This is the 29th annual seminar series, and as you know, this year we're working on the topic of disparities. The series this year is co-sponsored by the Urban Health Initiative, the Global Health Program, and also by Dr. Chin's Robert Wood Johnson's Disparities Program along with the McLean Center. This is the first actually of 27 seminars on the topic of disparities, divided into roughly nine each quarter for the fall, the winter, and the spring. Many of the speakers are from the University of Chicago or from the city of Chicago, but there will be 10 or 12 visitors from other groups nationally. We're delighted that the opening session today will be presented by Professor Rick Kittles. Professor Kittles is at UIC in the section of hematology oncology, and his research utilizes novel methods to uncover genetic changes leading to the onset of prostate cancer and its progression in treatment. He studied health disparities and how genetic ancestry can be used to map genes, looking at common traits in diseases. We all know Professor Kittles and worked with him when he was here at the University of Chicago in the Department of Genetic Medicine. Also, he serves as the scientific director of the Washington, D.C.-based African ancestry incorporated group. I've reviewed a number of Professor Kittles recent publications, and they're really quite remarkable. Published in 2010, a paper in gastroenterology on genetic heterogeneity and colorectal cancer in Americans of African versus European descent. A paper that Professor Kittles published in cancer in 2010 looked at gene sequence variants in relation to prostate cancer risk among men of African descent doing a case control study. The papers are really many and very deep and fascinating. Rick, it's a delight to welcome you back to the University of Chicago, and thank you for being our first speaker in the seminar. I must say, it's always good to be back at the U of C. I treat the U of C as my Chicago home. Just so you know, I'm not going anywhere. You'll see me every now and then. Good, thanks. I had no idea that the date that I proposed would be the start of this seminar series. Yeah, well, hopefully I won't do any harm to the rest of the series. But today I'm going to talk about some topics that are near and dear to me, race, biomedical research, and the politics of trust. And I use the term politics of trust because very often we don't think about what we do and how it impacts the average person, people on the street. When you deal with genetic information and health information of individuals, it's about trust. It's about respect, and some of us think of, if you're a clinician, you think of yourself as providing a service, but it goes beyond that. You really are entrusted with this information, and I don't think we think about that often enough. And so I want to talk some about that because there's a history of trust across the varying communities that we deal with. And some there is greater trust, others there's a lack of trust. And I think it's about how not only we interact with these communities now, but also how we understand the history and try to reconcile issues that may have arose previously. So we talk about genetics. I get really excited because things are rapidly advancing in genetics. And all of you, I'm sure, remember the project, the International Human Genome Project, where scientists all over the world were involved in sequencing the human genome. And we found that there were about 20,000 genes in the human genome and 3 billion of these nucleotides, those chemical bases. And there's about 14 million SNPs, which is a class of polymorphisms. These are variants in the sequence. And so if we compare the genome of any two people in this room, it will be different. And we've cataloged close to about 14, about 12 to 14 million. I have to get the actual number because most of them are rare, seen only once, okay? And so after the human genome, we then went on to the mouse because this was big science, right? Think about it. I mean, it cost tens of millions of dollars, if not hundreds of billions of dollars, actually to sequence the human genome. And so the machinery, the personnel then went on to the next question, which was the mouse and then the rat and then the dog genome in 2004 was completed. The dog genome, I tell people all the time, is very important because the dog is a good animal model for cancers, human cancers. Like prostate.  Yeah, naturally. And the women always smile and laugh when I say that. The guys look at me funny. But seriously, naturally, human male, the dog. But it also was important in understanding, you know, our best friend, right, the dog, the canine genome, right? And we found that there's about 19,000 genes in the canine genome, which is why some of us resemble our pet dogs. After sequencing those five individuals across the genome, we found out that it was important to understand variation, genetic variation, because genetic variation impacts not only what we see physically, but also things we don't see, like risk for disease. And so then came trying to study as much of the human population diversity as we can. And so we have a lot of technology that allows us to do that. And so, for instance, we can look at a sequence and a gene and look at it in three different people. And they may have a different allele. What we call this is a SNP. This individual may have a CC, a TT, or the third individual may have a CT, a heterozygote. Now, for the most part, many of these polymorphisms have no major implications in terms of health. But for some of them they do. Think of a disease called sickle cell, where it's just really one polymorphism, one substitution of one of these bases in the beta-globin gene that creates so much havoc in those individuals that have sickle cell trait or disease. So instead of having a circular red blood cell, they have a sickle-shaped red blood cell, right? It doesn't flow through the vascular system as well. It can get caught up in capillaries and have a crisis, all because of one polymorphism. That is quite common in West Africa, some parts of West Africa. Not all of West Africa, but some parts, parts that historically experienced malaria. And so here's a situation where polymorphisms may provide advantage for survival in a population, but then in another environment, a vastly different environment, it could create problems. So this is something that we see a lot when we think about the evolutionary history of these polymorphisms. And so as I said, the technology is rapidly advancing. So I get excited when I see these. These are my toys, but they're costly. They're costly. We can answer a lot of questions. In fact, we can answer a lot of questions faster than we ever could imagine. The sad part is we're asking the same questions using the new technology. You see what I'm saying? But this is expensive. Each one of these machines here costs about the same amount as a condo in Chicago. So just think about that. When that happens, you have a situation where you have the haves and the have-nots, right? So some universities, institutions, medical centers, research labs have a lot of these sequencers and genotypers, platforms. Many of them. And then others have none. And so the rift is widening even more and more because the technology is very expensive. And so, you know, I tell the students when I'm here, when I was here, I used to tell the students, you should be excited and grateful that you're in Chicago because this is a have institution. All right? You go down the street, Chicago State, it's a have-not, right? So I think we need to understand that this technology, while it's important, and can answer some very interesting, exciting, and important questions, it does deal with the economy, you know? So in terms of the benefits of this technology, it's not really equitable. That's what I'm trying to say across all communities. And so we have this era of genetic and genomic ancestry and challenges related to health. I use genomic ancestry because we're moving away from race. I'm going to talk something about that. Why race is not really that important anymore. Race captures some information, but not what we want to do in terms of getting to the next level as it relates to disease. And so what are these challenges after we sequence the genome? We know that one of the biggest challenges is how do we define ourselves? Group definition and membership. Identity has been shifting ever so much as the technology has been increasing. Think about what I'm saying. Science and society are intersecting in ways that are quite exciting, but also uncomfortable. Folks are redefining themselves. What does it mean to be an African American? What does it mean to be a Hispanic American? Why are we using these terms defining people by language? What does that mean biologically? So this tension is exciting right now because it has to be reconciled. And people reconcile that differently depending on how they were raised, how they were socialized. What's important? What's the value? What's the utility of the technology? So I'll get into some of those stories. Can we accurately assess genetic ancestry? How does ancestry relate to issues of skin color and SES? For a long time we thought that we could just type these markers for ancestry and go away, put away with race. Don't even ask people what they are, just type these markers and put them on some scale of genetic ancestry. But we find that ancestry is related to issues of skin color. And skin color modifies the social interactions. So while you may have high levels of let's say West African ancestry, like I would say myself but I thought I had high levels. Why don't we use Wesley Snipes as an example. High levels of West African ancestry. Pretty dark skin, right? So we say okay well we don't have to ask him what he is, we can just type these markers. But skin color modifies his interactions with society. So that has to be taken into account too. How useful is ancestry for informing us about disease risk? The issues of health disparities? Are they due to biological differences? That's the big million dollar question, right? And we're finding