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All engine running, I'm so genius.
Get this. Welcome to the show where we bring you science.
What that which I mean is discovery is the most questions we've had.
Technology unbelievable.
Without further ado, this is the Naked Scientist.
Hello, welcome to the Naked Scientist podcast.
The program that brings you the biggest breakthroughs and also talks to the major
movers and shakers in the words of science, technology and medicine.
I'm Chris Smith and coming up this week.
A massive meningitis outbreak in the UK.
What's behind it and what's being done to stop it?
Also, how thousands of old tumour samples could help scientists fight
rising rates of bowel cancer in young people
and a sound way to save the much-loved European hedgehog
that's falling victim to road traffic.
Up first this week, health officials have described a sudden outbreak
of meningitis in Kent as unprecedented.
It follows the deaths of a university student and also a sixth form pupil
in the English County with more than a dozen other cases reported.
At the root of the outbreak is a strain of the
Nasirium meningitis or meningococcus bacterium called Men-B.
It usually sits harmlessly in the noses and throats of a significant proportion of the population,
maybe a quarter of some age groups carry it,
and it spreads between individuals through close personal contact.
Occasionally, though, for reasons we don't understand,
it becomes virulent, invasive and deadly,
entering the bloodstream to cause septicemia and the tissue layers around the nervous system
to cause meningitis. It's a public health emergency
and officials are now racing to identify potential contacts and offer them protective doses
of antibiotics. Dominic Kelly is a pediatric infectious disease consultant and vaccinologist
with the Oxford vaccine group. The meningococcus comes in different types and we give them a
letter to differentiate them, A, B, C, W, Y, things like that. The letter refers to a capsule of the
bacteria. Historically, back in the 1990s, Syrogroup C, we call them Syrogroup C,
meningococcus was a big cause of disease, but we had a vaccine for that introduced in the late 1990s,
which really has controlled that type of the meningococcus very well. The types were left with
the type in the UK that has caused most disease over the subsequent years has been the type B.
Infants and young children have the highest rates of disease,
but there's also been a higher rate in adolescents, students over the years. We think that is
something to do with transmission rather than perhaps a weakness of immunity in that age group
that in mid-adolescence, early adulthood, people are having many more social contacts and perhaps
are more close-knit nature. So their exposure and ability to meet lots of people
means that they transmit these organisms more readily and that's probably why you have
a higher number of cases of disease anyway in that age group.
Extraordinary thing though is that if you go and pick people at random from the population in
this particular age group, you can find as many in some cases as one in four who are carrying this
bacterium in their nose and throat and they don't have meningitis. So why do we have this
situation where some people can just have this nasty bug in them and on them and they're completely
fine and then the next person gets it and they go down with meningitis.
Well that's a really interesting question and I guess the first point you make reflects the fact
that this organism for the most part causes very little trouble to most people and passes from
person to person without causing disease and the disease is only in a minority of people exposed,
probably even in this outbreak where disease rates are much higher, it's only a small number of
the people who actually had the organism that get disease. Why a particular individual gets disease
is still not well understood. There are genetic factors probably about their immunity,
there may be things to do with the dose they get. There are some risk factors such as smoking which
make you a bit more susceptible but if we don't understand especially well why a single individual
gets disease when others haven't but yes the organism normally exists just as a commensal almost
a carinizing organism just passing from person to person and disease is almost an accidental by
product. How are they managing the outbreak? What's the the strategy to protect people in the short
term and then stamp this out in the days to weeks following? People who are ill, the priority is
to get into hospital, give them antibiotics and deal with their immediate illness but very rapidly
after that because this organism is spreading from person to person, the public health organization,
the health security agency would be informed of the case from the hospital and their first
priorities identify close contacts of those individuals. So often in the hospital we're contacted
while we're still managing the case by public health and either we're asked to try and compile
this or they will talk to the individual or their families and identify who's been in close contact
and the reason for that is so they can give antibiotics to reduce the chance that their contacts
who may well be carrying the organism will actually get disease and what's interesting is it's a
disease with a very short incubation so if you acquire the bacteria and if you're going to get ill
usually it's we're going to be within a week or so of that initial contact so there's a real
priority on public health identifying contacts quickly and offering them appropriate antibiotics
