Member Statements, the member for Windsor to come see. Good morning, Mr. Chairman. I rise today to bring birthday greetings to a dear friend of mine. Steve Sernick is turning 94 today. That's right, 94. He was born in 1926. Back in the days, we used to call him the Roaring Twenties. And Roaring is certainly a descriptive word that describes Steve for most of his life. He slowed down a bit, but just a bit, Speaker. If you're a new Democrat in Windsor and Essex County, you likely work with Steve Sernick on an election campaign or two. If the kids were tearing down election signs, Steve would be the first to scramble up a tree and put the sign up there so they couldn't get at it, Speaker. The member for Niagara Falls may have the best mustache in the legislature, but Steve Sernick has the best mustache this side of Croatia. It's a handlebar without the handle. It's big and bushy like the one you'll send me, Sam. The Looney Tunes character has it just droops down. All the better to match his ponytail, of course, Speaker. It's also a convenient way just to reach out very gently and pull him in for a big kiss. And, Speaker, I'm not ashamed to say I have done that on more than one occasion. His wife, Dr. Madeline Sernick, used to be an analyst on my old Percy's political panel back in the old CBC days in Windsor. So, Steve, happy birthday, buddy. I hope the next time to get together with you, we're doing shots of slivovits. Member Statements, the member for Haldeman, Norfolk. Yes, thank you, Speaker. And the days over the past several months have been tough for many and certain professions. We value and respect those essential workers who showed up and continue to show up. And, you know, Speaker, one field where challenges have been plentiful is farming. I know many people took to growing their own food this spring and summer, including myself, and it's not easy as it seems. And that's just on a very small plot. Imagine trying to produce and harvest food to feed many, many people in Ontario and across Canada. The pressure is immense. Weather, too much rain, then not enough. Pest and, of course, early frost is always something on a farmer's mind. And farmers, of course, are not immune to the challenges a global pandemic has presented. In my writing of Haldeman, Norfolk, labor-intensive agriculture is dealing with some of the strictest rules in North America for housing seasonal workers. I know my farmers cannot endure much more as they've been put in a precarious and unfair situation. They're clearly at a competitive disadvantage. And the risk, as well, is they may not be able to adequately feed the rest of us. Farmers don't ask for much. What they do ask is to be treated fairly. And, more importantly, they ask for support. We ask for support for our farm families who put food in our tables. Thank you. Thank you. Member Statements, the Member for London North Centre. Thank you, Speaker. Today I remember a great man who taught many about kindness, thoughtfulness, and life's second and third acts. Jerry Lehey was a wise soul, an impassioned writer, speaker, and devoted friend to many. Last week, he met his final rest. The loss felt in London is colossal. Jerry used his undeniable charm and zest for life to push for greater accessibility for everyone. After both his legs were amputated due to complications from diabetes, Jerry showed Londoners what life was like for folks in a wheelchair. He pushed to prioritize sidewalk snow clearing, AODA standards with teeth, and parking enforcement so walkways and bike lanes weren't blocked by cars. Jerry and I also had many conversations about insufficient ODSP funding. He felt that many years of government neglect were pushing more and more people deeper into poverty. COVID has only made these flaws more apparent. ODSP recipients hardly received any assistance during the pandemic and are struggling now more than ever. Jerry reminded us that ODSP recipients deserve to live with dignity and that we almost do our part to ensure Ontarians with disabilities are not left behind. He taught us all that if we don't look outside ourselves, we will never see what others need. Jerry, you are one of a kind and we miss you terribly. Thank you for sharing yourself with us. Thank you. Member Statements, the Member for Willowdale. Thank you very much, Mr. Speaker. I rise this morning to lend my voice in bringing awareness to a genetic disorder which affects thousands of Ontarians including in my community of Willowdale. Cystic fibrosis, or CF, is the most common fatal genetic disease affecting children and young adults in Canada and at present there is no cure. It's estimated that one in every 3600 children born in Canada has CF. The disease causes damage to the lungs, digestive system and other organs and in many cases leads to the destruction of lungs and a loss of lung function that is fatal in the majority of people with CF. Speaker from Onts, I have been meeting with members of CF community in Willowdale and representatives from Cystic Fibrosis Canada including Jennifer, whose 8-year-old daughter Allison is living with CF. Jennifer's daughter is often unable to play with other kids, attend school or enjoy many of the activities that make being a kid great. During this pandemic it has been especially hard for her to be away from her friends or receive necessary care. In September Jennifer and I met with Willowdale MP Alia Sassy to discuss ways both the federal and provincial governments can help approve and make available life-saving treatments for CF. Speaker, at the moment there is no proven cure for Cystic Fibrosis and I know that our government is negotiating with pharmaceutical manufacturers to make new treatments available in Ontario but we all have a role to play in ensuring that Ontarians living with CF have access to new treatments, the best care and breakthrough medications. Let's all work to help Allison, Mr. Speaker. Thank you. Thank you. Member Statements and Member for Trottles Centre. Thank you Speaker. Today is International Tenants Day, a day to highlight the challenges facing tenants around the world. This year tenants organizations are calling on governments to take action to ensure housing for all. In the fight against COVID-19, access to housing has become a matter of life and death. For those without stable housing it is impossible to isolate and as many tenants have lost their income and their jobs more and more people are struggling to keep a roof over their head. COVID-19 has compounded the housing and homelessness crisis that many of our communities are facing. Too many tenants are being renovicted, receiving massive above guideline rent increases and waiting decades on wait lists for affordable housing. Liberal and Conservative governments have let tenants down over and over again and have ignored the housing crisis for years. And now instead of helping tenants during this difficult time, this Conservative government has managed to take things from bad to worse. Tenants urgently need rent relief. They need a ban on commercial evictions and real rent control that's going to put a check on the sky-high rents we're experiencing in many of our communities. We need substantial investments in affordable housing and to repair the existing infrastructure of housing that we have. We need significant changes to the Residential Tenancies Act to ensure that tenants have faith that their landlord is properly maintaining their units.  Thank you. Member Statements, a member for Ottawa 7th. Thank you very much Mr. Speaker. Vision problems can really create a problem for young people when they're trying to learn. 80% of classroom learning is visual. So I remember in 2013 I was here in this building and an ophthalmologist said to me, we don't actually check children's vision in school anymore. I said that's not true. I found out it was true. And literally nobody was checking the box. Parents don't often see it. It didn't always happen in the physician's office. And it was a problem with the perception of perception. It's hard to tell when someone can't see. So I was pleased to be able to do some work as a parliamentary assistant to bring vision screening to schools in Ontario on September 2019. The Ottawa Public Health Unit started doing that. Now it's been pulled back because of the pandemic. It's really a critical thing. It can affect a child's brain development. So I just want to mention this to members in this house that once we get out of this pandemic, we'll have to refocus on this effort to ensure that every child has their vision screen before they get to school, go to see an optometrist, get the glasses if they need it. Thank you, Speaker. Thank you. Member Statements, the member for Stormont, Dundas, Southland, Geary. Thank you, Speaker. I rise to say to recognize the achievements of the Williamstown Fair Board for their centuries-long commitment to their community and especially for their dedication this September to hold again Canada's oldest annual fair, the 209th edition of the Williamstown Fair. On September 5th, the Williamstown Fair staged a wonderful experience by hosting a drive-through experience along with a horse riding and cap, dairy cap competition. It was gratifying to see the work put in by the many volunteers and resulting support from the residents. They were able to bring together more than a thousand feet of displays that everyone could enjoy from the safety of