out that for the most part the bulk of health disparities have very little to do with biological differences. They have more to do with social determinants. But there are some like prostate cancer that have a strong genetic underpinning. And then how do we prevent repeating the negative past abuses of race? So with the challenges come the promises, right? The technology is advancing. We have increased research in diverse populations. So I meant to tell you guys Ghana today is a studying white man. You know, we're now looking at women. We're looking at Africans, Asians, Indians. So it's important to understand not only the biology of these and the genetics of these populations but also the social-cultural variation that's within those groups and between those groups. And so then becomes the integration of epidemiological, cultural, and population history. So that's what we're seeing more and more. We're not just saying, well, these are some West Africans and these are some Chinese samples. But people are trying to investigate much more about the history of these populations and how they define themselves. And so with the technology, I think it's very exciting because, as I said, we have these ever-emerging new sort of disciplines. Like, for instance, pharmacogenomics, right? Which really wasn't, you know, it's been pretty recent that that's been advancing. And it's advancing pretty rapidly. And so I put this picture up. Anybody know what this picture is? It's a cell dividing. It's a very important cell that's dividing. It's the HeLa cell. HeLa, H-E-L-A, stands for Henrietta Lacks, African-American woman from Baltimore, Maryland, who died of cervical cancer back in, I think, 51 or something like that. And when she died, her cells were, before she died, her cells were taken in several biopsies and her cervical cancer cells. And they were growing up in the laboratory at Hopkins. And she had no idea. Her family had no idea. And those cells were quite important. In fact, they were one of the first cells that were immortalized and that were continually growing for decades at that time. So folks were trying to keep these cells growing continuously, but they would die. And then when they got ahold of her cells, they kept growing. And so that presents these ethical issues, right? The ethical dilemma, right? The advances of HeLa that the HeLa cell has provided has been enormous. I don't even think most people in this room could fathom the amount of information that we've gained just from that one cell line and the amount of money that companies have earned based on this one cell line. However, her family, many of them still, illiterate, poor, lack health insurance or underinsured, have gotten absolutely nothing. So that's the ethical dilemma, right? And so from a historical perspective, we know that this isn't new. This wasn't new. This was going on before 1950 with the war tribunal, the Nuremberg war tribunal, where the German scientists were accused of experimenting or doing research on individuals. The syphilis study in Tuskegee, Alabama, everybody knows that one. In fact, most folks in the black community who know very little about research know about the Tuskegee study. It's as if it was like imprinted in our genes. There's no sort of Sunday morning breakfast discussion about this, but we know about it. We know something bad happened. We know that we were exploited. And so there's some serious implications still today. And so this is back in, it started in 32 in Tuskegee, Alabama, and the public health service actually wanted to find out what was so different about African-Americans and the natural history of syphilis in the African-American population. This was an interesting study. They actually had an African-American nurse who was engaging the community, the men. She made them feel very comfortable. They provided medical service to these men, medical exams. But then when penicillin came about, they didn't give them penicillin because they wanted to see the natural history of this pathogen in the body, the natural history from start to finish. And so they were denied penicillin. And then the study was stopped in 73. This is Nurse Rivers, the African-American nurse I was telling you about. And what's very interesting about this study is it was actually CBPR before we knew about CBPR. And what do you mean by that? It was community-based participatory research. There's an institute, a college in Tuskegee called Tuskegee Institute, it was called Tuskegee College at the time. And there was a lot of important federal officials who were on the board of Tuskegee at that time. And they were having a discussion about what are some of the issues in Tuskegee County. And the folks at Tuskegee said, well, if it wasn't for this bad blood, this syphilis, we would probably do better. We'd be better off. And so that's how this whole study emerged. It was actually a discussion among the community members. And then they determined the best way to get those individuals to participate in engaging the community. So CBPR at its worst though, in a sense, because the outcome really wasn't beneficial for those individuals. At the same time, there was a woman named Henrietta Lacks who was having some woman's issues, went to the doctor, and was diagnosed with, I think it was stage three or four cervical cancer. She was born in 20, she died in 51. Her and her husband were Southern tobacco farmers. First cousins, they were related. It wasn't uncommon. They lived in Baltimore. They had five children. Now, they were poor. They litter it for the most part. And he was, what do you call those guys? He liked to go step out. What word can I use here? Philander. Philander? Okay, let's use that word. Philander. So he gave her several STDs multiple times. And ultimately, I believe, and many believe that he gave her HPV, which led to the development of the cervical cancer, which is why those cells continued to grow. They were immortalized at that point by the virus. And so the story is quite interesting. And it was written up by a woman named Rebecca Skloot recently, Skloat, who spent a lot of time with the family and wrote a very interesting story. However, she didn't really deal with the racial issues at the time, race, which was very, very important because Henrietta, when she was sick and went to Hopkins, which was a major hospital on the East Coast, it still is, they had two, at the time, two wards, the black ward and the white ward. Had she have been white, she would have went to the white ward and probably got a little bit better treatment. And more than likely would not have been a research subject. But pretty much all of the black patients, since they couldn't pay, ended up being involved in research. So think about that. Since you were illiterate, you really didn't, you lacked the education in terms of research literacy and health literacy. And you wanted a service provided medical care.  I don't know if that's coercion or not. I would leave that up to the ethicist. The fact that she didn't know. So in 51, as I said, diagnosed with cervical cancer, oh, I'm sorry, it was stage one. Within a year, she was gone. The chief gynecologist, Tallinn, when he did the biopsy, he took the cells to Dr. Gay, who was a major researcher doing tissue culture work and was trying to have these cells grow, trying to immortalize cell lines. He got ahold of those cells and they just took over the lab. He became very well known for those cells. Now, probably one of the most important results with the HeLa cell line was the polio vaccine development. You know, you have to grow up these, the polio, it has to grow in cells in order to develop the vaccine. And for many of the cells they were trying to use, they couldn't, it wasn't stable. They were unable to grow. But then they used the HeLa cell and it was quite successful in growing up the polio virus. That's when the vaccine was, it became very important in the development of that vaccine. Now, where did this happen? At Tuskegee. At Tuskegee. So, and a lot of people don't realize that the first mass production of the polio, of HeLa cells for the polio vaccine was done at Tuskegee Institute. They were growing up tons and tons of HeLa cells. And there were scientists involved, students involved, all of them of color. Not having any sort of clear connection in terms of where these cells came from. And they were shipping those cells all over the world so that countries all over the world could develop the vaccine. And in fact, if it wasn't for that, polio wouldn't have been eradicated at the time. It was also useful in studies on the effects of the atomic bomb, advances in vitro fertilization, cloning, gene mapping. In fact, I used it when I was in graduate school and we're using it now currently in the laboratory. Cancer research, viruses research, all surrounding HPV. Not all, but many of them surrounding HPV. Cells brought and sold for billions of dollars. So this is the book I was talking about. Very fascinating book. Spent a lot of time with the family, but really didn't deal with the politics of race much. Now, one of the reasons why HeLa cells have been so important in terms of biomedical research was because she was African-American and part of her gene pool was from West Africa. In fact, she has a common maternal lineage. Her mitochondrial DNA actually goes back to Sierra Leone. We were able to look at the mitochondrial DNA of HeLa cells and look at where an African may have arisen from. What's fascinating about this is that the variation, genetic variation is much more extensive in people of African descent. This is a study that was done recently where they resequenced 250 genes in Hispanic-Americans, European-Americans, Asian-Americans and African-Americans. And you'll notice here, the African-American bar, a larger number of these polymorphisms, these snips that were found in those genes, the number of them were much more higher among African descent than the others. And it's not until you get to the common polymorphisms, those that are greater than 30%, that you see sort of an equal distribution. But the low-frequent variants and the rare alleles are much