and begin to look at the spread and whether any common themes common places those people have been to
and I think the interesting thing in Kent was that identified a nightclub where a lot of them
had been to so could begin to look more closely at the spread and identify a wider group of people
who might get risk. Where do vaccines come in then? Because that is also being spoken about
quite a lot. There's also a big campaign to vaccinate thousands of students in the Kent area
and it's also leading to a run on people accessing the vaccine privately in pharmacies and so on
across the country to the extent that some have actually now said they've run out of vaccine so
where does vaccination come in in the fight against this? We have vaccines for many of the strains
of the meningococcus but men B which is this strain has been more difficult to develop vaccines
but over the last 20 years there's been extensive research and development of a vaccine against
men B so we're in a very fortunate situation at this point in time to the last 10 years where we've
actually got two different men B vaccines that cover around 80% of the strains and we have an
infant program in the UK offering vaccines to infants and vaccines haven't been offered to add
a lessons up till now as routine because the number of cases in adolescents and early adulthood
have been low enough that it actually was not felt to be worthwhile to immunize hundreds of
thousands of people a year to prevent very very few cases. The situation changes when you've got
an outbreak like this there is an increased rate of disease for some time after an initial index case
and there may be ongoing chains of transmission and so if you've got an outbreak that's continuing
on a scale that's likely or could go on for weeks and months then vaccines coming to play
and the strategy for vaccines requires quite a lot of thought on the public health authorities part
to identify groups of people who in the weeks and months ahead may be at higher risk because of
the communities they're mixing in that have had a higher rate of disease and so what I understand in
the the kent outbreak is that they are doing a targeted vaccine program around the groups of people
who've been most likely to to to contain cases of meningococcus. The interesting thing about
vaccines though is they are particularly for the men be vaccine you probably need two doses
for full effect and you only begin to get real protection two three four weeks after the vaccines
so one dose four weeks later you have a little bit of effect but you need a second dose and it'll
be two or three weeks afterwards so these aren't the main stay of the immediate response which is
detecting cases treating them antibiotics for close contacts Dominic Kelly with the Oxford
vaccine group and the current guidance is that the risk elsewhere in the country hasn't changed
so there are no grounds to seek vaccination for people who are farther afield but everyone should
nevertheless remain vigilant for signs and symptoms which include a flu-like illness fever headache
next stiffness photophobia that's pain caused by exposure to bright lights and a purple rash that
doesn't disappear when you press on it with a glass if you have any of those symptoms please don't
delay ask for some help we're going to discuss schizophrenia now which is a chronic mental health
condition characterized by hallucinations delusions and disorganized thinking there's currently no
diagnostic test for schizophrenia though so the diagnosis is usually made clinically and this
can limit our ability to tell apart different disease processes that might have different prognoses
and also different treatment responses but now US researchers have identified two potential bio markers
which do appear to signal the condition Bonnie Firestein conducted the study so many years ago
we started researching schizophrenia but we were looking at things like how chemicals and cells
change when you have schizophrenia so we used what we call post-boredom or after death brain samples
from patients and we found that some of these molecules in cells were elevated so then we ask
the question well what if we looked at living human beings who are experiencing schizophrenia
and could we somehow detect the increases or even other types of changes to these molecules
or chemicals in cells without having to wait until unfortunately they pass we want to be able
to figure out can we help diagnose early on can we help figure out what medications will help them
and that's what led to this study do we have a problem doing that at the moment then diagnosing
people who actively have schizophrenia yes we do so there are different ways that or different domains
that psychiatrist will use to diagnose somebody with schizophrenia and in these domains they look
for things like hallucinations or hearing voices or not having interest in the things that people
used to have interest in or having memory problems but the problem is that they're two-fold one is
that it's difficult and more subjective to say that someone has schizophrenia in fact schizophrenia
is on a spectrum there are schizophrenia effective disorders meaning that they're similar to schizophrenia
but not quite schizophrenia the second problem is often medications that are prescribed do not work
and it's trial and error and the third and biggest issue is that let's say Chris you and I
unfortunately both have schizophrenia the reasons for us having schizophrenia could be different so there
is a component that is genetic and there's a component that's also environmental but the genetic
