Jim: Welcome to Science in Focus. A free public lecture series showcasing the latest research from prominent UTS scientists. I'm Jim McNamara, Deputy Dean of the UTS Faculty of Science. In accordance with UTS custom, I would like to acknowledge the Gadigal people of the Eora nation upon whose ancestral lands our city campus now stands. We pay our respects to their elders past and present, and acknowledge them as custodians of traditional knowledge about this place. Now I hope you enjoy science in focus.
Laura: Hello, I'm Laura McCaughey, and I'll be the moderator for today's event. We have a great turnout, both Australia wide and internationally for what I'm sure is going to be a fascinating talk by Dr. Georgina Meakin. Before I introduce Georgina though, I have a few housekeeping details to cover. If you have any questions during Georgina's talk, then please use the question marks, question and answer box down at the bottom of your screen. This'll allow you to type in questions and I can take note of these and ask them to Georgina at the end of her presentation. There's also an up voting function as part of this Q&A. If you really like a question someone else has asked, then please click the little thumbs up and this will let me know that more people are interested in hearing the answer to that question. This talk will also be recorded. We won't be filming any of your video or audio. And if you have any queries or you want further information of this recording, please e-mail science.future@UTS.edu.au.
Laura: So now to introduce tonight's speaker, Doctor Georgina Meakin is a senior lecturer at the Centre for Forensic Science here at UTS. The main focus of her research is in the transfer and persistence of DNA and how this affects the interpretation of DNA evidence in criminal casework. Georgina moved to UTS from University College London's Centre for the Forensic Sciences, where she set up the forensic DNA research facility with whom she continues collaborations. Georgina has also practised as a forensic scientist working at the Forensic Institute in Glasgow, which is my mother city, and for which she continues to provide advice and consultancy casework. I'd like to now hand over to Georgina, for her to tell us more about the fascinating world of forensics.
Georgina: Well, thank you very much, Laura. And thank you all for attending. So in order to set the scene for today's talk, looking into this, are the issues and challenges of forensic DNA evidence. I'd like to start first by giving a little bit of history of forensic DNA profiling. It essentially all started in the mid 1980s when Sir Alec Jeffreys at the University of Leicester discovered the scientific basis of what he termed to be 'DNA fingerprinting', what we tend to refer to as 'DNA profiling' nowadays.
Georgina: I hope you're all familiar with this image of the cell from your high school biology. Within the cell we have the nucleus that houses the majority of our DNA. As humans, we have twenty three pairs of chromosomes, and our DNA is coiled into these chromosomes housed within the nucleus. You may also be familiar with this double helical structure of DNA. Within the backbones of that double helix, we have these chemical structures called nucleotides, which we refer to by the first letter of their chemical name, A, T, C and G. And that's really all the chemistry I want to get into in today's talk. My point of telling you about these nucleotides is that, it is locations within our DNA where we have repeating sequence motifs of these nucleotides, the number of which differ between individuals. And this is the scientific basis that Sir Alec Jeffreys discovered. So, for example, here you see the motif TCTA, repeated eight times. And that number of repeats can differ between each of us.
Georgina: We are aware of different areas within our DNA that have different sequence motifs that repeat different numbers of times and each location on each chromosome is referred to as a locus or plural loci. So let's take two individuals, for example, say we take this first individual and we examine and analyse a specific area or locus of their DNA. And we might observe that there are nine repeats of a particular sequence motif at that area. And we refer to this is as marker nine or allele nine. But I mentioned earlier that we have pairs of chromosomes, and that's because we inherit one set from our father and one set from our mother. So we have one marker from one parent. And then when we analyse, we'll see another marker from the other parent. So, for example, this individual might have 10 repeats or marker 10, as their other copy. When we analyse DNA in the laboratory, we generate essentially a graph of a series of peaks. So this will look like two peaks on that graph and the software will label it as 9 and 10. So let's take the other individual. We may analyse their DNA at the same location and see 11 repeats, or marker 11.
Georgina: It is also possible to inherit the same copy of ... it's also possible to inherit copies of the same marker from both your mother and father. And in this situation, for example, they might also have eleven repeats in their other marker. And in this case, we would see one peak at that location on the graph representing two copies of that allele. So when we look at a full DNA profile, we analyse DNA at a number of different locations. And this is an example that's generated by a particular chemistry called MGM select that is used by some casework laboratories within England and Wales. But the number of locations that are analysed, and the specificity of the different locations that are used depends on the kits and depends on the jurisdiction and country that is doing the analysis. But in this example, we see 17 different areas being analysed. 16 have those short tandem repeats, those repeating motifs that we're interested in the number of. And then an additional location that we refer to as amelogenin which examines the gender of the person who donated the DNA. So, for example, this DNA comes from a male because we see that X Y present at this location. But if we were to only see an X, then this DNA would be coming from a female. So within this profile we see and these grey bars at the top, which indicate the location of the DNA that's being tested, we see the peaks that are labelled with the numbers of repeats. And as I mentioned earlier, you expect to see two peaks, one representing a mark inherited from the mother, one from the father, although it is possible just to see a single peak. But if you were to see more than two peaks at one particular location, this would indicate that you're actually recovering DNA from a mixture of more than one individual.
Georgina: So going back to our timeline, we see that in 1986 was the first time that this form of DNA analysis was used within forensic casework. And it was ultimately used and lead to the conviction of Colin Pitchfork for the rape and murder of two girls in Leicestershire. And then what proceeded after that is what I like to refer to as the 'heyday' of forensic DNA profiling. This is when DNA profiling was used a lot and very effectively to aid criminal investigations. And at that time, you needed visible body fluids. For example, a coin sized bloodstain or a semen stain. And therefore, you could be confident that the DNA was coming from that body fluid and therefore was deposited during the commission of that crime. And then in 1997, a landmark article was published in Nature from scientists at the Victoria Police. What they found was that when you touch an item, you can also leave DNA that can be recovered and analysed.
Georgina: So let's see that in a case. So this is a case in 2012, in which Ravesh Kumar and his companion were at home. Intruders broke into their home and they tied up Kumar and his companion, and they used duct tape across their mouth and nose. Intruders then spent a couple of hours ransacking the house and during which time the companion was able to get free and call for help. But unfortunately, by the time paramedics arrived, Ravesh Kumar had suffocated to death. Samples were taken from his fingernails as part of the criminal investigation, and DNA was recovered. And it was, these samples were targeted because it was believed that Kumar had, had fought back with this one of the intruders who had tied him up. So they were hoping to find DNA from the offender. And they did find DNA from another individual on those fingernails. And that DNA matched the DNA from Lucas Anderson.
Georgina: So what I'd like to do is ask you a question. Now I'd like to run a poll and I'd like to ask you, do you think that Lucas Anderson should be charged with this murder? Simple yes or no. I'm just going to launch that poll now. Hopefully we'll see it on your screen. So please indicate yes or no. And I'll give you a few moments to respond.
Georgina: Most of you have answered now. Numbers are still going up just a little bit. So I'll just give another moment or two. I'm going to end the poll now, and just show you the results. So as you'll see the majority of you said no. A few of you said yes. You probably could tell from my tone of voice or just simply your interest in actually being here for this talk, that perhaps it's not as clear cut as this. So how about I gave you a little bit more information? What if I were to tell you that at the time of the home invasion, Lucas Anderson was unconscious, drunk, in hospital with a blood alcohol level of five times the legal limit for driving. If I relaunch that poll, what would your answer be now? Should you continue to prosecute Lucas Anderson? Or would you perhaps seek elsewhere for an answer?
Georgina: The rest of you have answered. I'm just going to share the results now. OK, so now we shifted to an even greater majority saying no. Still a couple of you thinking that you would proceed to charge, charge him. Interestingly, the prosecutor shared that view . I'll just stop sharing results now. So interestingly, the prosecutors did continue to share that view, because you know, they questioned the validity of the alibi. However, assuming that all of the hospital records are correct, then his alibi was ironclad. He genuinely was in hospital at the time of the invasion. So, of course, this raises the question of how did his DNA get to be on the fingernails of Ravesh Kumar? So if we return back to that key Nature paper that essentially revolutionised the way that we do DNA. Thew way we look for DNA evidence at crime scenes. Not only did they observe that when you touch something, you leave DNA. But they also observed that when you touch something that someone else has handled, you can transfer their DNA onwards. And this is known as 'indirect DNA transfer'. So going forward then, the number of researchers started to do some more experimentation to try and figure out under what circumstances does this happen, and what do we expect to see? So, for example, a number of the early studies looked at clean items, so they clean them free of DNA. So for example, a glass beaker or plastic tube. They then asked volunteers to shake hands, for example, for a minute or even as long as two minutes. And then one of the individuals handled the glass beaker, for example. And then it was swabbed for DNA. And what they observed was a whole variety of different results. It could be a single source profile coming just from the person who handled the item.
Georgina: It could be a mixture of DNA, in which the major component, the majority of the DNA, was coming from the person who handled the item and a minor profile being indirectly transferred from the handshaker; or it could even be a mixed profile with a major profile as the DNA from the handshaker and the minor profile was coming from the handler or even a single source profile from the handshaker and no DNA from the person who actually touched the item.
Georgina: So this led to obviously questions about this concept of indirect DNA transfer. And what do we expect to see? And when we recover DNA evidence at a crime scene, do we know whether the DNA got there directly or indirectly? Now, clearly, these were very controlled laboratory experiments. And so we wanted to do some research to kind of step in the direction of being a little bit more realistic. So this study comes from a student of mine at University College London from a few years ago. And what we did was we asked volunteers to initially handle the item so that we could have some sure background level of DNA on the item. We asked the volunteers to handle knives and they handled them in a particular way to leave this background level of DNA. We then asked volunteers to shake hands. But this time we asked them to shake hands for just 10 seconds. So a somewhat shorter handshake than what had been previously looked at and perhaps something a little bit more realistic to kind of the levels of casual contact that you might have with people on a day to day basis.
Georgina: And then we asked a volunteer to take one of their own knives and stab it into a foam block for a minute. So we had four pairings of volunteers. In the first instance, we only saw DNA from the what we refer to as the regular user, so the person who'd regularly use the knife and then stabbed it in the foam block. For that pairing of volunteers, we actually only saw DNA coming from that one person. We didn't see any DNA from the handshake.
Georgina: But with the other three pairs of volunteers, we saw about 10 percent of the DNA coming from the handshaker.
Georgina: So not only did this demonstrate that even when you have a background level of DNA, you can still detect indirectly transferred DNA from the handshaker.
Georgina: But it also showed that even with a 10 second quite short contact with someone, you can also transfer that DNA onwards. But more than that, we saw a certain amount of unknown DNA that these participants were bringing in to the lab with them. In particular, one pairing of volunteers, we saw quite a lot of unknown DNA, about 10 percent of the DNA that they left on the knife. And it was a particular male profile. So we asked the volunteer, did they have any idea where that DNA was coming from? And they said, "Well, I walk into campus every morning holding hands with my boyfriend". So we asked for his DNA profile. And yes, indeed, we found that the DNA matched his DNA. So this was DNA that ended up on those knife handles from someone who had never handled those knives, never even been in the laboratory where those knives were set up. So, again, providing further evidence of this concept of indirect DNA transfer under normal everyday circumstances.
Georgina: But what researchers have shown subsequently in a number of different papers is that we're commonly carrying around other people's DNA on our hand. And it can be up to 10, 15 percent of the DNA on our hands coming from someone else or several other people. Just to give you another research example, again from researchers from Victoria Police. They set up a clean room essentially where they cleaned down so that it was free of DNA so that they could observe where DNA was being brought in and where it was moving to. And they asked three participants to sit around this table for 20 minutes, whilst sharing, pouring out drinks from a shared jug into their own glasses, drinking the juice, having a chat for 20 minutes. Now, what this image shows is that the arrows indicate DNA just from Participant One. So Participant One has brought in the DNA obviously from their hands, they've handled the jug handle. And from there, the DNA has been transferred to Participant Two's hands when they've handled that jug, poured out their own glass of juice and from there onto the table, on to the chair, onto their own glass, etc. This is giving an illustration of how DNA can move around within a social situation.
Georgina: And then more than that. The researchers also identified again that unknown DNA that we brought in on the hands of the participants. And these arrows here, for example, show the unknown DNA that Participant One has brought into the room that they've then left on the table, on the glass, on the jug, etc. So, again, illustrating how easily DNA can be transferred.
Georgina: So what does this mean for casework? Well, firstly, there was quite a long debate as to whether indirect DNA transfer would actually occur within casework. Was it only within these kind of strict laboratory setting it was probably not until about the mid noughties that it was gradually accepted that indirect transfer is an issue and it is something that we need to consider within casework.
Georgina: So what about Lucas Anderson then? How did his DNA end up on the fingernails of the deceased? Well, as I mentioned, he was in hospital due to alcohol consumption and he had actually collapsed within a store and paramedics had been called to attend to him.
Georgina: So yes, you've guessed it, the same paramedics then attended the deceased at the crime scene. And what they think is that this little device that's used to clip onto the end of the finger to test for oxygen saturation in the blood, that that's the culprit that transferred the DNA from Lucas Anderson to Ravesh Kumar. Clearly, once this was identified, Lucas Anderson was released, having spent a number of months in jail awaiting trial.
Georgina: So in general, what does this mean for casework? Well, firstly, we need to think about contamination. When investigators attend the crime scene, they can't go dressed in ordinary clothes. As you can see, there is an example for those of you who might be fans of CSI Miami. She looks like she's dressed for a night out. She's probably examining her own hair in fact. For those of you in the U.K., might be more familiar with Silent Witness. And at least they're dressed in the right kind of crime scene suit that we're more familiar with. But still, the hair is on display, the face is on display, there's potential for DNA transfer from the investigator to crime scene.
Georgina: So what we need is that people dress appropriately when they attend crime scenes wearing a full crime scene suit with the hood up the mask on and ensure that the gap between the glove and the sleeve is appropriately sealed. Back in the day when we just needed a visible body fluid to get a DNA profile. It's no longer the case now. Yes, we would obviously still target visible body fluids at a crime scene that give valuable information. But now we can target items that we think have been handled within a crime scene and therefore get DNA, potentially get more mixed DNA profiles. And we need to start asking those questions of how and when did the DNA get there. Obviously, the most obvious explanation is that someone has handled the item. But we need to also consider indirect DNA transfer and also the possibility of transfer just by speaking, coughing within the vicinity of the item.
Georgina: So what do we need in order to answer these questions? Well, we need empirical research. We need to have more studies conducted under more real situations investigating different variables that we know can impact transfer and persistence of the DNA. In 2013 I co-authored a review article. Looking at all the publications at that stage, that had been studied in view of giving empirical data on DNA transfer. And we observed that more data was needed to inform and help forensic scientists give evidence on these matters. Then co-authored another review article in just last year. And although there's been a lot more research done on this subject, we still noted that more research is needed. There's still a lot of unanswered questions. And I'd like to illustrate the kinds of questions that we're tackling at the moment.
Georgina: There's essentially four different areas that we need information on in order to better understand DNA evidence when it's recovered from the crime scene. The first is transfer. Now, this can be direct transfer, ie. When you touch something and you leave DNA.
Georgina: So one of the key factors that we know can impact the amount of DNA you leave when you touch something is, your 'shedder status'. This was first identified in 2002. They basically showed that some people could be really good shedders and leave a lot of DNA and some people can be poor shedders and leave little DNA. A number of studies have been published investigating this, but I particularly like this one from researchers in Adelaide who have used DNA binding dye that fluoresces green. So when we see someone who is a really good shedder, he might be referred to as a heavy shedder. When they touch an item, so this is for example, a fingerprint on a glass slide. We see that there's a lot of DNA material present, a lot of green fluorescence. And then someone might be classed as an intermediate shedder. And as you can see there's less DNA present. And then someone might be considered a light shedder and even less DNA is deposited when they touch something.
Georgina: However, subsequent research has shown it's not quite as clear cut as being able to categorise people so easily and that people can leave DNA, different amounts of DNA, at different times of the day. And depending on whether they use the right or their left hand or other activities that they might have been doing immediately before touching something.
Georgina: In addition, the condition of someone's skin can impact how much DNA they leave. It's been shown that if you have a particular skin condition such as psoriasis or dermatitis, then they can leave, you can leave more DNA when you touch something because of those conditions.
