How Stem Cell Research Is Curing Heart Defects (Interview w/ Cenk Uygur)

How Stem Cell Research Is Curing Heart Defects (Interview w/ Cenk Uygur)

Welcome to TYT Interviews, and we’ve got
a fascinating one for you guys. This is actually three different doctors who are gonna talk
to you about stem cell research. We’re here in YouTube space New York. Let me introduce
you to the doctors first – first actor, Todd Evans, and doctor Jim Cheung, and doctor
Albano Meli. That’s right. OK, as good as I could get it. Ok. So, this
is a fascinating story. It involves a couple of different countries, and one person’s
heart, and how we’ve…. So these doctors have tracked the mutations, and hopefully
fix some of the issues that are at hand and involve stem cell research. It’s enormously
fascinating. The more I talk to them off air, the more I get a sense of how much I love
science. Ok, so in my mind, these are the good guys.
And so let’s have an interesting conversation about how it all works and how we all came
to be in the same room. So doctor Cheung, let me start with you. We have someone on
staff, Praveen Singh, she is head of business development for The Young Turks, and she had
an issue with her heart, and she came to you. So, what was her issue? Actually what happened was that Praveen – several
years before seeing me – had actually had an event when she just completely blacked
out while at her office on the phone. And she… it was actually quite a significant
event and she ended up getting hospitalized, she found she’s having arrhythmia, had several
procedures done, and actually done well on treatment but as it turned out she had found
out that her mother actually had the same condition. Then fast forward few years later – that’s
when she met me in my office. She had explained to me and she was actually an advocate for
herself, because she really… you know she was actually pregnant at the time and said:
Look, you know, I really think I have a genetic problem here. At that time her diagnosis was
called short couple torsades de pointes – quite a mouthful but what it really is is a form
of arrhythmia that tends to affect patients who have otherwise normal hearts. You know,
she was young, otherwise healthy, no other medical problems, but she passed out from
arrhythmia. So it turns out that her mother had the same
exact condition, so two very rare occurrences, so she was thinking this could be genetic,
so what can we do to maybe find out if there is an actual mutation that we can identify,
with very direct implications for herself – she was pregnant at the time with a child
and she was worried – is it possible that I might pass this along to my child and future
generation. So that’s really how it all started. So let me understand this. It’s pretty scary
for a lot of people. You might not realize you have this condition? That’s right. And you might simply have… is it a cardiac
arrest you’re going into? Yes, pretty much. Do we know if it’s the same thing, or not
necessarily same, but similar to conditions we see on TV from time to time – if you
are a sports fan, you know Reggie Lewis died suddenly while playing basketball… And do
we know how many people it affects, is it similar, and how much overall does it affect
the country. Thankfully, it is very unusual. A lot of patients
who have cardiac arrest tend to have prior heart problems. Like, patients who have Myocardial
infarction, meaning they had a blockage to a part of their heart, a part of their heart
died as a result. Or a patient has a very weakened heart, what we call a cardiomyopathy.
So that’s just to put it in perspective. It is still the vast majority what causes
cardiac arrest. However there is a distinct subset of patients who have otherwise totally
normal hearts – young and otherwise healthy – who may have some unbeknown condition
that predisposes them to have cardiac arrest. Exactly like the examples you’ve mentioned
– Reggie Lewis had something called hypertrophic cardiomyopathy where he had a thickening of
his heart. Obviously, it led him to have electrical abnormalities
of the heart but he was an NBA basketball player, so obviously it was not affecting
him so much that it would prevent him from competing at the high level. Every so often,
absolutely, we would hear stories of marathon runners or other athletes, who are otherwise
very much high performing – people who pass out suddenly or even have a life-threatening
arrhythmia. So again, in perspective it is relatively infrequent. So for example, the
most common form of this kind of disorder, it’s called long QT syndrome – it affects,
you know, one in a thousand, one in two thousand let’s say, it’s not super rare, it’s
definitely out there but it’s not super common, but it’s definitely something we
need to know about. About 280 thousand people die in a year from
heart attacks. But it’s a smaller subset that is affected by this. I mean, what scares
a lot of people, is that it seems to come out of the blue and there is no other indication.
We all know we need our cholesterol checked, we all do our check-ups, so you have a sense
of how to make your heart healthier, but if you have this – boom! You’re either – in
Reggie Lewis’ case you’re exercising, and all of a sudden you get…. Or in Praveen’s
case you’re at rest, and it’s even scarier in some way. You didn’t even know that that was possible.
So now in her particular case, they know what it is, you guys know what it is, and you know
that it’s a mutation, right? So we think it might be genetic but we don’t know. So now how do we find out more about it, how
do we then transition to doctor Evans? With Praveen’s urging actually, we decided
to send off genetic testing. Actually, to be honest with you, I was quite skeptical
in the beginning, because I felt that her story did not fit. The list of disorders that
can cause sudden cardiac arrest in an otherwise healthy heart – so there is a list. And
her condition did not fall under the known list which has been known to be associated
with specific mutations. So obviously, there are genetic anomalies that are out there,
we just don’t know what genes they are because we haven’t explored every possible gene
out there. So at that time I was a bit skeptic about