more common in African people. That's big. That's very, very important to understand because many of these genes that were sequenced were either drug transporters, metabolizing enzymes, or known genes that impact risk for disease. And so here's a situation where we know a lot about the variation in European-Americans with very little about African-Americans. So we're not really capturing much of the variation that's contributing, that could contribute to disease and drug efficacy. So now the race is on, right? To study people of African descent. So this is a recent dump from HapMap. The HapMap project is a project that the federal government put together to collect samples from different parts of the world and sequence, discover polymorphisms, and find the frequency of these polymorphisms in these populations. The populations are Yoruba from West Africa, Han Chinese, Sef, French, Sef. They're French Europeans. I guess that's the prototype of Europe. It's French, France. And then there's another Asian population, the Japanese. So we actually have two Asian populations in HapMap, Chinese and Japanese. And I find that interesting. That was really about political power. It's interesting because you can say, oh, well, maybe the Chinese could represent us. They said, no, they can't. We're unique. Genome is unique. And they still believe there. Okay? And so we have two Asian populations at HapMap. And so from the, and then after HapMap, build one, there were several other iterations of HapMap. And so we now have African-Americans. We have some mixed groups, Hispanics, a lot of other groups. But anyway, the recent dump of data showed a very large number of SNPs that were found. But when they looked at where they came from, of course they came from the African populations. So still, when you hear, oh, we know all about genetic variation, we still know very little. There's a lot more that we're still, there's a lot that we're learning daily. And so this is important because there is a study design called genome-wide association studies that allow us to interrogate the genome to look for risk alleles or genes for disease. And in fact, there have been a large number of these GWAS studies over the last five, 10 years. And we've been quite successful in finding genes for Celiac and atrial fibrillation and colorectal cancer, breast, prostate. We just submitted a paper on prostate cancer, the first GWAS in African-Americans meant for prostate cancer. It took 10 groups across the country to get together to do it, but it was just submitted this week. Very interesting findings. Crohn's disease and others have been quite successful in terms of mapping genes using GWAS approaches. However, one of the things we do know is that the genetic architecture across populations varies. So risk alleles discovered in one group may not necessarily confer the same level of risk in others. This is important because genetics and clinical practice are becoming more and more situated together. This is that new field of personalized medicine, individualized medicine, genetic medicine, right? Better diagnostics, pharmacogenetics, new drugs, new biology, and better risk assessment so that we can then ultimately come up with good ways of modifying that risk. This is what's going on. Over the next five or 10 years, you're going to see a lot more of this happening, especially now that we're finding these variants, these risk variants across populations. Now, why should you care? Well, many people will say, well, you can take an active role. You can take an active role in clinical decision-making. Genetic tests are currently available. Many of them deal with cardiovascular disease, heart disease. And so how do you make informed decisions based on these risk alleles? Genetic medicine, however, may actually increase health disparities. And that goes back to what I said earlier about you have the haves and the have nots because this is not cheap. This is not cheap. So you'll have a clinic. You'll have two clinics. You'll have one on the Gold Coast and you'll have one near Washington Park. And where's the one where you will see folks getting the genetic tests? However, the genetics alone will not help us. I like this. It must be in the genes somewhere. This is why the new thing are genes and environment. Looking at populations and trying to understand risk, not only biological risk, but environmental risk, too. This is important because they work together to produce almost all phenotypes. You may have alleles for height, height, height alleles, height genes. But if you don't eat, something's going to happen. The environment, particularly important for geneticists because of issues of selection, if you know the history of these populations. They may be informative gene environment interactions, may be informative for treatment or modifying effects of genes. We can mass detection of genetic effects if not controlled for. And environmental effects may vary across populations. Now, let me give you an example. This is a study from the NHANES group where they looked at vitamin D levels, by sex and age and all of that. The three groups, non-Hispanic whites, non-Hispanic black, I don't know what that means. And Mexican Americans, right? And they looked at 25-hydroxy vitamin D in the serum in nanomoles per liter. You'll notice that whites have, the average is about 80 nanomoles per liter. African Americans almost have, about 50, 49. Mexican Americans in between, right? This is important because vitamin D actually is made in the skin due to exposure from the sunlight. However, if you have dark skin, it blocks the sun from getting into the lower dermis where the conversion of 7D hydrocholesterol occurs. So, biology and the environment are interacting there, okay? Good, perfect example. You can also take dietary supplements for vitamin D. Do like I do because I live in Chicago and I have dark skin. You know, the sun is only out about three days a year here, right? So, I take, I go to CVS and I take D3. I take over 3,000 units a day because that's about what you would get. No, you get a little more if you went outside with your shirt off for a half an hour. Midday. Not in the winter, right? In the summertime here in Chicago. But nobody can do that. I would love to see more women do it, but I'm just saying nobody would do it. Nobody would do that. Now, vitamin D is important. In the blood, it goes to many different organs. Breast, it's implicated in breast, colon, and prostate cancer because it's involved in apoptosis. It inhibits angiogenesis. It goes into the kidneys where it could actually regulate blood pressure. There are some really interesting clinical trials going on now where they're looking at blood pressure regulation by vitamin D supplementation into the pancreas where it's involved in blood sugar control. So, not only does it implicate cancer, but also hypertension and diabetes. And then also is involved in parathyroid hormone regulation. Now, as I said, you can get it from natural sources. If you were to eat salmon, fresh, wild salmon, you get about 1,000 units in the serving. Most folks in here are saying, well, what about milk? Because you're always taught milk. Milk has very small amounts of vitamin D. Fortified milk is about 100 units. We actually need several thousand a day. You can get it from shiitake mushrooms. You can get about 1,600 units from that very expensive shiitake mushroom. Good serving of that. It's always good. However, exposure to sunlight for half an hour, which is sure it off, about 3,000 units. Or you can take, like I do, vitamin D3 over the counter. Now, this didn't come out, but what I wanted to show you was the environment is very important. Had my figure come out on this slide, it would show that along this axis is BMI, and along this axis is percent hypertension. So from low to high hypertension, and BMI goes from low to high. And there's a line here that goes across these three regions. There's two populations in West Africa. There's two populations in the Caribbean. And then there's one population in Maywood, Illinois. And these are African descent populations. Nigeria, and Cameroon, Jamaica, and I think Barbados, and Maywood, Illinois. These are blacks. And you'll notice... Oh, you won't notice it, but... Imagine. You can imagine. The line goes from low BMI to high, and also increasing hypertension. In fact, hypertension is pretty low. It's about less than 10% in West Africa. Less than 10%. But if you go to Maywood, Illinois, it's closely approaching 40% prevalence. Now, what's so different? I mean, these are all African descent populations. What's so different? Very little. The environment's a big difference. You know, because they don't drive cattle-like escalades in Nigeria. Well, not everybody. They don't drive, you know, as much. And they don't stop at windy drive-throughs. Eat five meals a day, some six. Or... And they exercise a lot more. So, that's very important to understand. Because one of the biggest ways of modifying risk for hypertension is to just walk a mile a day. Take the elevator. I mean, take the elevator. Take the stairs. Take the stairs instead of the elevators. Contributing factors for health disparities, as I mentioned before, many of them are socially determined. So, while there's gene-gene and gene-environment interactions that could impact, like, for instance, vitamin D levels, which could impact risk for disease, but also stress, because stress is real. Life course selection, cultural factors, behavioral differences, and there are some. Even within groups, there are serious behavioral differences. Right? Think about how one copes with stress. Some people are very cool with coping with stress. It's like water on the back of a duck just flows right off. Others get stressed out. Start smoking. Start drinking. Erratic sexual behaviors, all kinds of things emerge because of stress. And so, I think we have to understand that in order to fully understand these health disparities, we have to look at the environmental, these social determinants in ways that we may not have in the past. Racism is also real. And then, of course, SES, an institutional