Georgina: The age of the donor can have an impact. As you age, you leave less DNA. And this has been particularly observed for males rather than females.
Georgina: And I mentioned earlier the idea of activities prior to touching. So when we touch other items, we might be picking up more DNA from other people that we can then move on and leave when we touch the item of interest. Alternatively, we might also just be essentially touching ourselves: our hair, our face and therefore loading our hands with DNA material then therefore we might leave more DNA in that situation. But these are things that we still need to research a lot more. There's also a number of other factors, such as the type of surface or the nature of contact. For example, if you put more pressure, you'll leave more DNA. And these are all things that we need to research more. And there are more factors that perhaps we've yet to discover. What about indirect DNA transfer? Well, clearly the amount of DNA that's initially present on the surface is going to impact how much DNA is available to be moved on to another surface. So therefore, the amount of DNA that is initially present is going to completely depends on this fact, as I just mentioned. It's also going to be dependent on the biological source of the DNA and whether that is wet or dry. I mean, you'll know yourselves if you've had a nosebleed, for example, that when you have wet blood, that's going to transfer easily onto other surfaces and between surfaces. Whereas when it's dry, it's not ready to transfer so readily, although perhaps the blood, it might start flaking when it's dry and that is an additional variable to consider.
Georgina: And then the number of transfer steps. So talking about handshaking, we're talking about just one intermediate surface, and that's referred to as 'secondary transfer'. But tertiary transfer and other onward transfer is also possible that each time a transfer step occurs, less DNA is transferred. So this, again, affects the amount of DNA we might expect to see. And again, there'll be a variety of variables that we have yet to identify. So in addition to the ways in which DNA can get onto an item, we also need to consider how long the DNA has been on an item. Could the DNA have been at the crime scene before the crime occurred? So was it deposited completely irrelevant to the crime that occurred? So I'm commonly asked, how long does DNA last on a surface? And my answer is, how long is a piece of string? The challenge with persistence is that there is an awful lot of variables involved, and we don't really know them as fully as we would like. Hence the need for more research. So, for example, one key factor is the biological source of the DNA. And you'll be aware from news article that crimes, particularly sexual assaults, can be solved decades after the event occurred. And this is because sperm cells are really hardy. And they're hardy, they require an additional step during the laboratory analysis process to release the DNA from sperm cells so they can last for a long time and protect the DNA. And that's why we can get DNA from sperm cells literally decades after it was originally deposited.
Georgina: And similarly, if it's say, a lot of body fluid present, there's more DNA to persist for longer. But then on sort of touched or worn items, it tends to be less DNA and it may not last as long, although we need to do more research on this. The type of surface will impact how long an item, how long the DNA will persist for, environmental factors will affect it. So, for example, in summer conditions, when the temperature is hot, when there's a lot of UV and longer hours of daylight, the DNA is not going to persist as well as during wintery conditions when it's cold and darker. And we've demonstrated this being the case using a climate chamber from a student's research a couple of years ago. However, we also found the type of surface had an impact even on the ability of environmental factors to affect the persistence of DNA. And then whether the DNA has been treated in a particular way, by which I mean you might encounter a crime scene where the offender has tried to cover up the crime. So, for example, they've cleaned down the surfaces or perhaps they've set fire to it. And so when it comes to cleaning, again a student project from a couple of years ago, we looked at the impact of cleaning mugs and knives. And we saw that even just simply rubbing with the surface without any kind of cleaning product was enough to kind of physically remove a significant amount of DNA.
Georgina: So in addition to transfer and persistence, we also need to consider prevalence. Let's take background DNA. I mentioned earlier we don't live in a clean environment, there's going to be DNA on the surfaces around us. So on everyday surfaces, but also on like regularly worn items of clothing that might get left at crime scenes and regularly used tools that might be used as weapons. And then finally, we also need to understand more about the recovery of DNA.
Georgina: So, again, from the kind of TV shows, you might be familiar with this idea of using a cotton swab to recover DNA from the surface. And that probably is one of the most commonly used recovery methods. However, there is also a range of different kinds of swabs both in terms of shape, material and size. And therefore, how we go about swabbing can have an impact on the amount of DNA that we recover. In addition to the type of swab, how long you swab for, how much pressure do you put on the swab, whether you use one or two swabs, whether you wet the swab first, all of these variables have an impact on DNA recovery and I currently have a student working on this at the moment.
Georgina: And investigators might choose to cut out a sample, be it say from a bedsheet or an item of clothing or a cigarette butt, and recover DNA directly from the item. And then investigators might also use an adhesive piece of tape and within the UK this is routinely used for the recovery of DNA from clothing. So there's a variety of different methods and this is going to impact how much DNA we get from item of interest. And therefore research needs to be done to help inform the decisions being made about the type of method to use and what's best to maximise that DNA evidence.
Georgina: The other thing about recovery is a consideration of whether using a different method or targeting a different location on an item might give different information about the how and the when the DNA got there. I'd like to show you a piece of research that we're just in the process of finishing up that's trying to shed some light on this. And this is within the context of worn items of clothing, which are common items that are recovered from crime scenes.
Georgina: Now, ostensibly, when you recover an item of clothing, you're seeking DNA from the item of the most recent wearer, i.e., the person who committed the crime.
Georgina: But when we have mixed DNA profiles from an item of clothing, how do we know which DNA profile came from that person?
Georgina: And what about if the defendant were to provide the defence that yes, that is their item of clothing, but they gave it to a charity store the week before, for example. Or perhaps they lent it to a friend or left it on public transport. What then? How do we judge who was the last wearer of that item. Though it has been reported within the scientific literature that there are occasions when the last use or touch are results in the major contributor to mixed DNA profiles and that this has been observed in clothing.
Georgina: However in casework, I've also observed forensic scientists saying something like a major profile matching the defendant is what I would expect if he was the regular or usual wearer of the jacket. Now, clearly, it's possible that the regular wearer and last wearer are the same person. But what if, as I've just mentioned, the defendant provides an explanation and we as scientists need to try and evaluate these explanations?
Georgina: So a few years ago, we started the experimental work for a study at University College London that we are continuing on with the data analysis here at UTS. And in this experiment, we asked volunteers to regularly wear a brand new hoodie for four weeks. In order to do that, actually turn it into a regular worn item of clothing. And we tried to keep it fairly controlled so we could make comparisons across the different volunteers. And we asked them to wear the hoodies two days a week on Mondays and Wednesdays for six hours each day. But the six hours could be intermittent. At the end of the day, it's a hoodie, you put it on when you're cold, you take it off when you're hot. And we wanted to be as realistic as we could make it. We then asked volunteers to wash the hoodies on weekends with their, with the rest of their clothing in their routine way of doing their laundry. We then targeted one half of the hoodie for DNA. We sampled the inside collar, and inside cuff. These are areas that are routinely examined within casework for items of clothing and then also targeted underneath the arm and within the pocket, perhaps to see if these different locations could give us different information.
Georgina: We then asked a second person to wear the hoodie for four consecutive hours. And so again, we're envisioning that they just put on the hoodie, committed a crime and dumped it. And then we sampled the other half of the hoodie in the same locations being the inside collar, cuff, underarm, pocket.
Georgina: We used two different recovery methods. Firstly, we cut out a section from those different areas with the hypothesis that perhaps cutting out a section would give more DNA from the regular wearer, which might become a bit more ingrained into the item of clothing. We then used a second method, a mini tape, as I mentioned earlier, an adhesive piece of tape with the hypothesis that perhaps this would recover the DNA on the surface of the item and therefore give more DNA from the second wearer. Now, unfortunately, what we observed is very similar results across the different areas and across the two different methods. So unfortunately, neither of those hypotheses were ... the data didn't support either of these hypotheses. So just for the interest of simplicity, I'm just going to present to you one set of data. And this is looking at the inside collar and inside cuff using the minitape. So the way in which DNA is routinely examined from clothing within UK casework. So just to show you the results from one pair of volunteers. So from one pair of the volunteers, we saw the majority of the DNA was coming from the second wearer on both items with a little bit of DNA coming from the regular wearer.
Georgina: However, when we flip these two volunteers we saw a majority of the DNA is coming from the regular wearer with an even smaller amount coming from the second wearer. And what we observed, the reason for this is because coming back down to that concept to of shedder status that different people can leave different amounts of DNA. And with this pairing of volunteers, what had happened was we just by chance have paired a very good shedder with a very poor shedder. So when the very good shedder was the second wearer they left the most DNA, but when they were the regular wearer, they also left the most DNA. So having seen these two extremes with the other pairings of volunteers that we had, we saw everything in between. But with just four volunteers in this experiment, so it was a very small scale experiment, essentially a proof of concept study, what we showed was that neither of those earlier statements was true, or rather or alternatively, both of them are true but depending on the circumstances involved. So sometimes we see the major profile coming from the second wearer and sometimes we see the major profile from the regular wearer. So clearly, there's a lot more variables involved here and a lot more variables at play that we need to investigate further and better understand.
Georgina: So essentially, if you remember nothing from my talk today, I hope you remember this one concept. The finding of DNA from an exhibit does not necessarily come from the person who committed the crime, ie. DNA does not always equal guilty. And for those of you members of the public who live within jurisdictions that have juries, you may well serve on the jury one day. You may well be faced with DNA evidence. I'd like you to remember to think about the how and when of DNA evidence. And thinking about whether someone is guilty of a crime.
Georgina: And then finally, for those of you interested more broadly in the forensic sciences rather than just DNA, please do go check out our website at the Centre for Forensic Science at UTS and see what other kinds of fascinating research my colleagues are up to. Thank you very much.
Laura: Thanks Georgina. That was a really interesting talk. There's been lots of questions on the Q&A. Before I get to these questions, just to the audience, if you have any questions, pop them in the Q&A and I'll still be going through these as we ask Georgina the list we've already got. So to start off Georgina, are there any complications with X and Y peaks if the individual is intersex?
Georgina: Ok, so there are chromosomal alterations that can impact whether someone has, for example, an additional X chromosome. But here the area that's targeted, you're still just going to see a single peak for an X. So you're not going to see two peaks if there's two X chromosomes, if that makes sense. So perhaps the height of the peak might be informative. However, that's going to very much depend on whether you're seeing a mixture anyway. And also, there's a certain amount of variation that happens during the analysis process that can impact the peak height. So you don't always see exactly the same peak heights from two components as coming from the same individual.
Laura: Nothing in science is ever clear cut is it.
Georgina: No, not at all.
Laura: We've got a few questions about COVID. So can COVID-19 be transferred via DNA? And following on from that, do you think that because of COVID-19 and social distancing will help reduce contamination and confusion of DNA?
Georgina: Ok, so firstly, I'm not an expert in viruses at all, so I couldn't comment on whether the virus is transferred with the DNA or not. I'm afraid I can't help you with that. However, it's a really interesting question about whether social distancing is going to impact the issues of DNA transfer. Clearly, if we're not contacting people so much, we're not going to be transferring that DNA on so much. Similarly with the world that we're now living in, obviously we're cleaning a lot more, we're disinfecting a lot more, we're washing our hands a lot more. So I would hypothesise that this is going to have an impact on the amounts of DNA that are present due to the prevalence of DNA on everyday items. I would also hypothesise that it is going to impact the DNA that we're leaving on an item, whether the amount of DNA or perhaps we might be leaving less of other people's DNA simply because we're washing our hands. I don't know this is something that we're definitely going to want to research more going forward. And it also is going to make it even more challenging for forensic scientists simply because we rely heavily on the research that's currently being published to help inform decisions on the how and the when of the DNA. But now going forward, as crimes are committed in our essentially new world of being a bit more cleaner? Will that research still be relevant or do we need to do a lot more research in the new way that we're living in this cleaner environment to better understand prevalence and transfer of DNA? And I think we do.
Laura: I guess following on to that answer then is how far can DNA transfer via sneezing or coughing? Because it would seem hard, a bit hard to eliminate this from a crime scene.
Georgina: This is something that's been barely investigated. So there was an initial study. Well, I can't exactly when it was published. I think it is in the early noughties, so quite a long time ago that looked at the concept of coughing and talking at a crime scene and whether it was likely to contaminate a crime scene and the importance of being able to wear a mask to help prevent that. Or help to minimise it, sorry. So it's something that, you know, I've actually wanted to do some research with sneezing. And I started trying to do some pilot studies on this at University College London some years ago. And it's actually notoriously difficult to make someone sneeze on command. So that was the problem I was having using myself as a guinea pig obviously, of trying to make myself sneeze in order to get, trying to understand what impact sneezing might have on DNA position. So at the moment, it's more of a hypothesis that we believe that DNA can be deposited in this way and then there's a little bit of research to demonstrate that it can under very specific situation. But we definitely need to investigate that more. But like you say, it's a little bit a little bit challenging to investigate. But some people have started looking at speaking, in terms of what DNA can be deposited through speaking.
Laura: Yeah, there's a lot of research now regards to COVID, how far it can transfer via speaking and stuff, so -
Georgina: I saw a paper on this and they had a particular device that was simulating sneezing. And I thought that would be really great if I could get my hands on that device and use it from a DNA perspective.
Laura: Well, if only one good thing comes out of COVID, that could be it. Um, a lot of people like the question of what if there are identical twins? Can you tell them apart at all? And has there ever been a case where a wrong twin was convicted?
Georgina: Ok, so first part of the question. So the routine DNA profiling that I explained to you today, because it only looks at a number of different areas. So the example I gave you, 17 different areas or in some jurisdictions, perhaps 22 areas or even more. For identical twins, that DNA profile is going to be the same. However, we do have more advanced technology where we can sequence every nucleotide of the DNA, so all those letters we can actually read that sequence of the DNA. And there are occasions where even identical twins might have the odd letter that's different due to mutation. And then in addition to that, DNA goes through chemical modifications through life. So it has, it can gain what we call 'methylation' and the pattern of the methylation on DNA varies depending on a variety of habits.
Georgina: So, for example, if you smoke, what your diet is, if you drink alcohol, even the environment within the womb when you were developing as a baby, all those things have an impact on your methylation pattern. Which means that an identical twins will have a different methylation pattern. And that's a way in which we can also distinguish between DNA from, uh between identical twins. Whether there's been a case in which the wrong twin has been convicted, I don't know. That said though, I did work a case once some years ago in which there were identical twins. So it can happen.
Laura: We've got a couple of questions I'll ask them one at a time just to make it easier for you, though, that are all related to sort of contamination. Do police get proper training in DNA contamination?
Georgina: I hope so. I mean, I get involved sometimes and I've certainly given presentations to police officers on contamination minimisation and how best to wear the protective personal equipment. Obviously, we train our students as best we can to try and do it properly and they obviously go on and work within, some of them will go on and work within the police, but I don't know how routine it is. And I guess it will depend on the jurisdiction as well.
Laura: Do forensic labs collect and sequence the DNA of their staff and of police or first responders so that contamination can be identified?
Georgina: Yes and no. So I think the majority, if not all DNA laboratories, will have the DNA profiles of their staff. I can only speak for the UK on this, but I know that there's been a push by the forensic science regulator for crime scene examiners and police to provide their DNA and have a reference database for that. In terms of first responders though, when you think about a paramedic, I'm not sure. But certainly crime logs are kept. So anyone who has attended the crime scene will be recorded. So even if there isn't a database they can, if there's concerns over contamination, they can go and ask the person to take a sample of their DNA and make comparisons that way.
Laura: Well, that's good to know. Are there any problems with contamination of supplies from manufacturing? So in the labs, do you run unused swabs or materials to rule out any contamination?
Georgina: Yes, yes and yes. So there was a case again back in the day, I can't remember exactly when it was in Germany, and they referred to it as a phantom because they had this DNA profile that was coming up in all sorts of different cases all across the board. And it turned out that, yes, it was contamination of a particular tool that was being used at the manufacturing stage. So it is possible for that to happen. Only, we've learned more over the years. So manufacturers and suppliers have quite rigorous quality control processes in place to ensure that their supplies are DNA free when they're being used for forensic science purposes. And similarly, within forensic science laboratories, they will do background testing of the laboratories to ensure that their cleaning processes are appropriate. They'll do testing. You know, every test you do, you have a variety of negative controls and certainly with extraction blanks. So there will always be a test of kind of a blank tube from the start of the DNA extraction process to ensure that contamination isn't introduced at any point. Similarly, the kits that we use have serial numbers and they're always recorded within casework to ensure that if any contamination was discovered, that could be linked back to a particular serial number, it could be tracked. There are a lot of procedures in place to, to monitor for the risk of contamination because clearly DNA does get everywhere and we do have to be monitoring that and hopefully minimising it as best as we can.