doing a genetic testing because I felt, you know, what’s the likelihood of us finding
something? This could be low. There are actually downsides of finding something, because if
you find something, that mutation, the alteration of genetic code may or may not be what’s
actually causing the condition. So what happens is that the downside during
genetic testing when you don’t know what you are testing is that you may find some
abnormality which is actually totally benign, you know it’s just as benign as the difference
in hair color, but then you link it to some potentially you think fatal condition, without
the full scientific knowledge of what’s going on. In any case, just a backtrack. So in Praveen’s
case we did the genetic testing, and we found a mutation in a gene, which is really quite
surprising, because that mutation is associated with arrhythmia generally with exercise, and
in her condition, it occurred purely at rest. So at the time I was, well, that’s interesting,
and we tested the mother, and the mother had the exact same mutation. Now that does not prove anything. So that’s
the thing. Now we have two patients with relative uncommon presentation, with relatively rare
mutation, and then now, however, the hard work begins, which is making sure we can prove
that we have the science to make the association between the actual mutation and the actual
medical condition we’re trying to make the diagnosis for. And that’s where doctor Meli
and doctor Evans step in. Where they can actually give us the scientific evidence to support
that hypothesis. So already this is really interesting and
a little scary for people if they have this. So they’re rooting for you, I think, to
get this right. But I think what is more interesting is to see what doctor Evans and doctor Meli
have done. So you sent Praveen’s blood to doctor Evans. Doctor Evans, what did you do
with the blood? What our group did with the blood was… we
are actually turning them into stem cells. What we like to do – to be able to study
Praveen’s cardiomyocytes or other cellular components of her heart, but of course we can’t
do that. A physician can study various clinical aspects of her condition but we actually like
to understand the molecular basis for what’s going on, to actually be able to understand
the biochemistry in terms of how the proteins are functioning in her heart. And there are certain things we can do now
that even five or six years ago we could not do. A lot of times, for example, you could study
somebody’s blood cells and try to make an assumption about how a gene being dysfunctional
there relates to the cardiomyocyte but that’s a big stretch. We’d actually like to be
able to do is generate a cardiomyocyte, replicate what we call the “disease in a dish”.
Actually create functioning cardiac tissue in a dish which has the exact same genetic
makeup of the patient. And we can do that now. So what we do is we can take blood cells and introduce four genes that are called “pluripotency genes”, they are genes that are important
form of parting phenotype of a stem cell, similar to an embryonic stem cell – that
allows these cells now to become reprogrammed. So they forget basically that they are a blood
cell. Actually one of the beauties of this process
is that blood is easy to obtain just from the periphery. Everybody goes to the clinic
and gives blood. We need very little blood. We use the blood cells that would normally
make red blood cells, which is the most abundant cell in your body. So we can expand it in
a Petri dish these what I call a erythroblast. And we introduce a virus, an engineered virus. That virus is such that it will go in these
red blood cell precursors and express these pluripotency genes. Essentially, erasing the
memory of that cell as a red cell. And the culture conditions are such that we can capture
cells as they transition and reprogram to become a stem cell. The reason that’s important
is that one of the great features of a pluripotent cells is that we can grow them in a dish,
and make as many of them as we want. We can grow them up, grow them up, grow them up. So that’s occurring actually right now at
the Weill Cornell Medical School in the incubators. Now the beauty is that over the last five
or ten years – something that my own group is very much involved in but many other laboratories
are working on actually using these embryonic… these are actually called “induced pluripotent
stem cells”, IPS cells. That does not do that much good, just to grow lots and lots
of them. We have to do something with them. And so a lot of people had been working on
the protocols to then differentiate them into different cell types. You could start with
a blood cell, reprogram it back to the stem cell, make a lot of it, and now induce it
to turn into whatever cell type you like. And one of those, which we now have a very
good protocols for are cardiomyocytes, the cells that make the beating heart. We are
also very interested in making other cells of the heart, like the cells of the conduction
system that’s involved in controlling rhythmic beating, and very actively involved in that
as well. So we can make those cells in a dish. And
as doctor Cheung was saying, it’s just absolutely true – even if you took a cell and for example,
put in that mutation, even a cardiomyocyte, it’s not really where we want to study.
Because the genetic background will be different. And genes interact with each other. So what
we really need to do is have the exact genetic background to understand how that affects
cardiomyocyte function. OK, so let me try to break this down, and
I love this because a lot of times I deal with politics. And you guys are so much smarter
than the politicians, that it’s exhilarating to talk to you guys. And I’m trying to learn
as best as I can. Now you can turn the red blood cells into stem cells, and so already
that’s amazing. It is amazing. As we were chatting earlier,
this is one the pioneering events, it did lead to the Nobel prize in 2012 by Shinya
Yamanaka and his colleagues. So when you got the stem cells, can you … if
I’m understanding this right, and that’s why I need help here, you can make them into
heart cells of that particular person, right? Can you do other cells – liver, kidney?