their motor vehicle. The Fair Board also collaborated with their partners, the World's Finest Shows, the Raising River Conservation Authority, and the Township of South Gun, Gary. World's Finest prepared cotton candy, candy and caramel apples to serve to visitors in each vehicle, while the Raising River and South Gun, Gary work together to give away free trees to the first 500 vehicles. This example of community spirit in these troubling times is what makes the riding of Stormont-Dundas and South Gun, Gary the special and strong place that it is. Thank you, Speaker. Member Statements, the Member for London West. Thank you, Speaker. I rise on International Teachers' Day to celebrate the amazing work that Ontario teachers are doing in the age of COVID-19. As public health experts emphasize the critical importance of physical distancing and gatherings of no more than 10, in-class teachers are in cramped classrooms with as many as 30 students, while rooms down the hall sit empty because of this government's stubborn refusal to reduce class sizes. Online teachers are grappling with challenging technology issues. I talked to London West parent Anna Foutt, whose two sons, age six and nine, are learning online. Anna says, we have every advantage. A mom who has flexible work and time to do IT support. Sons with their own Chromebooks who are being taught by brand new enthusiastic teachers. Yet they are all frustrated by provincially mandated digital tools and systems that do not work together by login and authentication errors that regularly reduce her sons to tears by unrealistic expectations that parents will download, print or reproduce worksheets, then upload or use a webcam if they have one to record the assignment. Speaker, this government had six months to plan for the safe reopening of schools. Instead they chose to ignore crucial public health recommendations for safe in-school learning and to flood schools with uncoordinated remote learning devices. We are profoundly grateful for the dedication and professionalism of teachers who are rising above the chaos and doing everything they can to help students learn. Thank you, Speaker. Member for Burlington. Thanks so much, Speaker. Every year Canadians buy over a billion batteries and according to Environment Canada only 5% of them are being recycled. When batteries break down in our landfills chemicals get into the groundwater and can contaminate the supply. That's why I partnered with Call to Recycle Canada's national consumers batteries collection and recycling program. I'm pleased to report that during two weeks in September, my Burlington office collected over 160 pounds of batteries. In addition, my paint recycling drive took in 872 cans of paint including 103 spray cans. Recycling paint and battery protects our environment by keeping hazardous waste out of our landfills and it's something everyone could be doing. Speaker, I'm pleased to be working with the non-profit electronic recycling association and the pediatric oncology group in a six week long collection drive. We're accepting used laptops, computers, monitors, printers, cell phones and tablets from now until November 6 at my Burlington office, Speaker. Electronic devices will be refurbished and provided to children undergoing cancer treatment. I want to thank the Burlington community for always stepping up and supporting these efforts. Thanks so much, Speaker. Thank you, Member Statements. The Member for Scarborough Center. Thank you, Speaker. And I just wanted to give a shout out to the Scarborough Rib Fest that happened a few weeks ago and was put on by the Rotary Club of Scarborough. We had over 2,800 cars drive through the Centennial College campus on progress so thank you Centennial College for lending us your parking lot and my family and I were one of the cars that went through and we went to Camp 31 which is a family favorite and got ribs, mac and cheese, chicken coming onions and funnel cakes with strawberry and ice cream and my daughter enjoyed her first Scarborough Rib Fest meal and she loved the sauce as she says the most so next year I really look forward to coming out with all of you Rotarians at Thompson Park and waiting in one two-hour line-ups in the blistering heat because let's face it that's part of the experience. So I thank you Rotarians so much for putting on this event this year and for ensuring that Scarborough still had this really great community event and it was really nice to see so many of your familiar faces so thank you for the work you did on the Rib Fest and thank you for all of the volunteer work that you do for Scarborough. I understand the member for Guelph has a point of order. Thank you Speaker, I rise with a point of order. I'd like to congratulate Anami Paul for not only being elected the leader of the Green Party of Canada Thank you but I also want to congratulate her for her historic election. She is the first black woman and the first Jewish woman to lead a major political party in Canada with seats in the House of Commons. Thank you.


Te uru kertu. Te ambisyon of this panel is not so much the rather easy gesture of thinking outside the box, but rather to collectively think through some of the consequences of that box that is the shipping container. The shipping container is an object or better an empty space into which a vast multitude of objects can be placed that is of enough interest in its own right. In 1957, the standardised shipping container has revolutionised not only shipping, but has brought international and intranational trade and with this the work and activity, the lives of other people into closer contact than was ever before imaginable. As you'll hear from the speakers on the panel today, the shipping container is vital in global supply chains and work on and off ships is a key locus of struggle in contestation of what we call logistical capitalism. Further, and perhaps less obviously, the shipping container is now widely used to home surplus migrant working populations and also bears its own quite specific box print in terms of its impact and the casualties caused with boxes moving across the globe. In some ways the shipping container is an interdisciplinary or what is perhaps better described as an interdisciplinary object. Brings with it a vast set of technical, economic, social and ecological questions. The character of this object is shared by a range of other objects that are of interest today from climate change, migration, oil, transportation, housing to finance, logistics and the algorithm, the technical and social composition of the present, and the future is radically calling into question the borders that were constructed between academic disciplines in the 19th century and were extended and expanded through the 20th. If the world today consists of relations, connectivity and flows, while the academy thinks principally in terms of discrete particulars, then this is an academy that has little to say about our world. This is a charge that weighs on the social sciences and the humanities that issue the technical as it does on the physical and technical sciences when they are unable or unwilling to think the social, economic, political and philosophical significance of their objects. Indisciplinary objects such as shipping containers do not call for networked teams of researchers bringing together the latest from each of their separate disciplines. Rather, they propose a fundamental challenge to disciplinary isolation as such and to the defensive postures taken by the presumably safe identity of the professor of this or that. They disrupt the identity and the local interests of the observer. And in doing so, they promise anew the prospect of science, science being, of course, only meaningfully a discourse without a subject, a language irreducible to the particularities of the observer. In this sense, the challenge of indisciplinary objects such as the shipping container and arguably most every object of which we've spoken today is that these objects call challenged disciplinary silos and radically challenge the separation of the scientific and best-gatter from other people. I therefore like to thank and to welcome my colleagues who have taken up the challenge of their disciplines and took themselves to speak today about the shipping container and its movements. Each speaker will take up one thing. Richard Leharon will speak about mapping and machining and thinking movements. Christina Stroud will speak about working on ships. Natalie Jacques will speak about resisting and striking against logistical capitalism. Francis Collins will speak about the use of shipping containers to house surplus populations and constantly about the impact of shipping on the most ancient mammals of our seas. In business, it's a common platitude to speak about the importance of thinking outside the box. It's just as well known in business that, as the saying goes, the easiest way to think outside the box is to make sure that the box is really, really small. I thank you then for being here and for my colleagues who are joining me in reclaiming what it means today to think big. And in asserting that this box and by extension outside of this box, many other apparently empty spaces today is even bigger than might at first be thought. And beyond this, we assert our capacity, this finite mortals to have the capacity to think big. Thank you for being here and welcome.