arrangement. Now, why did I say all of this? Because, you know, you can teach people to eat healthy, but if there's no place to eat, like on the Chicago South Side, to get, not no place to eat, but no place or very few options to get healthy foods or food, then you're going to have issues like this where the South Side area and the West Side, which are areas where these food deserts are in the city, are also areas where there's high BMI and the food balance score is worse. Now, this is real. This has absolutely nothing to do with genes. So, like for instance, I couldn't do much with this, right? I couldn't solve this myself. This is economics. This is politics, you know. This is legislation. And so, one of the things we did do, though, was we set up two farmers markets right around here. We helped these community organizations develop these farmers markets. Now, that was real. Folks went out there on Saturdays or Sundays and got all kinds of fresh produce from farmers from the southern Illinois. You know, I forget that Illinois is big. You know, I've just been here for years. I've only been here for years. There's a lot of farmers down south. Many of them are black in southern Illinois, Missouri, all the way down to Oklahoma. And so, many of them come up and set up at these farmers markets. Those are real. Discrimination. If you want to know anything about, if you want to know some good studies about discrimination in health and outcomes, check out the journal Black Psychology, this issue in 2009, which was February 2009, it came out. The whole issue dealt with studies looking at racism, trying to quantify the effects and outcomes on health. And one of the things that I found very interesting in that journal was this study where they looked at correlations of perceived discrimination. Not even, you didn't have to say it was real or not, just the perception of discrimination on health in these clinics. And what you notice here is that, and these are quite significant, if the patient perceived discrimination in terms of with the physician or his office or her office, there were negative correlations with health. General health pretests after four weeks, after 16 weeks, the only thing that was positive was a number of chronic diseases. But this is what I find interesting, the fact that the idea that you and the doctor are working together as a team to better your health, all of those negatively correlate. So this is real. The problem is trying to quantify this and then also trying to reconcile it so that we can overcome that issue. I mean, we talk about cultural competency, I don't hear that much anymore, we used to talk about it a lot, but it's about perceptions. Now, why community participatory research? Because you can build and maintain trust. When I came here in 2006, I spent two and a half years out there in the community talking to folks, finding out what the issues were, what was important to them. One of the biggest issues was nutrition. We started working with some of the medical students, some of the undergrads and grad students to develop programming around nutrition with the communities. It was very important that they saw that we can. And I think that's part of the framework in which we can operate successfully. And this is important because as this technology and the information is emerging, the new technologies I was saying, the new treatments and interventions that could helpfully eliminate disparities, if they're not involved in that, they're not going to accept it. You have to bring them into the mix. And there are many different levels. I'm not going to get into this, I'm sure you guys know, to CBPR. But know that the Tuskegee study of untreated syphilis was a classic example of CBPR. And of course the barriers deal with respect, willingness to share power, that's major. I talk to researchers all the time and I say, well, you know, if you really want to get access to this group or if you want to increase your numbers or whatever, you should go talk to these individuals, this community. And many times they'll say, I don't, you know, I'm not sharing any information. And so that's something that I think is major. Accepting another's perspective also is big. But what's also big too is the fact that there are very few blacks and Hispanics doing this research. Now, this is a representation of grants from NIH by race and ethnicity. Now you'll notice that since for the last, and this is up until 2010 actually, the numbers haven't changed much. Last 10 years have been pretty much the same for African Americans. About 1.7% are funded researchers. Hispanics, about 3.5%, and then others, about almost 20%. This is real. And so we talk about these pipelines, we talk about increasing the numbers, but we're doing, it's not really having an impact. At least I don't see it. So back to race real quick and then I'll end. This historically has been the problem in biomedical research. We've used race as a proxy. So you go through the literature and you'll see there'll be a study looking at stroke or heart disease or prostate cancer. And it'll say race is the biggest risk factor. Ancestry is the biggest risk factor. What does that mean? African Americans highest risk for stroke. What does that mean? Does it mean that there's some genes that blacks have that's contributing? Or does it mean that the environment, some diet, chicken and watermelon or something? What is it? It doesn't allow you to tease apart the risk factors, the biological and the environmental risk factors. What we're doing now, more and more, is that we're actually, instead of using race, we're actually looking at genetic background, we call that genetic ancestry. And we're measuring the environment better because geneticists are now talking to other people. Geneticists are very fickle. I don't know if I wanted that recorded, but very fickle people. And they say, well, they don't know, they don't understand what I'm doing and I don't understand what they're doing. But the social scientists actually have some good ideas. And so when you think about complex disease, you have the risk coming from the biological and the risk coming from the environment. Then you have an interaction. And the only way you can accurately measure that is by studying them individually and not confounded by race. So how do we do ancestry stuff? Well, this was a good study that came out of Ohio where they had two groups, two cohorts. One that self-reported as black, the other one that self-reported as white. And they typed genetic markers and estimated African ancestry from zero to 100%. And you'll notice that these individuals here had less than 10% African ancestry. Those who said that they were white. But then you look at those African-Americans, look at that distribution, look at that spread. There's a significant number, even though it's not a lot, but it's still real, of African-Americans. These are folks who self-report as African-American. They go to black barbershops, at least most of them do. Who genetically have more European ancestry than other African-Americans. On average, it's about 80% West African ancestry. So it's a very heterogeneous, macro-ethnic group. High genetic heterogeneity due to the antiquity of being African, the African ancestry, but then gene flow or admixture with non-Africans. And mainly it's white men. Mainly white men. I got to tell you guys this story. You'll hear about it more after today. So all African-Americans have some level of European ancestry. So even me, okay? Even me. But recently I actually looked at some prominent African-Americans, you know, like Martin Luther King's lineages. And we find that one of the biggest civil rights leaders in our time has a European Y chromosome. Which a lot of people would be shocked to hear. They'd be like, wow. So he had on his paternal line somebody who was of European ancestry. And that's about 40% of black men that we test. We look at these Y chromosomes. 40% of them have European Y chromosomes. That is major. Because when we look at the other side in terms of the female contribution it's only about 5%. So that's called sex bias gene flow. And that's because of the behavior of slaveholders during the beginning of slavery and then through slavery. And then after, for the most part. And so when we look at across the United States the pattern of genetic variation in African-Americans differs depending on the history, the local experiences in those communities. So anyway, I'm going to go through this real quick. But I'll leave it here. So this was a study where we looked at colorectal cancer here at UFC. And we did this, I did this with Nathan Ellis and Sonya and Anthony Skoll. I mean Anthony, Andrew Skoll. And what we wanted to do was look at some genetic risk factors for colorectal cancer. But before we could even look at genes we had to really estimate how much variation was it within those so-called racial groups, African-Americans and European-Americans with colorectal cancer. And then control for that variation. So look at the spread here for those African-Americans and then those that are white, European-Americans. And these are the French seph samples in green and these are Nigerian-Europe. But there is no clear dividing line. I mean there's back and forth here. I think that's very important for us to understand because as we start talking about individualized, personalized medicine, we're going to go beyond the whole by-deal of the race-specific drug. Because there's a lot of variation even within these groups. So it's important for us to estimate that. And I think that's probably been one of the biggest contributions of these ancestry markers in biomedical research is allowing us to just move away from race and rather interrogate genetic variation. This is another way of showing some of that data. So a triangular plot of West African, Native American, European ancestry. And so in this red square, could be somebody like Holly Berry who has her mother's European and her father may not be 100% Mandingo. But there are some blacks who have more European ancestry than some European. So there is no dividing line. Hispanics also vary heterogeneous, grouped