You can do all that? And so then you can begin the study how that person’s heart cells
react when you introduce a disease to be able to track it. Is that roughly right? Yes, that’s roughly right. Now there are
many caveats because of course even though you can make, for example, heart cells, cardiomyocytes,
that really are from the patient essentially, I mean, secondarily derived, but they are
not a heart. And so they are not affiliated with the whole physiological response that
occurs in a living human being, so it is very much of a surrogate assay. That’s why we
call it “disease in a dish”. But they do function, they beat, they have,
hopefully, the same physical characteristics as they did in the person. You can now as
many of them as you want. And so you can look for what other proteins or genes might be
altered in those cells. They are very easy now to add drugs to, to test the screen for
whether or not drugs give certain responses. It’s a way of boot strap from a patient into essentially
a clinical trial in a dish to think about pharmacological approaches to working on a
disease. So, I’m gonna make it personal for me, I
have a fairly rare skin disease. It’s called Pemphigus vulgaris, I don’t know if you
guys are familiar with it, you wouldn’t be, it’s not in your fields. So could we
then take my kids’ red blood cells and test them? Is that a different course of action?
Or to see if they would have it also because it is genetic, and then how we can treat it
afterwards? My point being – forget about me, forget about Praveen, can this be applied
across the board with other genetic diseases? Very widely. There are many scientists now
actively engaged in that type of research, whether it is for example, neuro-degenerative
disorders, diabetes, complex genetic diseases. Cystic fibrosis is a very well understood
disease but one of the things we have been working on recently is generating, for example,
pancreatic ductal cells that are the target of this disease. There are many mutations
that can cause Cystic Fibrosis. But now you have a screening platform to actually
look for drugs for not only “cystic fibrosis” but for the cystic fibrosis that person has
because not only the mutation in the known disease gene but all other genes in the genome
will interact with that. This is what now is called “precision medicine”, the medicine
that is really designed for the patient, not for a disease. OK. No, we’re not done yet. It’s about
to get more interesting. Now we take the heart cells that doctor Evans has made and we ship
them over to France to doctor Meli. And what do you do with that? So basically based on the clinical features
that doctor Cheung can reveal, we focus on some mutation occurring in some particular
protein, what we call a “calcium receptor”. We focus on all the calcium that needs release.
Calcium is a major component to allow the contraction actually, precede the contraction.
And what we do back in France, we focus on all the properties that are related to the
calcium into the cells. And for that we basically we use different techniques. And also based
on what we did with doctor Cheung so far, we know which part of the cells and which
protein in particular we should really focus, and eventually do model the disease. So basically
from the initial patient through the IPS via doctor Evans we get cardiomyocytes, and we
try to model some features of the disease, still in the dish. Then what we can do once we have those features
of the phenotype, we basically can try different drugs that are under clinical trial, so FD
approved and see which drug would basically prevent or treat any of these features that
we can reveal. So again, let me try and see if I got this
right, correct me where I’m wrong. Red blood cells, then stem cells, then heart cells?
OK. And then once you’ve got that person’s particular heart cell, you then introduce
the disease to it, and then you test it against a control to see what the difference is. Basically, the idea of patient specific cardiomyocytes
is that the mutation is there already. And thanks to doctor Evans’ expertise, we actually
can correct some of the stem cells to the a perfect control. So the only difference
between two cell types is just one mutation. OK, so let me pause there because the audience
might not quite understand that, cause I had trouble understanding that in the beginning.
So normally you would find a person who is about the same age, who is also female around
Praveen’s age. And that would be your control group to see how that reacts differently as
opposed to the one with the mutation in it, which were Praveen’s cells. But you guys
don’t do that anymore. Doctor Evans actually fixes the mutation, so that it’s Praveen’s
heart cells but that are fixed, and that’s your control. And then you test it versus
the one that has mutations. Absolutely. Phenomenal! All the rest of the genetics is the same. So then you introduce the disease… I’m
sorry, you have the one that’s mutated, and then you… what do you do? You experiment
what happens and how to fix it? I mean, in layman’s terms. We try to exhibit some of the features of
the disease in the dish, and only with the cardiomyocytes. Try to reveal some of the
features either by applying some sort of pharmacological compounds that will activate some proteins,
or we try also to improve the matter of the cells by some physiological or patho-physiological
stimuli just to reveal the disease. Once we have those features, once we characterize
the cells and we can reveal the features, we then go to the second step which is basically
testing different drugs and see which one would be the best for the patient – in the
dish – and maybe eventually at the clinical level. So doctor Cheung, would that then come back
to you and say, ok, doctor Meli says this is the one that’s most likely to work for
Praveen, so do we eventually try it and see how it works for Praveen? Is that roughly
right? Right, I think that…. Thankfully, Praveen
is doing well right now, so there is no… she’s doing ok with the current therapy
based on the previous procedures she’s had, so she’s doing quite well. But it has obvious
