Webinar: Human Skin Microflora: DNA Sequence-Based Approach to Examining Hand Disease

Webinar: Human Skin Microflora: DNA Sequence-Based Approach to Examining Hand Disease


Julie Segre: Hi. This is Julie Segre. So today
I am going to talk about my own research project specifically examining the microflora, which
are the bacteria, the fungi, the viruses so on that live on your skin and also give an
overview of the larger projects. So what is really important to remember about
this, and on slide 2 I do not seem to have control over the slides Sarah. On the next
slide of this presentation, I wanted to – okay. I wanted to introduce some of the goals
of the larger NIH Roadmap for Medical Research Human Microbiome Project. And what is really important to realize here
is that we tend to think of ourselves as humans, that we are these human cells. But in fact
we are really made up of human cells that are living together with bacteria, fungi and
other small microscopic organisms. And it is really remarkable because in and
on our bodies, these microbial cells actually outnumber the human cells by about tenfold.
So for every human cell that there – you have in your body, you actually have ten more microbial
cells. But it actually – it is not that they outnumber
us but they do not actually outweigh us because each human cells has about 1000 times more
DNA and is about 1000 times bigger or – than – or at least 100 times bigger than a microbial
cell. So we actually outweigh them even though they outnumber us. Now as an example, the bacteria that live
in the gut, in the intestine, we think that because of this microbial diversity and these
large number of bacteria, that the bacteria and the other fungi and the other small organisms,
they probably have 100 times more genes than our own human genome. So there is a tremendous amount of diversity.
And this microbiome is really the – microbiome means the total microbial DNA – is really
an important part of our genetic landscape and also of our bodies. So for example, when you take a drug, you
probably think that it is your human cells that are metabolizing the drugs. But in fact,
the bacteria that live in your gut are part of what metabolizes this drug. And so it is really important for us to understand
the complexity of our human DNA, but also to understand the complexity of our microbial
DNA. So the overall goals of this project are really – the Human Microbiome Project
– are really to understand how the microbiode of the small organisms interact with our human
cells and how that maintains health and disease. So I just talked about drug metabolism via
bacteria, but of course these bacteria also break down food and aid in digestion and on
our skin, they can break down the proteins that are made by the human cells of the skin
and create sort of a, you know, contribute to creating natural moisturizing factor that
keeps your skin supple and smooth. It is true on the skin they also have waste
products that create part of what we think of as body odor. So, you know, we have to
think about the full range of how the bacteria contribute to our health and to disease states. And that really is the goal of the larger
Human Microbiome Project written here. We are bringing in 250 normal individuals and
sampling them at five different body sites – the gut, the nose, the oral cavity, the
vagina for women and the skin. And this giving us a baseline so that other
investigators including myself are then doing clinical trials, we are examining the skin
microbiota in people with common and rare skin disorders. But in order to know what the differences
are in a disease state, we have to first know what is normal – how much variation there
is between people and how much variation there is between different sites of our body. So
in order to do this, we are assessing the microbial diversity of 250 individuals. And then skipping ahead to the third point
here, our ultimate goal is metagenomics. Let’s say that I could just scrape the, you know,
the dead layers of my skin off that sort of white flaky stuff that makes those dust bunnies
in your house. If I could scrape off those dead cells or could take, you know, a swab
inside your nose, I would like to just directly sequence them. But the bacterial diversity is so complex
that we need to take some baby steps to get there. And that is why point number two is
that we are sequencing bacterial reference genomes. So that means that we are determining
the entire bacterial sequence for different isolates. And using that to then form a springboard
for future microbial studies because with metagenomics where we analyze the combined
coating potential of a complex mixed environment that is what we would ultimately like to achieve.