component it's not like when you have a certain disease where you have a problem with one gene
and that's it your diagnosis to develop that disease in fact it's a lot more subtle so we can
have different genes that confer what we call a risk for schizophrenia and the basis the biological
basis for your schizophrenia could be different than mine so they might converge and have different
what we call pathways in the cells different ways of signaling that might be very similar between
you and me but the reason for it could be a little bit different and what you think you have some
markers that can be used to diagnose people who have schizophrenia yes so what we did is we
grouped different ages races and both sexes and then we looked for these biomarkers or these chemicals
or markers or molecules in cheek cells that were elevated in patients with schizophrenia versus
a population of control patients without schizophrenia who are age, race and gender matched
how many of these markers are there well we focused on two of them so right now we have two
that we were able to confirm are indeed increased in patients with schizophrenia and correlate with
symptoms and also with learning and memory issues so for example if you look at patients with
schizophrenia and they have an elevated level of something called sp4 that's just the name of the
chemical and it's mRNA which tells the cell to make that chemical for example we see that the
more that a patient with schizophrenia has the worse that they do on learning and memory tasks
and the worse their symptoms of schizophrenia are so there are two of these there's the sp4 mRNA
which I just described and then there's something called heat shock protein 60 which is a molecule
or chemical in the cell that helps and acts as a chaperone for other chemicals and takes them
throughout the cell and puts them where they should be or helps them degrade and go away and so the
more of this also marker we see that patients with schizophrenia do worse and they have worse symptoms
one of the interesting but also frustrating things about diagnosing schizophrenia it's one of those
disorders that comes on a bit later in life once people get into their teenage or late teenage
early 20s and then again there's a peak later in life as well isn't there do you see your marker's
correlating with the behavior changing or are your markers always positive and therefore they
could help us to spot people early so that is an excellent excellent question we do not know
so this was considered a very large pilot study although it's not a large study overall
we had 27 patients who were already diagnosed with schizophrenia and what we'd like to do is now
extend this for either patients who are showing signs or looking at just patients who are of adolescents
or late teen age which is probably easier to do in a double patient so we would say 18 to early
20s and be able to screen and see if people develop schizophrenia the other question we have is
do medications alter the amount of these chemicals these biomarkers or markers in the cell
we would hypothesize that perhaps if there is a medication that helps somebody with their symptoms
or with their running in memory that somehow that would decrease these markers but these are
things that we have to look at going beyond this initial study and how sensitive and specific are
these markers just for schizophrenia because when we look at a range of other things like the genetic
risk for effective disorders like depression for example there's a huge overlap in risk factors
environmental risk factors family risk factors genetic risk factors have you got discrete markers
here or do you think that the lines are going to get blurred and so you're going to end up diagnosing
some depressed people with schizophrenia by accident so I think part of it is that we need a
combination of these biomarkers it's not a single biomarker it might not even be the two we found
it might be five or ten I think that they're going to be overlapping biomarkers because a lot of
these neuro we call neuro cognitive disorders so disorders where you have changes to personality
or changes to learning and memory there's a lot of overlap and so the question is how do you
diagnose one versus the other it might be that we have to combine with symptomology but it's an
excellent question and I think that one of the control groups for the next study would be
patients with bipolar disorder for example or patients with depression what are the differences
between the patients with schizophrenia versus one of these other disorders and that will help us
narrow down again my guess is that it's going to be more than two markers that will allow us to
distinguish between schizophrenia and one of these other disorders but do I think it's 10,000?
no I do not I think that it's going to be manageable we just need to extend this study
really interesting that was Bonnie Faustine she's based at the University of Kentucky the study
was recently published in Science Advances
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Chris Smith still to come how researchers are trying to keep much-loved European hedgehogs safe
from road traffic but first we're in London where researchers say that thousands of tumour samples
which have been stored in a hospital for over seven decades could help us to understand why
bowel cancer cases are on the up among young people under 50. The scientists at the Institute
of Cancer Research are examining these samples to determine what is causing the current uptick
and how we might be able to tackle it in future. I've been speaking with the ICR's Trevor Graham.