No, I always joke that they can't use video of me unless they use the Michelle Pfeiffer filter. But geez, Mary Claire did great, Helen Hunt, hats off. So inspired by the picture motif, I'm actually going to consider art as in some metaphors for really looking at big picture progress that we've made over the past 10 years. I was fortunate enough to be part of the celebration 10 years ago for the sequencing and it's just an incredible time to be in science. I just feel so lucky to be part of this now where we're able to witness these discoveries as we have over the past 10 years. I don't think any of us at the celebration 10 years ago would have believed where we'd be even today knowing how fast things were moving. So I am going to be talking about sort of at a 35,000 foot overview some of the things that have happened. Association studies via high throughput genotyping which I'll make the analogy to cave painting since people think that that's sort of like where genotyping is now. That's from exome and whole genome sequencing, maybe minimalism still at this point in time. Omics beyond DNA sequence, abstraction, a word that has many meanings and getting functional information using additional omics technology I think is a very important part of where we are now. Prediction, causality, heritability, I'm going to talk briefly about. Modernism is the metaphor I'll use there. And the more complete synthesis, mockingly, I've used the metaphor of postmodernism because of course we never really get there. We're always trying to get a real synthesis of the information that's being created to really use the discoveries to get new knowledge and it's always imperfect and we're always trying. So of course we spend a lot of our time now, people like me, doing the analysis of all the genome data, trying to relate phenotype to genotype and we started out of course with a lot of high throughput genotyping now, very old hat. The sequencing is of course a much sexier way of generating a lot of this data but I think we really have to move away from thinking of these as separate things. We need to think of this as just genome interrogation and at some point this will be done probably exclusively by sequencing but right now we have to keep in mind for the DNA variants that we already know about, genotyping is still a very cost effective way of getting that information and particularly from the informatics perspective, the data storage, data management, information extraction, genotyping is still very inexpensive in comparison with sequencing for the things that we know about. Sequencing offers us the opportunity to get the things that we don't even know about yet and there's substantial value added to that. Also our cave painting, we have learned a tremendous amount from the era of genome-wide association studies. As Eric mentioned this morning, we have a thousand fold more discovery for common diseases and related complex human traits. For those of us wandering in the wilderness before this era started to actually make discoveries has been an entirely new experience, a tremendous experience but the fact is that we haven't learned as much novel biology as we might have expected given the number of discoveries that have unquestionably been made and part of that is because the signals that have come out of genome-wide association studies tend to be from non-coding, the lead signals tend to be a non-coding sequence variation and we're often unsure even what gene is being implicated by that very reproducible and highly significant association. So when you don't have a handle on the gene it's hard to get a handle on the biology. Moreover of course we've spent a lot of time picking the cherries and that's the right thing to do. I mean it's the low hanging fruit, we need to grab every bit of it that we can but it's by really mining the data that we'll start to get a better understanding of the driving biology for some of these underlying some of these discoveries and the fact is, we're learning now as you'll see, we've got clearly orchards of cherry trees to pick. The things that have been highly significantly and reproducibly associated with common diseases and complex human traits to date really are the tip of the iceberg of what there is in even the genotype level surveys that have been done. So we're on now to minimalism, so whole genome and exome sequencing has really given us an unprecedented understanding of human variation. It's been dazzling to see this unfold, the things that Sarah Tishkoff talked about this morning, the evolutionary, our understanding of human population evolution and the importance of recent demographic events in shaping genome biology has really been a product of the ability to get an unbiased view of human genome variation and it's really been fantastic. As Eric mentioned, it's enabled a successful assault on the remainder of Mendelian disorders not yet ascribed to genes and that's ongoing and continues very productively. But of course, we're learning lessons that we weren't necessarily keen to learn about the effect sizes of rare variants contributing to common diseases and their associated quantitative traits. We might have hoped for larger effect sizes even for the rare variants and it's important to note sort of all of first generation technologies we tend to have not adequately addressed power issues because we don't know where to pitch in the first generation of the studies. And so you inevitably pitch too low, we don't have the sample sizes in the first generation of studies to make all the discoveries that will eventually come when we can put more sample sizes into this, larger sample sizes into the studies. But the fact is, with thousands to tens of thousands of genomes, at least exome sequenced for some common diseases, there are not rare variants with huge effect sizes routinely falling out and generating novel biology. When it does occur, we get outsized, we get disproportionate biological information because that information is coming at the level of genes and genes where we learn biology. And so whatever proportion of human disease will turn out to be driven by rare variants, there is huge value in getting that information because it drives disproportionate knowledge of biology. But of course exome sequencing, for example, has not enabled gene discovery for all Mendelian phenotypes or pedigrees attempted. And that's a message that hasn't necessarily come through in the literature but comes through in the meetings. So people will talk about these 50 pedigrees that they ascertained in the same way for this rare Mendelian disorders. And they've got discoveries in 20 or sometimes 30 or sometimes only 10. And part of that may be the capture. And we're learning how much more we get with deeper sequencing. But part of that may be more interesting and complex models than we've appreciated even for disorders that can look Mendelian. There may be multiple contributing loci in some cases. And of course, non-coding sequence variation can have big consequences, can lead to effectively Mendelian disorders. And so we will be learning more about that as we move from exome to whole genome sequencing on a routine basis. And as I say, exome sequencing, whole genome sequencing studies done to date have not been adequately powered to enable discovery of novel contributing genes and applications to complex disorders at thousands to even 10,000 or so cases and controls. Although in the follow-ups, novel discoveries are starting to be made. So again, we need to move beyond this first generation. The very first studies are partly underpowered because the technology is very expensive at the very beginning. As costs drop, sample sizes increase, and discoveries go up exponentially. So now our abstraction, the abstract art analogies, the advances in sequencing technologies are enabling a lot of additional omics technology. So people talked about epigenomics today. It's going to be an incredibly important part of future omics efforts in understanding and pinning down the relationship between gene and environment. It's one of the ways that the environment talks directly to the genome. Protein omics, it's not proteomics, but protein omics. Rich Jones likes to call it at the University of Chicago, assay through micro-western assays. In very high throughput, he can look at actually get protein levels measured in many different tissues. And the ability to really look at genetic variants associated with protein levels I think is a very cool thing telling us a lot of new biology that we hadn't fully appreciated from just the transcriptome biology, which everybody is more familiar with, and which I think is hugely important in allowing us to draw more nuanced inferences about the associations that we have made for common human diseases. And here I think the foresight of NHGRI to invest in G-TEX, the Genotype Tissue Exchange, is extraordinary. So this is an NHGRI-led effort, including many other of the institutes, to really develop tissues from many different parts of the body and then make that available for research. So a lot of the initial studies have been on the transcriptome, but there