And we would like to achieve that, as stated in point number four to correlate the changes
in the microbial community with disease states. And the – another arm of the study is really
to explore the (ethical), legal and social implications of this new field of research
because every human genome project that we embark on, we devote a cert – you know, we
devote time and energy to understanding how this information is going to be communicated
to the public and how this is going to be absorbed by people in understanding that there
may be a contribution of their microbial communities to their health or to their disease. And as such I will get to, at the end, what
are really the questions that we would like the – we would like people to think about
in terms of how this research is impacting their own lives. So let me now take you into my laboratory’s
specific research project which is to really understand that the skin is a barrier to infection
of pathogenic organisms, but the skin is also an intricate home for microbes. And those are what I will call the commensal
microbes, where the healthy microbes, the good microbes, the ones that just normally
live on your skin and serve the role of breaking down human proteins and keeping your skin
moist and also serve the role of keeping pathogenic organisms from being able to adhere to or
attach to your skin. So when people think about the skin, they,
you know, it is actually – I show you here a cross section of it. And underneath your
skin are these blood vessels which are the red and the blue. And you know that because
if you scratch yourself you can bleed from your skin. Overlying that are these orange cells which
are really the stratified epidermis, the top layer of your skin. And these go through a
process where they lose their nuclei and they become dead cells on the top of your skin
that provide the skin barrier. That is what you see on the upper layer of your skin. Well, this is really – we think that there
is a relationship between the skin cells, the immune cells that can sense if there has
been like a wound or an abrasion because as you think about it from an evolutionary perspective,
of course it is very dangerous to have an open wound. You could have a bacteria get in and your
body could, you know, develop sepsis. Well now of course we have antibiotics to treat
that. So, it is less of a risk but antibiotics have only been around since the 1940s so the
body still responds as if this is a tremendous risk. And so the third type of cells that we will
be talking about today are really the microbes, these small microscopic organisms. Well, we
asked the question about how do you know what microbes live on your skin. And the way we
traditionally do this is by looking on Petri dishes and seeing what we can culture. Well there has been a new method that has
been developed, but this is new and old and just being altered so that it has greater
specificity. What we do is that every bacterium has a 16S rRNA gene. Now the 16S – r stands
for ribosomal. It is a ribosomal RNA gene. It does not get made into a protein. What
it does is it stays as an RNA and it helps guide other RNAs through the ribosome. The
ribosome is where proteins are made. So mRNAs are translated into protein. This stays as
just an RNA and is a guide. But if you examine the sequence of the 16S
rRNA, the ribosomal RNA which is shown on the left here, what you see is that it actually
has these stem regions which form a lot of double stranded basic base pairing. And from
those, that actually puts a fair amount of conservation constraint on those base pairs.
And then there are the (loop) regions which are more variable. Now, when we look at the sequence of the stem
regions, those are conserved. And that serves as what we consider an evolutionary clock.
So if we looked at the conserve regions we can say well there is some change in them,
but that allows us to say this is a staphylococcus, this is a streptococcus and assign what type
of bacteria it is. The sequences in the loop region will change
even faster than that. But these sequences of the 16S gene allow us to identify what
type of bacteria it is. So the orange highlighted sequences are how we amplify this gene out
of a bacterial genome and also we use the purple sequences. Those are highly conserved
and then we examine the intervening sequences. And that allows us to identify what type of
bacteria this is. Now here I show you an example of how we compare
the data that we obtained with our DNA survey sequence identification with our culture methods.
So what we did here was he had healthy volunteers come in. And we looked at two different sites
of them. And actually we did 20 different sites of them as you will see. But I am just
showing you the examples of two different sites here – from the face and from the belly
button. Now, on the right side of each bar graph,
you see what we found when we brought these swabs down to the (microbiology lev) and tried
to culture everything that we could. Well the dark blue is called propriona bacteria
from the face. And that is an oily loving bacterium. And so the skin is a little bit
oily and that would make sense that those are the types of bacteria that live there.
