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Gregg Semenza 2019 Nobel Prize Winner | Press Conference

(audience applauding)
(audience cheering) (audience whistling)>>Great. Good afternoon, and welcome. My name’s Landon King, and on behalf of the School of Medicine, I wanna thank you for joining us on this extraordinary, exciting day. I wanna thank all of
you who have come here to celebrate with us
today including faculty, staff, lab members. A particular Welcome
to Gregg’s wife, Laura. Congratulations. It is a family affair. We’d also like to thank members
of the (mumbles) families for being with us today. They are among the many
who have contributed to Johns Hopkins and allow
us to pursue the things that we seek to achieve. I’d also like to thank
the members of the media who have joined us here today, either in person or on by
phone or through social media. First, I wanna offer the
heartfelt congratulations from our Dean and the CEO
of Johns Hopkins Medicine, Paul Rothman. Paul is traveling today
and very disappointed that he could not join us. But he’s incredibly proud
about this accomplishment, what it means for you, Gregg and what you’ve been able to achieve and what it also means
for our institution. We’re here today to celebrate
the groundbreaking work of our colleague Gregg Semenza. But I wanna make sure to mention
another Hopkins connection to today’s prize. Gregg is sharing the award
with two other scientists, William Kaelin of Harvard and the Dana-Farber Cancer Institute, and Peter Ratcliffe of
the University of Oxford and the Francis Crick Institute. In particular, Dr.
Kaelin did his residency in internal medicine at
the Johns Hopkins Hospital where he also served a
year as chief resident. So as we gather to celebrate Gregg’s tremendous achievements, we want to offer our
congratulations to doctors Kaelin and Ratcliffe as well. This is the 14th Nobel Prize associated with the Johns Hopkins University School of Medicine, one of the many Nobel Prizes
awarded to the university. The Johns Hopkins University
School of Medicine received more than $700 million
in federal funding last year and has been one of the top recipients of NIH funding for many years. As a university indeed,
we are the top recipient of research funding. That funding supports work
across the full spectrum of biomedical research. This award and our celebration today highlight the critical importance of fundamental basic science research in advancing our understanding of biology and our opportunities to improve
the lives of our patients. We are investing it significantly
in basic science research because of our commitment to
the importance of this work in advancing medicine. The recognition of the work
of Dr. Semenza and his team also provides the opportunity
for reminding ourselves of the process and the time required to move from initial
observations at the bench to understanding the potential
impact of these discoveries on our patients. As Gregg will attest to,
work of this sophistication and importance takes a village
and we wanna take a moment and also congratulate the
numerous trainees and colleagues who have made contributions
over the many years. In a few minutes Gregg will
talk more about his work but I wanna briefly provide an overview. Gregg and his colleagues
discovered how cells sense oxygen, an essential process for survival. Oxygen is carried to tissues
and cells by red blood cells and when oxygen levels are low, the body generates a hormone
called erythropoietin, which signals to boost
red blood cell production. In the early 1990s, Gregg and his team were trying to understand
how oxygen deprivation, called hypoxia, triggers
production of this hormone. They identified a segment
of DNA and enhancer element that is responsive to low oxygen. When put in front of any
gene, the enhancer element causes that gene to be turned
on when oxygen levels are low. Gregg proposed that a
protein binds to this element to turn on a specific gene or
genes and named this protein, hypoxia-inducible factor 1 or HIF-1. In 1995 Gregg and postdoc Kwang
Wong, purified HIF-1 protein and found that it contains
two sub units, alpha and beta. In cells, HIF-1 alpha is present
in low oxygen conditions, but disappears when oxygen
concentrations are high. In 1996, Gregg demonstrated
that HIF-1 activates a key gene involved in blood vessel formation called vascular endothelial
growth factor or VEGF. This showed that HIF-1 helps the body cope with low oxygen conditions by triggering not only RBC production, but new blood vessel growth. Gregg’s discovery of HIF-1 and
the research that has ensued has opened up new doors
to developing therapies for a number of diseases, including cardiovascular
diseases in different organs, metabolic diseases and cancer. Many tumors draw nutrients by
growing extra blood vessels. So being able to turn off HIF
may slow cancer progression, and at least one compound
is in clinical trials for kidney cancer. Gregg, we’re extremely excited for you as you receive this highly
deserved recognition, and proud to call you
friend and colleague. And with that it’s now my privilege to introduce Ron Daniels, the president of Johns Hopkins University. (audience applauding)>>Well, thank you, Landon. I think it’s fair to say it truly doesn’t get any better than this. And today, I’m thrilled to be here with Nobel laureate, Adam Reese. Where is Adam? Sitting over there. And it’s good, you’re fine. We got a chance to say
hello to one another now that you’re both in
this illustrious club. Is Peter Agree here? I know Peter saw you earlier Gregg, but no, Peter was hoping