together because the federal government says they speak Spanish. So we have Mexican-Americans from Colorado, a high level of Native American ancestry and Spanish-European. But then we have another group of Hispanics who if we're doing a study on asthma would be grouped together with them, Mexican-Americans. These are Puerto Ricans and look at the distribution. Much less Native ancestry, much more West African ancestry. So I think that this has been a lesson for a lot of folks looking at risk for disease and then also, like I said, treatment outcomes. When we look across the United States at different African-American communities, we see a lot of variation. A lot of variation. And it's not all sort of this homogeneous group. The lowest level of European ancestry we saw was in the Gullah Sea Islands of South Carolina. We published this, we looked at the Gullah folk, Charleston and Columbia, South Carolina all in one state, vastly different numbers there in terms of European ancestry. The lowest is in the Gullah, the highest in Seattle, Washington. Almost four out of every ten folks that we recruited in that study had one white parent. So just socially, it's a different group. And these African-Americans are socialized much differently out West than they are in the rural South where the history of race has been quite strong. Which is why when I was younger and I used to go to San Francisco, I used to be like, something's wrong with these folks out here. It's different. They're just different. It's different because they don't necessarily see themselves like, I saw myself as a black male in New York. Okay? If you think about multiculturalism and diversity, all of that emerged from where? Out West, the Pacific Northwest. Washington State, Sacramento, Sacramento, all of that stuff. Tiger Woods is a perfect example. What did he say years ago? He said he was Cable Asian. He's not black, he's Cable Asian. He wanted to say, he was saying he was mixed. And he appreciated all of his mixtures. Caucasian, Asian and black. However, he was quickly reminded that he's black. Now some of y'all are wondering what's going on in South Carolina, right? From low to high levels of European ancestry. So Columbia had the highest. It's a major highway. It's a capital of South Carolina. The University of South Carolina is in Columbia. But most importantly, Strom Thurman was in Columbia, South Carolina. So remember what I said about the local experiences? Those are very important. Local histories, really important. We can't just group these all together. But one of the things that has been a problem for a long time is when we do these genetic studies we set up these consortiums where people recruit and put all of these samples into one analysis. But they're different environments and also biology. And so because of these markers we can now control for that heterogeneity in these big consortium studies. I'm going to end with this here. And I apologize for having so many slides but I always do. This is why I have sort of... I'm kind of ambiguous about pharmacogenomics because these big drug companies don't necessarily... While they say they want to go more personalized and individualized, that's not how their economic plan is, their business plan. Their business model is set up around marketing to populations, to everybody, and not just to individuals. But anyway, this was the by-deal publication of the combination drug, the clinical trial, where they looked at isorbidinitrate and hydrolysine in blacks with heart failure. This is a very, very important study. I was excited because I said, wow, they're studying heart failure in blacks. This is very important. But then I read the paper. And okay, it says here, studies suggest that people identify themselves as black may have on average a less active renin angiotensin system and a lower bioavailability of nitric oxide. So you look at the literature, that's pretty consistent. I mean, there is some differences there. They haven't really been able to identify what's going on, but there are some differences there. But then they say their trial represents a departure from the recent approach to the design of cardiovascular trials. A large heterogeneous population, we examined a specific population because they said, you know, those blacks. A heterogeneous population may have substantial variations in genetic and environmental factors that influence disease regression and response. Now based on everything I've said, does this make any sense? No, it doesn't. And so we have to really go away from that. This actually is that whole racial sort of model. And while it was important to see if in fact this drug did have some level of efficacy in the African-American population, we also have to understand that not all blacks are going to respond to it. And in fact, not all did. There was only a 43% improvement in survival. So what were some of the issues? Who was black, race was this crude proxy, just self-report, skin color, whatever. The trial didn't test other groups, so we don't know if actually by-deal works better. And then, of course, while great, there are important functional variants there. What did those individuals have in terms of genotype that made them respond while others didn't? That's where this should be going. And that's where I hope this is going. Because if not, then we're going to continue to stall on our route to personalized medicine. So with that, I will end and I will say this. This is the future paradigm. We're going to be, hopefully, more opinions, predictive, personalized, to preempt, but none of this will happen unless everybody participates, because those communities that are not part of the discussion are not going to benefit. Thank you very much. So, Rick, I have a question. When you do research, like on the south side of Chicago, how do most south side residents self-identify when you talk of ancestry versus race? First thing I say is, how do you define yourself? Because that's important. I'm not saying we throw away race, because when somebody says that they're an African American or a Hispanic American or whatever, that means something. And so there's some that could, those variables could be important in the study. I then also have them go deeper though. So I ask them, what is your mother's ancestry and what is your father's ancestry?  So they go back to their grandparents, and they'll do just like they did for themselves, African American or whatever, and then you can really see sort of the complexity in that family. I mean, in that individual, based on the family history. Okay, and so the last point that about a week ago, or two weeks ago, and I don't know if you saw it, the Chicago Defender ran an eight-part series. It was called the Legacy of Tuskegee Clinical Trials in 2010. Right. And so you're right, because there have been several studies actually two studies done one in 1990 and then one in 2000 that said most African Americans and Latinos don't know about Tuskegee and that's not their reason for non-participation in clinical trials. But even if they cannot articulate that most that are involved in research will tell you we don't want to be guinea pigs and be experimented on. So the interesting thing I thought about the Defender's eight-part series is they're trying to put out in the community this whole push towards personalized medicine. The person who did the series is someone who has participated in clinical trials herself, but her caveat is the community does not know the questions to ask and also she herself being a freelance writer doesn't always have insurance so she signs up for studies so that she can get the free healthcare particularly in depression and when she brought up the issue of race to her white therapist the whole structure of the trial and the therapy changed because the person back to what you said had a different perception of what is racism as opposed to the person and she then felt there wasn't this trust between the two of them. That has big implications as it relates to that trust. But engaging the participant and learning as much we want to learn as much as we can about the community and the individuals in the community I just always found it much easier and you gain much more information when you ask them sort of these questions about their parents and their grandparents and it also because sometimes people say I didn't show this data but sometimes African-Americans say that they're Native American they will say that and look just like me they say I'm Native American and then you got to walk them through because being a Native American is important to some people actually it's important more and more for some people because of what's been happening in terms of reparations and all that for moving them on these reservations. Yes. Stand up off the floor to ask the questions. The first is a little maybe scientific and that's the question of whether or not it's more complicated just genes and environment I thought I heard you say at one point that the same gene in a particular racial group might behave differently and so aren't we even talking about gene-gene interactions at that level too it gets very complicated. You can have not only gene environment but also gene-gene or you can have more working together gene-gene environment it can be quite complicated but with more and more disparities work is going towards looking at that looking at how where the direction of risk is coming from and all of that and the complexity of that. And then the second question is I think a very significant one for anybody who wants to work in community-based participatory research is your judgments or advice about who stands for the community right right well I mean historically I mean early on people you know folks thought that you could just go to the head honcho and he'll give permission or she'll give permission but I mean it goes beyond that it really depends on the on the on the structure of that community and the history of those communities so it's complicated it's not just a you know who's gonna who can consent you know it's much more than just going to that one person I think we really have to