As well as the orange is the staphylococcus. That is like staphylococcus epidermidis which
is one of the most common healthy bacteria that we can grow. And if you compare what we found on the face
from culturing versus survey, you can see that we did a pretty good job, but we completely
lack the cornflower blue and the lighter blue. Those are actinobacteria and you can see the
chart on the right hand side. We failed to culture them. These bacteria are actually the (carinobacterium)
and other actinobacteria are very hard to culture because they take – they are very
slow growing. Sometimes we grow them after about six days. But by six days, the staff
and the propriona bacterium grow so well that they have almost overgrown the culture plate. And you see this even more when you look at
the samples that we collected from the belly button of this person. Well culturing it seems
like the orange and the red are the firmicutes. Those are the staph and the strep and other
bacteria that fall under the greater taxonomic name of firmicutes. And, so that is what we can culture from this
person. But when we look at the survey, what we see is that really 50% of the bacteria
are the (carinobacterium). And as I said, we just had a very hard time culturing them. So the take home message from this is that
we can get greater information and different information if we use this DNA based surveys
that are less – that are – that have less of an ambiguity to them and there is less
of a bottleneck that the strains go through. So the information is more precise. Now, let’s talk about how we would use this
type of information. Well I am just going to show you one example of an animal model
that we made and then I will get into our studies with human subjects. So as you can see from this mouse, this mouse
has scale skin. And you can best see it on their ears. In the bottom corner of the picture
of the mouse, I show you what a wild type or what a normal litter mate would look like.
And you can see there is smooth skin on the ear. When you look at the histology of this mouse,
you can see that the dark purple and pink layer on the top is thicker in the mutant
mice. And then it has where the arrow is pointing is that sort of thick basket weave, and that
is the scale. So the question is, is this related to, you
know, how does this then contribute – how does the bacterial community contribute to
this because we were using this as an animal model of the very common eczema which has
that sort of scaly rash-like skin. So now here I show you what is the bacterial
survey that we find by sequencing. Well if we consider this an animal model for eczema,
one of the things that we know is that in eczema patients, there is a large amount of
colonization by the staphylococcus. And now the staph is the firmicute, so that is the
third over. And what you can see is that the mutants,
this is – the mutants have about 11% firmicutes. So they do have an increase in firmicutes
over what one bar over you see is the wild type litter mates. So that is what we pick up when we culture.
These mice have an increased amount of these straph – staph and strep and other types of
firmicutes. But in fact, even though that is what we pick up on the culturing, that
is not the whole story because if you move over to the actinobacteria, what you see with
these mice is that they have a huge increase in the (carinobacterium) which are shown as
the green bacteria. Well I just told you, those are really hard
for us to culture. So if I did not know to look for them, which my survey data tells
me that there is an increase in (carinobacterium), I would think that there is an increase in
the firmicutes and I would miss the fact that there was an increase in the actinobacterium. And perhaps when you give antimicrobial treatment,
you know, antibiotics, you decrease the amount of staph and you think you have cured, you
know, the person’s microbial disorder. But in fact, maybe it is really acting on
the (carinobacterium). And so that is an equally plausible hypothesis. From this data, I cannot
tell which is more likely to be causative – the increase in firmicutes or the increase
in (carinobacterium), but I now have two hypotheses to test. And in fact I have a third hypothesis to test
because if you look at the first set of bars, the proteobacterium, when you see is that
we have had an increase in firmicutes and an increase in actinobacterium. But they have
come in and they have selectively pushed out the pink bacteria, the pseudomonas. If you look at the bright blue bacteria, that
(genthina) bacterium, that is about 35% in the normal litter mates and about 32% or 31%
in the mutants. So those levels have stayed the same as have the other components of that
bar, the dark blue, the orange and the yellow. What has changed is that the pink, the pseudomonas
have been pushed out. Well what about if those pseudomonas provide some beneficial effect
to this skin. Then that is a third hypothesis to test. So it is really about generating more ideas
to test. So now let’s look in human skin. And as I have shown you before, there are
different levels to the human skin as there are to mouse skin. And this is the histology. So to assess things from the human skin, we
took a swab which goes up to the very superficial bacteria. Then we scraped off – without drawing
blood, we just scraped off the dead cells from the top of the skin. And those (pellets)
what live inside that scrape. And then we took a punch biopsy from a few
sites to look at the full thickness because there are bacteria that live all the way down
in the hair follicle that dwells – goes all the way down into your thick into the dermis. And what we found is that if we used a swab,
we could recover 10,000 bacteria per square centimeter. If we used a scrape, we could
recover 50,000 bacteria per square centimeter. And if we use a biopsy, that yields 1 million
bacteria per square centimeter. So that means that when you are washing your
hands, you know, like a swab would be, you are really only removing 1 in 100 bacteria.