to be able to join us. Provost Sanjog Kumar. Of course, if I could,
Vice Dean Landon King. Laura, it’s great to see you
here and celebrate this moment and all of you as we join the
Nobel Committee in honoring the remarkable, remarkable
scientific achievements of Gregg Semenza and co winner Peter Ratcliffe and Dr.
William Keitlin who as Landon noted, trained here at
Hopkins as also a resident. I know we have a lot
of people here to thank and I’m sure Gregg will
have many in his comments for arriving at this moment. Starting, of course with Gregg’s parents and going forward from there. But I’d like to call out
one who might be missed and that is Rose Nelson. She’s not a winner, not
a previous noble winner related to Hopkins or
indeed hasn’t won a Nobel associated with any institution. Rose was in fact, though,
really instrumental in bringing this, to bring us to this day. She was Gregg’s high
school biology teacher who herself held a PhD, I understand and understood the power, the importance, the allure of basic curiosity-driven
scientific research. Gregg has often credited
her with, as he says, transmitting the wonder of
biology and the excitement of understanding the subject
at its most fundamental levels. And clearly, Gregg, you have
built an extraordinary career from exploring that wonder
at the highest echelons, and digging in deeply, incrementally to the fundamentals of human physiology. Indeed, it was your commitment
to exploring and explicating these fundamentals with your
own post doctoral student that led to the discovery
which Landon has referred to that we are celebrating here today. A discovery that I understand
could have been missed had it not been your drive
to scrutinize punctiliously and unrelentingly the many
results from your many, many, many experiments over the years, and an effort to discern patterns that would generate
insight and understanding. One day of course, while pondering the meaning of
a series of negative results, you held up a gel shift to
say and saw a faint image. And there it was, HIF-1. As we know from what Landon
said a few moments ago, hypoxia-inducible factor
1, a protein that helps direct the cells response
to low levels of oxygen has informed our understanding
of a staggering array of biological processes,
or as you so simply put it, in ways that even a law
professor could understand, hold your breath for 20 seconds and you know right away
how important oxygen is. I got that. More than 30 years ago you
asked that central question, how does this system regulate itself? It’s a double delivery system that makes Amazon
Prime’s look rudimentary. But thanks to your tireless efforts, we are closer than ever
to understanding it and all its richness and complexity. And as you well know, your discoveries have led to momentous
advances in human health and well being for people suffering from cardiovascular disease. Of course, a condition that
causes veins to (mumbles) and heart tissues to be starved of oxygen. HIF-1 can play a life-saving
role by activating genes that support the creation
of blood vessels. And thanks to you, your co
winners and collaborators we now know that HIF-1
can help us formulate novel treatments for
everything from deadly cancers to diseases related to aging. So today, we recognize and celebrate a career marked by a passionate
commitment to the wonder of basic science and
its profound connection to improving and saving lives. But we also celebrate those
mentors like Rose Nelson, and most important like you, Gregg who have instilled in others
both the wonder in science, a capacity to pursue its
fundamentals day upon day upon day, in order to advance knowledge
that serves humanity. And we know Gregg that though
this honor is a profound, indeed a momentous one for you, that you will be right
back in the lab tomorrow, if not later this afternoon,
to continue doing the work that you have done for decades, and continuing to honoring
that great pursuit. So, Gregg is the 28th Nobel laureate associated with Johns
Hopkins, a prestigious list that gives great pride
to our entire community. I’m delighted that we can pause here today to applaud this matchless accomplishment, together with his friends,
colleagues, students, and of course, his family. Without further ado, I’d like to introduce Johns Hopkins newest Nobel
laureate, Gregg Semenza. (audience applauding)>>Thank you. (audience applauding) It’s a good day for Hopkins, I think. Thanks everybody. Thank you very much. Believe it or not, this has been a really lousy year for me. May 31st, I somehow ended up
walking through the hallways of my home in the middle of the night and fell down a flight of
stairs and broke my neck, fractured four cervical vertebrae. And it was a pretty serious injury. Fortunately I got to Hopkins and a very talented
neurosurgeon named Ali Biden put me back together again. And it was funny ’cause
he told me afterwards that when he operated on me,
he didn’t know who I was. And he said, “If I knew who you were, “I would have been so nervous.” (audience laughing) But the point is, he did a great job and I have very little, very little deficits as a
result of his great surgery. And for me, that’s sort of the way it’s been my whole career here. There have been lots of
times when I needed help, and there was always
someone on the faculty or the staff here who helped me. And yeah, I’ve been able to
do what I’ve been able to do here at Hopkins. And I really don’t believe
that I would have accomplished this anywhere else. And that’s why I’ve stayed
here my whole career because I think this is the