was just an RFA recently to enrich G-TEX with other kinds of technologies to really get more information from these tissues. The individuals from the studies are very high throughput genotyping and exome sequencing has already been done. It's not hard to see that eventually I wouldn't be surprised to see whole genome sequencing of the DNA samples from these subjects. But having many different tissues really provides a lot of additional information. So just a teeny bit of some of the results. So these are QQ plots from the Wellcome Trust case control consortium genome-wide association studies. One of the first generation large-scale genome-wide association studies published on seven different human diseases. And what I'm showing here are the QQ plots. So this is the expected number of P values at any given threshold versus the observed number. And what you see is that for, instead of using all of the SNPs in the genome-wide association study for this effort, they're using just the EQTLs, just the SNPs that are associated highly significantly in cis with transcripts estimated where this has been done from whole blood. And so you can see that for the autoimmune disorders, if you look at the scale here, you're talking about P values of 10 to the minus 100, 10 to the minus 200 for Crohn's disease, type 1 diabetes, rheumatoid arthritis, that's a huge signal from cis-acting EQTLs identified in whole blood. And you can take chromosome 6 out of this. You can take HLA out of it. And while the scale will come down some from the 50s and 100s that you're seeing, it doesn't come down much. There's huge remaining signal that you can pick up by looking exclusively at these highly significant EQTLs from whole blood. And nobody would be surprised at that for autoimmune disorders. They have done disproportionately well in genome-wide association studies. So consider hypertension, which is much less tractable in the context of common variant associations. In blue, we show the QQ plot for all SNPs. And in red, the QQ plot for only those SNPs that are characterized as EQTLs in adipose tissue. And you see a much stronger signal coming off the line fairly early. So you're talking about hundreds of contributory signals here for a phenotype that has been otherwise hardly tractable in common variant associations. So I think the opportunity to look at these functional variants across many different tissues is going to inform about biology in ways we otherwise wouldn't have been able to imagine, apparently. This is not true for all EQTLs. Adipose EQTLs are working unusually well in hypertension, and that may be telling us something important about the biology of hypertension. Causality, polygenic model and prediction, I also had put under the rubric of Impressionism. I think one of the things that we have been able to learn about sort of stepping away a bit from looking directly and only at the highly significantly associated and reproducible common variant associations. So the work of Peter Vischer and colleagues to say, okay, let's look at the totality of what we are learning from not just those highly significantly associated, but everything that we measure in large-scale genome study. Proportion of the inter-individual variability in liability to disease is accounted for by all of the variation that we measure. And so looking in this way allows us to get a completely different view of how the genome is contributing to disease and quantitative traits and makes clear that part of the heritability that we were worried about having missed is there. It's just hard to see. We just haven't pulled enough of the signal away from the noise of the very large volumes of data that we're generating. So now for many traits, we have not only the previous estimates of heritability from family and twin studies that we can consider, but what's sometimes called chip-based heritability or the proportion of the phenotypic variants that we can see attributable to all of the additive effects of the genome variation that is interrogated in the large-scale genome studies. So where, for example, in height, everything that had been identified and height was better than many because they could put very large sample sizes to it. For the first 180 or so loci identified as contributing to the inter-intervigil variability in height, that accounted for only still a small proportion of heritability. Everything that you interrogate in the genome when you look at height accounts for closer to half of what we expected to find, a little more than half actually. And so the next generation of these studies I think will be really interesting. I wanted to show a few examples, and of course heritability is a very old concept. And we have done it frequently in the past by just looking at the relationship of phenotypic similarity to genetic relatedness. And that's exactly what we're doing in these mixed model approaches developed by Visher and colleagues and extended by others. But here, rather than relatives whose genetic relationships are established, we're estimating the genetic relatedness from all of the markers in the genome. So I wanted to tell you just a little, draw your attention to some interesting kinds of second generation studies that these models allow us to do. So these data for Tourette syndrome and obsessive compulsive disorder were generated by the Tourette syndrome consortium and the OCD consortium. And because Tourette syndrome and OCD were considered to potentially have some overlap in the genetic architecture, the data were collected and put together at the same time. So they were intercalated on the same plates for the genotyping studies. All of the analysis and quality control studies were done at the same time in exactly the same way on all the same data. GWAS have been published for both of these studies. But when we apply the Visher et al approach, what you see is that the heritability estimated in Tourette syndrome for the rarest of the variants is both disproportionate and quite different from the heritability estimated for the rarest variants in OCD. This is not any possible artifact of data cleaning or data quality differences. The data were generated at the same time in the same way, all QC the same way. But you see a very different pattern between the two disorders in the proportion of all heritability contributed by rarer variants. Both disorders in a sense are outliers because for many of the disorders to which these models are applied, you estimate heritability that's largely proportional to the number of SNPs in whatever minor allele frequency class you're looking at. Here, there's disproportionate heritability being estimated in Tourette syndrome for the rarest variants and much less than you might expect and then is seen for most disorders for OCD. A really interesting observation that I think is going to be interesting to follow up. And this is true despite the fact that there's substantial genetic correlation that can be estimated for the two traits. That is in a bivariate analysis of heritability, there is evidence for a significant component that's shared between the two disorders. In bipolar disorder, again, second generation for some of these heritability sorts of studies, heritability estimated from previous twin and family studies for bipolar is in the range of .7, at least .7. Some studies estimated it to be even higher. Heritability estimated by CHIP studies, so in this particular example from the gain and the bipolar genome studies was around .35 and that's similar to what's been estimated, I think, in the Wellcome Trust data. And that's with about 600,000 SNPs being included in the analysis for the estimation of heritability. But for just 27,000 SNPs that are identified as EQTLs from BRAIN, you can estimate a heritability of .2, so almost 60% of all heritability that we can estimate from the entire genome can be accounted for by just a small number, a relatively small number of C-C-QTLs from BRAIN. And that doesn't have anything to do with there being some bias in just being an EQTL. If you take EQTLs from lymphoblastoid cell lines or EQTLs from muscle, you get almost no heritability estimated for that set of C-C-QTLs and it's about the same number as the C-C-QTLs estimated from BRAIN. So again, these are the sorts of things that can give us more information for prediction, more information for biological understanding, more information potentially to take forward even into the analysis of rare variation. Causality was also, it fell in my impressionist metaphor and remains a hugely challenging issue for rare variant discoveries in Mendelian diseases for common and rare variant discoveries in complex disorders. And the beautiful work that was discussed this morning and the stickleback fish. So with the pace the discoveries are being made and the number of discoveries are being made, it's just not going to be possible to get knockouts and knock-ins in every situation to really validate discoveries. And models are not always adequate. Even, you know, some mouse models don't work for human phenotypes. Some model, we just don't have model system models for all human diseases. And it can be