Laura: In terms of cold cases,DNA evidence stay around indefinitely if it's being collected appropriately?
Georgina: It won't stay around indefinitely. It will degrade. But that rate of degradation is going to completely depend on how much was there in the first place, the biological source, you know, I mentioned earlier about sperm cells being super hardy and can hang around quite a long time. It'll depend on how the item has been packaged, how it's being stored. So there's, there is a lot of variables involved. And this is something that we don't fully understand and don't have complete research to fully understand the lengths of times involved. So that generally means that when you have a cold case, that we would sample it for DNA now, you probably would get a DNA result, but the question comes back to the: well how did the DNA get there and when did it get there? Is it a more modern sample because some form of contamination's happened during the time the item's been stored, so these will have questions that need to be asked when thinking about cold cases.
Laura: On that theme. Can you watch Netflix documentaries that focus on like bad forensics, the ones like the Innocence Files, or do you just get too annoyed?
Georgina: I do struggle with watching them. And I think, I think these days, because for me, DNA evidence is really about thinking about the how and the when did the DNA get there, these questions aren't commonly asked within these kinds of documentaries. That said though, the second season of Making a Murderer, I actually really enjoyed and it's because they actually did go and start doing some kind of some experiments to try and evaluate the different explanations for the findings of the different evidence. So I did quite enjoy that one I have to say. Guilty pleasure right there.
Laura: That's good. There are always our guilty pleasures. DNA was always seen in courts as being 100, well, never a hundred percent, but always like the golden standard for evidence. But now you're saying that it's not this silver bullet. So how are lawyers treating this? And what weighting is now given to DNA evidence in light of your research?
Georgina: Ok. So firstly, just to caveat that for a moment from saying, you know, using DNA from a visible biological fluid where we know the DNA, we're confident that the DNA came from that biological fluid for example blood. And we're pretty confident that that blood was deposited during the commission of the crime. That still means that DNA has a lot of power in those kinds of situations, so that that hasn't gone. But now the issues are, this idea of DNA being recovered from items that we think have been handled, that we're getting mixtures that we don't actually know which DNA is coming from who from the person who touched it or when it was deposited on there. And so now lawyers from a prosecution perspective are going to have to start thinking about these questions, you know, and thinking back to that case that I presented this evening. The prosecutors need to think about, is there sufficient evidence to go ahead with the prosecution? And the key question is, is there corroborating evidence? There really does need to be other evidence than just DNA when it comes to prosecuting someone. And then obviously from a defence perspective, defence lawyers are going to also be asking these questions because they're going to be trying to evaluate the evidence that's pointing towards their client and their defendant to see whether any scientific challenge can be made to it. So certainly in more recent years, these questions of the how and when are being asked a lot within the courtroom now when it comes to DNA evidence.
Laura: We've got another question here. One of our audience watched a crime TV show set in the future where the perpetrator sets off a little DNA bomb like a flea bomb, and it disperses hundreds of people's DNA into the air to provide a kind of anonymity. Do you think this could become a reality or is it too far fetched?
Georgina: That's an interesting one! I don't know. I mean, if you could spray DNA in that way, then certainly it would hamper the interpretation of DNA findings. But whether you'd be able to set off some kind of bomb to enable that, I really don't know. I think that's, that requires some physics knowledge, right there and I'm afraid I don't have that.
Laura: What samples can extract DNA from. You've mentioned a few, but can you extracted from things like sweat or any of the less obvious bodily fluids?
Georgina: So, sweat contains DNA and in essentially two ways that we're aware of. So one is that as the sweat comes out of the ducts, it brings cell, cellular material essentially from the ducts into the sweat. And so within those cells there'd be DNA. But there's a couple of researchers have shown that cell-free DNA exists within sweat as well. So this can also be detected and therefore will be deposited via sweat. But essentially, most biological materials you're going to get DNA from, but just to varying degrees. So, for example, you can get DNA from hair, specifically from the root of the hair. Although you can get different kind of DNA from the shaft. You can get DNA from urine, from faeces, from vomit. But it all depends on how much cellular material has been deposited within that fluid as it's come out the body essentially.
Laura: Well, unfortunately, we're all out of time for more questions. I'd like to thank Georgina for such an interesting and thought-provoking talk. And I'd also like to thank all of our audience for attending and for asking such great questions. If you want to watch this talk again or if you want to get your friends or colleagues to watch it, a copy of this talk will be available on our website, pretty soon. Have a lovely day, everyone, and keep safe.
Georgina: Thank you very much.
Welcome to Science in Focus. A free public lecture series showcasing the latest research from prominent UTS scientists. I'm Jim MacNamara, Deputy Dean of the UTS Faculty of Science in accordance with custom. I would like to acknowledge the Gadigal people of the Eora nation upon whose ancestral lands our city campus now stands. We pay our respects to their elders past and present, and acknowledge them as custodians of traditional knowledge about this place. Today, it is my pleasure to introduce Dr. Lana McClements, who is speaking on the miracle of pregnancy and new life. Lana is a lecturer in biotechnology in the UTS Faculty of Science. She researches women's health with a particular focus on understanding pregnancy complications, such as preeclampsia. Her research has had significant impact in creating new monitoring strategies for women who are at risk. We are pleased to present Dr. Lana McClements.
Hello, I'm Laura McCaughey, and I'll be the moderator, for today's event, collecting questions and asking our speaker, Dr. Lana McClements, questions both during and at the end of her talk, I'll now hand over to Dr. Lana McClements to hear about her fascinating research into pregnancy and its possible complications.
Thank you very much, Laura. Hello, everyone. I'm delighted to be able to talk to you about pregnancy and also my research, which is in relation to pregnancy complications. So I'd like to start my talk by showing you a picture of myself with my second born daughter. This is two days after I've delivered Emily and I looked very happy and relieved at the same time. But I'm not sure if you can notice. I do have a bit of a yellow tint in my face, even though this is this is one of the two most happiest days of my life. The first one being with my first born. So the events coming up to it were a little bit stressful, to say the least. So I actually was diagnosed with gestational diabetes in pregnancy. So this was my second time that I had gestational diabetes because I also had it in my first pregnancy. It was a bit of a shock in the first pregnancy because I didn't expect it. I did expect it in the second pregnancy because there is increased risk of developing it, developing it sort of in, when you when you have had it in your first pregnancy.
But in addition to this, I also developed towards the end of my pregnancy obstetrical cholestasis , which is the liver dysfunction often linked to the hormone secreted from the placenta. And we'll talk about the placenta in great detail later on as well. That obviously meant that I have to have induced labor. My children were not premature, so they were full term, but I was lucky. The good news was that they didn't have preeclampsia. So you will realise, you will learn about preeclampsia today in my talk, whilst I had quite a few other complications, preeclampsia was not one of them. So we'll go back to the very start and will give you an outline of actually how pregnancy starts with embryogenesis. So I'd like to thank my talented honours student, Claire Richards, for providing these pictures to me. So this is part of the female reproductive system and this is the ovary where ovum or 'egg' gets released. It travels down the fallopian tube to meet sperm cells. So spermatozoid, which actually then implants, fertilizes the egg and travels down definitely a particular tube and gets implanted into the uterus. But during this travel from sort of meeting the the egg to actually implanting itself into the uterus, there are quite a lot of changes happening. So following a fertilisation, zygote is formed, which is a single cell which contains fusion of sperm cells and egg cells. And these zygote undergoes a number of divisions until it forms 'morula'. Morula is a structure that contains about sixteen cells at this point that have been divided and containing both genetic material from the mother and the father.
And then further on, on day six, a blastocyst is actually developed, which contains all of these cells. But as you can see, it's a little more organized structure and it contains outer layer of differentiated trophoblast cells. Now, remember this name 'trophoblast' cells, because we will talk about them a lot. They actually end up remodelling maternal vasculature to allow supply of oxygen nutrients to the baby. But also they form this organ called placenta. There is this inner cellular mass within the blastocyst where the foetus will be formed from. The rest of the blastocyst is actually filled with fluid that will form on the attack on the amniotic fluid that will keep the baby floating inside. And mothers and stock interests. So what happens then. Well, once we have the blastocyst form, it travels down fallopian tubes to reach the uterus. And these trophoblast cells on the outside of the blastocyst are quite sticky. And they secrete, they secrete chemicals that actually attach to these endometrium, which is the lining, the mucus lining of the uterus. So whilst the blastocyst actually attaches to the endometrium. It travels down. And these trophoblast cells then start dividing and forming this layer of cells that travels further down to actually reach a spiral uterine arteries of the mother and trophoblast... what happens then is that trophoblast actually invade these foreign uterine arteries, remodel them, which is our next part of the talk. This is the cross-sectional and the magnified section of this spiral uterine artery within the uterus or the myometrium of the uterus.
So normally in a non-pregnant state, these spiral uterine arteries are just sitting at normal, they are supplying uterus with blood and oxygen, nutrients, etc. But in pregnancy, so once the blastocyst travels down to the endometrium trim and then further down to the myometrium, which is this part of the uterus, it actually starts to remodel these spiral uterine arteries by allowing trophoblast cells, which formed the outer layer of the blastocyst that we talked about in the previous slide. And what this does actually allows for these spinral uterine arteries to remodel, and to become elastic and to allow and restrict the supply of oxygen and nutrients to the placenta and then further the baby. But what this means for the woman's body is that there are a lot of changes. So both cardiovascular and metabolic changes. So some examples of these include an increase in maternal blood flow hundreds of times, which is substantial. As you can appreciate, blood volume also increases 30 to 50 percent and heartbeats increases 10 to 15 beats per minute to meet the demands of all these changes and the growing fetus. So until placenta develops from these trophoblast cells and what placenta actually does is delivers oxygen and nutrients to the baby so the baby can grow in utero and also removes waste products. But also another important function of it is partial protection of fetus from teratogens and pathogens in the maternal circulation, I would like to thank my other honor student, Ingrid Ataman, for providing this to me for this presentation.
What is interesting is that placenta is actually an endocrine organ. What this means is that it actually secretes hormones to substantiate the development of the fetus. So the hormones that are secreted include estrogen, cortisol and human placenta lactation. So what these hormones do, while they do wonderful things, and enable pregnancy, really, the progression of pregnancy. They also have the function of inhibiting the insulin and the work that insulin does within the body.
So insulin is not very effective anymore in utilizing and breaking down glucose and metabolism. So that means that women actually have to produce more insulin from their pancreas, which is at this leafy structure underneath the liver.
But in some women, this is actually not managed very well. The body can manage this excess insulin demand and this develops into gestational diabetes mellitus. Gestational diabetes occurs all in pregnancy, and it is a major concern nowadays, particularly because there is increased risk of obesity. And nowadays, with a change in the lifestyle and the number of women actually having Type two diabetes as well before pregnancy is increasing to. So currently, over 21 million women have some form of diabetes in pregnancy. So we could easily say that hypoglycemia or the presence of high blood glucose in pregnancy is actually one of the most common complications in pregnancy. And this complication in pregnancy does lead to increased size, increased baby size because actually glucose passes through the placenta very easily and it can be easily absorbed by the baby. However, this leads to sort of increase in the size of the baby.
But it's not a good thing, actually, because fat around your organs can be formed and other complications as well. And in fact, what we've been seeing over the last 10 years is a two to six fold increase in the incidence of gestational diabetes.
So what are the complications of gestational diabetes and macrosomia, which means a big size of the baby that can cause complications during delivery, such as so shoulder dystocia but also other complications, such as preeclampsia and preeclampsia is the focus of these talks. And my research as well, in addition to preeclampsia, I also research diabetes as a risk factor for pregancy.
So what is preeclampsia? Preeclampsia is the leading cause of maternal and fetal death in the world, and it affects about five to eight percent of pregnancies. The number of women experiencing preeclampsia in pregnancy actually is on the rise because there is increased number of women with obesity and diabetes.
Also, after preeclampsia or after the pregnancy has been finished.
And women are at increased risk of developing future cardiovascular diseases and also diabetes. And two out of three women will actually die from cardiovascular disease. Cardiovascular disease in general is the biggest killer in the world, accounting for 31 percent of deaths. Even more in cancer. But these women in particular increased risk in the future. So it needs to be monitored closely. Knowing all this, it is shocking that we actually don't have any any effective treatments or effective monitoring strategies for women who have preeclampsia, at pregnancy and afterwards as well. This is the area that we focus on. So preeclampsia still kills over 70,000 women and five hundred thousand babies every year. Most of these deaths actually occur in developing countries, and this is because women don't have access to care so easily and they live in remote areas. The health care systems are not very well developed, etc. and that leads to fatal consequences. Short term complications from preeclampsia during pregnancy includes preterm birth. And these this is general. This is before 37 weeks of gestation. HELLP syndrome, which is the hemolysis, elevated liver enzyme and low platelets, a very dangerous syndrome that lead to organ damage and other complications as well. Eclampsia, eclampsia are seizures, which can also be fatal. Stroke. Neonatal respiratory distress syndrome is another short term complication associated with preeclampsia and long term, like I said in the previous slide, it's diabetes. Women have increased risk of diabetes, cardiovascular disease and stroke as well. It is possible that these some of these women already had sort of underlining risk factors for developing these diseases later on in life that actually get unmasked during pregnancy. So actually, whilst pregnancy is a stress test for the body, it's also an opportunity for intervention early on to prevent any complications and death further in the future.
To make things even more complicated, they're actually two, at least two in fact, phenotypes of frequency that we know of. We are still research and trying to understand this condition better. But what we know so far is that there is early onset preeclampsia and there is late onset preeclampsia. These two types of preeclampsia are subdivided according to the time of gestation of their diagnosis. So, for example, early onset preeclampsia is diagnosed before 34 weeks of gestation, and it is normally associated with difficult complications in placental development and also intrauterine growth restriction, just as small babies, in fact, whereas late onset preeclampsia, which is which actually consists 80 to 90 percent of preeclampsia cases, a lot more case women would have this type of preeclampsia, that early onset preeclampsia. Whilst it's potentially milder, it actually occurs after thirty four weeks of gestation. And often it is not associated with placental placental complications and restrictions in the growth or the development, in fact. But still, it is... There are some overlapping features between the two different types of preeclampsia. Hence it is not so straightforward to identify one or the other type. Also preeclampsia, what we know so far is often associated with sort of underlining complications such as diabetes and obesity and other vascular complications in pregnancy. And I'd like to thank Ingrid again for providing this slide for me.
So how does preclampsia develop what we know in terms of sort of placental development, where placenta is actually involved in its development, is that if you remember from our blastocyst slide where we had our trophoblasts that traveled down the spiral uterine artery to remodel it. So in normal pregnancy. This is done properly. And the spiral uterine arteries are remodeled. They're wide, they're elastic, and there is unrestricted supply of oxygen. and nutrients to the placenta and the baby. However, in preeclampsia, this process is actually restricted, leading to a restricted supply of oxygen and nutrients to the baby potentially restriction in the growth of the baby, but also other complications, because what these trophoblast cells have to do. And these are fetal cells, if you remember, from the blastocyst that we talked about earlier on, they have to remodel this artery. And by remodeling, they actually have to interact with endothelial cells.
Now, endothelial cells are cells that line the blood vessels in our vasculature through through which blood actually flows and supplies various organs, including placenta and the baby in pregnancy.
So these endothelial cells, if they're not functioning well because there is an underlying vascular risk factors that women have without ever knowing, it can cause this inappropriate development of the placenta. Also inappropriate spinal uterine artery remodeling, as we call it. But if the fetal cells, on the other hand, as well are not functioning well, this can cause problems, too. And therefore, a lot of our research will actually focus on identifying factors that can influence the function of the trophoblast cells, but also the function of the individual cells as well. So before we go on, I'd like to pass you on to Laura for any questions that you might have to break down the talk into two sections.