When you are scraping, which I promise you is, you know, less – I mean it is less harsh
than even washing your hands, you can remove about 1 in 20 bacteria. But it is these bacteria
that live down in the hair follicles that can then come back and repopulate and those
are the healthy bacteria. So we looked at the 20 different sites on
the human skin to say – and now this is all done with scrapes because we decided that
scrapes were as effective as punch biopsy and certainly less invasive. So when we look at the scrape, what we see
is that there is a great variety of bacteria. But in fact, the bacteria are determined by
where you are on the skin. So the blue sites are what we consider oily
sites. And those are very similar to each other. They share a lot of the dark blue and
light blue bacteria called the propriona bacterium, but can live on the lipids. But then what you can see is in the middle
of the body, there is a lot of moist sites that are more sweaty. And in those sites,
those are – have a lot of the green bacteria, the proteobacteria. And then you can see the cornflower blue which
is the (carinobacterium) more at the base. There also are sites that have a lot of the
orange bacteria, the staphylococcus. And what we found was that the human body
is really an ecosystem. So imagine it like a dry desert, but then there are sites that
are streams. Those are the moist sites, the creases. And then there are the oases. Those
are places like inside your nose or inside your umbilicus that really just harbor a huge
amount of diversity. And what we found is that the site like the
left arm and the right arm are most similar to each other on the same person. But then
my left arm is most similar to your – or my arm is most similar to your arm. And my arm is more similar to your arm than
my arm is to my chest region. And I have given all the anatomical correct terms, so I –
instead of saying chest, we call it manubrium. But you can see here that the manubrium, which
is five sites down on the left, is more similar to the side of my nose because those are both
oily sites than either one is to the axilla – the axillary vault, the underarm which
is considered a moist site and not an oily site. So this is – another example of this is –
of the data is just shown here on the next slide where what you see is that the back
of every person is very similar. Retroauricular crease is behind the ear. It is very similar
to each person although you can convert. So you can see that healthy volunteer number
4, that site has been converted to being really staph colonized and that is a term that you
sometimes will hear from your physician if you have a sort of what we call really below
threshold infection where this is, you know, it is not causing you any problems but that
site has become overgrown with staph. (Cansia) the antecubital crease which is the
bend of the elbow is really a lot of the proteobacteria. And then actually what you can begin to see
here with the nares which is inside the nose and the umbilicus which is the belly button,
these are really diverse complex sites. And that is shown actually in the next chart
where you can see that there is a range now here where I show you these different anatomical
sites and then they match up with a two letter code. There are sites that are really very complex
like the volar forearm which is the – the forearm has about 44 species on – each person
has about 44 species living there. The site right before that is the umbilicus, the belly
button. That has about 40 sites on every – 40 species for every individual. Where some of the sites, like all the way
over on the left behind the ear, the retroauricular is actually kind of simple. And the back is
the next site. So those have about 15 species. And so there is a variation of the complexity
of these different sites. So I would like to just give as a summary
how we think about the microbiome project and how we hope that this can serve as an
educational tool. First of all we would like this to really
put forth the idea that as I showed you on slide number six, if you compare the survey
and the culture data, they are both accurate. When we culture, we culture (multuly) staphylococcus.