particularly difficult to deal with causality when you have a single family or individual with a really rare phenotype. And a group, again, in efforts initiated by NHGRI has been working on a manuscript. It's been going back and forth. A number of members of the authors are in the room. Really interesting issues that remain under considerable and heated discussion even among attendees on how to think about causality in these contexts. And I think some of the lessons that we're seeing from insulin, a molecule that we perhaps know better than any other as it was one of the first human genes. It was cloned for obvious commercial reasons, has great value. We know with near certainty for any given possible insulin mutation, whether it has functional consequences or not, the assays are, and we have very detailed assays for looking at the function of the insulin molecule. So we have a huge amount of information. As you can see, many of the mutations, there are many mutations that are characterized that cause different kinds of rare Mendelian diseases that have diabetes as part of the name. Insulin is probably the central molecule for glucose metabolism. So the black indicates mutations that can in dominant fashion lead to permanent neonatal diabetes and the yellow recessive mutations that can lead to permanent neonatal diabetes. But you'll also see in the purple mutations that can lead to maturity onset diabetes of the young. So here we have a molecule that we know rare mutations can lead to Mendelian subtypes of disease that have diabetes as part of the name. And yet there are lots of variants, lots of mutations that have been seen that we know are functional, that we know have some function in terms of altering the functioning of insulin, some of these even altering the function of cells, altering other kinds of cellular function besides just the activity of insulin. And yet they don't appear necessarily to have, to impart any risk for garden variety type 2 diabetes when they occur in the individuals in which they occur. So, you know, we sometimes think, well, okay, we see a mutation in a gene that is clearly involved in some biological process and rare variants at this gene have led to Mendelian subtypes of disease, these rare functional variants must increase risk of, no, they don't necessarily. And so we have to keep these lessons in mind as we try to move forward in interpreting and making the distinction between functionality and pathogenicity. One of the things we've learned is that there's tremendously more variation in the human genome than we have appreciated in the past. And tremendously more functional variation in the human genome than we had appreciated in the past. But it's not necessarily the case that for any given disease or phenotype, most of the functional variation at a gene at which some of that variation can lead to disease will lead to disease. So that my last metaphor was postmodernism and getting to a synthesis, of course, is something it's just like you never reach the horizon. We're always trying to get there. I think some of the main lessons that we have for today is that we've got to consider what we have in its entirety. We need to do whole genome interrogation. And even when we've got exome sequencing, we almost always also have genome-wide association data in a lot of those same samples. And so we need to be moving beyond just genes into other functional units and using all of the information that we have. I mean, among the things that we're looking at now is the ability to take, for example, the polygenic predicted quantitative trait value against the observed and see if that doesn't give us better information for identifying the effects of rare variants and for identifying the effects of contributing environmental factors. So we need to use more, ideally all, of the available information simultaneously. We need to use all of the information on genome function, all of the information on common and rare and structural variation if we're going to pull meaning out of the genome for the things that put people into hospital beds. And of course, part of the postmodernism is the recognition that we have a huge issue with respect to computing over the genomes that we have now. And so at the University of Chicago, we have moved very aggressively into cloud computing. And we believe that this sort of cloud computing needs to be made available to the public community at large. And they've actually been able to become an honest broker, for example, for NCI and the TCGA project. And this is an open resource for the scientific community even now. You can apply to use the cloud at the University of Chicago to analyze TCGA data. For those of you who've tried to do that, there's a lot of data to download and you can basically then just move up into the cloud, not have to download anything and do your computes in the environment. And I think that is part of what we are going to need to move to, to really integrate genome information into further discovery work. So I'll take questions now. These are the people in my lab who work on all of these things. The Tourette syndrome, nitty gritty analysis group. And while I take questions, if I can, I'll show you some pictures made from billions of bases. We're going to have this up on the website for my lab. You'll be actually able to take sequences. And I hope sequences of your choosing, like any given gene, any piece of your own genome and photograph, it works better, it works much better with high resolution photographs and see your genome in action. So happy to take questions. Putting together all these individual pieces of information, baby pointillism is a good metaphor. And the other question was, do you think that the reason for Mona Lisa's enigmatic smile is that she understood causality and... I would like to think that. I mean, you know, she has two X chromosomes, so it would be a good thing. I think that the genome integration, so not just integrating everything we know about the genome, but going across theomics, is really the next frontier. We have to do that. And I think pulling together the information will hugely enhance prediction, which is something that we haven't spent as much time on, because for a while we thought we couldn't do it. For many disorders, prediction would be a huge thing. We talk about the diagnostic odyssey for these kids. People with bipolar disorder, on average, spend seven years from the time they first start seeking medical care for this condition until the time they're diagnosed and treated properly. Seven years where they're going from specialist to specialist to specialist trying to get some relief. If we had the ability to do good prediction with genomics and or other kinds of omics, I think we could, you know, you'd like to think we could cut short that diagnostic odyssey, offer relief much sooner, and save a lot of health care dollars. I mean, I think there's a lot of opportunity yet for prediction. And importantly, this will come back to the ELSI, because we didn't think we could do it, we may not be so prepared to be able to do it now. And this is an area where I think we need a lot more research. Yeah, I'm a big fan of the mixed models and all the stuff that's come from animal breeding and plant genetics into this. I think they're great. But I do worry in a case control scenario, it's not quite the same. It's not kind of a closed system. There's some confounders and some ascertainment problems that could really bite us in this. And so it's not like I don't think it's a good thing to do, but I'm interested in your response to how do you deal with, especially in the rare variants, you know, the difficulty of case control ascertainment in this. Yeah, so I think it's not perfect and it's clearly less perfect in dichotomous phenotypes, particularly in a case control situation, where of course, rather than a cohort situation where you've got the whole thing. On the other hand, you know, for example, in the particular comparison between Tourette and OCD, there you've got exactly the same genotypes having been generated in the samples at the same time, on the same plates, QC the same way, and clearly a very different inference on the contribution that variation in different minor allele frequency classes are making to the inter-individual variability in risk of those diseases. And I would be much less confident about comparisons in other contexts. But in this context, these data were generated in order to be analyzed together in exactly this way. The fact that you see such a difference between the two disorders, but also between those two and many others that we've looked at, where the inference is very straightforward, you see about the same proportion of heritability in each minor allele frequency class that you expect based on the number of SNPs in that class. So I think we will see differences among disorders, and this is what I mean by we didn't learn a lot as we rushed through picking all the cherries, but as we go back and focus more, look at these data in more kinds of ways, I think we will learn more important things about genetic architecture, about driving biology.