Thanks for a fascinating introduction into pregnancy Lana, we've had a lot of questions come through the Q&A and also from the event registration. And I'll try and get through as many of these same will permit. Our first question is from Deb, and she wants to know. Do we know what causes preeclampsia?
That's, that's a great question. Thank you very much Deb, for asking that.
So a lot of the mechanism and the causes of preeclampsia are unknown. We're still trying to to investigate and understand why this happens. So that is the big problem, why we haven't really been able to come up with very effective preventative treatments or curative treatments and also monitoring strategies. But what we do know is that diabetes, for example, is a risk factor and that can lead to and that increases the risk of preeclampsia. So, for example, women who have pre-existing diabetes before they become pregnant, they have up to fourfold increased risk of preeclampsia. If a woman has a higher BMI as well, that is a risk factor, too. Sometimes. And age can be also of older age, but is not a significantly increased risk. But it is associated with the risk of preclampsia and other auto immune diseases, chronic hypotension, for example. It is interesting the first time mothers actually have a sort of background increased risk of preeclampsia, rather than the second time of it, for example. So there are some things we know about it. But there is also a lot that we don't know and we need to find out going forward.
I have another question that you touched upon there. The question is, is there a higher risk for people who are older? And if so, why?
So that there is an increased risk potentially of preeclampsia as you get older and age is one of the risk factors, too, generally over 40 years of age. We don't really know exactly why this happens. It could be to do with the vasculature and sort of more stress that the body has gone through and the aging process itself.
But again, it's not it's not very well understood. And we are trying to sort of understand how these aging processes can actually affect and are linked to it. Again, coming back to vasculature there is sort of underlining the issue with the vasculature and the fetal cells are not working so well, etc. That could be one of the reasons, too.
We had two questions from Marina. She wanted to know, what does a one hundred fold increase in blood flow mean? Do you mean that it circulates faster? And also, could you clarify what you meant by two out of three women who have had preeclampsia will die of cardiovascular disease?
Sure. No problem. Thank you, Marina. So a hundred blood fold... actually, more blood is produced to substantiate the development of the fetus. So the body has to go through all these changes, more haemoglobin in the red blood cells, etc. So it's it's a fascinating machinery, really. And what women's bodies going through. In terms of future. So. So as I said, cardiovascular diseases are actually the leading cause of death in for everybody. So the 30 percent of deaths account for... come from cardiovascular complications.
So these women, for women, cardiovascular disease, anyways is the number one killer too, but because preeclampsia can actually cause this inflammation and oxidative stress and will go in the second part of my talk about these sort of stress factors that can remain after pregnancy and therefore lead to damaged to blood vessels, etc, that can lead to cardiovascular disease.
We've got a question from Kathy, and she wants to know what are the first symptoms of preeclampsia to watch out for?
That's a great question. Very difficult. Preeclampsia is sometimes also very difficult to diagnose. It's not straightforward in some women we have typical symptoms. Symptoms of high blood pressure. So high blood pressure is what one of the compulsory, you would call them symptoms. But in addition to high blood pressure, there has to be other symptoms as well. Otherwise, if it's only high blood pressure in pregnancy, that's called gestational hypertension. So in addition to high blood pressure, we also have organ damage, for example, kidneys or liver. So if there is any liver function tests showing a sort of abnormal results or for example, there is protein in the urine where it shouldn't be, damaged kidneys are not working so well, etc. Other symptoms, in addition to high blood pressure, could be a headaches, swelling in the feet around the ankles and other, other organ damage. Platelets could be also affected. In addition. And it is generally, what is why we are working so, so hard to actually try and figure out the way to monitor women from the early pregnancy and to pick up preeclampsia early is because it comes on so suddenly. In a lot of the cases, the pregnancy is going really well, nothing is wrong. And also then all of a sudden, all this happens and women end up in the hospital, etc.. So we are trying to actually find a way that we can monitor it from early on in pregnancy so that we can diagnose any changes or foil any changes early on without complications and sudden onset of severe symptoms and early birth of course.
Thanks, Lana. I'll let you tell us about your research now. And we'll have some time for more questions at the end.
Thank you very much. Right.
So we'll go on about the details of of my research and the research of my team. Of course, it's a team of collaborators and collaborators and students and postdocs students to help with this research. So our focus is actually trying to understand the mechanisms underlining preeclampsia, what happens early on in pregnancy with a placenta or with other cells. That then leads to the development and manifestation of preeclampsia later on in pregnancy. Bearing in mind that pregnancy, that preeclampsia gets manifested sort of after 30 weeks of gestation, any time after 20 weeks of gestation actually can occur, but in most cases, it will be after 30 weeks of gestation. So we are actually investigating some novel proteins and microRNAs. MicroRNAs are a small nucleic acids that regulate translation of genes into proteins and proteins are very important because they actually are key for the changes in our bodies. So whatever is the result of molecular changes actually comes through changes in the protein expression or differences in the function of those. So we are using placenta as a model, and to understand any molecular changes and how these can be leveraged and used for developing, for example, tests. Inflammation being one of the one of the very common undermining process in preeclampsia as well. So we are understanding how these proteins in my property can affect information, lead to development of inflammation, etc. Angiogenesis is the vascular development. So obviously there is a lot of angiogenesis happening in the body during pregnancy because extra blood is needed to supply a fetus. Endothelial dysfunction. So cells that line the blood vessels and we talked about as well, we want to understand how these proteins and microRNA affect their function and also cellular processes, because all these cells trophoblast, endothelial cells and other cells that are actually present within the placenta. And these include sort of other cells such and such as mesenchymal stem cells, immune cells, etc. They all have down the road proliferation and differentiation. So maturation as well. And aptopsos is a celld death, really.
So obviously there is increased cell death potentially in preeclampsia that we are trying to understand why this happens and what regulates these processes.
So I just wanted to show you some of our work. So this is this the cross section of the placenta. So we took a little chunk from the placenta, from a mother who delivered a baby and placenta is a massive big organ. And so, therefore, a really expensive tissue to be, to be investigated and used for for research purposes. And what we did actually, we made little slides of these placental tissue and we looked at the expression of trophoblood cells and also blood, blood vessels or endothelial cells that line our blood vessels. So this is how placenta looks inside. It's actually composed of many of these Chorionic villi, which are surrounded by trophoblood cells. And within these chorionic villi, we can see blood vessels as well, which are shown on this picture. So, for example, when we want to look at the differences in the expression between one one or many proteins that we are interested in, we can actually look at the differences in the expression of these proteins in healthy placenta versus placenta.
That was from a woman with pre-eclampsia. And this picture just depicts an example of how this particular protein is actually overexpressed, increased in preeclampsia compared to healthy pregnancies.
So because it's very, it's not so easy to get early placental tissue during pregnancy. The procedures are invasive and it's not something that we can do routinely. We're trying to actually develop models of the placental development in the lab using trophoblast entity or cells. So this is the work of my very talented honours student Claire Richards. She actually was trying to develop these mini placentas into tissue. So it's a 3D. This is a 3D placental structures and composed of trophoblood cells. The first trimester trophoblood cells that actually organized themselves into these spheroids or organoids. And you can see that there was we've stained them with different proteins to show the nuclei of the cells or to show other features of the cells that are important in the development of these sort of mini placentas. When we actually take those out of the culture and cross-section them, so we cut the company in half or across. And we looked at inside the cells to see whether we have different types of cells. And it's not just one type of cells because it is the multi-tier rock called organized structure of the placenta. We actually realize that we have many different cell sizes within each spheroid or organoid. Some are bigger. Some are smaller.
Therefore, we have the heterogeneity in terms of the same structure.
But further work that I've done with Professor Warkiani from biomedical engineering is to try and develop these mini placentas in a more dynamic way. So having sort of been able to kind of see the development and measure changes in real time as cells interact. So what we are doing at the moment, we're trying to culture these trophoblast series that I showed you on the previous slide together with endothelial cell so we can mimic what's actually happening with the with this with placental development, inspiring uterine artery remodeling where these cells actually interact together. So this is a fascinating platform that Professor Warkiani actually has in his lab where we can put many different cell types on this chip. So it's almost as if we're building placenta on a chip. And we can put these in the single cells in the middle, for example, trophoblood cells on the side and or other cells that are of interest to us, as well as other treatments or collect super natans, which will contain changes in the protein expression that we can use as biomarkers. All of these then represents sort of more dynamic structure, and we are using this to elucidate and... Mechanisms affecting early preeclampsia and also early placental development, but also to test some treatments that we could potentially develop and use either to prevent preeclampsia or to treat preeclampsia. A specific project that we've been interested in elucidating its role in preeclampsia is called FKBPL. So we started this work five or six years ago. And we realized that all these processes that have been well-established in preeclampsia, including impaired vascular response or antiangiogenic response, which means restricted vasculature, also abnormal trophoblast invasion or abnormal trophoblast function oxygen changes when there is sort of restricted vascular development and there is obviously low oxygen potential and we call this hypoxia or reduced oxygen concentration and inflammation of the immune system play a big role. And actually, this protein that we are interested in plays role in all of these processes. And we have been exploring its role as a biomarker, but also potentially as a treatment for preeclampsia too.
So we filed two patents in relation to this work, which are currently being commercialized and validated and developed further as new tests of preeclampsia. So what we propose with our biomarkers and we have developed an advanced algorithm, not just including one protein, but a couple of proteins and other critical characteristics, they can actually we can identify changes in these, in the level of these proteins in combination with clinical features such as blood pressure, or proteins etc.. And then when we measure this sort of towards between second and third trimester, which is still sort of before preeclampsia develops, we see that the increase levels of this of these proteins. And then when preeclampsia is actually diagnosed, the ratio goes down. So if we can detect these changes early on before full blown preeclampsia occurs and manifests, we could potentially do something about it and reduce premature births and deaths, even if it just means monitoring women closely and giving symptomatic relief therapy as well. It can prevent complications.
So because most of these deaths associated with preeclampsia occur in developing countries due to poor access to health care and monitoring, etc., the best way to actually translate these tests into something that can be beneficial for all women and babies all around the world is to develop a digital health solution, which means that remote monitoring is something women can actually do from home and be monitored remotely by the clinicians or the health care team who can then intervene if they see any changes in various parameters that could stipulate that there is something going on that could indicate preeclampsia. So our proposal is to sort of be able to connect many monitors and also point of care devices. Point of care devices means that it could be like a pregnancy test... In the form of a pregnancy test. But it could be lined with various sort of proteins that we think could have a role in preeclampsia. So therefore, at home, patients can do their own testing and upload this information onto the app or the cloud where clinicians can remotely check it.
And then others patients, if there are any changes that could be indicating development of preeclampsia.
And then we've be doing this work at UTS with another collaborator of mine, Professor Dayong Jin. And he has a fascinating platform as well. Point of care test platform that can be translated into so many different diseases in testing and monitoring among many different diseases.
We've been working on actually translating our biomarkers into this platform that then can be incorporated at this digital health. This work is still in early stages, but t is promising.
So then shifting gears, we want to monitor women in pregnancy and also, detect if there any changes which can prevent serious complications. But actually one of the treatments, can we actually treat preeclampsia? How can the all of this be prevented or treated? And like I said, there are no effective treatments so far.
But what we do have is a limited, limited therapies. So, for example, aspirin, low dose aspirin calcium are used in some cases in high risk pregnancies, for example, that we know have underlying high risk of developing preeclampsia, such as, for example, women with diabetes.
However, aspirin has been shown to reduce the incidence of preeclampsia, but mainly of early onset preeclampsia. So that is a low stronger for that. And not so strong for late onset preeclampsia, which, if you remember, actually consists of 90 percent of preeclampsia cases. Calcium is also used as a supplement for women who have particularly lower calcium level in the blood. So if they have normal calcium levels, it might not work so well if they have lower calcium levels. So these are two options that we currently have and a lot more is in development. And then what happens when preeclampsia gets diagnosed? There is high blood pressure, there is organ damage. Then all we can do really is symptomatic relief. So we give we can give women the potential to bring their blood pressure down. Magnesium can work well for that as well. Just to kind of get a get a pregnancy to term so that we can prevent this preterm birth, which is associated with complications.
And often we don't have a choice but to deliver the baby and the placenta, which in most cases would stop.
But again, there is that residual risk of future complications. So we've been working on this novel Treatment Strategies, which consists of using mesenchymal stem cells and they secreted vesicles which have a lot of beneficial effect. At this pre-clinical stage, it hasn't been tested in human, but it has been tested in various models of the disease. So Mesenchymal stem cells, are probably one of the widest used stem cells. Some stem cell type tech therapies at the moment. And there one of the safest stem cell therapies at the moment. Many clinical trials in different diseases have been carried out with these type of stem cells. They can be isolated from adipose tissue, placenta itself or bone marrow. And what we've kind of been realizing over the last few years is that these mesenchymal stem cells actually don't necessarily differentiate and form different types of cells, but rather secrete these vesicles called extracellular vesicles that contain all the proteins and microRNA and sort of all the genetic cargo that has all these beneficial effects and therefore can improve the anti genesis or can improve that vascular restriction that can happen in preeclampsia. It can reduce inflammation. And also it can act as an antioxidant as well, potentially reducing the symptoms and curing this condition in preclinical models of preeclampsia.
They have been shown to have a beneficial effect and to be able to induce hyper high blood pressure and an organ damage. And we have actually recently reviewed this in the current hypertensive reports. If anyone is interested, you can look at our paper on this.
So what happens after preeclampsia develops and the baby's delivered and preeclampsia, this appears, there's that residual risk of cardiovascular disease that women are.
That two out of three women will actually die from the future. So cardiovascular disease is the single biggest killer in Australia, but also worldwide accounting for up to 30 percent of deaths.
So women who have had preeclampsia after preeclampsia is gone and the baby is delivered a few years later, even within the first five years postpart, they have three point seven fold increased risk of developing hypertension and a two point two fold increase risk of developing heart attack, for example, or ischaemic heart disease and one point eight percent and one point eight fold increased risk of stroke.
So therefore, what we should be doing really when women have suffered preeclampsia in pregnancy, we need to make sure that we are following them really well more closely in the future and trying to prevent or delay or manage these diseases better. So there is surprise.
We have been working on this paper, which is also published in the study with collaborators from Queens University, Belfast and also Mayo Clinic, where we wanted to look at the overlapping mechanisms between pre-eclampsia, hypertension, and HFpEF, which is heart failure with preserve ejection fraction. It's a form of heart disease. So because we know that these women have increased risk of cardiovascular, well, cardiovascular diseases in the future, we don't actually know what the mechanisms are. Again, coming back to the molecular levels and understanding what happened so that we can actually leverage this knowledge and develop tests or treatments, etc. And we have identified about 30 different mechanisms that could be overlapping and therefore they are worth pursuing further and trying to sort of understand, understand these links better and develop tests, for example, or treatments for that matter.
But other work that we've been moving, developing in collaboration with another colleague from biomedical engineering at UTS, Dr Carmine Gentile. He's trying to develop cardiac spheroids and so similar to what we're doing with our placentas, developing mini placentas, he wants to develop hearts in the dish. So Dr. Gentile has this amazing platform that is capable of bioprinting, these cardiac spheroids, and they're shown here.
So it's, again, that they would represent heart tissue by using blood from patients that can be converted into stem cells. And stem cells are pluripotent so they can give rise to many different types of cells. And by using a patient's blood, for example, to develop and make these stem cells, we can actually then make these stem cells produce other cell types which are a main or key cell types within the heart. And these include cardiomyocytes, endothelial cells and cardiac fibroblast, these three cell types of very important within the heart tissue and cardiomyocytes in particular, they compose most of the heart cells on tissue.
So we mix these three different cell types in a tube, for example.
And then they organized themselves and formed these sort of heart, cardio spheric, mini heart tissue that we can then use to understand mechanisms again. Or we can test some treatments to see whether certain treatments were working in a certain group of patients or not.
And this is sort of just by using blood from women post preeclapmsia for example, post complications in pregnancy so that we can understand if they have any if they will have any complications. Future complications, cardiovascular disease.
And then when Dr. Carmen stained these cardiac spheroids, then you can see that they are there cardiacmyocytes are actually in the red and they consist most of these cardiac spheroids. And then the green on the cardiac fibroblast and the blue endiothelial cells. And they organize themselves very similarly to what we would see in real heart.