implications for other patients like her. So again, with doctor Meli’s work – that
will first at least establish that the mutation is indeed disease-causing. That’s the first
thing. That’s what we need to do. We need to prove that it really is, this mutation
really is causing a problem here. And if he can recreate the disease in a dish, then it
ups the evidence level for the fact that, ok, this mutation is causing a problem. And
if on top of it, as doctor Meli says, if he can find the best compound to treat it, then
that will be again, even greater significance. Then it comes back to me, and we can think
about things. We can think of a more big picture. How many people are out there with this disease
that we don’t know about? They may have the same mutation. Then you may talk about
employing ideas about screening all patients. Now it’s a relatively rare disease. This
is something where we require multiple… you know, across the nation, and international
effort to identify patients with her condition. And then we are doing more wide-spread screening. And if we find that hey, certain percentage
of patients – usually never 100% but let’s say a good substantial percentage of patients
with her similar condition have this mutation, then that would – or at least of the same
gene, the same gene is affected – then you can think about using that same drug that
tested so well in the Petri dish in a say clinical trial. And if you already had a parent that has these
kind of conditions, you are far more likely to know that you should test. And so what
it might do is for the people who had been dealing with this, and it’s a mystery and
they don’t know why, they have to live in panic for the rest of their lives, that I’m
literally gonna fall down one day and not get up, have a heart attack in a way that
could not be predicted – well, now we can test for it. So one more part of this that I have to understand.
You guys build this whole system for understanding it, for mapping it, etc. Then when a person
comes, is the medicine personalized for them? Is there a process you build, or you take
the blood and it becomes easier? You guys are building the beginning of it, but it’s
gotta be easier to go through all three of you for each patient, right? How do we make
this process a little more efficient? The hope is that down the road this will become
more of a wide-spread approach but right now this is just one case. We just fighting the
battle on one particular patient who said, hey, test me. There are tons of people out
there that we don’t have this… or they don’t have the resources, we don’t have
the technology, we don’t know which gene. So the thing is we need to take a step back,
we don’t wanna whole scale start screening everyone who has a genetic condition for something.
Because then you’re gonna pick up random things that we don’t know whether they have
significance or not. But yes, down the road, as we sort of start
cataloguing more of the genes that are associated with these genetic disorders, then we can
sort of do more of this approach. But you know, it’s still in its infant stages, but
obviously, it’s hopefully something that, as doctor Evans has pointed out, this idea
of personalized medicine which President Obama had raised in the state union address, it’s
kind of that idea. So doctor Evans, once you’ve mapped all
this, you still take somebody’s blood from them, and then you bring it through this process
for medicine to most likely to work given the research we’ve done in the past, is
this? Is that how?.. I would say that of course there are two aspects.
One is that the screening we are doing now is physiological screening in a dish to try
replicate the disease. You’re not gonna want to screen people like that generally.
But if for example this mutation is identified for really being responsible for the patient’s
disease, then it’s easy to screen for that genetically. You would just add it on as a
part of standard genetic testing ultimately. If it was a really strong indication of the
disease. So genetic screening… you know, there are
standard genetic screenings right now for far more common diseases. We all imagine that
at some point it would become standard protocol to have your genomes sequence. It’s controversial
because there may be… first of all, there is a lot of issues about protecting patient
privacy, and that information is patient’s own, and newborn’s own – genetic information.
But ultimately I think we all believe that at some level that would become standard of
care. But it’s still very complicated because of the fact that – as we brought up several
times – even the identification of this allele – I can pretty much guarantee, and
probably that was the part of the reason why there was skepticism, and we’re still very,
not skeptical… you know, we’re gonna test a hypothesis and we don’t know if it’s
correct. But that same allele – let’s call it a
mutation, a difference, a gene difference in a different person might not have any consequence
at all because of other protective genes for example. Doctor Meli, you are trying to find out what
different medicines could work to help if you already have this condition but you were saying earlier to Doctor Evans fix the mutation in order for you to have the control test
on it, right. So can we fix the mutation in the body without treating it with the medicine? That’s a really good question. There is
a lot of fantasy around such a possibility. I am sure in the future it might be possible.
Currently this is not the case for many reasons. But like you just said, indeed what we try
to do is that we try to get perfect control. Perfect control over just a single mutation
is the only difference between the two samples. Because if you pick one patient, you always
have a genetic background that differs, some genes might be more expressing one side to
the other side and so on. The question in the future, can we just fix
the mutation like this in the whole patient, in the whole body. Technically it might be
possible in the future. And doctor Evans might be more of an expert than I am to answer this
but I think currently this is not possible. So right now it’s enormously complicated
because of what you were saying. There could be different things that can be reacting within