And that is true. But that is based on culturing. When we survey, we can find that there is
an increase in the amount of (carinobacteria). So that – what we understand about scientific
facts is really relative to the methodology that we employed or how we determined that
information. And as science evolves and we find better
tools, we can also find out new things. This is a real process of exploration for us. So
we can learn new things about our microbial contribution when we have new tools to examine
them. And that is really the process of science, understanding what is known and what is unknown. We hope to use this project as a way to educate
consumers about what is health. And in that regard, I think we need to lose the language
of warfare with pathogenic microbes. We need to not just think about all bacteria
as bad, but remember that bacteria also do contribute to our health and that our goal
should be to promote the growth of the healthy bacterium while maintaining, you know, low
levels of exposure to any pathogenic microbe. And of course our goal is also to educate
physicians about how to make better diagnosis and treatment decisions. And so I will ask
you, you know, really, why is – I mean this is sort of at the crux of it is we have to
have this relationship between health and disease. And I see in the culture right now that (Ubberland)
wants to sterilize their exterior with using these hand sanitizers but then eat probiotic
yogurt or take probiotic pills. And I think we need to really balance this and to understand
that our goal is to balance the healthy bacteria and the pathogenic bacteria. But it is not really just to sterilize our
exterior because the bacteria will come back. And it is really about promoting the growth
of healthy bacterium while maintaining the pathogenic bacteria. And so finally in conclusion, I want to emphasize
that this study is a very thorough relationship and trans-disciplinary investigation that
is being led by the Human Microbiome Project, so HMP. But it is a scientific endeavor pursued
by physicians in clinical medicine and in infectious disease combined with colleagues
in microbiology and colleagues who have an expertise in sequencing DNA and analyzing
that information. So these are all the groups who are involved
in the study, but it is really a three legged stool between DNA sequencing, microbiology
and clinical medicine. And it is the strength of that three legged stool and the scientific
disciplines that really is powering this project. So thank you very much. Sarah Harding: All right. Well thank you Julie.
That was excellent. And I definitely learned a lot about things I never knew. So I want
to open the call to any questions that we might have from the group. And I need to just
let our hosts know that that is what we are doing. So if you would just hold one minute. Can everybody hear me? No. Julie Segre: Well I could. Sarah Harding: Oh you could? Julie Segre: Yes. Sarah Harding: Well potentially they can hear
me but we cannot hear them yet. We are just waiting to open the lines to be able to ask
questions. And so what we will do is we will have an open session. People can ask questions
to Dr. Segre and we will just ask that you obviously go one at a time. One question that was emailed to me Julie
that we can probably talk about before we get everybody else on the line is just whether
there is – you – I think you did this to a certain extent but whether there is more
– can you translate. The question is could you translate some of
the bacteria speak into more of the diseases that we typically hear of in a… Julie Segre: Right. Sarah Harding: …every day, public health
kind of… Julie Segre: Right. Sarah Harding: …the laundry list of terms… Julie Segre: Right. Sarah Harding: …that was a… Julie Segre: Yes. So there are several projects
that are being investigated. Here we are looking at common eczema and what is the contribution
of bacteria to eczema. And we are also looking at patients who have
recurrent infections of MRSA, the methicillin-resistant staph aureus. And we are looking at whether
there are some people who are exposed to MRSA but never develop an infection and other people
who would develop an infection, and is that related to the MRSA that they are exposed
to or is that related to something else in their micrbiome. If you get exposed to MRSA but you have a
(carinobacterium) that the (carinobacterium) can actually keep the MRSA in check because
actually bacteria have a lot of ways that they have figured out to control the growth
of other bacteria. So that is an interesting question for us. Now other projects in skin are exploring acne,
psoriasis. And then in the gut there are projects about inflammatory bowel disease, Crohn’s
disease, a lot of these diseases that are being treated with antibiotics but we do not
really see a clear infectious agent. So we do not really understand but we know
that if we treat with antibiotics that the disorder, you know, can get better. So, that
is what we are really trying to understand a lot of is what are the infections really
– what are the antibacterials really treating. So we are looking at projects that have to
do really with all of the systems. The, you know, the gut, the esophagus, the – all of
the digestive system, the oral cavity and trying to understand really a wide variety
of diseases. Sarah Harding: Excellent. Okay. Now I was
told that the lines should have opened. So if somebody has a question and they want to
try asking it, hopefully we can all hear you. Okay. Well we actually – I have gotten a number
of questions over email. And if that is something that anybody would rather do that is fine.