There is a lot of evidence that recent warming of the planet is caused mostly by human emissions. This evidence is so strong that an overwhelming majority of climate scientists accept that the warming seen since 1950 is mostly man-made. However, there's a certain climate change myth that chooses to ignore all this research. The myth claims that the recent warming is just a continuation of natural processes that enter the little ice age. Here we'll see that the evidence shows that natural factors were indeed important to begin with but since 1950 human influences have become dominant. First, what was the little ice age? Well, it lasted from about 1450 to 1850 although some scientists think it started as early as 1250 at the end of the medieval war period. Just how cold was the little ice age? In Europe, Central Asia and North America the average temperatures are now 1°C that's about 2°F higher than the temperatures that prevailed during the little ice age. This warming might not seem like a lot but it has been enough to cause the majority of the world's glaciers to shrink. Most of the rest of the world has warmed up since then with the exception of small areas that are slightly colder than they used to be for example, off the southern tip of Greenland. Glaciers advanced during the little ice age, not only in the Alps and Rocky Mountains but also in New Zealand and the southern Andes although the exact timing of these advances varied but after that as the cool period ended glaciers nearly everywhere started to retreat. The little ice age had its best known historical impacts in Europe so mud weather patterns in North Atlantic made the already cool climate there even worse in some years. There were some bitterly cold winters and there were also some very wet years that led to crop failures and famines. Famously, river Thames in London froze over and frost fairs were held on the ice. Despite cold average temperatures the hard freezing in the Thames was still a rare event it froze over thick enough to hold a frost fair just 21 times in 300 years. What do we know about what caused the little ice age? First, small changes in the tilt of the earth helped cause a gentle decreasing trend in temperature over 5,000 years. The rate of cooling was about one-fifth of a degree Celsius that's about one-third of a degree Fahrenheit per thousand years. The little ice age occurred towards the end of this long slow decline. It ended when temperatures started to go up sharply after 1850. Second, there were at least two large lows in the output of the sun which we call the Spira and Monde Minima. Third, there was an unusual number of really big volcanic eruptions that through small particles highens the atmosphere. These acted like little mirrors that reflected sunlight back into space and cooled the earth for a year or more afterwards. An example was the huge Mount Tambora eruption in 1815 which caused what came to be known as the year without a summer. Scientists are not completely sure about the exact size of the cooling effect that volcanoes and solar lows had on the earth but even so, a range of calculations for the northern hemisphere shows a very good match with what the evidence suggests the temperatures were. Researchers estimate the temperatures of the past by analysing records like tree rings, ice cores and the growth bands of stalactites in caves. In this graphic, the red and blue lines show the calculated values and the grey shading shows the range of reconstructed temperatures. The long-term trends match very well including following the rapid upward trend into the 20th century. Volcanic eruptions and solar variations carried on after the little ice age but they were generally smaller and were dwarfed by ever bigger human influences. More people and growing industries produced more and more greenhouse gas emissions. This graph made with the data taken from the recent IPCC report shows the relative importance of volcanoes in black and the sun in green as well as natural variations which are shown in orange. These variations are mainly caused by fluctuations in ocean currents like El Niño. Note that the natural factors sometimes cancel each other out and they do not show any lasting trends unlike the steadily climbing human influence which is shown in red. When we add together the natural and human factors and overlay the natural variation as the faint background that jumps around we can see that it would be hard to distinguish a clear separation between human and natural causes before about the 1930s. Now let's compare these factors with the thermometer record. The monthly temperatures are shown here as a grey wiggly background and a smooth version of this is shown in black. The match is good when we look at all the factors combined but it's terrible if we exclude the human influences. Back in 1914 it would have been possible to argue that the recovery from the little ice age was almost entirely natural but now, 100 years on, it's clear that humans are playing the major role and by far. To claim that what was once arguably true 100 years ago must still be the case today is to introduce the fallacy of jumping to conclusions which is to say that just because a factor was once significant does not mean that it's still important. Times changed and over the past 100 years human influences on the climate have grown enormously and they continue to grow. They are now the main factor causing the warming of the earth.


Hi everybody, it's nice to be back with you on this Monday for our daily briefing and on our Facebook live. Today, I want to give you a couple of numbers and then just make a couple of points about the weekend. Today, there are 52 active cases in Fort Worth and three recoveries. That's up from 41 on Friday, but it's not at all unexpected. We knew the numbers were going to climb some. Hopefully, we'll get up to that apex shortly and begin to flatten it because I want to thank you all who are sacrificing so much and who are following the recommendations that we have in place right now. I know the weather was beautiful this weekend. I had a chance to be out on my bicycle, my husband and I. We were six feet apart and we tried to stay that far apart from everyone and many of you are doing that and many of you really want to be out and about with your friends, but remember the safety of our entire community depends on how close we practice the stay-at-home order. You could be contributing to the spread of this virus even if you don't have symptoms or if you're just beginning to feel those symptoms. We can stop it and we can slow it down and we can prevent our hospitals from getting overrun. And that is one of the first and foremost. Even if you aren't at risk of having COVID-19 and most of us all, our loved ones could be and you certainly don't want that and they would require medical attention or potentially a family member might have a broken leg or some other medical event and if the hospitals are overrun, they won't have the treatment. So everybody, let's take this seriously and let's try to wind it up sooner rather than later. I'll make a note that over the weekend, we got lots of messages about basketball courts and volleyball courts and how many folks were owned those playing basketball and playing volleyball. That's not really social distancing. The City of Fort Worth Parks and Recreations Department made the decision today that they would be closing basketball courts and volleyball courts. The nets at both will be removed to keep people from being there. There are over 100 basketball goals in our park systems and those will be removed and I don't know the number on volleyball but the volleyball nets will be removed. We take no pleasure in having to restrict your use of those courts but when they get overrun with kids and adults, we just simply can't risk the spread of COVID-19. You got to take it sooner. You got to take it seriously folks so sooner or later we'll begin to stop this and we can all get back to our freedoms. But today I've got a little bit of happier news. On a good point, I've got Cara Waddell, the CEO of Child Care Associates with me, to announce something that a press release went out on earlier today. You will really find this amazing. It's called Find and it's about finding child care help for first responders and for medical professionals in this crisis who often need to work long hours, additional shifts, and many times into the night. We simply need it to come together to find them the resources for child care. So Cara, would you like to join us and talk a little bit about Find? Welcome. Well it's a pleasure to be here. I'm Cara Waddell again with Child Care Associates and I'm here to give some bragging rights to child care programs today. Child care in Fort Worth, Arlington, and Tarrant County have remained open to provide child care to the children of essential workers and we're really pleased today along with Mayor Price to announce Find, a feature to support our essential workers. And so basically parents employed by essential businesses during COVID-19 can now access on their mobile phones or on their computer a searchable engine to find an available child care program near either your work or your home and then search to see immediately if your age of child is going to have an available child care slot. And we're very excited. You can you can visit find.bestplaceforkids.com. Again, find.bestplace number four kids.com. And parents who are deemed essential workers during the COVID-19 response can easily search and find available child care on their mobile devices. So as of Friday we have 50% of our licensed child care programs open and over 7,700 available child care slots. And Mayor Price I know you know since our community is committed to becoming a best place for kids we have rallied in the last few days and we've built a platform that today serves the need of essential workers but tomorrow can help all Tarrant families find available child care. So again all essential workers in Tarrant County can now go to find and find the free child care tool at find.bestplaceforkids.com. Now for our community's hospitals, first responders, or agencies with essential workers you're welcome to call us at child care associates on our main line at<PHONE_NUMBER>. And we'll have a specialist work directly with you so that you can identify the child care assets in the vicinity of your hospital or other locations. We've got one other announcement as well. Tarrant County, along with the cities of Fort Worth and Arlington have released guidance and recommendations for our child care programs that are open and operating. So this was emailed to all licensed care this afternoon and we have shared this also with your child care mentors. This will work to ensure that no classroom exceeds a total of 10 children or adults as well as give guidance on basics like disinfecting toys and classrooms and physical distancing. With toddlers we don't social distance but we're trying to keep the space it's a hard thing to do. So lastly let's continue to support our essential workers many of whom have young children and we want to make sure that your children are healthy and safe and learning.  And I'm thrilled that we're able to support working parents by making this available as well. So Mayor Price we're excited to make this possible. Very exciting. Great. Kara, thank you. It's really exciting folks and when we come out of this crisis this tool will still be available and be expanded. I do want you to know we visited earlier about this these are licensed child care providers. These are not just people who came on board and agreed to do child care. These are trusted vetted child care employees.  A lot of time is going into this 1200 hours, Kara, correct? Kara's nodding her head over there. And how about that? They got the program up and running in a little less than two weeks. All typical Fort Worth people come together when we have a crisis. I just want to thank you all for tuning in and listening to us daily for being with us. And once again I want to thank our first responders, our medical professionals and everyone at the EOC who's out there working on your behalf and keeping you stay. So y'all stay safe, y'all stay healthy and y'all stay home.