greatest place to do research. It has the greatest colleagues, and the greatest sense of
collegiality of any place I know. So there are places where
there are lots of smart people and know how to do all sorts of things. There are places that are,
everybody’s very friendly, but there are very few places
that have both of those like Hopkins where there’s
always someone who knows what you need to know and
they’re willing to help you and that really started for me in postdoc. When I started this project
kind of from scratch, and this is like a crazy
thing for a postdoc to do ’cause a postdoc doesn’t come into a lab and just start a project. They work on something in the mentors lab. And I was very lucky that I
had mentors in Haig Kazazian and Stylianos Antonarakis that allowed me to pursue this project, even though it was not part of their
general research program. And we were lucky in terms of being able to make some discoveries and
we would have hit the road because we had identified the factor but we were trying to clone the DNA and we were trying to use
expression library cloning and it didn’t work and we had
screened millions of clones and guess I had several choices. We could continue screening and continue to get negative results. And that didn’t sound like a good idea. We could give up and
let somebody else do it. That didn’t sound like a good idea. Or we could take a different approach, which involved the biochemical
purification of the protein. And that was daunting because my lab was a
molecular genetics lab. We didn’t know anything
about protein purification. We didn’t even own a fraction collector. But Tom Kelly’s lab was across the street and was one of the first
labs to purify a protein based on his binding to DNA. And with the assistance of his lab, we’re able to purify HIF-1
from 100 liters of helix cells found ina suspension culture. And we know the heritage of
(mumbles) here at Johns Hopkins. So it’s been a great time
for me here at Hopkins. And as I said, a lot of people helped me. I’ve tried to return that
by mentoring students. And that’s one of the major enjoyment. So I have, in addition
to doing our research is to mentor students both
in my lab and elsewhere. And the message that I have
for everybody who’s here who’s training today, is that I was once where you are now and someday you will be where I am now. And I think that we’re very
lucky to have this career where we get to follow
our interests and dreams and crazy ideas wherever they lead and people will pay us to do this. We have friends all over the world that share our passion for research. So it’s a really great career. People often complain about grant writing but I always say that’s the
only bad part of the job. And the rest of it is fantastic. And when you think about it, we’re very fortunate to have a career that we actually enjoy doing because so many people have jobs, to pay the bills, basically. And people say, well, you work very hard, but come on, it’s in, we
enjoy every minute of it. So I’ve been very fortunate in the sense that I was
brought up by my mother, along with my four other siblings. She was an elementary school teacher, and she was very supportive
of me all along the way. And I was fortunate to be able
to get involved in research fairly early on in high
school and then in college. And really fortunate to come
to Hopkins to start work. We originally started work
by making transgenic mice that express the human EPO
gene with John Gearhart. And again, I was a postdoc
coming to John with an idea and there was no reason
that he had to say yes, but he did. And that started things along the way. I’ve been very fortunate
that the administration here has been so supportive. Ron Daniels invited me
to lunch at Homeward I think seven years ago, and we had a great talk
about what I was doing. And Ron and Paul Rothman I’m
sorry that he’s not here today ’cause I know he would like to be here. I have been incredibly
supportive of the work as has Dave Valley, who’s now the chairman of the new department of genetic medicine. And Dave has been my boss
for quite a few years, and has been, again, very supportive of all
the work we’ve done. So I’m really blown away by
the number of people here. Thank you all for coming. It’s been a really amazing day. And like I said, this is a
award that’s shared by everybody at Johns Hopkins, past and present because I couldn’t have
done it without you all, including all of my trainees. I’ve just been really
fortunate to have a long list of superb postdocs and graduate students and undergraduate students
who work in my lab. And the great thing is that
the students come and go. And every year there are new students. They remain young. And as long as I don’t look in the mirror, (audience laughing) there’s no aging going on in the process. So it’s, yeah. I enjoy it so much and
have so many great people who have worked with me and
are working with me now. And everybody who knows our
lab knows that it’s filled with great people who are
always willing to help. So thank you again for coming. I know I’ve forgotten to
thank a whole bunch of people and I apologize. I’m sure it’ll come to
me about two seconds after I leave the podium. But my day started before 4:00am and it’s been non stop since then. I did have a little bit of champagne. I must confess. (audience laughing) Thank you very much. (audience applauding) Thank you, everybody. (audience applauding) (audience cheering)>>So, before I turn the
microphone over to Landon King who’s going to preside over
some questions for the press, there’s just two things I
need to share with you Greg. The first thing is that