study these populations a lot more deeper in order to understand that. I really appreciate your insight about Tuskegee being a community-based research program I think that's a I didn't know that and I think it's an interesting way of looking at it. There were a lot of discussions back and forth before it even started Right right but I don't think it's been positioned like that until I mean I haven't heard it before but I think it's interesting now to think because we see this as such a positive you know a positive thing now that we're doing and so I would and I'm sure the people who are doing it especially the black woman who's involved with see themselves as doing a very positive thing for the community at the time. So my question is 30 years from now 40 years from now how do you think we'll look back at the community-based research we're doing now in terms of you know was it a good thing was it you know what were the possible I think the jury is still out on that I think that there's sporadic success but it's not everybody's not enjoying this right now you know there are some institutions that do it quite well and they have been for a long time and so while there's others that are just trying to catch up now so it'll be interesting to see after 10 years sort of how but the successes that I do see are very important and exciting so I'm not saying we should stop I just you know I think we have to be very very careful you also have to understand too now it's an education that goes both ways and so the community may not understand a lot about research and they definitely don't understand the pipeline the research pipeline because I'm sure folks at Tuskegee knew that papers are going to be published that they were not going to be given the drug penicillin once it was found to be efficacious for syphilis they wouldn't have said do this you see what I'm saying so we have to understand the whole pipeline too or we have to describe that in a way that the community understands it because a lot of times the community thinks that they're going to get data back right away you know I have people I've recruited for several years ago here in Chicago who try saying you know where's my data you know I'm like this is a research study you don't get that back we don't give that back so that pipeline is important the whole research pipeline because I think Heela is a perfect example of when things get out once you give it up and then most people will tell you that it is highly unlikely that the Lax family her descendants are going to get anything from this even though we know it was wrong because of there was no protection there so I think that's an important new sort of dimension that we should really look at in terms of CBPR is making sure the community understands the full gamut of the research because they have a research they have issues and sometimes their issues correlate in terms of their research questions and we get all excited but we have something else we're going to do with it than what they want so I would like you to speak to a little bit to using race more as a social standing and the interaction with social environment I used to think that race was this it could be looked at in terms of social standing but I don't know when you have an example and I'm just talking now like Barack Obama these examples where it doesn't necessarily hold and there's these sort of issues with it race is real and they'll get me wrong and politically social politically in the United States historically it's been used a lot in terms of across many different institutions but using it as a measure for social standing I'm not sure Rick I apologize for not telling you that you were going to be the keynoter in this series it was by oversight but you did a fabulous job and I want to thank you so much


Guys, that moment we have all been waiting for, Alden Ring DLC has been confirmed and today I bring you all those juicy details. As it going guys, my name is DPG and if you do enjoy the video, leaving a like really helps out and if you like what you're seeing and want to see more, be sure to subscribe. Ok so on screen now we have a beautiful looking wallpaper, I mean if you want to download this for yourself guys, I will link the original image in the video description because it is a pretty one, but they tweet this out, Alden Ring themselves tweets out stating, rise tarnish and let us walk a new path together. An upcoming expansion for Alden Ring, Shadow of the Erd Tree is currently in development. We hope you look forward to new adventures in the lands between, guys I walk up to this, I mean I had goosebumps when I saw this, I couldn't believe it, I could not believe it people. It's finally happening, a new DLC for Alden Ring, wow I mean, so looking at the image people we can speculate, I mean nothing has been confirmed here, I mean it is like I said just speculation, take it with a pinch of salt, but we see a horse rider, we see the Erd Tree, we see like a golden goo, a golden liquid leaking from that Erd Tree, I mean we can speculate on these things guys, I mean add your opinion down below, what are you seeing here, let me know, but that does look a bit like Mikaela on that horse back, I mean is it even a horse, yes it is, we also see that golden liquid like I said, could this indeed be that death blight, I mean we don't know, but I mean it is an interesting thought, don't you not think, but yeah guys I mean I can speculate all day about this, I'm not even going to lie to you, I'm just so excited about finally getting an Alden Ring DLC, I mean this is massive news, I mean Alden Ring in my opinion probably one of the greatest games ever made, if not the, especially for me anyway, but yeah the DLC, the shadow of the Erd Tree looks absolutely incredible, we'll also see in many of those spirits too, look like a lot of gravestones here, but what is this all about, the shadow of the Erd Tree, this is going to be so good people, from software do not mess about, being quiet for absolutely ages and all of a sudden, get us all hyped up and then bam drop confirmation of a DLC, this is just going to be utterly incredible people, now as of right now we have absolutely no idea about release dates, any further details, nothing of that sort has been released, as soon as it is guys, I will have you covered right here on my channel, you know this, as soon as any details are dropped on this DLC I will have you covered, but yes a short but sweet one for you guys today, I apologize if a notification woke you up, because hey I mean it's definitely worth it, is it not, I don't think the DLC people, yes this is going to be good, guys let me know your opinion on this down below in that comments section, the shadow of the Erd Tree coming, probably late this year if I had to guess, but hey we can all hope, couple months, come on, come on, come on, no it ain't happening, it ain't happening, guys if you enjoyed the video leaving a like really helps out if you like what you're seeing, want to see more be sure to subscribe and hopefully guys, I will see you on that next one.


Welcome to the BSC Dev Room. So, let's talk about FreeBC Graphics Tech. Yep. Hello. I'm going to start with a question. How many in here are FreeBC's users? That's, well, two-thirds of the room maybe. How many of you use FreeBC on a desktop or laptop? Or in some sort of graphical environment? Well, most of the people who raise their hands for FreeBC users actually use FreeBC on a desktop or laptop. That's great. So, today I'm going to talk a bit about the Graphics Tech on FreeBC and I'll talk a bit about the team behind it and what we're doing, what we have in FreeBC today and what's coming up next. And the person doing the talking, my name is Nicholas Seising. I'm Seising at FreeBC.org, so you can reach me there. And I've been part of the... I'm an IT consultant in Stockholm, Sweden and I've been working on FreeBC for over 10 years and I've been a Committer since 2012 and for most of my work on FreeBC has been on the Graphics Tech. So, the purpose of this talk is to present what we're doing and a bit about the team and who we are. Before I start, I'd also like to thank my employer B3Init because they make it possible for me to do a bit of this on paytime and they also made it possible for me to get here. So, thank you to B3Init. So, starting with the agenda. As I said, I will talk a bit, present the team. Then I will walk through the actual Graphics Tech what's in FreeBC today? What's the Graphics Tech in FreeBC? I will talk a bit about the challenges we face. What's making this job, what's making this perhaps less than trivial? And if there is some time, I will see if I can find my crystal ball and gaze a bit into the future and see what I think is the things we need to do to make FreeBC a better desktop platform. So, let's start with the Graphics team. So, this is quite a small team. It's me. It's two guys named Johannes, both of them, to confuse things. We get some help from Warner Rush on Core to do some Lia Song and things like that. There's a guy called Pete that's helping out, keeping some things up to date, writing some documentation, things like that. So, we have a fairly small team. Then Manu, who is not in the room, is here today somewhere. He's working on the ARM platform and Graphics on ARM and we get some help from Matt Macy, who's been involved before and he's also helping out with the PowerPC64 platform. So, the workflow, we use GitHub. We have a GitHub team, I think it's called, in GitHub terminology, where we have our development repositories, so we have a fork of the FreeBC ports tree where we can have experimental updates and things like that. We have a copy of the FreeBC base tree for things that need to go into the base system eventually to support driver updates and things like that. This is where most development takes place and then we move it into the official FreeBC repositories. You can find the team here on GitHub. It's github.com slash FreeBC desktop. So, you can find all the things there. This is also where you find sources for our ports of the drivers as well as some library shims for some Linux compatibility. So, all the sources there and you can open issues there if you don't want to use FreeBC, or you can make pull requests there. So, what is the team maintaining? So, it's about 300 ports. It doesn't sound like very much. I did an experiment once and I broke one of them and almost 30% of the FreeBC ports tree stopped compiling. So, even if it's not that many ports, you'd rather not break them. If you break the wrong one, then you're in a bit of a mess. There's also some ports infrastructure. This makes it possible to easily depend on FreeBC X11 libraries using use underscore Xorg if you're familiar with ports. This also uses GL, things like that. And then we have the kernel drivers. That's also our domain, so to speak. So, the stack on FreeBC, as I said, we have the core libraries. This is all in ports. We have the core libraries, your lib X11, your lib XCB, your lib whatever basically. The X servers is, of course, something we're responsible for. We also maintain the FreeBC support of Wayland.  