Sorry for the inconvenience, science problems. So, okay, nice black screen, very interesting. Does anybody know what's going on? It's passing here, but I don't know. Yeah, yeah. Okay, cool. So the first thing I would like to tell you is about this interesting equations on the screen. So we'd say that the first is Faraday's Law of Induction, the second is Faraday's Law, and so on, and so on, and so on. And by that time, some years ago, I was into a electromagnetism class and the professor came in and said good afternoon and started showing these equations as if they were extremely natural for us. I mean, for me it was weird. So what's this triangle and what's the sign? So how many of you had this weird experience of learning things like this without context? I mean, how many of you had at least one experience like this and it was totally frustrating? So I see many people here who had frustrating learning experiences. I don't know if it was intentional, but I might talk right after I talk about teaching kids, but I'm talking about teaching adults, which can be frustrating too. And this can lead to three different reactions.  You can feel totally lost like this panda, or you can feel like I'm in the right place, or you can feel delighted. Maybe some people can understand at the first glance, but it's not everyone. So I'll quickly talk about what I do. I am a developer. I like all of these extra things in my free times. Organized meetups like coffees and gifts. This is a quick disclaimer. I know that we are from different place of the world. So for some of you, education might have been different. I know some people in Norway and Finland had a totally different background from mine, but I have some friends in the United States and Europe, and we had a similar background when we talk about learning and learning, especially science, math, physics and so on. So if you don't share this experience, just be aware that I'm talking about some examples that I have lived and some of friends have lived similar experience too. So why I'm talking about math and physics? I don't know about your graduation course, but I studied engineering and I had all these subjects related directly to math and physics. Did you have similar subjects? At least one or two? So some of you had similar subjects and my learning experience for them was a bit frustrating. I mean, yes, they were okay. I had nice professors, but they rarely contextualized me about what I was doing or why I was learning that. And that became really sad and scary. So every time I was in a calculus lesson, usually most of the professors came, said good morning or good afternoon, and they showed us some crazy equations and I always asked, why? Why are you teaching me this? Why do I need to know this? Shouldn't I be writing code or why do I need to solve this equation or where I am going to use this? Have you ever made this question to yourself when you learn something? Even for a framework, sometimes you ask yourself why I'm learning this or why I'm learning this into this way? And anyway, I usually had bad experiences. I was almost expelled of some classes by asking this, but still I kept these questions. I think they are very useful. So most of my professors and friends, they really provide context of what was going on, why I was learning that. So this made, I mean I was really frustrated by that time. And sometimes this lack of context confuses us. Think about yourselves. How many times you tried to learn something and you got totally confused. When this happens, we are human beings and especially if you don't have a context, like sometimes someone starts a conversation and you don't have context and you get into the middle of the conversation and you understand totally wrong. This happens. This happens with math and physics too. So it could also motivate us. How many times have you heard a friend saying I hate calculus? It's horrible. Sometimes I open Instagram and I search for the hashtag mathematics and move us then like I hate math. And there is a giant list of homework and someone posting photos of the list and saying that hates math or same for physics. It's scary. Statistically the number of hates associated with math is higher than love associated with math. Why? It's such a beautiful work. And then something word started happening. This was a feedback for me. I started doing some courses and we needed to provide feedback for each other and then I thought I was becoming a machine. I started putting numbers and formulas and proofs and my colleague who gave me feedback we were all into the same course. He studied philosophy and he gave me a feedback after analyzing my document and he was like please be more human. I didn't understand you. I didn't provide him any context and I started putting numbers and proofs and weird structures and he got scared and it was when I started thinking I should be changed this way because I am frustrated and I am doing nothing to change this reality so I need to do something. And then I started to think about some techniques to humanize the teaching of math and physics. I was able to put some of them in practice during my undergraduate course and after my graduation course. So the technique number one that I would like to show you, I don't know if everyone can make something but at least we can try. The first technique that I saw that it's really useful is to tell the story behind what you are trying to teach. After all we are all humans behind science. It's the guy who created a math equation for something.  So I started telling to the professors hey could you please tell the story of this equation? And some of them were like sure. So let's start the class. In the 16th century this guy wrote this equation. Not this kind of history, I mean life story, not history. And I was surprised because most of them didn't even knew or most of them were like why do you want to know this? I want to know this because I want to understand how this person achieved this result. There must be some reason for this person to have studied this topic. So telling the story of the human being, not the word history behind it. So I figured out that it was very important. So I have some examples that I would like to share, but as we are all human beings, I mean as I started studying the history of some science and the history of some topics and I could figure out we have very interesting stories. We have family dramas behind it. We have a tragic event of really young mathematicians, for example. We have amazing random facts of, you know, someone was studying a subject in mathematics and then he discovered a very interesting subject into biology. So this is very interesting to know. Because this becomes a bridge between the topics. So let's try an example. What comes to your mind when I say the name Kepler? Kepler's Laws, right? How many? Three Kepler's? Good, good. But personally, it was interesting. Who is this person? I mean, who is this Kepler guy? I mean, he didn't take two laws of his pocket. Hey, I have two laws here. Let's share. No, that's awkward. I don't want to think about this. So when I think about Kepler, Kepler has a very interesting life story you should read. This person was chased by Catholic Church during his entire life. Do you know Kepler's history? I see a few hands here. During the time that he was doing his research about his Kepler laws, the Catholic Church wanted you to believe that the Earth was the century of the universe. Which we know it's something like weird. But by that time, they wanted to force everyone to believe this. And one important figure that started saying, hey, the sun is in the center was a person called Copernicus and Kepler was following Copernicus' ideas. And that's why he was a chaser during his entire life. Another random fact but very interesting. Do you like Star Wars? Star Wars is a classical science fiction movie and probably Kepler is the first person in the literature story to write a science fiction book. Did you know this? He wrote a book about an expedition to the moon and I'm talking about 17th century. Which is super cool. I mean, so we can tell that he has a strong relationship with the creation of science fiction. And nobody tells us that. Why? This is very, very interesting. So Kepler, he came from a very poor family. He had a horrible childhood. And luckily he had a very rich friend, Ty Ho Bray. And this guy provided him instruments to make his research. But his guy passed away. And Kepler was alone again. So Kepler had a very lonely life and he was being chased by a Catholic during the entire time. And even though he was able to make his research and prove with mathematics and physics that the orbit made by the planets were elitid, that was incredible. Because that time people were also forced to believe only in Euclid's book. And ellipses are not in Euclid's book. So Kepler spent a lot of time trying to prove that the orbits were a circle. And then he ended up giving up after 10 years of study. And after 10 years he had that magical moment of, aha! It's not a circle. So it's something that is not into Euclid's book. So anyway, Kepler has a very interesting life story. And this could be a bridge to teach about