each person. So even if you figure out that one mutation and you try to fix that, it might
affect other things in your body. Is that right? Well, there is two issues. One there’s that but I think more importantly right now, technically it’s feasible to do. It certainly has been done in animal models, in mice, single mutations have been corrected and “cured the mouse”. Currently the recommendation coming through the NIH for federal funding is that we shouldn’t be even doing this experiments in humans because it’s just too early, we need to take the
time to think it through. Because if you can correct mutations, you can do any kind of
editing that you want in the genome. And that has serious ethical consequences. So currently,
at least in the US we are not doing any types of experiments like that in people. Other
than for use in a dish to actually study the biology behind the specific changes in a genome. But somebody could? Somebody could. Even if we’re not doing it here, somewhere
in Outer Mongolia… There has been a report that a Chinese group
have modified the human genome. Of course doing it in a manner where there would be
no opportunity for the embryos to survive or emerge, to actually grow. At the very very
early stage of embryogenesis. And there is a bit of outrage about that. I think generally
scientists worldwide believe that this is very powerful technology. It’s ok, we have
so much to do, so much we don’t understand, there are so many great experiments that can
be done – we can do those for a while. We work through these ethical issues and what,
where and how human genome should be modified. Now we’re gonna get a tiny bit into fantasy
world here. The work you guys are doing is super real, it’s very important and has
real consequences for people in the real world. But now that we’ve opened up this interesting – I don’t wanna say Pandora’s box – I do wanna blow people’s minds a little bit. If you “fix” a genome within a person – if they have kids later , they would actually pass on the new genome that you corrected. Correct? It depends on how you corrected it. You have to correct it… you can correct it in every cell in the body. If you didn’t correct it in the germ line, so the cells will give rise to either the sperm or the oocytes, then you’re not gonna pass it on. So it’s very possible you could imagine – in science fiction world – coming up with strategy that fix a gene in every cell in your body or in some cells in your body. What we would call “tissue-specific” correction. If fixing genes in all the cells of the heart, because that’s in fact that’s the only place where this gene is being mutated is important. Other genes may be important in all cells. But if it’s done with strategy where you would not modify the germ line, then it wouldn’t be passed on. Could you – if you were so disposed – change a genome in a way where the person would be taller? That should not be probably difficult. Stronger? Stronger. Oh-oh! Absolutely. These are so-called “designer genes”. There are certain physical characteristics that are fairly straightforward to alter. Knowing what people know about growth and development, hormones systems, etc. One last piece of fantasy, and then we get back to the real world. When would they do that? Let’s say you wanna do it. it’s 38 years after, it’s not here, it’s in Outer Mongolia, somebody says “I wanna make a super fast, tall, strong person, and I wanna do it for whatever reason”. Would you do it when it’s a fetus, when the baby is born, can you do it to an adult? We’re in super fantasy land here. It’s always going to be easier to fix something with current technology the earlier you do it. because there is just less cells to fix. So if you could fix – genetically edit – from one cell stage, or what’s called the zygote, the fertilized egg, that would be by far the easiest place to do the editing. Then it would fix every cell in the body. That would only work if you start from one cell. If you start from a grown adult, then it’s much more challenging. For example, it should be very feasible right now if you had a… there is a way that you can mix stem cell biology with gene therapy. There are trials ongoing right now that are basically adding genes for example to your hematopoietic stem cells that make all the blood cells of your body. You can take those out of the person’s body, genetically alter by adding a gene, and those stem cells will be put back in, go back to the bone marrow, repopulate your entire body. You can cure diseases that way. There are clinical trials to cure blood diseases like thalessemia for example. It should not be difficult, today it would be feasible to use the same approach, instead of adding a gene, go in and fix the mutation in that sense. And then all the blood cells would be fixed, and it would not be passed on. So those kinds of therapies, probably in the next 10-15 years, may be moving all the way to clinical use. So that’s the perfect way to come back to today and the work you guys are doing. It has both very specific purpose. For example, doctor Cheung, if it turns out, knock on wood, one of Praveen’s daughters has the same mutation as she does, all this work can hopefully find medicine to be able to more effectively treat her if she needs it. Correct? Yes. And that’ll be feasible very soon. Five year window or so? Roughly speaking. That’s great. We might be saving people’s lives. Your work saves people’s lives today. So that’s phenomenal. And then secondly, there are broader implications. That’s just one example. And then you can take this and multiply it out, as doctor Evans was talking about, to other diseases, and and see the cases in which you can specifically design medicine or perhaps even fix it within the body. Is that right? I think so, yes. That’s phenomenal! I have to say it throughout the interview. I kept thinking my head, because I am a goofy guy. Science! I speak for the entire Young Turks community and our audience in saying thank you, we really appreciate the work that you do. On behalf
of not just people that we know but humanity. So thank you doctor Evans, doctor Cheung,
doctor Meli. It’s been a great pleasure talking to you.