The small applications that used to be distributed together with the X server when it was a big monolithic thing and these days are separate packages. Window managers and desktop environments and things like that like KDE and GNOME, those are maintained by other teams. That's not what we maintain. That would be just too much. So we try to make a foundation of FreeBC graphics that you can build on and you can maintain your graphics driver or you can maintain your desktop environments and window managers on top of that. So let's look into the FreeBC graphics stack. And I will do this. I will start at the bottom with the drivers and then I will work my way through the graphics stacks all the way up to the user interface you're seeing right now. So for drivers, we have a legacy driver in base unless someone did something tonight. We still have a legacy driver in base. And this driver, it's a complete port of the Linux KMS graphics drivers that was done in 2010, 11, 12, 13, something like that. So they've taken the driver, they've made a complete port. This was done by Kostik Beliso where he basically changed all the things that was Linux specific in the driver and used FreeBC kernel interfaces for that. This port has then been updated a bit along the way and in terms of hardware compatibility, it's somewhere around Linux 3.8. This driver is planned for removal in FreeBC 13. It's already disabled in the default build and it will be replaced by DRAM legacy Kmod, which is a port of the driver. It's basically we're taking the source that's in the FreeBC base system and we've made a port out of it. We have had to made some small adjustments to make it work as support and that's it. So it's basically what's in the base tree today. And the reason we're removing the DRAM legacy drivers is that some of them are conflicting with the new drivers that we are developing. So they attach to the same hardware because they support the same hardware and that makes it so that it's hard to figure out which driver is being used or using the old driver or the new driver and that makes documentation hard. It makes support hard. So that's why we're removing the driver. And as I said, it's planned for removal in FreeBC 13. I don't think it's happened yet but it will happen soon trademark. So the new drivers or DRAM next or I think it has similar names or it has a multitude of names. These new drivers, they exist in port and they will only exist in ports as kernel modules in ports and of course packages, they will never end up in FreeBC base. Part of it is because of licensing issues. Part of it is since they're based on Linux kernel code and the Linux release cycle is very different from FreeBC, it's very hard to maintain the driver entry. These drivers, they use the Linux KPI or LKPI and LKPI and FreeBC is a kernel module that implements or translates Linux kernel APIs to FreeBC kernel primitives and APIs. And the LKPI was first invented by, I think it was developed by Mellanox or something like that for their fiber channel drivers, something like that. And we build on that infrastructure, we have added things to the KPI to make graphics drivers work. And this makes it so that we can take, well in theory at least, so that we can take code from the Linux kernel, the graphics driver from the Linux kernel with very, very few changes, we can take them and we can run them on FreeBC. In practice, Linux really likes to change their KPIs, so you have to update the Linux KPI while you're doing this. So there will be some changes forever at least. As you will see, this makes it possible for us to keep fairly current with what's going on in Linux, in terms of hardware support. As I said before, the legacy driver, it's still on Linux 3.8, it was very hard to maintain, it was very hard to update since you had to go through the drivers and change Linux specific bits into FreeBC specific bits. These days, this is primarily done on AMD64, that's our primary target because that's basically what everyone is using. So our primary target is AMD64 or x86 underscore 64 in Linux land. Secondary targets are E386 for people with old hardware and PowerPC64. I would also say that ARM is a secondary target and ARM is a bit special, so there is some development to get better graphics on ARM as well. It's done by Manu. And this is also the reason why we made a legacy port or a port of the legacy driver because the legacy driver is working on 8V86 and perhaps other architectures as well. We have in FreeBC 12 stable, I'm not sure about the release. We have support for E386 for the new graphics drivers, but it's kind of an alpha-beta stage and it might be a bit unstable. PowerPC64 support is being worked on. It's done by Matt Macy and others and I think it's kind of working, but it's not stable mature yet, but hopefully it will be. So the new graphics drivers in ports. We have multiple versions because different versions of FreeBC have different support in the LKPI for different drivers. That's basically it. In short, use the meta port. That will select hopefully the correct driver for your version of FreeBC and your FreeBC architecture. Drivers, they are available in FreeBC 11.2 and 12.0. Earlier releases will not work because there's not enough support in the Linux KPI. They're not supported anyway. Perhaps they've run out of support, yeah. Okay. 10.0 or 10.4. Okay, so these are the only supported drivers or supported versions of FreeBC. So moving on upwards the stack. Drivers, moving upwards through the stack. We have the libraries. The biggest library is probably the OpenGL library called Mesa. This library has fairly quick development and it's important to keep it working because if you break it, things like that, things stop working. It's used for very many ports. You also have the libdrem library, which is a library to access the hardware in a device-independent manner. So it's a translation library between the user and the kernel driver, so to speak.  As I talked about, this is the Libx11 and LibxB and, well, hundreds of others, I don't know, 50 others. Then on top of that, this is the foundation on which you can build a graphical environment. On top of that, we have the Xserver. And the Xserver in FreeBSD is out of date. It's current with 1.18.4. This is an area where we need to do more work. We have had to get the drivers and things working upwards the stack, and then this is the next step. The Xorg server, it uses two ways. It needs to communicate with the graphics hardware some way, somehow. There's two methods of doing this. So you have the DDX drivers, as they're called. These are the DDX stands for device-dependent execution, I think. These are the old XF86 video intel, for instance, or XF86 input mouse, things like that. Those are still around. Upstreams seem to be heading towards something that's called mode setting or kernel mode setting, and using that to talk to the kernel directly to fiddle with graphics. And mode setting is part of the Xserver itself. So right now, we have a choice between the two. It seems like Upstream is heading towards the mode setting in the mode setting direction, but at least AMD is keeping their DDX driver up to date. There's new updates for it. Intel, well, there's co-developments. This hasn't been released in quite some time. Next step, Wayland. It's the new, not Xserver, but the new way of doing graphics on Unix and Linux systems. I believe this has been the focus Upstream for quite some time. And this is where most of the new development happens. The old Xserver is, you know, I guess a bit of a maintenance mode. Previously recently gained support in the default package bill 4 for Wayland. And this means that everything in the ports tree and the package system are built with Wayland support enabled by default. For instance, the GTK toolkit is built with Wayland support enabled. Same goes for Qt and other toolkits that build on graphics. The Mesa package is built with Wayland support out of the box. This makes it possible, makes it much easier to try the Wayland. And the Wayland library implementation itself is mostly up to date. We also have Sway, which is an i3 clone available if you want to try Wayland. However, Wayland, to use Wayland, you need the FDEV support in the kernel. And FDEV is the new Linux way or newer Linux way of handling input drivers or input devices. And this support is in the kernel for at least freebies to 12 and current. I think the code is also in freebies to 11. However, it's not in the default kernel configuration on the releases. So if you're running freebies to 11.2 or 12.0 you need to have a custom kernel. In freebies to stable and freebies to current, this FDEV is enabled by default. Unfortunately, there were some fixes that needed to go in that were not in time for the freebies to 12.0 release. So to run this, you need either a more current version of freebies to or a custom kernel. The whole Wayland stack, it needs more testing. It's fairly new. It's not very much used, as I said, until around Christmas. I think you needed to compile your port tree specifically with it enabled. So you needed to build your own packages and stuff like that. Now you can get