following a tradition that has been inspired by Elizabeth Warren at all of her rallies, and now
apparently a set of standards and expectation for those in receipt of the Nobel Prize this year, you’re gonna be expected
to stay until everyone here gets a selfie with you. (audience laughing) So, he’s got nothing left to do today. So the self–>>Just 450 emails to respond to. (Gregg and audience laughing)>>But the selfies are part of it. So that’s the first thing. The second thing is
Landon’s gonna officiate, but I wanna get the first question. Of course, it has to do with
the call you got this morning. Is it true that you slept
through the first call?>>Yeah, I am a deep sleeper so, (audience laughing) I did wake up eventually. But by the time I got to
the phone, it was too late. And so I said to myself, oh boy, I wonder if this is
somebody’s idea of a bad joke. So I went back to sleep or tried to and it was quite a few minutes. I think they were debating
whether to call me back or not. But fortunately they did.
(audience laughing) And I was a little faster to the phone the second time around. So this is why we say
it, same as in research. My first advisor, when I was an undergrad, he used to say search and research. So you’re not always gonna
get it right the first time. (audience laughing)>>Gregg, thank you for
the inspirational words, and certainly for the work. And thank goodness they
didn’t say who’s next. (audience laughing) So we’re gonna open it up
for questions from the press, and we’ll start with those
who are here in attendance. You have questions?>>Woman: (mumbles)>>Yeah, that’s a great question ’cause that’s really what it’s all about. And so, it turns out that
because oxygen is so critical to life, many of the common
human diseases have derangements in the ability to maintain
proper oxygen levels. So for example, in a cancer, the cancer cells divide very rapidly, consume a lot of oxygen, and the cancer cells become very hypoxic. And what we’ve learned is
that when they become hypoxic, they turn on genes that enable
them to invade, metastasize and spread throughout the body. And whereas most of the chemotherapy drugs are designed to kill dividing cells that are well oxygenated,
there are no treatments that are approved to
treat the hypoxic cells within the cancer. And we believe it’s these
cells that survive the therapy and come back and kill the patient. So one of our major goals
is to try to identify drugs that will inhibit HIF
activity as an addition to existing cancer therapies. And we hope that that will
help to improve outcome in a number of solid cancers where once the cancer has metastasized that there aren’t really
effective therapies. Then on the other side is
the cardiovascular disease where the blood vessels
for example in the heart can become narrowed, reducing
the blood flow to the heart causing the heart to have ischemia, which is injury due to the lack of oxygen. And this of course, can ultimately result in a heart attack. And we know that the
hypoxia-inducible factors stimulate new blood vessel growth. They stimulate the
remodeling of blood vessels to increase flow to tissue. And so we hope that there
may be the possibility for new therapies to
increase the perfusion of ischemic tissue in diseases
like coronary heart disease and also limb ischemia which is a major problem
particularly in diabetics, leading to, in some
cases, limb amputation. And so there are a number of disorders where we hope to make an impact. The one that’s gonna occur first, I think is chronic kidney disease, where individuals with
chronic kidney disease cannot make EPO and as a
result, they are anemic. They originally Of course
required blood transfusions, and often came down with
transfusion-associated viral illnesses like AIDS and hepatitis. When EPO was cloned, it was possible to generate
the EPO protein in the lab and that’s now given by injection. There are drugs now that
are in clinical trials that will induce HIF activity, and these drugs can be
delivered as a pill. So, this will be, I think, a major advance in the
treatment of anemia. And there are over 25,000
people in clinical trials now for these drugs. So I suspect that one or more
of these drugs may be approved in the next year or so. So I think that there are
some clear applications and many more, I think that will follow.>>Woman: (mumbles)>>Say again?>>Woman: (mumbles)>>Yeah, I think that we have sort of a new target for therapy. And the hope is that
by having a new target, we may be able to
significantly improve outcome in a number of diseases. But again, as you heard,
research is a process that occurs in some leaps and bounds
but mostly in small steps, and particularly when it comes
to developing new therapies, the road is a tough one. So and we understand that, that it would be difficult to
develop these new therapies. But certainly in my lab,
that’s what we’re focusing on now is to try to move these
discoveries to the clinic.>>Additional questions from the media?>>Man: (mumbles) Get that call.>>Woman: (mumbles)>>Yeah, so, Rose was an amazing woman. She was under five feet tall, and always had a beatific
smile on her face. And she had, as you heard, received a PhD and done a postdoc at Walsall so she knew what research was about. And so when we learned
biology, we didn’t just learn the facts we learned
who made this discovery. When did they make the discovery? What were the experiments that they did that led to the discovery? And what a wondrous thing
it is to be able to learn something of fundamental
importance in biology. And she used to say to us. She used to say, “Now, when