  1. I have a disease called Sarcoidosis. It has given me stage 3 ckd, high blood pressure, and destoyed my liver. Is this something i should look into?

  2. It's okay, fellas. You don't need to go to all this trouble with this. I prayed for all disease to end, so I got it covered.

  3. By the way to everyone watching – today is the FIRST ever International Summit on Human Gene Editing. Gene editing is about to become a huge issue (you heard it here first!) and is the only hope of a total cure for diseases like Short-coupled torsade de pointes. Please use your voice to advocate for more research into human genetics – people like Praveen shouldn't have to fight solo!

  4. Another fan-fucking-tastic interview coming out of TYT interviews! Man this channel not only constantly meets my expectations, often exceeds them. Really exciting and amazing advancements for humanity, thanks for getting some real scientists on to talk about an issue that doesn't get nearly enough play elsewhere.

  5. The implications of this are huge.. I only hope that the technology can be made accessible to everyone, whatever their condition is.

  6. Great interview. These guys are the warriors of our future. The legislative restrictions on stem cell research is akin to condemning/killing millions in the future to diseases easily cured/mitigated by the work of stem cell researchers everywhere.

  7. very important petition on mental illness and the wrongful labeling of people that goes on in hospitals today

  8. Heart attacks tend to be from the plumbing – blocked arteries/cholesterol. Sudden cardiac death is the electrics – rhythms etc.Two different types of things.

  9. Try interviewing Liz Parrish of BioViva, I am sure she'd jump at the chance to discuss what gene-therapy she is doing and her and the BioViva team's goals are. Aubrey De Grey would be an incredible watch too.

  10. please make a concise summary in a fun short clip format in the future. this info is too good to be falling asleep listening to docs explain technical info

  11. With greater power comes greater responsibility (no reference), but can we handle it right in the first time? history tells us, no – we just going to do, whatever we "feel" like it.

  12. Im 17,and im in a bunch of advanced placed science classes so this interview was fucking amazing for me.this shit was very interesting and i learned a lot.GO SCIENCE

  13. funny the 2 doctors in the brooks brother suit did not mention the word stem cell not once. do they even know what a stem cell is. embryo did his lawyer just whisper that word in his ear.

  14. So stealing cells from a unborn baby so old rich people can be cured, so kill a child so someone can live longer.. Fuck you young Turks.

Leave a Reply

Your email address will not be published.