So it's it's an excellent model for trying to investigate the mechanisms, biomarkers, but also treatment strategies for women who are at risk of developing cardiovascular disease post preeclampsia, for example.
So in summary, what I've sort of tried to give you an overview of pregnancy and our research and what we've been actually working on in my lab with many collaborators. So we are working on a new test for preeclampsia based on a novel mechanism that we think we can leverage to potentially early diagnose preeclampsia or monitor women from early on in pregnancy. We have developed or we are developing actually the heart and placental tissues that are representative of the human tissue. And we are also trying to understand the mechanisms between pre-eclampsia and future cardiovascular complications so that we can develop better monitoring and treatment strategies for these women and working on new treatments as well to treat preeclampsia and pregnancy, which are related to mesenchymal stem cells and secretive visicles. So this work doesn't happen very easily, and simply, and by myself.
So a lot of collaborators are involved and students in this work and would like to thank them all for all their effort and excitement to actually work on these projects and many different universities and organizations here in Australia, but also abroad also involved.
So thank you for listening and for attending my webinar as part of the UTS Science in Focus events. The webinar will be recorded and available on this link.
So I'll take now some questions from the audience, is there any further questions.
Thanks Lana. That was a really interesting talk. And we do have many, many questions from the audience. First question came from two different people, very similar question from Dana and Pada. Are there any groups or subpopulations of people who are more susceptible to preeclampsia? And is there anything that can be done to prevent it
So the women with diabetes, for example, particularly with type one and type two diabetes, which has developed before pregnancy, not as a result of pregnancy, would have increased risk of preeclampsia. Also, some women with auto immune diseases or if they have chronic hypertension before preeclampsia kicks in. They would be at increased risk of developing preeclampsia. So in this in these women that we know, when they when they come in for their twelve weeks plan or early on in pregnancy to obstetricians, we actually, they would normally be started on aspirin.
Aspirin is the only really preventative treatment there is to potentially prevent in high risk women in preeclampsia. But again, it's not so effective. That is the problem or particularly is effective for early onset preeclampsia, preeclampsia rather than late onset preeclampsia. So what we are trying to focus on that. We're trying to just increase that monitoring in women using low-cost and remote monitoring. So just by monitoring the blood pressure closely and most women wouldn't because they wouldn't know or it wouldn't be at risk of developing anything, they could potentially pick up these changes. So it doesn't mean that everybody should be doing that. But if anybody is at increased risk, if they're tested and they have increased risk, for example, of developing preeclampsia, they should be monitored closely, for example. And that can that would mean that they could they could diagnose it and prevent complications and preterm birth. Also another another way of sort of trying to not prevent and to reduce the risk will be by not making sure that women do not put a lot of weight in pregnancy as well. So the weight is managed well.
Traditionally, it's been thought that, you know, we can eat whatever you want in pregnancy. But as it is, you can see from right from my talk, there are a lot of hormonal and metabolic changes and cardiovascular changes. So weight has to be sort of managed well, whilst obviously it has to be a certain amount of increased weight if it's too much. That's also not good.
Are there any ethnic groups that are more likely to develop diabetes or preeclampsia?
Yes. So generally ethnic groups such as, for example, you know, Aboriginal and Torres Strait Islanders in Australia are indigenous groups that they tend to have increased risk, not just necessarily of preeclampsia, but a diabetes in pregnancy and beforehand. And that could be sometimes linked as well to the increased risk of increased levels of BMI.
And also, sort of some genetic predisposition to and if there is some, there is a familiar link as well with preeclampsia. So, for example, if if a mother or anybody else in the family had preeclampsia in their pregnancy, then that could potentially be also a risk factor for preeclampsia in your own pregnancy.
We've got another question from two people that's very similar. And have you tested FKBPL in urine from pregnant women? And could this be done like a pregnancy test, or do you need to use blood for your tests?
So far, we've only done it based on blood. So we still have to obtain blood. We haven't really measured it into yurine. Right. We don't know if we can pick it up into your urine. Urine of course, will be the least invasive way of doing it. But because women are getting blood tests done for various things throughout pregnancy, especially a 20 week scan and 20 week checkup. Then it wouldn't be necessarily an extra as a blood sample, but it will be sort of part of the regular regular monitoring.
Do you think that the increase in telehealth due to COVID-19 will help encourage the use of apps like the ones you've described?
That's a great point. It has actually come, it's coming to light with COVID-19, they are really promoting the use of digital health and telemedicine. And in fact, they they they have acknowledged that as a service that that clinicians can actually provide and get reimbursed for. Which is a big step forward for digital health. In fact, and I think it is now is the time when it when we realize how important this is. I mean, just going by my personal experience when I had gestational diabetes in my both pregnancies. I had to go in every week or every two weeks and that would have required half a day off work and two hours travel each way and then two hours wait in overcrowded waiting rooms and areas just to see somebody for ten minutes. So I would much rather have done this from home whereas I can still be monitored by by a clinician and escalated if I neeed to be but actually sitting at in the comfort of my own home or even from work.
Do you think there could be any risk of over monitoring by nervous first time mothers if they can do it themselves in their homes?
That is very true. And that is one of the points that we have to acknowledge, is that I guess, as a limitation because everybody's quite nervous in pregnancy, especially first pregnancy, everything's going well, etc.. So, yes, there is tha, but again, clinical staff will advise what is the most optimal number of test or monitoring points that you have to report. For example, for blood pressure it could be twice a week for blood glucose. For women who have gestational diabetes or onset diabetes, they will have to monitor their blood sugar six or seven times a day. That's a lot of breaks and difficult. So it's just it is just how, you know, you have to do it whatever the clinicians actually advise you to do it.
We've got a question from Alison, and she wants to know how are microRNAs being explored in preeclampsia.
Are you focusing more on their role as biomarkers or their biological roles in the development of preeclampsia?
So whilst biomarkers are actually generally used as a test to predict the likelihood of a disease or to actually diagnose diagnose a disease. They also give good insight into the mechanism and why this is happening. So they have the most of the time they have biological role. In some cases, it could be just an association and not necessarily a mechanism of the disease, but a lot of the time there would be a biological link as well.
There's a follow on question from that, from Glenna, and she wants to know, would you be transecting cells with extra cellular vehicles containing specific microRNAs to promote or demote specific protein translation?
Yes. So what we do generally, we collect these extracellular vesicles from the secreted medium or mesenchymal stem cells. And then we add them onto the cells. But we can certainly manipulate the protein or protein or RNA, or microRNA expression, if we find that MicroRNAs will make these vesicles more effective. That is also possible to do before we actually put them on the cells and test them.
Another question from Alison is what is the reason for Proteineuria in preeclampsia? Is it due to damage of the kidneys or the blood vessels and the kidneys?
Sure. So proteins shouldn't be present in the urine. And so when the kidney actually filters all these proteins, it puts them back into the body, essentially. So if the proteins are present in the urine, obviously certain amount is OK. This is above an allowed amount then that can suggest that there is damage to the kidneys.
It could be many different causes of that. But it's generally the glemroical damage, which is the small cells or small cells within the kidneys which is due to many, many different reasons. But it could suggest kidney damage. Obviously, the kidneys are not actually filtering these things efficiently.
Any long term risks associated with preeclampsia for the baby and has a genetic link been observed?
Yes. So actually, everything that I've talked about, including the risk of future cardiovascular diseases for the mothers, the same risks are actually applicable to the offspring and the children as well. So there is increased risk of developing cardiovascular disease, diabetes, obesity, etc. for the offspring as well because of this, because fetal reprogramming, intrauterine fetal reprogramming that happens during pregnancy.
So we have a question here and it is whether the stem cells that you talked about need to come from the mother or whether they come from an anonymous donor. And then also, are stem cells safe to give to pregnant women?
So stem cells.
Actually, there's some evidence that mesenchymal stem cells in particular, that we are interested in, in women with preeclampsia. They have actually impaired function. So this is the work that has been done by our collaborators in the Mayo Clinic. In fact, Professor Garwich and her team, and they actually take out and extract these mesenchymal stem cells from the adipose tissue following the birth of the baby. And they have shown by characterizing the function of these cells, of these cells appear to have a different or impaired function. So hence that might suggest that it will be better to use a healthy donor mesenchymal stem cells from a bank, for example. And more so using these secreted vesicles from the stem cells will be an even better option in the future, because it is it will be a cell free therapy. So any risks or problems that are associated with this cell based therapies would then then disappear as well. Again, we are a long way from knowing exactly how safe these will be in humans, in human trials. But we are, there are a number of preclinical trials that are showing promising results.
Excellent. We've got a question here from Marilla, and she wants to know what is the difference between diabetes and gestational diabetes?
So gestational diabetes occurs in the second half of pregnancy. So women would develop it in pregnancy as a result of placenta secreting those hormones and the body not being able to adjust and generally disappears after the pregnancy is finished and the baby is delivering, a placenta is out, whereas other types of babies, such as type one diabetes and type two diabetes, they develop sort of outside of pregnancy in women who are not pregnant. And that's the main difference. Now, gestational diabetes can sort of turn into type two diabetes after the pregnancy is certain in sort of 30 to 40 percent of women who have had it or sometimes in pregnancy, the type two diabetes can get unmasked because of the tests and the stresses that the body's going through. That wasn't diagnosed before pregnancy. So that is the main difference.
We've got a personal question for you here. Given your knowledge about how scary the complications in pregnancy can be. Were you worried at all about having babies?
Absolutely. I was terrified in both my pregnancies, but I'm that kind of a person as well, I worry too much about things. Tt was a worry.
But I think you just kind of had to trust clinical staff and people who are monitoring me. I was lucky to go to the same hospital with my first and the second one so they have my records. And they they knew my history from the first pregnancy. So this was monitored closely because I had gestational diabetes in my first pregnancy. So I would certainly recommend that if you are changing hospitals to make sure they have the full history from the first pregnancy, for example. So I was worried and I just was hoping that the second one would be better, but unfortunately wasn't. So now I'm done.
If you experience preeclampsia and your first pregnancy, what is the probability in your second and subsequent pregnancies?
Great question. There is increased risk. So if you had preeclampsia in the first pregnancy, there is increased risk for having it in the second. Again, you have to, your clinical staff and people looking after you, obstetrics and gynecology, the staff from the antenatal clinic and other health professionals. They would, they should have that information and then they would, if you have any concerns, by all means, speak to them because they will manage it the best, in the best way possible. So there is.
What are your thoughts on the placenta's medical benefits post pregnancy?
And a very controversial field. A lot of it is unknown. So I really couldn't really comment too much about it.
Is their a genetic link to preeclampsia?
There is so I mentioned that I think earlier that if so, this is somebody in your family, your mother or aunt, would have had pre-eclampsia, there is increased risk. So if you are worried about a thing like that, to me, if there is I guess preeclampsia runs in the family, then you should most certainly speak to, speak to the doctor who's looking after you during pregnancy. And they would generally ask you these questions anyway as part of the first checkup. So speak to them and they will answer all your questions and concerns you might have.
Are there any treatments to be preeclampsia once you've been diagnosed with it?
That is the problem with preeclampsia, that we don't have sort of treatments that will cure the condition and that would cure sort of all these apparent processes that are happening and all these problems that are happening with the vasculature, with other cardiovascular effects. But the only option, once somebody is diagnosed with preeclampsia is to manage the blood pressure with antihypertensives. And there are certain types of antihypertensives that can't be used in pregnancy because they're dangerous for the baby. So there is an approved list of that antihypertensive drugs, which can be used for the margins of preeclampsia, but they would only really manage symptoms until the woman is ready to give birth. It's in the halls of strategy will be around trying to delaying that, prevent preterm or premature birth, really. So this is an area that certainly needs to be improved and researched more. And we have to come up with better and more effective treatments to actually cure this condition.
You mentioned that diabetes contributes to an increased risk of preeclampsia. But does it work in the other way if you have preeclampsia? Are you an increased risk of diabetes further down the line?
Absolutely. So preeclampsia increases the risk of future cardiovascular diseases, but also diabetes in both mother and offspring. So there is a risk. So whilst there is a risk for preeclampsia and general diabetes in adult life is a risk for future cardiovascular diseases is all intertwined and interlinked. And a lot of it is unknown. But certainly the epidemiological link between preeclampsia and future cardiovascular diseases such as diabetes has been established.
If apoptosis is reduced, preeclampsia, then will that impact on other disease states that are controlled by apoptosis?
So quite often. Again, this is under, under research and still a lot more that we don't know about it. But there is an increase in, you know, apoptosis potentially of trophoblast cells. So we are trying to actually prevent this from happening, whereas, for example, in some other conditions, such as cancer, we have tried to kill cancer cells. It's sort of the opposite of what we're trying to achieve here. Prevent that apoptosis.
How does nature or nurture influence gestational diabetes and preeclampsia? What lifestyle choices can help with dietary deficiencies that may contribute.
Sure. Very good question.
The gestational diabetes is very much, links to obesity and high body mass index. So there are some studies which have shown that in women who are at risk, for example, of gestational diabetes in general, for example, that have had gestation liberties in the first pregnancy, and they will be naturally at increased risk of it in the second, pregnancies, if they lose weight or manage weight better before pregnancy, and bring their glucose control within the required and desirable limits. That that reduces the risk in preeclampsia. So by managing your blood glucose and your body weight well and eating healthy and balanced diet, which allowed exercise, preventing that sedentary lifestyle, all of these things have shown to improve healthy outcomes of preganancy
Do you know anything about the implications of COVID-19 on a fetus's growth and development?
It's a very hot topic at the moment, and unfortunately, there's not much evidence coming through.
So far it has been reported that there is not necessarily an increased risk than any other pregnancy, but this is still to be confirmed and firmed up as more women, pregnant women actually have it. And we have better evidence to support these these findings. I mean, in terms of influenza, for example, influenza can be or for the flu, for example, it can be dangerous for the baby and the pregnancy and the mother as well. So pregnant women are encouraged to have their flu vaccines during pregnancy to prevent themselves in the flu. But in terms of COVID-19 so far, the reports are saying that it's not any more dangerous than the general population. But still to be determined.
You've talked about mesenchymal stem cells and they are different according to their different types of tissue, their stage and the proteomic or genomic profiles. So what types of cells were you planning to use?
So we've been working on in particular on bone marrow derived mesenchymal stem cells, bone modernized mesenchymal stem cells actually have been the most widely characterized.
And they're being used in clinical trials for patients with different conditions, not necessarily in pregnancy, but sort of outside of pregnancy for cardiovascular disease, respiratory diseases, etc. And they're sort of the gold standard ones that we will refer from. But a lot more work now is being done with the umbilical cord-derived mesenchymal stem cells. They're the second most popular ones. And then also adipose tissue and the placneta itself.
So far, we've been working with bone marrow. But we are planning to also use the placental derived stem cells in the future, research and articles derived stem cells as well.
Well, thank you for a brilliant talk today, Lata. And thank you to everyone who attended. So thank you again for joining us. And have a great afternoon. Thank you, everyone.