renaissance period. We could connect better the subjects that we study. We also could teach facts about inquisition, about chases, about other important person who suffered during this period. So we can connect these facts with a lot of stuff. And we can connect math with literature which is beautiful. Because sometimes when I studied it, I saw things very unconnected. And we can start building bridges to this. Another example Euler. What do you think when I say Euler? This question, what? Yeah, we can actually think a lot of things because Euler was a present person in many, many, many, many areas. So Euler has a very sad story too. He got blind. He was totally blind and he was still able to do math. He is an example of someone who had incredible memory. He could memorize like the multiplication tables for more than 600 numbers which is weird. Anyway And when we talk about Euler we have a very interesting example of a person who wasn't happy with just one area. He made studies into biology, into medicine, into physics, into geology. So it is amazing. When Euler died, the publishers still had material for the subsequent 50 years. After 50 years this guy passed away. There was still new content unpublished. And the publishers were releasing things every 15 days. So you can imagine how much things he wrote about. And it's very interesting and it's so so much professional because he was blind. So imagine that he was blind and he solved equations about the moon orbit. And he was like blind. So you can start motivating people that physical disabilities shouldn't stop you to do amazing things. This also can teach us about magical issues. So if you are studying medicine or we have biology into the school we could connect math and medicine again. And this can be also used for children as an example to do not provide bullying because sometimes we see someone who is different. I had some colleagues who had visual disabilities and we can show the children like hey we have amazing people and they were blind. So start from the beginning show bullying questions. I mean I think Euler's story is a story for a movie. But also talking about movies a second move, a second technique would be producing more movies about science. But not about like a drama based on a figure but a movie where you can show the amazing things done by a science. So one movie that I really think we could make is a movie about this guy Aloua. Have you heard about him? I see a few raised hands but this guy is very amazing. I mean his life story is amazing. He died by the age of 20 by the way and we could still make a movie. He was very involved with French history. He was really good at math and he was also very involved with politics and he was famous not only for math but for being involved in how to say that, the rebellions and he went arrested several times and he was being chased by the government and he was there still doing math during his free time and that's amazing. Imagine how many things you can teach related to history and also related to math and he produced a lot of interesting things about math but everything that he created unluckily was ignored and not only unluckily but he submitted his papers to the Universes and they were like he's just a revolutionary. He can do math. So again he's stereotyped just after 20 years after he passed away his work started to be recognized. That's very original. Anyway we have very interesting things related to Galois and if you don't know about what he has done for math, he's the creator of group theory which is the basis for modern algebra. Just that it is so amazing and almost nobody talks about his works. If you google for group theory you are going to see amazing applications. So it is important to remember that behind science there are human beings. We must start thinking about this. This movie technique works for Alan Turing. By the way there is the movie imitation game which ran very well and it was selected for the Oscars. So movies can change the way our culture sees science. The final part that I would like to present is how to connect math and physics to change to computer science subjects. So the first experiment that I've done was to teach numerical methods into algorithm analysis. They are very connected and so what is a numerical method in mathematics? You won't solve the equation by the traditional way. You are going to do some different arrangements, discrete arrangements and it's just algorithm applications. So it was a good connection. We joined two subjects which was the numerical methods class and algorithms class and we got a very great result. Luckily we had very open minded professors who accepted to work together and we made this run pretty well. Of course, don't forget to tell the story behind the numerical method analysis and the story behind the algorithm. It's very important. The second thing that ran pretty well, we started teaching statistics with UI and UX. So we usually have AB tests which is a good case to study statistics. Can you see that how these two topics are very connected? You need to analyze the data when you are studying. Hey, is my UX good? Do I need to change anything to the UI? So you need to analyze the statistics when you are trying to improve this matrix and it's a good case to teach statistical instruments. So we also had an experiment where we could join part of this subject. It also ran very well and we saw that these students were also happy to be able to apply a theoretical concept into something related to computer science. Of course, we are humans. We are making science and sometimes we make mistakes as many of you said in the previous talk. But it is important to try. I mean, if you are unhappy with something, we need to try to change it. So the results that we saw is that these students were much more happy. I mean, I have never been a professor at university. I made this by being an observer and trying to help the professors to organize the content. But what I saw from my colleagues is that they were really, really satisfied with the results. And which was good for the subjects and which was pretty sad because when they were tending the regular calculus classes which had no connection with anything, he started to perform very bad. I mean, very, very bad. That was the bad experience that it had. And it shows that we should connect the subjects more. I mean, if it makes people happy, we are not connecting them more. So my last quote about this is like, I have seen that in software engineering, we try to connect the areas. So we are trying to bring DevOps people, with software engineering people, with UI and UX people and make them work together because we know that if we bring different people to different areas to make a team, we get amazing results. Why can't we make this for traditional university teaching? We should be doing this. And my personal feeling about this after some time of trying to connect the areas is that we are not fully ready yet. We should keep fighting. I mean, sometimes I feel isolated from the math department. Sometimes I feel that they don't want contact with me. The same for physics. And we should be all working together because the boundaries of research of computer science, which is quantum computing, quantum physics, they are all connected. If you start studying quantum computing, it has a lot of math. A lot. But it has a lot of algorithms. So we need to work together to end up the session. A friend of mine, she sent me this and she was like, hey, I'm not using algebra today. So that was not cool. And I told her, hey, you're using your phone and share that behind your phone. There is a lot of math. And this works beautiful. There is beauty behind it.  We won't solve anything by blaming people. We need to make our own contributions. I mean, after doing this work with some open-minded professors, I tried to do my best there. But I started writing what I knew about math history in a personal blog. And then I wrote tips on how to humanize each section of the things that I had studied in history. So it might be useful for someone. It's a small contribution, but it's better than spending my time blaming that professor is boring. It's not like that. We are all humans behind it. So the same way I make mistakes, they also make mistakes. And if they had a bad instructor education, the chances of they provide you a well-structured education are lower. We need to do our jobs. We need to tell them, hey, we are unsatisfied. Let me help you to change this. I really believe that if we are working and putting our efforts to make software development community work together, why not put science as a big picture to work together? I mean, I really miss attending a programming conference and see people from physics and see people from math. I mean, we should be working together. And I would like to ask you to make your small contributions, invite your friends who are sometimes not direct connected with program development to attend conference because sometimes we have ideas that they don't have and they can help us to solve the problems that we have and vice versa. We can help them. We should start working with science people in general. So thank you very much.