biologists were after that. In medicine, I think the really smartest people are the immunologists, and then the hematologists, and then the infectious disease people. I think that’s the order, because immunology is so intricate. And the story here, it’s—you almost always—whenever anybody tells you an immunology story, they’re always giving you the simple version, (laughs) because they can’t give you the full version. It’ll take too long. But the very simple story around macrophage is in order for the—the macrophage-activating factor is made by T-cells --and the T-cells need to know when to make it, because if they made it all the time you’d get what is called HLA, which is this hemophagocytosis syndrome that we just had a case in Morning Report last week about, where it’s called macrophage activation syndrome. These patients have this syndrome related to the uncontrolled activation of macrophages. So you want to be careful about when the macrophage gets its signal. Well, the way it gets it in the setting of TB is the organism is phagocytosed by the macrophage, and the macrophage does a little bit of digestion of it, and sort of chops it up into pieces, and puts some of those pieces onto what’s called the major histocompatibility locus, HLA-DR. And the T-cell comes along, and if it happens to recognize, having gone through all this evolution to recognize that antigen, it gets the signal to activate, and it expands its number, and it produces the macrophage-activating factor in that local environment, activates the macrophage. The macrophage then becomes more effective at killing the [bacteria?], and you control the infection. So we were—Jerry had shown that individuals who don’t have that—don’t show that ability, have the TB but they don’t do this process, have … He was interested in knowing why, and he asked me to do this project where I would take—they had just described HLA-DR. It turns out Benacerraf up at Harvard had just gotten the Nobel Prize for transplantation antigens, and transplant immunology, and although the context I’m explaining it in is microbiology or immunity to organisms, it turns out these antigens are very important for transplantation, because if you have mismatches across this antigen, the T-cells then kill the organ that has the mismatch. But Jerry realized, as many people early on, that that same antigen that’s recognized as foreign when you transplant it does this presentation to the T-cells in the context of this infection. So he had the theory: he said, “Why don’t you explore the hypothesis that that antigen is not expressed on the monocytes of patients who have TB and are energic?” It’s this concept of—we’re very familiar now with tumor energy here, right? Because we’re now reversing tumor energy, and Jim Allison got the Nobel Prize because of the understanding that he had in how energy develops, but at that time we didn’t know what Jim knew. And there was a good reason to think that maybe those antigens were not on the surface of the macrophage. And, indeed, what I was able to show was --I was able to get monocytes from patients, or get blood from patients, isolate the macrophage precursors called monocytes, and show that those cells didn’t have as much HLA-DR on their surface. It was reduced about 50%. And then, this is, again, just … And then when you incubated them—and I developed a way we could incubate them and still study them the next day—they grew. The macrophages had a burst of this—expression of this energy. It turns out that—we thought there was something being produced, and it might’ve been macrophage-activating factor. So we basically wrote a letter to Genentech and said, “Can you please give us some (inaudible) interferon gamma? And we’ll see whether it is—interferon gamma has the ability to cause a sprouting, if you will, of this antigen.” And we got it, and it did. And then the other thing it did, it did everything: it activated any test that we ran in that laboratory, that I ran and my colleagues ran. It just—you got a positive result. So the lesson in science that I learned when I—now what I train everybody is if you want to get somebody interested in science, and for a real commitment, give them an experiment that works. (laughs) And so this worked. It affected a white cell. I was very interested in white cells. It wasn’t the neutrophil; it was a different lineage, but closely related. And the cytokine that did this was cloned.
Tacey. A. Rosolowski, PhD:
Why don’t we leave it for today there?
David Tweardy, MD:
Okay, yes, yes.
Tacey. A. Rosolowski, PhD:
Yeah, because we’re at four o’clock, actually.
David Tweardy, MD:
My God.
Tacey. A. Rosolowski, PhD:
I know. And this is a good cliffhanger moment with the lesson learned. (laughs)
David Tweardy, MD:
Yeah, I’ll tell—yes, thank you for your—(laughter) I had a clock right in front of me and I’m not even looking at it.
Tacey. A. Rosolowski, PhD:
No, you’re not even looking at it, because you’re into your story. (laughs)
David Tweardy, MD:
Well, you’re a very good audience. You’re a very good audience. And I have to say, it’s been—it’s fun doing this.
Tacey. A. Rosolowski, PhD:
Good, good. No, it is fun. Yeah.
David Tweardy, MD:
Good. I’m glad you’re enjoying yourself. (laughs)
Tacey. A. Rosolowski, PhD:
Yeah. Well, I want to thank you for your time today.
David Tweardy, MD:
No, my pleasure.
Tacey. A. Rosolowski, PhD:
And I want to say, for the record, that I am turning off the recorder at about three minutes after 4:00.
Recommended Citation
Tweardy, David J. MD and Rosolowski, Tacey A. PhD, "Chapter 05: Medical School Leads to a Research Focus on Cytokines" (2019). Interview Chapters. 1387.
https://openworks.mdanderson.org/mchv_interviewchapters/1387
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