So Isaac Newton once said, "No great discovery was ever made without a bold guess." So this is supposed to be true for all the great discoveries that mankind has ever made in history. Fire was one of our first technology that humans have ever made, and it seems a long time ago since that was discovered, but what have we done with it? In the ninth century, gunpowder was discovered, and that set the preface for this modern-day rocketry for our space rockets. 17th century, smallpox was eradicated, and this was the first time a disease has been eradicated by human intervention. 20th century: satellites, spacecraft, internet. That led to 1961, the first launch into space. In 1969, this allowed for a man on the Moon. In the 21st century, nanotech, biotech, which is amongst the first discovery in the first decade. We're now in the year 2019 and right now we're on the verge of allowing us to allow gene editing to allow our bodies to be enhanced, to eradicate diseases, and for the first time in human history, medical and space technology are converging together to allow us to make plans and to realize visions to allow us to go and colonize, explore other planets. So for all those people here tonight that knows me, you know my vision is unlimited, and for those who do not know me, please allow me to introduce myself. My name is Dr. Joshua Chou, and if you indulge me, I would like to show you how I plan to change the world. So good evening, everyone. Thank you all for coming today to my talk, on tonight, on "Curing Diseases in Space." I realize a couple nights ago that the title might, can be interpreted as curing diseases that are in space, so if you're here for that talk, it's probably not the right one. So I'm actually here talking about curing diseases on Earth through space. Now before we embark on this journey tonight into space, there's one word I want everyone to forget tonight, and that word is the word impossible. The world is round, that was thought to be impossible. We want to fly in the skies, impossible. We want to reach for the stars, impossible. How many times in human history have the impossible been shown to be possible? And that is one word that we try to forget, especially when we're doing research in places like Harvard. The impossible becomes the possible. Like many of you tonight, you're here coming to this lecture because you're curious about space, the curiosity about space, the wonders of space, the impact of space, and more importantly, the mysteries of space, and like you, I'm also a sci-fi person and I love space as well. So it all started with E.T. trying to phone home, and I was actually thinking the other night, it's actually really bad luck for E.T. To have landed during that time because if he landed now he wouldn't have a problem phoning home. He would just go up to anyone, grab a phone, and he'll be able to dial home. But what I'm trying to say is that sci-fi has always been embedded in our society, whether it be in culture or in films, and often times, a lot of things start with sci-fi, but then it soon after becomes reality. So, for example, "Armageddon", you're talking about, whoops, oh, wow. Sorry, I just got this new one so trying to use it. "Armageddon" talking about the impact of asteroids and we constantly hear news about asteroids that might be hitting Earth. Life in another planet, are we alone in the universe? These are real questions that we've always been wanting to answer. "The Martian," that has been held as one of the movie that most depict the realistic space exploration. It's so real, when I was in Boston, I had to argue with my Uber driver that it wasn't a documentary, it was just a movie. He actually thought it was a documentary, I was like, "No, bro, you have to look that up. "It's really not." But it was so real it felt like a documentary. And, of course, coming I think in the summer, "Ad Astra." Brad Pitt is in it and they have proclaimed that it is the most realistic depiction of space travel. So you can see that the fabric of space and the mysteries of space have always kept humanity really interested in it. Just last month, the front cover of "Time" magazine, "The Next Space Race." So we've already know about the first space race and that was going into space, going to the Moon. What is the next space race? The next space race is really about colonizing. Landing on the Moon, colonizing the Moon. Going to Mars, colonizing Mars, and beyond. You can also see that no longer space travel is limited to just countries like the United States or China, but we have started to see the privatization of space. So space exploration is just literally on the horizon. NASA and everyone else also have their own programs and programs to go to Mars. And how are we gonna build the science, the exploration, the technology to send people to Mars and live on Mars? So it actually all started with Isaac Newton coming up with the universal theory of gravity in the 1600s. Little did he know that 300 years later that there will be astronauts floating on the International Space Station. Just like me, when I first started studying, little did I know that here tonight I'll be talking to you all about surviving and curing diseases in space. So the first man in space was a Russian cosmonaut called Yuri, and since then, 560 people have gone into space, but what we don't realize is that these astronauts, or cosmonaut, or the space travelers, they've been carefully selected based on certain criterias, whether it be physical, mental, and so on. But that is no longer the case anymore. With the privatization of space, these criteria are no longer limited to certain space agency for each country, but rather up to individual medical officers. So one of the most famous picture that everyone relates to in space is the floating astronaut. Things float in space, and why is that? And that's due to a condition called microgravity. So these are either people or objects that appears to be weightless, and the effects of microgravity can be seen, an astronaut floating in space, and so we all see it in a lot of picture. So what is microgravity? So when we drop something here on Earth, it falls to the ground and that is due to the effects of gravity which is 1G. When an astronaut drops the same object in space, it is also falling, but it's just that because everything is falling, it seems like it's weightless, and we call that zero gravity or microgravity. So for those of you who plays a bit of game, you'll know that "Angry Birds," you know, you shoot the bird, "Angry Bird," when you shoot the bird, it's also due to the effects of gravity. So everything in our solar system, whether it be the planets, us on the planet, is all subjected to the laws of physics and gravity. So throughout human history, things have changed. The environment has changed, human evolution has happened, genetic knowledge has changed as well, but the one thing that has remained constant is gravity. That has not changed. The world around us has changed, physical, chemical properties have changed, but gravity has never changed, and that is a very powerful thing because it means that in our genetic code there is absolutely no memory of adaptation other to the gravity on Earth. So this is very interesting and it presents a lot of opportunities for scientists like myself to conduct research in biomedical research, commercialization, or even just fundamental science, and also for space exploration. So let's start with the beginning of the journey for astronauts. They go up in a spaceship. So this presents a lot of medical challenges in space flight. So if you see anyone sitting on the chair going up into space, they'll be subjected to different forces in XYZ direction. So whether it be a push sideway or up and down. So we live in three-dimensional world where there's X, Y, and Z, and these forces are present on the astronauts as they go up into space. Of course, the effects of gravity or microgravity is dependent on how long the astronauts are actually exposed to the microgravity environment. That simply implies how long they're actually in space for. So this year, these three astronauts are going up to the International Space Station, and Captain Hague, he made a very interesting statement: Getting there is only half the battle. We're just started to study those experiments here on the space station to see how microgravity changes the cell function. So he's acknowledging that we have the existing technology to get into space, but getting there is just half the battle. We actually have to survive it, and what he's saying is that they've only started to look at how microgravity affects cell function, and this is exactly what I'm doing in terms of my research, and also this reflects on our technology in the last decade in terms of space technology hasn't really matched our research in terms of how microgravity affects cell function. So what happens to the body when you're in space? So under microgravity condition. So in the short term, there are some short-term effects. Again, reinforcing that there are differences depending on the duration that you're exposed to microgravity, you have a lot of different medical challenges and effects as well. So whether it be hours, weeks, or months, they'll have detrimental effect on the body, but what you are see over here is that the effect is either radiation, yup, okay. It's either radiation or microgravity on the right hand side. So microgravity plays an important role in the human physiology when we're in space. What is very interesting is that it takes about 48 to 72 hours for the astronaut to start to feel the effects of microgravity on the human body. So we all know the one thing that we correlate astronaut and space exploration is bone, the loss of bone in space, and that is because bone is a very unique tissue and organ in your body that is responsive to mechanical loading, and what that means, for example, when we always tells our kid to go out, run around, and exercise, those are mechanical loading. When we're middle-aged men like myself, we're asked to do more weights. As we progress in life, we're asked to do a lot of sports, that's why we ask people to do sport, because of those mechanical loading help our body to build muscles, tissue, and maintain homeostasis. And in case any one is curious, this is a real life picture of me. I just cut of the head so that you can really see my body underneath here. So just to clarify that. So if that holds true, that your body responds to mechanical loading to sustain homeostasis, then the opposite must also be true. In the unloading environment where there is no more gravity, where there is no more force in your body, what happens to it? And that's where we start to see the loss of bone. So you can see that the percentage change in bone density per month during space flight is about one to 1-1/2%. You lose that much bone when you spend one month in space. So that is why astronauts can't stay in space for too long. Obviously there are certain areas in your skeletal system that are not that susceptible to the loss, but overall, and especially in the back, the hip, and the other areas, you lose a lot of these bones. So this actually causes a lot of problem because you can imagine even if we have the technology to say we can go to Mars tomorrow, what happens when we get there and we can't function, our body can't function to its full capacity. We're not able to colonize, we're not able to do work, and that causes a lot of problem. So that's why it's becoming very important to develop countermeasures to predict what type of side effects there is from long-duration space travel. So this is where my research comes in, in terms of the terrestrial musculoskeletal problems. So just like astronaut losing bone, it's also very similar to a problem here that's already prevalent on Earth and that's osteoporosis. So there are also other types of bone diseases like bone cancer, but, personally, my area of research is in osteoporosis. So to put things into context, I would like to show you how I've worked through my career to get to where I am today. So I started my bachelor's at UTS in 2001. As I mentioned before, the beginning of 21st century is almost all biotech or nanotech. So I was one of those people that did nanotech because that was hailed as the future. Then I followed through with a PhD in developing biomaterials for bone tissue regeneration. So what that meant was developing materials. When people break their bone, how can we put new materials in there to help improve the fracture time and healing time as well. Then I did my first post-doctoral fellowship at UTS. Then I went to Japan as a a JSPS Postdoctoral Fellow, in which I developed drug delivery system for bone tissue regeneration. So that's enhancing the biomaterials by adding different drugs into it to see if we can increase and speed up the regeneration process. Now at that point in time, I was not happy with it. There was only so much materials on planet Earth, and it's only so much we can do about it. It was not enough to cure osteoporosis, so I wanted more. So that's where I met my supervisor at Harvard and I decided go to Harvard, obviously, not I decided, people just don't decide to go to Harvard, but I decided to pursue in getting into Harvard, and that took a year or two before I actually got there to study bone cell signaling. Now what that means is we're studying at the cellular level how cells communicate with each other. It's no different than us humans talking to each other. If we can't understand how we talk, then there's no communication. So it's learning a different language but on the cellular level. So in 2017, I came back to Australia and went back to UTS. So I just have to show everyone what Harvard looks like. So that's me and my baby over that, over at the Harvard Medical School, and then I also was fortunate enough to be awarded the Dean's Scholar over at Harvard as well. So just a little insight into what is osteoporosis, like why is so important and why does this affect so many people? It's considered a silent disease because you don't really know you have it until you fall down and have a fracture, you go into the hospital, and the doctor tells you that you have osteoporosis. Or else, there's no other symptoms that shows on the outside, so a lot people don't know that they have it. So what is osteoporosis? So in a healthy person, your bone remodeling, which means the building of new bone and the destruction of old bones is in balance. When you have osteoporosis, obviously you have more breaking than building, so that tips the balance over to the other side and so you have more destruction of your bone. Similarly, the other can be hold true is that you can have more deposition than destruction. So you can see from the top right image, you can see the bone density of a normal, healthy bone, and also in the osteoporotic bone. I'm part of the American Society for Bone and Mineral Research, and they made a survey and found that more U.S. woman die each year from complicational hip fracture than from breast cancer. So you can see that bone problem, fracture, osteoporosis, this is actually quite a detrimental disease that hasn't gain as much attention as cancer. So back in 2001, a bunch of scientists found a very interesting person, this guy over here on the right. He has actually a lot, you can see that his cranium, his forehead, is actually very bulged out. He has really big jaws. I think he's also blind and deaf as well. This came from a mutation in one of the genes in the bone that's called osteocytes. So I'm not sure if this one, no, oh, here we go. Osteocytes, so there are three main bone cells in your body: the bone building one up here called osteoblast, the bone destroying osteoclast, and the manager cells called the osteocytes. So you can see that this man over here, poor man over here, he suffered from a condition that has overexpression of sclerostin. So sclerostin is a marker that is only produced by the osteocytes. So when they found that there was a mutation in the SOST gene, it means that he's suffering from a condition in which it keeps building bone, right? So that's why he's suffering from, his jaw's really elevated, his cranium's out everywhere. So that's what the condition where his body is constantly just making bone and that is not being replaced by the destruction of the old bone. So knowing that, this marker was able to continue to grow bone. What happened was the pharmaceutical company, Amgen, and together with NASA and Harvard, together they developed a sclerostin antibody. What this means was that it blocks the pathway of osteocytes creating this protein, and from there, they did this test in space. So we know astronauts loses bone, so they want to test it in space and see what happens to osteoporotic rats models that they took up to space for two weeks, and you can see, you can see, so this is the region of interest, so this is the part of the femur, the area that they're looking at. So this is the control group, this is the osteoporotic group, and then this is the osteoporotic with the drug being injected. You can see from the statistical analysis that the one with the drug, the bone density matches those of the control group down here on Earth, and similarly on the other side as well. So this was actually very important because for the first time in human history, we've actually used space to cure a disease that is prevalent on planet Earth. So as part of that, obviously they went through a lot of clinical trials to confirm those results. And as you can see, as of April 2019, which is only four months ago, this has been FDA approved for treatment of osteoporosis and postmenstrual menopausal woman with high-risk fracture. It was approved in Japan in February as well. It's been hailed as gonna be the gold standard for osteoporotic treatment in the coming years, and it does exactly what it was supposed to do. It blocks the sclerostin production in osteocytes and therefore increases bone formation and while decreasing bone resorption. So this is a very beautiful case study showing the potential of using the International Space Station to not only study diseases, but also study the human biology as well. So you can see that what they did was use the International Space Station to do this early target and screening, and also the pre-clinical studies, and then following on with the clinical studies back on Earth, which eventually lead to commercialization. So this shows that there is potential for using the unique environment of space to really study what's happening here on Earth. So I was very fortunate to be part of that project, I was very excited by it, and to be able to contribute to it, but then it left me with a lot of more questions. So how does the body, how does cells actually respond to microgravity? Are there certain mechanoreceptors that cells perceive these forces and so what are they? What is the normal threshold for gravity that cells can function or tissue can function properly? Why do gravity changes cell response, and, more important, how do they participate in the tissue growth, organ growth, and regeneration? These are very fundamental questions that we have yet to have any answers of, and these could be crucial and important if we want to do things like tissue regeneration, organ growth, and so forth. Before we get any deeper, I want to introduce to everyone the concept that your cells is more than just a cell. It is actually sensitive to the environment, just like you and me on the outside, but at a smaller scale. Just like us, we love to go to the beach and do yoga, have a lot of space, and stretch out ourselves. I was one of the fortunate people to experience the peak-hour traffic of Tokyo train lines where I have to be stuck in one of those trains, and I'm a pretty big guy compared to Japanese standard, and I feel like I'm almost gonna die in there, and you can imagine they have to do that every day. Similarly, cells feel the same. If they have space to spread out, they're happy, but if they're crunched up together, they also want to die, and that means if that is true, then that also means that they can sense their surroundings. But how do they do that? So as part of my research, I look, I study a signaling pathway called a YAP and TAZ pathway, and it probably won't mean anything to you, but it's a very important pathway because every single tissue, and organ, and cells in your body is governed by this pathway. Just think of it as a center for transducing or translating those mechanical signals that happens to your body. So organ growth, when you're a baby inside the mother's womb, how fast it grows, how much it grows, have you ever wonder how does your body and cell tell when to stop or when to grow? These are all governed through this pathway. So that's why this pathway is very important. Now I look at it from a perspective of bone, tissues, because that's my interest and that's my area of study. So a lot of people ask me, "How did it all start? "How did you get from bone into this whole space thing?" Well, it wasn't one moment in my life, but rather it started with my lunchbox at Harvard. So even when you're at Harvard, even lunchboxes aren't safe. We started talking, we started to write down ideas, on just brainstorming how we can measure these mechanical signals in the cells. Then when I came back to Australia, one day while I was picking up a delivery from the delivery store, the delivery guy for some reason drew a spaceship going to another planet. I was like, "Oh, that's interesting. "How does he know I have this interest?" And finally, my research partner, Dr. Peter Bevry who's sitting back there tonight, was also an inspiration for me, and we've talked a lot, and we're just two crazy people coming up with idea. And so put it all together, we decided to follow this dream on seeing, understanding how cells perceive of the environment. So the ultimate question came down to how do we create microgravity here on Earth that cells can actually perceive and we can do experiments on it? So there are a number of strategy and one is a neutral buoyancy. That's not really feasible. Magnetic levitation using super-conducting superconductors. That one creates the microgravity. It's not feasible to put cells in there for a long time. And then the most popular, your parabolic flights or drop towers. So you have those comet vomits, also drop towers, because the microgravity that it can induce is only about three to 10 seconds. So for cell study, they don't respond that fast, so it does not fit what we want to do. So the only thing left is the random position machine, or the RPM. The RPM is not a new concept. It's not a new technology as well. See, other people have attempted at building these type of devices, but you can see that they're very bulky. They rotated