The number of cases of bowel cancer in young people that's adults under the age of 50 and often
these people are in their 20s or 30s is rising rapidly. We don't know why this is the case and
if we're going to prevent this rising bowel cancer in young adults we we need to know what the
causes. When did we first spot this was happening? The data is really clear looking back to about
the 90s you can start to see the increase in the data and I think one of the numbers which I find
really striking is the number of cases of bowel cancer in adults under the age of 50 is doubled
since the 90s so in the data we have today it's extremely clear this rise is going on and what's
the study you have in mind to try and get underneath this? We know that something has changed in our
environment or the way that we live our lives that's causing this increase I mean it can't be
human genetics because that doesn't change over a few decades you know that something that changes
very very slowly through generations so there's something out there or something in the way that we
live our lives which has changed and we want to figure out what that is. Our plan is we found this
incredible archive of bowel cancer samples that existed in a London hospital and been kept in a
in a dusty basement room for many decades have been stored there we think for almost a hundred
years now and by looking in these old samples from cancers they collected and people have surgery
say in the 1950s and the 1960s and comparing those to cancers from people of our surgery in the
present day we can start to interrogate them and look at what's changed through the decades
we can do histopathology which means looking at the cells under the microscope and the structure
of the cells is really well preserved but we can also get DNA out and look at what's going on in
the genome of the cancer cells. Well that was what I wanted to ask because is it the same disease
although we're seeing more diagnosis of bowel cancer in younger adults now is that the same disease
that was knocking around 50-60 years ago or is there something else different and therefore
by comparing these older specimens are we literally doing an apples with apples comparison or
something else changed. Absolutely something has changed there are lots of hypotheses out there
about what's driving this increase in bowel cancer in adults under the age of 50 you know these
range from you know changes in our diet to perhaps the amount of exercise we do you know some people
think it could be something to do with microplastics there's even ideas it could be something to do
with air pollution there's a whole host of things that it could be one of the leading ideas where I
think the evidence is best is that there's a change in the bugs that live in our bowels the gut microbiome
and there's a particular kind of bug that's more common in people's bowels today and we think
was rare in the past although we're not entirely sure which is a type of E. coli and this particular
type of E. coli is known to damage the lining of the bowel and at that damage we think might be
the driver of our cancer in young adults and in the specimens you have can you get a cross
section of the microbes that that person would have had in their bowel when that specimen was
collected so you get both the microbiome as well as the person's genome can you see that
that's correct so we can see both the microbiome and the genome but actually where we're going to
look is not directly at the microbiome we're just going to try and look for the damage that the bugs
have done if they are indeed there so the kind of damage that the bugs do is to mutate the DNA of
the cells and make up the lining of the bowels that means to change the genetic code and once those
changes have happened they're fixed they're there and the DNA of course is copied and passed on
each time the cells renew in the in the bowel and produce the offspring cells to renew the
bowels so if the bugs do damage at some point in life we can see that damage later and because we
think the damage causes the cancers to grow in the first place it's changing the DNA of the cells
and the lining of the bowel that makes the cancers grow we can look in the cancer and ask are the
mutations we see in the cancer are they the ones that are likely to have been caused by the bugs
themselves if you do get a hit and it does look like that is the case that there is evidence that
something is shifted in the microbiome of today compared with yesterday and that's what's driving
the damage to the intestine and that's what's causing the cancers what does that tell us about
what we need to do to address the problem then that tells us we need to do something about the bugs
so the kind of things we might be able to do are to have a test where we can check young adults
possibly even children to see if they have evidence of this damage from the bad bugs and then
if people did have the evidence we might think about screening them later in their life to see if
bowel cancers are developing so we could have screening just for the people we think are particularly
at risk of early onset bowel cancer another thing to say is that our microbiome is shaped by the way
we live our life particularly by our diet and the amount of exercise we do is shaped by many of the
factors in our lives and so it may be that we can find some intervention you know dietary supplement
or something which promotes some bugs in our bowel and gets rid of the bad ones so we might be
able to change the microbiome to prevent their bad bugs getting hold in the first place how long
do you think it's going to take you to work your way through the samples and therefore when should
we be phoning you up next to hear what you found well research is an open ended thing so it's
very difficult to be exactly precise about the timescale here but I think within a few years time
we should have been able to look at the genomes of hundreds of cases collected over the many decades
leading today we're going to focus starting in the 1950s when the NHS was created and when lots of
samples started to be stored in the archive there and take samples from the 50s 60s 70s 80s so on
up until the present day and look across time and I think it would take us a few years to do that
well so yeah come back in a couple of years and hopefully we'll know what's going on and I
shall put that date in my diary to call Trevor back at the Institute of Cancer Research in London
and find out what he has found European hedgehogs are much loved but they've been engraved
decline lately largely because of road traffic which is leading to a third of deaths but new
research has now demonstrated that these animals can hear very high frequency ultra sound which