you win your Nobel Prize, “I don’t want you to forget
that you learned that here.” (audience laughing) And she just assumed that one
of us was going to do that. And it’s my great sadness
that she’s not still alive to share the moment because I know it would have meant a lot to her. But yeah, she was my inspiration. And I think that, boy, that’s
the importance of teachers to make that kind of spark. And certainly in this country, we need to give more emphasis to teachers and to reward them for
the hard work that they do which makes such a difference
in the lives of so many. (audience applauding)>>Other questions? I think there might have
been a second question from–>>Man: (mumbles) What were you thinking and (mumbles).>>Nothing (laughs).
(audience laughing) I was in a daze. And yeah, I was kind
of half awake and yeah, it was kind of just, I was not able to really
say much of anything, because I was so shocked and surprised. As I say, particularly given
the experience I’ve had over the last several months, It was certainly not
something I was expecting.>>Other questions from the
media that are with us here? Amy, do we have any questions
from the teleconference line?>>Amy: If you’d like to ask a question that is, one and then zero. And our first question
will come from Makino Asia India, Asia new service, please go ahead.>>Woman: Doctor, my question is, what does your work mean for patients who are currently undergoing chemo? Thank you.>>So the question is, as I understand it, what does our work mean for patients who are currently undergoing
chemotherapy for cancer? In the case of kidney cancer, there’s a drug that inhibits one of the hypoxia-inducible
factors, HIF-2 that’s in clinical trials and
showed some remarkable results in a phase one trial. So I think that kidney cancer
may be the first cancer where a drug that blocks HIF activity may be added to therapy. We certainly think that
there are many other types of cancers that may benefit
from a HIF inhibitor. We’ve spent a lot of time
and effort in the lab, all the folks in my lab
studying breast cancer, where we find that that HIFs
play a really critical role in the progression to metastatic disease and the ability of the cancer
cells to shield themselves both from the immune
system and from therapies. So in the long term, we hope
that there will be many cancers where a HIF inhibitor may be beneficial. And in the short term, it
looks like kidney cancer may be the first such case.>>Other questions, Amy.>>Amy: Yes, the next
one comes from Tina Fey. Science News. Please go ahead.>>Tina: Hi.>>Amy: Oops. One moment. Tina, you have dropped
off if you push one zero. And you may begin.>>Tina: Okay, hello Dr. Semenza. I was wondering if you
could talk a little bit about how your work intersects with that of the other two laureates, and whether you ever
worked directly with them.>>Yes. So, for the most part, the three labs have worked independently, although we have
collaborated on some projects along the way. So we discovered HIF-1, showed that it was induced by hypoxia. And then the question was, what
was the molecular mechanism by which the activity of
the protein was induced under low oxygen conditions? And Peter Ratcliffe and Bill Keitlin’s lab showed that the HIF-1 alpha sub unit, is subject to a
post-translational modification, which is the hydroxylation
of a proline residue. And they went on to identify
the enzymes that carry out this modification and they’re called prolyl hydroxylases domain proteins. And these proteins use
oxygen as a substrate. And they insert one oxygen
atom into HIF-1 alpha. And by doing so, HIF-1
alpha becomes recognized by a protein called the von
Hippel-Lindau protein, VHL. And when VHL binds the
hydroxylated HIF-1 alpha, it targets the protein for degradation. So when we’re under our normal conditions where we’re getting plenty of oxygen, the HIF-1 alpha is
hydroxylated and degraded. Then under hypoxic conditions, the hydroxylation reaction is inhibited, and VHL cannot bind to the protein and HIF-1 alpha rapidly
accumulates within hypoxic cells. Now, apart from showing
the molecular mechanism, the other part that was important here is that the enzymes that were
discovered use both oxygen and a small molecule called alpha ketoglutarate as substrates. And this is important because
it then became possible to develop drugs that were alpha ketoglutarate analogue, so they would bind to the enzyme but rather than activating
it would inactivate. And so the drugs that are
being developed to treat anemia and chronic kidney disease, these drugs bind to the
hydroxylases in the region that would ordinarily be
bound by alpha ketoglutarate. And that’s their mechanism of action. So really those discoveries
enabled a number of groups and pharmaceutical
companies to develop drugs that appear to be very potent
inducors of HIF activity and red blood cell production.>>Thank you. Amy?>>Amy: Thank you. And as right now, there
is no further question.>>Okay, thank you. Kristen, do we have any Twitter questions? No. Okay. Well, any other questions
from the media here?>>Woman: How did you
decide to start (mumbles)? How did that (mumbles)?>>Right. So when we started the
project, as I mentioned, we were working with John
Gearhart to making transgenic mice that express the EPO gene and
we’re interested in the fact that the gene is expressed in
the liver during fetal life and in the kidney in adult life. And we identified sequences
that were required for expression in the kidney and the liver in transgenic mice. And so after we had sort