the whole incubator. This one is just really gigantic, I don't know why. The closest one we could find was the Airbus one, and this has been built for the last, at least a decade, but no one has been able to use it because back then no one understand the concept of this, how cells perceive the environment, so it's kind of been lying there, kind of dormant, without people really using it while applying it to its full potential. For those people that are old enough, like me, who've seen the movie "Contact," that machine that they built, it also looks like an RPM, so I thought it was pretty cool. So I talked with one of my student who graduated. He knows he's a brilliant engineer. I'm a cell biologist, I'm not an engineer, so I can't make these things. So I talked to my student, "How can we actually build one of these "that fits the profile of what I need to do "in the laboratory to study cells?" So my student, Anthony, he went away for a few weeks and then after a while he came back and he made me one of these microgravity devices. So this is what it actually does. So you see that flask? That little flask with the blue lid? Inside there there are cells, and you can see that it's rotating on three different axes. And also here, down here, you can see that there's a graph. It accelerates at a certain rate and a certain angle that creates the microgravity that we wanted. What was really cool about what Anthony did was that he developed the algorithm so that we can actually produce the gravity from different planets. So that means we can actually mimic the conditions of gravitation pull from different planets and therefore study, and get a glimpse and an idea of how cells or tissues will respond under those type of condition. So last week me and Anthony were actually interviewed by ABC's "7.30" report. I think that's gonna be air either this week or next week, and he's also sitting there as well, so you guys can go take a selfie with him later. And so it was great. So we have this great device that can mimic microgravity. It's all good. Now I want to use it for my bone research, and that's great, but there was another question. So this was a point in time in my life where people around me started to also develop cancer. When I was a kid, knowing someone to have cancer was really, really, really rare, like you probably have to go to another city to even find anyone that might have it, but now fast forward 30-something years later, it's becoming widely accepted in our society to get different variations of cancer. So at my age, people around me, people I care, I love, start to either develop them or have the onsets of cancer, and that was, for me, that was not something I can live with. I'm a person of action and there was, but also I was very conflicted because I cannot restart a career looking into cancer research, and there are a lot of other brilliant people out there that do cancer research, so what can I do to help or contribute? So I thought about cancer. So we all know cancer starts of really small, like over here. So it starts out really small, and then it multiplies, and it gets bigger and bigger, and then it becomes so big, eventually it invades other surrounding tissue. That's a very basic model how cancer work. You also have to appreciate how well cancer can conduct modern warfare. It's no different than any types of warfare in history. You start of really small, you build a small base, you get more troops in there until you're so confident that your base is well-fortified that you send troops out to invade the rest of the country, and that is how cancer operates. So as I mentioned before, I study the YAP and TAZ pathway, and like I said before, it's preserved in all the organs in the human body. When I was at Harvard, even though I was working on the bone stuff, every single cancer-related research group there was studying how YAP and TAZ affect cancer biology. And then in recent publication, they've actually said that YAP and TAZ is the origin of all human cancer. So what that means is the ability for cancer to migrate in your body, that is also governed by YAP and TAZ. How it adapts to the environment once it gets there, that's through the YAP and TAZ pathway. How it multiplies and sense its surrounding, that is also through the YAP and TAZ pathway. So you can see that the cancer cell is one that is highly sensitive to its surrounding. So last week I had to actually go to my child's child care center to present what I'm presenting to you tonight, as I thought the best way to describe this was through Avengers. Thanos being the bad guy, the cancer, bad guy, and the superheroes are attacking him. We have in human history spent trillion of dollars in those years developing superhero drugs to combat cancer. And don't get me wrong, we've made a lot of progress, and they're very effective drugs, and they work to a certain extent, but, nevertheless, cancer still stands. We have yet to find any cure. We've done quite well, but we haven't got there yet. So the biggest thing in cancer therapy right now is personalized cancer therapy. So what that means is that we finally accepted that cancer are all different, each person's cancer is different, each individual is different, and therefore we cannot possibly make a drug to target different people with different types of cancer. It's just not possible. So now the big thing is about personalizing the therapy for a specific patient to a specific cancer. So if I say in this room everyone is different, right? You're all from different races, different age group, different sizes, and so on and so forth. There's no possible way I could develop a drug that can target every single one of you 'cause everyone's different, but I thought about it. Even though the individuals are different, the cancers are different, there's something that they all share in common and we all share in common. We all need to breathe, we all need to eat, we all need to sleep, and we all sense as well. So what if cancer also have these similar traits that they share amongst themself as well. So that led me to ask the question: Sp what happens if I put cancer in an environment where they can no longer sense each other? What happens to them? If they can't sense, how do they form a tumor? Can they still form a tumor? If they've already have a tumor, will the tumor disintegrate? Will it break down? These are really fundamental questions and yet no one has ever done it before. But before I can do that, I also need to have a good cancer model. So a lot of drugs and so on has been developed in the laboratory, but they don't hold up when it gets to the human body, and that's because of the different types of environment. But thanks to the UTS faculty of engineering, they were able to support us with a bioprinter in which I'm able to create an artificial 3D tumor model that mimics the biological environment. And this is one of the bioprinters. I'm printing little spheroids that eventually grows to look like these. So these are three-dimensional cancer tumor models, artificially created in the laboratory at a high-throughput production, allowing us to screen for drugs, and study cancers, and see how they work. So now I have both technology, a microgravity device and a realistic cancer model. So let's put cancer to the test. How do they hold up in microgravity? So I started off with a nasal cancer. You can see in normal gravity, normal gravity, these cancer cells are like this. After 24 hours in microgravity, there's less of them. That look really promising. Then I looked at ovarian cancer. So, again, you see a large population in the normal gravity environment, and a significant reduction in the microgravity. I'm happy with that, I kept going, breast cancer. Again, you see a large variety of cells, and after 24 hours, you have reduction in the cells and they look also different as well. So just what this tells me is that you have nasal, ovarian, breast cancer. Three different parts of your body and three different types of conditions, and yet all of them respond very similarly to microgravity in that they reduce in numbers and also in shapes and sizes. What was also very interesting is the surviving cell, cancer cells, if I return them back to normal gravity environment, after 72 hours they actually retain their full functions back. So isn't this really interesting? It takes an astronaut about 72 hours to adapt, to start to feel the effects of microgravity in space, and similarly, and then the opposite, it takes 72 hours for cancers to get its full function. So I don't believe in coincidences; there must be something there as well. So from this result, we looked at is the cytoskeleton a possible mechanosensor? So if you think of the cytoskeleton as a structure of the cell, it's no different than the bones of our body, so is this a possible mechanosensor? Are they sensing through their cytoskeleton? Maybe they are. So we dug a little bit deeper. So the changes in the cell number, is it because the cancer cells are actually dying or are they just, they can't fit, attach anymore, they're just floating around? What's happening to their cell cycle? So what we found was that, if you remember from high school when we did all those mitosis stuff? I had to go back because I forgot about it. You know how there's different phases of your cells on replication? So what we found was the cells were actually stuck in this G2 phase where they're actually unable to grow, and this is very interesting because just by using microgravity and no drugs at all, we were able to make the cancer cells not only come off, but they stuck in the state where they can not grow anymore, and this is very significant. So I wanna make it clear to everyone, we're not in it to create a miracle drug. I just don't think that's possible. But what we're able to do is to provide us with an advantage to coexist with current therapies and to make a more effective therapy for people suffering from cancer. The number one question, again, from people is, "So are you saying that if we have cancer, "if we fly out to space on say Virgin Galactic "we'll be cured of it?" That's not what I'm proposing here, and I've talked to a few ministers, they even propose, "Well, how about we build a big simulator "where we can put the cancer patient in there "and we spin them around?" I said, "That could be a problem "because the first thing that's gonna happen "is they're gonna vomit to death first "before anything actually gets cured." So that's not very feasible. What I am proposing is to, like the bone drug, into tricking the body, tricking the cancer, that it is in microgravity. So if they can sense the microgravity here on Earth, it means that there's some sort of sensory receptors that we can target and make it feel like it's actually out in outer space, just like virtual reality. It can be very convincing. So if we can convince cancer that it's actually floating in space, then how does it, it can no longer function and we can target it with current therapies and have a better much effect on them. So where do we actually go from here? So everything I've told you right now has been done in the laboratories. So this year I bought a new project called Project J.I.A., this is the patch, and what we want to do is actually conduct this experiment, in actually in space. So working with Airbus, Arlula, and Zertia, these are the first Australia companies that can help facilitate this type of mission launch, and the Airbus engineers will be coming to help us integrate with the air systems so that we can make a launch. Also I'm partnering with Harvard and MIT as well. Now when I say Harvard, MIT, I'm not collaborating with some young professors that just think space is cool. These are professors, these are well-renowned researchers, professors to be at the top of their game in the cancer field. These are people who you normally don't meet, and if you do, you have about five minutes of their time that they actually care to listen to you. But, yeah, when I first told them about my project, they actually gave me their complete support. So if I can convince professors, world-leading professors from Harvard and MIT, it means I'm actually doing, hopefully I'm doing something that's actually right. So what does this mission means? It's gonna be Australia's first research mission to the International Space Station. Now this is actually very historical because we, Australia has actually never launched a research mission to the ISS and this is gonna be the first one. Now initially I wanted it to be a mission where it's just promoting Australian innovation, Australian glory and everything, but I think that sends a wrong message, so that's why I partnered with Harvard and MIT, because I want this to send out the message that this is a mission for humanity and for all humankind. It's not just for Australians but for everyone that is on Earth. So in April, just a couple months ago, a company in the U.S. called Emulate, they also, too, started to send stuff into space, and to study brain, kidney, and lung as well on the ISS, and this how happens to be my supervisor from Harvard. It's one of his company, so I was a little bit upset that he beat me to it, but at the same token, there is no one else on Earth that can say that they're in competition with him because no one can be like him. He's just a person that thinks two steps ahead of everyone, so, actually, it's actually a good complement. It reinforces that what we're doing is actually really novel and, more importantly, impactful. So what are we doing as part of our Project J.I.A.? So what does it stand for? It stands for Joint International Astrobiology. So my friend calls it Josh in Action, which sounds cool as well, so either interpretation is fine. But not only is this gonna be Australia's first research mission to the ISS, it's also gonna be one of the most advanced cell biology study to be conducted in space. So there is not a lot of people in the world that has actually conducted this type of study in space. If you wanna send a satellite into space, that could be done quite easily, but what we're talking right now is sending live cells into space, that has to survive it, we have to maintain it, and we have to get them down back to Earth. So that adds a lot of dimensions of complexity and there are no current technology, so we actually have to build it from scratch. So luckily I have a lot of talented students that had helped me build all these new technology. And why is this the most advanced cell biology study? Is because if you look around, all the study conducted in space has been collecting samples upon returning. What we are able to do is to study the cells live while it's still in space, and that will give us much more accurate results and response than collecting the sample when it gets back to Earth. So we set a launch date to be somewhere in the first quarter of 2020, because launching a space mission is not as trivial as as one now says. So what will actually happen as part of this mission? So we've done the hard part, the developing the space module. We actually have to go to the United States 24 hours before the launch. We have to load the cells into the module. It gets launch, it goes to the ISS, it'll stay there for about 28 days, they'll return back to Earth, and then we process our sample. So you can see while this sounds really easy, it really is not, and then we have to go through a lot of rigorous testing and also regulatory approval. And for Australia to launch anything to the ISS, it actually has to get final approval from the prime minister himself because it's representing Australia. So it's not something that I just thought up and it'll happen. It actually has to go through a lot of process. So, in conclusion, I hope tonight that I'm able to give you a glimpse of what is gonna happen in the next couple of years in the space arena, especially in the space biology, space medicine, and space health care, and that the future for curing Earth-borne diseases might very well be found while conducting this type of research in space. So, finally, like I said, this type of project is not something that I can do by myself, but rather it's a collective work of a lot of talented people, so that's why I like to acknowledge and thank my past and current students for trusting me, having blind faith in me leading them into the unknown, and fortunately we have something to show for it. Also all the international partners that has worked with me to make this possible. And, finally, I would like to end, again, with Isaac Newton's quote, "No great discovery was ever made without a bold guess," and I hope that continues to hold true for moving forward, and I also would like everyone here tonight, if you'd like to follow us in our journey, into our space research, you can find us on Twitter, or follow us on our website, email us. And when I say support, it could be just even words of support. That means a lot to us to have those words of encouragement. We also have a Kickstarter if you're feeling, if you can support us financially, the students as well, that will also be great. So thank you very much, everyone, for listening and coming here tonight, and I hope you've enjoyed and learned something about space tonight.
UTS Science in Focus: Will coral reefs survive climate change? Professor David Booth
Thanks so much David and welcome everybody and it’s especially nice to see a bunch of old friends out supporters I guess you’d say. So tonight my role I guess is to not paint too much of a morbid picture of the state of the Barrier Reef, because it's still a wonderful place in this and fantastic diving and that sort of thing but to put these in the context of what's going on up there and what organisms that live there what options are they have, do they stay? Do they go? Can we can we repatriate etc so let’s just see if this works...
So what I want to try and get through tonight hopefully and certainly questions later will be welcome is what's going on up there and course I'm not going to summarise that fully in the next couple of minutes. I’m particularly interested in the phenomenon of coral bleaching which of course is very prominent in the news very few people don't know about it in Australia I would hope, and the bleaching response and how fishes might respond to this of course the charismatic and other tropical reef fishes are important fisheries for tourism etc and I what happened stuff and as David alluded were seeing him down here in that so I want my areas and some of the other people in the audience’s areas.
What happens to those fish that stay and suffer coral bleaching? Can they handle it and also what happens? Is there an escape from the reef to the extent that we might be able to save those horrible airfares and go diving in a coral reef off Sydney one of these days? So cast of important people here and others I'm sure I've left out that have a great deal of involvement in these sorts project and my project so I want to thank them at this early point and reefs in peril well I could put up 100 pictures of oceans and sadly there a lot of things to talk about here so we won't cover them all if I can just maybe go clockwise the top there you have the major ongoing issues of water quality so runoff from agriculture done poorly from urban areas out onto the reef and particularly during cyclones which is one of the other issues.
Sediment and whatever nutrients etc are absorbed onto the sediment get taken off shore and can really devastate areas. Federal government has pumped in lots of money into this and in fact there’s great gains and improvements in water quality in terms of what the farmers know and do in urban runoff.
Overfishing is a perennial a problem on the reef and you’d be pleased to know that 30 per cent of the reef is no take reserve a lot of people from overseas including my colleagues think it must be 100 per cent it's a national park isn't it but no it's only 30per cent but that 30 per cent gives a good foundation through reef fish recovery.
Sadly things like reef sharks are on the decline in spite of that so there are big issues with overfishing. Just human loving of the reef- the sepia picture over there suggests that that's an old picture we don't do the turtle rodeos anymore- gee they were fun but there’s lots of other issues with direct tourist impact, although tourism may save the reef as well, it’s an economic boom.
The crown of thorns sea star has been a problem for the last many decades, the eruption of this sea star, it’s amazingly voracious and it finds all sorts of coral delicious. It can attack a reef and make it look much like coral bleaching. We don’t know all the answers for the ups and downs of that, but that’s a big issue.
I put coal down there it's very prominent and it has many effects as we’ll mention in a minute. Coal export- what you've heard of the Adani plans that are going on up there, coal killing the reef is the headline there and coral bleaching itself and climate change and that's a global issue but you know where I suppose we are not really proud of the fact that Australia exports climate change the world through coal exports so for instance my wife and I who work on the Southern Reef were travelling up to the reef a couple years ago and this is not our picture but we certainly notice this I've been going there since 1978 that's 40 years and the port itself has always been a big industrial port but see the harbour looked like this a few years ago and now it looks like that a coal seam plant has been put there a huge industry there and of course it’s adjacent to one of the most wonderful parts the Barrier Reef so a bit of a handshake up there might help the country or destroy our beautiful Barrier Reef it's not too much politics don't worry I’ll save that till question time.
So focusing a bit more on climate change again there are many manifestations of climate change the ones I’ve shown you include the one probably most people know which is the rising ocean temperatures and our area here is a global hotspot as I'll mention.
Going down to the right here more intense storms they could be in the form of cyclones, we were just up at Hamilton Island and witnessed what was left of Hamilton reefs after a cyclone a year ago Cyclone Debbie but further down the coast as I'll explain also we have east coast lows that are bringing storms which can affect the fishes for instance.
Sea level rise can inundate areas that were otherwise not and finally one of the Insidious ones up the top, top left there is ocean acidification that is the CO2 to draw down from the atmosphere affecting the pH and other aspects of sea water and of course corals themselves calcified they sequester calcium from seawater and turn it into bone basically and it's interrupting that and the fishes have some interesting responses too.