raises hopes that in-car sound repellents might help to keep them away from roads and being run
over in the first place Oxford University's Sophie Land Rasmussen is dubbed Dr Hedgehog and she has
the story so the European Hedgehog is declining all over Europe and in the UK alone it's estimated
that three out of four hedgehogs have disappeared from the rural areas since the turn of the century
so it's a very worrying and massive decline their decline is caused by a multitude of factors but the
most important one is traffic it's estimated that one out of three hedgehogs are being run over by cars
every year so this was the problem I set out to try and solve to save the hedgehogs and how are
you going about it what's the solution apart from banning cars which is being practical
yes so I couldn't ban cars I wouldn't be very successful with that so I decided I wanted to
look into the possibility of creating sound repellents for cars to actually avoid having the hedgehogs
avoid thirping out in front of the cars for that I needed to understand what hedgehogs can hear
so we could actually target the sound repellents at hedgehogs
all right so what as the cars come along they're making some kind of sound
that the hedgehogs can hear and that warms them because makes sounds anyway so will this work
well we don't know that yet but we need to understand how to really target these potential
sound repellents at hedgehogs and we also need to investigate which sounds actually scare the
hedgehogs so it would make sense to just have the car emit any sound so this is something we have
to look into in the next step of the research what sort of sound do you contemplating using then
well I really don't know that yet but I know for example that the hedgehogs hate the sound
of juggling keys for example and also velcro but perhaps we could also use a distress call
from a hedgehog to warn off the others and have the sound repellents play that would this not
be extremely unpopular with people the amazing thing is that we discovered that hedgehogs can hear
everything between four kilohertz and 85 kilohertz humans can hear up to 20 kilohertz and everything
above that is considered ultrasound our dogs can hear up to 45 kilohertz our cats up to 65 kilohertz
and this means that because the hedgehog can hear such high frequency ultrasound we can actually
target sound repellents that wouldn't bother us or our pets that we wouldn't be able to hear
they might hit bats though might know because bats use same sort of sound regimes
yes so bats and mice and rats could be affected and this is something really important we have to
look into in the future to make sure that the sound repellents wouldn't have any harmful effects
to hedgehogs but also you know to bats we don't want to evict bats from our gardens because I'm
imagining that the sound repellents could also be placed on robotic lawnmowers and garden streamers
that may also hurt the hedgehogs so so we need to look into any potential negative effects of
these sound repellents as well why do hedgehogs hear these very high sound regimes what purpose
does it serve for them I mean it was a surprise to me to find that they actually heard such high
frequency ultrasound and they heard best around 40 kilohertz and this is really interesting because
I've often wondered why hedgehogs don't have that many sounds they have like a whistling sound
when the hoglets the juvenile hedgehogs are calling for their mothers and they have a hissing sound
like when they tell each other to go away and then they have a very high scream when they're
in worrying distress and this is of course an awful sound but other than that they don't
communicate a lot verbally or at least it seems so to us but since they hear best in ultra sound
they may also be communicating in ultra sound and we just can't hear it
do the hedgehogs react in the way you would hope as in if we had cars or vehicles going along the
road or lawnmowers or streamers producing these sounds does it deter the hedgehogs from coming near
would it make them run away because what we don't want is just to scare them and make them stressed
and then they'll still run in front of the car so this is the next step of the research and I'm
really hoping to catch the attention of the car industry here and have them reach out
finance the research and collaborate with me so that we can help each other save the hedgehogs by
creating efficient and harmful sound repellors for hedgehogs and have they made positive noises
about that not yet but we'll see what happens I'm really hoping to hear from them because to me
it's a no brainer to have them support this research as it is their products that are killing
most hedgehogs a year and and if we want to stop this decline of the hedgehogs if we want
the hedgehogs to be in the wild for future generations to experience then we need to stop this decline
and the most efficient way would be to reduce the amount of road-killed hedgehogs every year
so if you're listening and you think you can help out then do get in touch with Sophie
Lund-Rasmussen she's at the University of Oxford and she just published that work in biology letters
that's it for today do tune in on Tuesday though when we're going to be exploring the race to
return to the moon and what either the US or China are going to need to sustain the mission
regardless of who gets their first meanwhile thanks to all of you who are supporting our program
with your donations we really appreciate this we read all your messages and I do write back to
everyone personally to say thank you but here publicly thank you to all of you this really helps
and we're really grateful and if you're enjoying the program and you would like to get behind us
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hearing from you I'm Chris Smith thanks for listening and from all of us here at the naked scientist
team until next time goodbye
oh my perfect day at sand saltwater and friends but my moderate to severe plaque's
rises can take me out of the moment now I'm all in with clearer skin thanks to skyrizzy
risen chism at rissa a prescription only 150 milligram injection for adults who are candidates
for systemic or phototherapy with skyrizzy most people saw a 90 percent clearer skin and many were
even 100 percent plaque free at four months skyrizzy is just four doses a year after two starter
doses don't use if allergic to skyrizzy serious allergic reactions increased infections or
lower ability to fight that may occur before treatment get checked for infections and tuberculosis
tell your doctor about any flu-like symptoms or vaccines thanks to skyrizzy there's nothing
on my skin and that means everything ask your doctor about skyrizzy the number one dermatologist
prescribed biologic in psoriasis visit skyrizzy.com or call 1-866 skyrizzy to learn more