of explored the tissue specific expression of the gene, then it became obvious that
the other really interesting aspect of the regulation of the gene was the regulation by
oxygen concentration. And for those studies, we
went into tissue culture cells where we could expose cells to different oxygen concentrations, and other labs had shown
that in these cells, EPO was induced. And then using those cells, we identified the particular
regulatory element that was critical in the EPO gene, and then used that to identify
and then purify HIF-1.>>Great. Any the other questions from the media? You’re welcome to the audience?>>Sure.>>Dare we take some
questions from the audience? (audience laughing) Okay. Thank you, ooh. Ooh, hey Stewart.>>Stewart: (mumbles)
whether publishing science for cells major was
key to your early work? (Gregg and audience laughing)>>Thank you for that theory. (audience laughing) Now, we have to put a disclaimer there in that Stewart and I and the many members of the Johns Hopkins faculty
are the editorial board of the Journal for Clinical Investigation. This is a journal that’s run
by scientists for scientists. So the answer to your question is no. When we wrote our manuscript reporting the discovery of HIF-1, we submitted it to these so
called top tier journals, and they did not find to
be of sufficient interest to warrant publication. (audience laughing) (audience applauding) I was very fortunate that Victor McKusick was one of my mentors was a member of the National Academy of Sciences. And Victor had the
paper reviewed for PNAS, and it was accepted. And it’s been cited over 5000 times. (audience applauding)>>Do we have any other either
setups or general questions? (Gregg and audience laughing) If not, oh, please.>>Man: (mumbles)>>Yes, that’s a great question. So the ceremony will be on
December 10 in Stockholm, and anybody who’s been
in Stockholm in December knows that the sun is up
for a few minutes about. But I think it’ll be exciting nonetheless. I did have the opportunity
to speak at a Nobel forum maybe 10 years ago. So and then I was a speaker
at the Karolinska Institute a couple of years ago. That talk fortunately was in
the spring and in the daytime. So, yeah, it’s gonna be a very exciting, particularly because I’ll have my family and good friends with me. So I look forward to that.>>Other questions? Please.>>Woman: (mumbles)>>Well, yeah. I think the key is that
what makes it exciting is we never know which
way the work will turn. We never know what will be
the critical experiment. So we just continue every
day to try to generate data to move forward. And I think the joy has to be in those small steps every day. And then, of course, when
we write the papers, for me, that’s one of the best
times ’cause we get to see really how much progress we made, and then to share with the world. And I tell all my
students that your papers are your legacy. That they’ll live forever. And so we want those to
be really works of art. So that’s the approach that I would take is just to continue to focus on every day on your experiments and generating data ’cause that’s what we do. We generate data. We don’t try to show this hypothesis or that hypothesis is correct. We just use those hypotheses as a way of trying to understand
the universe right, past, present, and future. And so yeah, the key goal is to generate data that’s reproducible, that we know will stand up to other people doing the same experiment
and getting the same result and will move the field forward.>>Sounded almost like
a bridge to Adam Reese. Other questions, please.>>Woman: (mumbles)>>Yeah, I don’t know how it will affect my daily life and career. I’m very happy with my
life and career as it is at the moment.
(audience laughing) So I hope not too much (laughs).>>Other questions? Yes, ma’am.>>Woman: (mumbles)>>So, the question is about
the physician scientists, and that, I guess their
importance in research. And so I trained as an MD PhD, and my clinical specialty
was medical genetics which I was able to do for a few years. And I really enjoyed doing it. Because I think that first of all, patient care gives you a
very critical perspective on doing research. It’s why you do the research, at least it’s why I do the research. And when you see what families go through, for example, with diseases, it kind of gives you some perspective about your experiment that didn’t work, and you’re gonna have to do again. This is not a great tragedy
in the great scheme of things. So, first of all, I think it gives really certain
perspective and motivation for doing research. And I guess I felt that
by having both research and medical training,
that I was best suited to kind of be at the
bridge between the two, and to try to take basic science knowledge and hopefully help to have
it translated to the clinic. It’s very difficult to do both
research and clinical care. As many of the faculty know, I stopped doing clinical
care about 15 years ago. It’s just very difficult now. It’s difficult to do
research 100% of your time, much less less than that. And I do worry how much
it’s gonna be possible with all the pressures on people both in terms of medicine and research, to have those kind of dual careers, but I think they’re very
important for studying disease and for developing new therapies.>>Well, Gregg, thank you for being here. It’s an extraordinary day in recognition of an
extraordinary body of work. Thank all of you for being here. And if you’re interested,
we have a reception upstairs on the way outside of Turner auditorium. So thank you for coming. (audience applauding)>>Gregg: Thank you.