I'll focus mostly on temperature right now so these graphics are quite depressing to someone who's been looking at the reef for 40 years and this is from work done by Terry Hughes and his team who is one of the year the really big names in in this were thinking open mind if we in the whole Reef through aerial surveys and diver surveys and the years 2016/2017 back to back big warming and bleaching years and as you’ll see there the northern sector up north of Port Douglas was massively affected with over 80per cent of the reef severely bleached whereas the Southern Reef where we do most of our work really really did quite well, it dodged a bullet and the reason for that was really nothing particularly special but it was a miserably cloudy rainy period when this all happened so by virtue of clouds I think that was saved this time anyway.
Interestingly if you were to go up there to the Southern Reef a lot more tourists are going there, the tourists are voting with her feet and of course word gets around, this is Toronto Star where this came from but obviously they took it from somewhere else, so the world now knows that a lot of corals are dead in the southern and northern reef that has horrible ramifications for our tourism industry. Of course we should acknowledge that there are other respected scientists that have a different point of view, there they are there, last political comment, and of course you’ll always get denialists because of course not everyone can get out to the reef but I’m here to tell you it’s in very bad shape for the north, recovery we’ll have to wait and see.
So my little friends the fishes, which I’ll concentrate on mainly for most of the talk, how do they respond? Well you can stay or you can go I suppose are two options. So a little bit of physiology I guess you’d say- cold-blooded organisms like fish respond to temperature very much so, so their metabolism basically goes up, they crank up as the thing warms up like a car warming up after a cold morning and so if you can see the little green icon there we’ve got temperature versus their metabolism measured by oxygen. Oxygen is used in respiration and you’ll see that the basal metabolism like the idle speed of the fish increases sort of exponentially, goes up quite steeply with temperature, cranks up. Also the maximum they can do, their maximum ability to respire or take up oxygen goes up but not the same rate it’s at a decreasing rate so inevitably you get the clash of the two where the two clash, the animal has no scope to do anything- to breed, escape predators to grow etc - bad news.
In the middle here if you can notice the difference between those red and green curves that’s a maximum aerobic scope, that's kind of where you want to be in the in that case, it's where the fish wants to be and of course what's happening with increasing temperature where up on the reef is that aerobic scoop is dropping away so fish aren't doing as well in general. For example just some of the outputs here, this particular little spinal damselfish, we did some work with this guy and as you increase temperature in a laboratory situation its reproduction goes to pot. The size of the eggs it produces goes down, the number of eggs goes down, and overall reproductive success drops away and that’s only three degrees which is not a lot.
I cherry-picked some of the other examples from the literature, this is a good one and basically it’s suggesting that once coral is bleached, a consequence of rising temperature, little prey fish like little ambon damselfish right here are conspicuous against the bleached coral and predators like the psuedochromis here have much less trouble trying to catch them and killing them so and so this curve here down the bottom shows survivorship which is you want it to be nice and shallow, is steeper for the bleach corals than healthy corals so there's a conspicuous element here as well.
And there's Nemo everyone wants to know about Nemo but sadly anemones which are related to corals also bleach and so there's a nasty white ones they’re supposed to be lovely and pink, and for whatever reason those fishes that are in the bleached coral don't reproduce or reproduce very poorly and this example above the blue graph shows a year of a non-bleached anemone and then the red graph shows the drop off of reproduction in these fish when there was a bleaching event so yeah pretty dire consequences for poor old Nemo.
Also fishes can do different things at different temperatures and this particular bit of work that we did looked at three species of damselfish. This one up here loves live coral and once the water was heated up experimentally it still loved live coral. However, these two down here are what we call generalists, they’re quite adaptable to a range of habitat whether they be rubble or dead coral or alive coral. However, when we warm things up this guy in particular all of a sudden got a propensity for live coral, so it became a specialist, which is all very well but coral is a thing you really not want to be a specialist in in the future warming world. This guy maybe a bit better, will survive a bit better in warmer conditions it seems to like rubble a bit more which there will be plenty of in future.
So all in all without going through everything what we’re expecting to see and this is a very recent paper come out by some colleagues up north, a homogenisation of reef fish, a loss of all the different interesting things, functional groups etc as the reef deteriorates. Now for the bad news, nah. And we’ve been monitoring corals and fishes at One Tree Island the University of Sydney’s research Island for 25 years now, by monitoring fishes and corals, transect simple good old-fashioned biology, noting where bleaching’s occurred, noting numbers of fish etc.
And back in 1998 we were one of the first people to look at the impacts on the fish of bleaching because people had been very focused on the corals which is reasonable and we found that on and One Tree Island at these particular sites, the yellow sites were nailed by bleaching the horrible 1998 bleaching and never recovered, the green did better or the blue did better and as you can see up here the red box indicates those in the sites and the black to the grey shows the drop in life, which is quite severe those sites. And then I guess not too surprisingly the fish responded, the baby fish didn't come in in great numbers at those same nasty sites, the adult fish of these species also dropped off quite severely.
Now the yellow one of the top as I mentioned that's expected that loves live coral, the thing that worried us with the other two fish, these two here really didn't really care for live coral, they could be found in any old dirty old rubble, they also declined and that suggests to us that bleaching has a general negative effect on reef fish in the area which is a bit of a worry. Without going through too many more details things are looking up at One Tree Island, I have to say, after the initial drop in the early years corals have bounced back to a certain degree and so have fish so we may be looking at a slightly better news story at One Tree than in the Northern Reef.
So also one of the things that we certainly put this in every single grant we write not very successfully mind you, is that this particular region of South East Australia, there it is, is well known as a global hotspot for climate change, so I guess it’s a bit of a pun but the fact is that the temperature is expected to rise to this model by the end of the century by about 4 degrees and nearly as much on the reef and so it's a good place to do this work I guess you’d say and to ask a question what are the fish going to do? What are they going to do? Follow Nemo of course so one of the options are for fish is to travel away from the reef. Now fishes have a baby that lives in the plankton and most of those fishes have the ability to swim in lava form quite a long way for instance those little guys which about the size of a, I’m going to say 5 cent piece, are they gone now? $2 coin about that size most of them are about that size or smaller have an amazing ability to swim in spite of drifting with currents they can swim against currents and so this little graphic over here pretty much shows that some of these bigger lava fish in experimental situations can swim without food for 8 days and go over 100 km in that time- you try that and therefore they have an ability to choose where they’re going to be to a certain degree.
If we do a little graphic like so we might find and we are finding we think that a coral reef fish that has a distribution potentially like so with that red core where most of them are breeding and the little dottie line out there where the larvae go to don't survive. We might end up seeing a movement down the coast and we think we are to a certain degree whereby while on the move we have a trailing edge the guys left behind and a leading edge the brave ones upfront much like any invasive species you could argue, cane toads and then maybe finally relocating South so without going into detail we might see different aspects of the population and we might be finding the poor old trailing edge right at the top of the thermal abilities are suffering as a consequence directional selection smaller numbers in breeding etc so that could be the fate of those guys so they could change quite substantially if they stay there. The leading edge on the other extreme again has its challenges it's got to adapt to new areas and new temperatures and maybe low temperatures that it wasn't ready for.
So a big review that a bunch of us did a while ago asked a simple question who's getting through and why and I won't go into those details, you can look it up yourself if interested but it turns out a range of fishes, about 360 species out of about 5000 species so about 5 to 10per cent of species have a vagrant stage as we call it that is they can move outside the reef and we looked at which sort of species, there were things that had big larvae and various other features be quite a few fish make it from the reef and in this case in our case we presume and we think we're pretty sure they come down the coast, it takes in about a month to get down there with the advantage of the East Australian current of course but also their swimming ability and of course they come to an area that's pretty different from where they’ve left and enter to little vagrant tropical fish hiding down there.
So there's 4 or 5 climate change related things on their side- first of all the current itself as I mentioned is strengthening it's well known to be strengthening and it will continue to do so because of that mainly the sea temperature is rising towards the poles and habitat destruction, I already mentioned about the demise of the habitat on the reef but the flip side of that is the habitat, the useful habitat is expanding and that's mainly because they love rocks without allergy they love urchin barons covered in the thin film of coral and algae with lots of shelter holes and that's increasing because of a sea urchin that’s coming from the north as well.
Here is an example there are many many others but you can see these actually beautiful creatures that have been arriving through as far back as we know and whether they persist in Sydney we’ll talk about. A little video here shot by David Attenborough, no, telling some of the species just very quickly a lot of the butterfly fishes associate with the locals that is very quick a little triggerfish, they often like urchins and that sort of area some surgeonfish, unicorn fish, Sergeant Major damsels someone pointing, that’s me I think and you see that's a tropical damselfish a chromis it's quite happily living out there and spends quite a while there again a little butterfly fish friend these are quite common in Sydney and get quite large and some over winter this little surgeon fish, baby topical surgeonfish, some issues with surgeonfishes I'll mention in a minute they can cause damage there’s a baby olive surgeonfish scattering away from my camera, a baby damselfish, a cleaner wrasse and finally an iconic Moorish idol baby swimming around and so there's quite a lot, a grab bag of really cool fish I guess you’d say.
Our work over the years since about 2001 is simply going out and counting the. There’s a lot of experimental projects associated with that but the skeleton is basic surveying and of course what we’ve found over the years is generally an increase in early summer so don't bother going out December you won't see much at all, but if you go out in February you’re liable to see an increase in these babies, they’re quite beautiful but unfortunately they stop coming as the East Australian current drops off and most of them die over winter very few survive at the moment and what it means is at least easily Sydney’s fish fauna nearly a quarter of the fish are tropical visitors and with potential ramifications for the local fish.
So what we’re showing just very briefly here is over the years we've been particularly looking at Sydney and Merimbula on the South Coast but other sites as well and those two sites have shown a cumulative increase in the number of species but a lot more in Sydney but there's still quite a few come down to Merimbula in terms of what's happening through time we’re seeing the last few years we have now moved about the noise level and I think we see an increasing number of species in both Sydney and in Merimbula which has seen a huge boost in the last few years which I will mention more of in a second so just very quickly teasing that apart a little bit which fish the damselfish are on the increase the butterfly fish pretty stable ups and downs importantly these with this group here who I call surgeonfishes some of those at least are capable of destroying kelp beds you might say in a phenomenon known as stopping tropicalisation and it's happened in other parts of the world and colleagues at the University New South Wales are looking into more detail at this but they're increase the last 4 years is a bit of concern for the local environment and oddbods this is a beautiful little Luna wrasse and it was always around but it seems to be increased in numbers and last few years, difficult to explain but a fact.
And overall we’ve seen anything to the right of this line indicates an increase and obviously it's been increasing certain tacks are increasing more than others and worryingly the Acanthuridae or surgeonfish is right up there. How is this happening? Well the obvious no-brainer is it’s to do with the East Australian current, they’re all coming from up there so one would expect a really tight correlation between the strength of the current which varies year to year and the number of fish and of course you don’t really get that, you get something so years that had higher East Australian current strength on the right should have had higher numbers of species and numbers of individuals, there’s something there but it just reminds us there’s a lot of other factors in play.
Once they get there, that’s Step 1, Step 2 is meet the neighbours I guess you’d say, so I’ll talk a little bit about that briefly and one of the interesting things is seeing some very interesting interactions and they’re not just keeping separate, they’re integrating and this particular butterflyfish has a propensity for this territorial damselfish which is interesting. Also unfortunately as the waters cool down as they do every year, these tropical fishes start feeling the pinch and so this particular one here, some experimental work we’re doing on how quickly the fish can escape a predator, so the bigger number is better and as you can see if you look at the black bar this is a tropical one here and this is a temperate they’re about the same they both have the same escape speed but once you drop the temperature which is the grey bars the poor old tropical just doesn’t do and you get picked up by predators, so there's still a few issues here with winter survival and winter survival that's we think is a major bottleneck to the populations establishing so we published some work a number of years ago looking at how many fish survive the winter vs the temperature across the state and was quite interesting that above a certain temperature around about 18 Celsius all of a sudden a lot more survive so I sort of call that a threshold winter temperature so if the winter temperature in Sydney maintains itself at about 18 we expect a lot of those tropicals to survive.
Here is some temperature logger data just to reinforce the point and you can see first of all Merimbula over here, unfortunately if you’ve ever been in Merimbula in winter don't get in the water it drops 15-14 degrees every year not so good for tropical fish but Sydney, luckily for us, is in a very interesting spot. Some years it’s below and some years it’s above in the winter at the water temperature and indeed in those years its above we see more overwintering. And projecting into the future we are expecting an increase this is winter temperature across time, Sydney of course is there, there's our magic red line above that we think they might survive, so Sydney is a very interesting area at the moment whereby some of the winters are too cold some are just right but with a trajectory like that we might expect in my lifetime to see a continual influx of overwintering of these little tropical which is very interesting. Whose overwintering? Mainly damselfish on the left hand side there but others. Is it increasing? We’re starting to see signals above noise and we’re starting to think yes there is an increase in overwintering, very low numbers at the moment. Who’s doing it all? Damselfishes the top guys there, they’re increasing in a jaggardy sort of way, the surgeonfishes are up and down but they’re the ones we want to watch because they’re the one’s responsibly potentially for destroying kelp habitat which we want to keep and fisherman would like to keep as well. Are they breeding? That's the acid question, well someone out here might have observed it in Sydney, I haven't seen it as yet.
This particular species are a likely customer this is a Sergeant Major damsel breeding in that picture up north somewhere I've seen them change colour the males would change a breeding colour and I've seen that happening so we might be set to see some breeding. When you think you've got it all licked and worked out as far as temperature along comes another climate change factor. I mentioned intense storms and east coast lows have battered Sydney, you might know of the one June 2016 this here is a nightmare photo for my risk assessment and this actually happened in Sydney and in fact my study site the idealic Cabbage Tree Bay was reduced to rubble and the little toilet block in there was completely destroyed and dispersed over my study site so luckily we had done a survey just before so as soon as we got out after still we went out and checked out who was still there. Insights they were very exposed and somewhat protected from that horrible storm and as you can see here exposed sites we had huge drops in numbers of the surgeonfish particularly really nailed and there were very few fish left out there afterwards and so that's very negative consequence but interestingly what we also noticed was a lot of this nasty old kelp which isn’t nasty at all but a lot of our fish don't prefer it was replaced by this delicious habitat.
Now the habitat itself includes bits of toilet block as well which they also like and so that restored habitat at least the next year we looked in that habitat vs the other habitat and we found lots and lots of our little tropical fishes in the blues in that new habitat of those of barrens and compared to the stuff outside so there was a negative effect of the east coast low and then the next year was positive it just reminds us that climate change is a little bit sneaky and we don't know all the answers. But of course it’s still not a coral reef is it it’s just a bunch of fish coming down.
This grainy photo is form a colleague of mine Yohei Nakamura at Tosa Bay in Japan, which incidentally is 34 degrees north about the same as Sydney is south. This is a shot from the 70s, late 90s, early 2000s and now. Rapid change over 20-30 years, from a kelp environment which the fishing industry love to a coral environment and as you can see quite beautiful so this is at a place like Sydney so will this happen here? And they found being a fish person, the southern fish that is the fish in the tropics, because of course it’s the other way around there, the current brings them up, increased and the northern fish including fish they like to catch disappeared so the fisheries dropped out of there but we've got some nice corals. Finally will we expect this? Not the flying car I'm guessing maybe the rest of it in future. Well it turns out this not so far-fetched, and if you look at this particular video here are done by John [inaudible] don't know if you are out there in the audience anywhere yes and you'll see it ain't a coral reef but it looks a lot better than than nothing and there's certainly corals there now growing off Shelly Beach in fairly exposed conditions, phosphorus corals that support fish, that fish like branching coral and this has increased in the last 4 or 5 years very beautiful indeed and more importantly supporting some very cool fish that we hadn't seen here before like the little guy in the middle here so you know it's early days but it could well be that we’re seeing a transition in Sydney, watch this space, sadly we might lose some fisheries species but we might see some interesting corals in Sydney maybe not a coral reef but potentially corals can move south so there's the answer I guess you could say for now and that's all I’ve got for you thank you very much.
Medical and Biomedical Sciences