So I will just ask a couple more questions. And so one of them has to do with the slide
that – one of the last slides that you put up, and that is that there has definitely
been a – it has to do with the picture of the Activia yogurt that you have and why that
of all kind of yogurts of all, you know, what has made that special in terms of having a
pretty big campaign and you kind of see it. I think everybody knows the jingle. And, you
know, why has that necessarily been any more special than any of the yogurt we have had
before? Julie Segre: So, I think here we really need
to get into what is science based. And that is what we are trying to create the foundation
for is to understand really who would, you know, who would respond to these probiotic
yogurts and who is this really benefitting? And in the same way that we do double blind
studies, placebo studies and, you know, to try to test most drugs, we would like to,
you know, we would to have that same kind of science based, evidence based approach
to other things that we, you know, we consider that we are taking to increase our health. And I think that there is a great potential
for understanding probiotics from many systems of our body and to really understand what
on an individual level is making each of us healthy. But I just think that this is something which
we really want to understand not as marketing strategy but as a scientific endeavor. And
in that same way, what we have – I mean Activia is just adding, you know, a probiotic to a
yogurt. But the Purell, the hand sanitizer, has really
substituted now for soap and water and washing your hands. And so it is, you know, it is
great in that we often have access to having clean hands when we might not otherwise, you
know, if you are traveling or something in the airport or something like that. But we just need to, I mean we just need to
understand what these products are really doing and how they are affecting our health
and how they are preventing us from getting sick. Sarah Harding: Great. Thank you. Are there
any other questions from participants? Okay. Then I have one other question that has come
in. Jay Gee: …hear me? Sarah Harding: Oh. Yes. Hi. Jay Gee: Oh, okay. This is Jay Gee and the
CDC, just a simple question. Have you all gotten to the point where you can see if natural
microbiota, the composition is preventing certain infections such as MRSA, I mean the
ideal being the bacteria, the natural ones would occupy a niche preventing colonization?
Have you gotten that far yet? Julie Segre: So we have not gotten to the
point where we know which bacteria are really having an effect of keeping others out. We
recruit those patients to use the NIH Clinical Center. And patients we recruit are at an
increased risk for developing staph aureus infections in some cases because they have
eczema. And we recruit the entire family, you know, in to try to see if anyone else
who has been exposed to MRSA is also a carrier for MRSA. And so that is really the goal of our study
is to do an in-depth analysis of exactly that type of question – how do we control the transmission
of MRSA and can that be controlled by other microbes and promoting the growth of other
microbes because you can imagine that it could be very effective to try to over grow the
MRSA rather than trying to wipe out the entire bacterial colony. And so those are the goals and even ones that
– harder than that is going to be to figure out what is causing these diseases. But if we could even just figure out what
is correlated with a protective effect, we could start to target that. So no, this project – I should have said that
– this project was launched just one year ago with the goal of trying to develop the
basic understanding that would enable us to treat disease and also to control infection. Jay Gee: Okay. Thank you. Sarah Harding: Great. Any other questions
from our audience? So I did just receive one question from (Tim
Burke) at Access Genetics. And he had a question about – he mentioned you had three hypotheses
about skin flora and their cause for skin disorders, which is assuming that eczema is
caused by a lack of some bacteria or an overload of others. And so he poses the question of what if it
is because – what if it is the other way around, if the skin disorder is causing a certain
variety of bacteria? Julie Segre: And so I completely agree with
that. And that actually takes us back to the first slide that I used to launch into the
question about what are the types of cells that inhabit the skin. And there are the human
cells and, you know, the skin cells, the immune cells and the microbes. And that it may very well be that the skin
disease, which is caused by a defect in the human cells are then causing this scaly skin
and that causes the microbes to be different. And the – if it is only the skin cells, then
affecting the microbial flora would not change that. But we know that in the case of eczema,
what are the most common treatments for eczema are steroids, corticosteroids, antibiotics,
sometimes even giving the kids bleach baths so that we can just reduce the microbial load.