Robin Kshlerin



  1. David Omondi Posted on October 7, 2019 at 7:20 pm

    👣 thats the step in science

  2. JAM JAM Posted on October 7, 2019 at 10:22 pm

    This is amazing!

  3. 7.756.935 Posted on October 7, 2019 at 11:03 pm

    C-O-N-G-R-A-T-U-L-A-T-I-O-N-S! ✌🤩👌

  4. Vincent Wang Posted on October 8, 2019 at 12:20 am

    So lucky to be there, today…….Big day of JH!

  5. vaishnavi ramakrishna Posted on October 8, 2019 at 2:52 am

    Congratulations Sir!! Congrats to all who contributed to the success 👍👏👏

  6. Ashish Jumde Posted on October 8, 2019 at 5:42 am

    Congrats sir

  7. Jamie Park Posted on October 8, 2019 at 8:35 am

    Congratulation! It’s really amazing.

  8. Medico factz Posted on October 8, 2019 at 12:23 pm


  9. Amir Ciba Posted on October 8, 2019 at 5:20 pm

    Please stop using plastic bottle.

  10. Connie's Community Posted on October 10, 2019 at 9:20 pm


  11. ابوعبدالله Posted on October 11, 2019 at 9:48 pm

    اتمنى الأخوه العرب لديهم فخر بالعروبه ويكتبو بالعربي

  12. Tamara Voronina Posted on October 24, 2019 at 12:53 pm

    Congratulation! It’s really amazing. Now NHS may start to use Intermittent Hypoxia Training!