And that seems to make the kids look and feel a lot better. So it is true that the root cause may be something
in the human cells that maybe makes them make a less good barrier. But we already know that
the treatments that we use are more likely affecting the microbial than they are the
human cells. So, it may be that the primary cause is something
in the change in the human DNA. But what I am looking for here is how to really affect
the greatest health for people with skin disorders or other disorders. And so if I can intervene and give them a,
you know, a topical therapy that increases their health even if it is not getting at
the root cause, even if it is just getting at some other part of the pathway, I still
think that that is our goal is to really be promoting health. And so it will be very difficult to untangle
what is causing the disease but really the outcome that we are looking for is to improve
the health. Sarah Harding: Excellent. So I appreciate
this. There are a number of you asking questions over the Web portion of this webinar which
I think is excellent. And I will just bring it to your attention to those of you who maybe
haven’t seen it. But we did get a question from Ke Chen at
Boston University. The question is, are you considering the impact of environmental factors
such as the level of sun exposure or living in an area of more damp or dry area in to
the relationship of human cells and microbial cells, sorry, in your study population? If
so how, and what type of impact would these environmental factors have? Julie Segre: So sounds another – and these
have all been just great questions. And that is another thing that just makes this so complex.
When we are trying to capture what is normal, of course we are finding individuals who live
in a dry community, people who, I mean, even a dry environment like, you know, living in
Arizona and people who live in a moister community. And even that can change between if it is
the winter time and you are spending your days inside, you know, a heated environment
which dries out your, you know, is a dry environment. So there are many variables here. It may be
important, you know, just the sun exposure, all those things may really be important.
And we are actually trying to capture as many of those variables as we can. And we are asking people, you know, who they
live with. We are asking them do they have a pet. It turns out people have a lot of contact
with their pets. And so we are asking them all those questions. I am not sure that we will have a great enough
population that we can determine if there is statistical significance to any one of
those factors. And it may be that what we find out is that the variance is just so great
that you really cannot tell a difference. But we are capturing all of that information
in our questionnaires to see if there is a correlation between where someone lives and
who they live with and, you know, what they eat and what allergies they have and those,
you know, those types of questions to try to get to see if those are affecting their
microbiota. Sarah Harding: Great. So are there any other
questions from the audience? All right. Well I want to thank Dr. Segre for speaking today.
I think this was very interesting and certainly added some insight into one of the many programs
that are going on here at the NHGRI. This is a series of talks that we will be
holding pretty much every other month for the next – for the significant future. And
so we will be announcing more of these webinars as time goes on. So we hope to see you again. There is a Web site that I believe went out
with some of the emails that you would have received from me that would have information
on our other webinars that happened last year. So again we look forward to seeing you in
future webinars and if in fact you would have other ideas of other topics that you would
like to hear from, I would be very excited to hear about those as well. So you will receive more information from
me. But again, thank you very much for participating and I hope you all have an excellent afternoon.
Thanks very much. Bye-bye.

3 Comments

  • DuJuan Ross says:

    Jumping genes and pseudogene in-stitching as well as some carcinogenic mutantcy,ALL may have had their origins in the retrotransposable impact viruses have had on the organelles of eukaryotic lifeforms down thru Geologic Time.

  • Darrick Baxter says:

    Judy, love the video and notes. I wanted to get my DNA sequenced, do they give me an electronic file that I can save? do you have a sample file of a DNA sequenced?

  • Kamlesh sharma says:

    got bored!!!!!!!

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