it by just installing it. And that makes it much easier to try it. So, how do I try this then? I've talked a bunch about X-ray and X-server and I've said that you should try Wayland. How do I get started with this? I mean, most of you in here are already running it. But for those of you who might want to get started to try it out to help out testing, it's fairly simple to be honest. At least it should be fairly simple. You need a freebies to installation. Quite obvious. And if you want to release, I'd recommend freebies to 12.0. If you want even better support with FDEV enabled by default, things like that, freebies to stable or freebies to current is available. Then you simply install Xorg, like this. You install your favorite window manager or desktop environment. So, PQA install GNOME or XFC. We have a whole bunch of them. Window maker, i3, VM, things like that. Lumina. Of course, we have Lumina. Then you need the driver. As I said, yes, PQA installed there and came out. This will select the right driver for you. A bit of a caveat. If you're not running a release version of FreeBSD, and if you're running a custom kernel, and especially if you're running current, instead of installing the package of the driver, build it from ports. It needs to be in sync with your kernel, because kernel interfaces might change and things like that, and data structures might move around. So, if you're not using a release, you need to build it from ports. It's fairly quick to build. It's located in Graphics-DRM, Kmod, and you will build it for your kernel, together with the firmware needed to use the graphics card. Then, you start X. You might need to fit a little bit. If you want your favorite window manager, you might need to set up XInitRC. The default is TWM, as has been the default since forever. This should work. If you're running on Intel hardware, I think most of the bugs are sorted out. You should not need a configuration for Xorg. You should find the hardware and drivers you need to start. If you're running on AMD hardware, you might need to fit a little bit until you get the driver to work. There is currently a conflict between the EFI frame buffer, so if you're using UEFI, you might need to disable console before the driver loads. There is more documentation about this on our Viki, for which I have a link later. In general, to get a graphical environment on FreeBSD, this is what you need. It sounds very simple. What are not so simple in this? Testing for one is not very simple. It turns out it's very hard to emulate graphics cards, graphics hardware, which means you need to have the actual hardware laying around. There is quite a lot of different graphics hardware, so you can't cover all bases. This means that we need help with testing from, I'd say the public, but from users, we need help. We need to help with testing. We need help to cover our bases. This also means that sometimes it's very hard to reproduce problems. For instance, I have a friend who had a freeze when he loaded a graphics driver, and I was like, well, it works on my computers. It works on the rest of the development team's computers. We have no idea why it's not working on my friend's computer.  Another challenge which is perhaps easier to solve is build times. It takes time to build a graphic stack. I do most of my development on my laptop. I have a fairly modern laptop. It still takes quite some time to build, which makes build test cycles fairly slow, and I hope to be able to set up some way where we can commit things to GitHub and get the package in the other end. And doing that would also make it possible to an easier way give testers access to development packages so they just can install on their laptop or desktop and test. The third challenge is developer bandwidth. We're a small team. Upstream moves fast. Sometimes life and work happens, and this means that sometimes updates have to wait a bit. This also goes again with testing. Sometimes we don't have time to test everything. In the end you have to make the jump, but sometimes it's better to be a bit safe and perhaps stick around with an older version that's known to work instead of updating to something that's not at least a bit tested. In the future, this is me getting into the crystal ball, but I think what's going to happen in the future we never know. First off, input devices. I've talked a little bit about this, about FDV, about blip input, things like that. This is an area where Linux is changing how they're doing it, and we kind of need to tag along. I would guess that we need to improve our input device handling and somehow have a translation layer so that it looks, at least for X server and for WLAN, looks a bit Linux-y. Today it's the FDV kernel code I talked about earlier, but I think this is an area where we need to improve both in regards to what we support and also become better at automatically configure things. Mouching keyboard works, but touch screen, track pads, for instance, wake-up tablets, things like that. We also have to do something about theorem legacy. As I said, it's going away from freebies database, at least in 13, but then should it live on forever in freebies ports at some point when the new code is stable enough or when I386 is not as much of a thing, it probably needs to go. The next thing that needs to happen is outload. Today you install the kernel driver, you need to load it, and this needs to happen automatically. It does sometimes, it's not always. And previously the DDX drivers I talked about earlier did the loading of the kernel module. That's not happening anymore, so you kind of have to do it from your startup. I would like to see this happen automatically. There is a facility in Freebies D to handle this, but the graphics drivers aren't using it yet. And since the graphics drivers come from Linux, they look a bit different than native Freebies drivers, so this is something we have to look into. We also have to look into support for more architectures. I mentioned ARM and PP64, PowerPC64 as the most important ones. Support and work is ongoing. We probably have to support I386 for at least some time more, at least in 2038 or something. It was at least one person who got that joke. So, looking further into the future, and this is things that's needed to get Freebies D better as a desktop platform. We need to get a better way to manage our network on our desktop, or at least laptops, where we run them around and use them everywhere. So some sort of tool for this is probably needed. We need to become better at power management, and Wi-Fi support is always something that can improve. It's working pretty good today, but there's always some Broadcom chipset that doesn't work and things like that. So in summary, we talked a bit about the Freebies D graphic stack. I worked through it from kernel to what you see today, basically. We talked about the drivers and what we're doing there today. We talked about the libraries, the Xorg server. We talked a bit about Wayland, and we talked a bit about what I think we need to do this year and the years to come to keep Freebies D a viable desktop platform and to make it a better desktop platform. If you want to help out more resources, you can find our, as I said, we have our GitHub space where you can find us. We have a GitHub chat that integrates into GitHub where you can find us there. You can always email our main list, and we're also available on IRC, at least some of us. You can also talk to me, if you like. I know this has been fairly dry. I wouldn't say boring, but fairly dry. There's no demos or anything. In a way, this whole thing is a live demo. This whole presentation was made using Freebies D. It's done in open office on Freebies D. I'm running Freebies D. I'm running a fairly recent version of Freebies D. Thank you CFS. That makes it possible to upgrade, and then, oh, it broke, okay. Revert to the last snapshot. That was what I had today. Are there any questions? Oops, that was not meant to happen. Any questions? We have one minute for questions. I'm around here today, and I'm around here tomorrow. Let's start with the gentleman in blue. Currently, I don't know. As you've noticed, I haven't talked very much about NVIDIA drivers at all, because we used the binary blob from NVIDIA, so we're basically forced to do what NVIDIA does there, or forced, but we're using what NVIDIA provides. And I don't know if NVIDIA provides, I don't think NVIDIA, the NVIDIA driver provides the libraries needed today, but I haven't tried. Over there. Does that even work on Linux? Pardon? I don't know. I don't think optimal support is... Well, it should be doable if someone sits down and do it, but I think you have to pick either the Intel driver or the NVIDIA driver.


Capitalism is violence. Notes from the edge of the narrative matrix. A system which financially coerces those who have nothing to sell but their labor to work for companies for a fraction of the value they generate is violent. It is aggression. It is simply legalized theft. The only reason this isn't obvious to everyone is centuries of capitalist propaganda. And if people ever manage to free their minds from that indoctrination and begin moving to redistribute wealth the capitalist class has stolen, guess what will happen?  This is on top of the global war on communism that has been going on for generations. The entire thing is violence and is held in place by violence. Capitalism just means free trade. No it doesn't.  Capitalism means what the Marxist who coined and popularized that term have been saying it means since the 1800s. The owners of the means of production exploiting workers by paying them a fraction of the wealth they generate. Capitalism is a system which financially coerces those who have nothing to sell but their labor to sell it to the owners of the means of production. Necessarily at a price that is far below the amount of value they generate and with no influence over the industries they are powering with their work. It is inherently exploitative and leads to corporations with no human interest pursuing profit at all cost even at the expense of the ecosystem we all depend on for survival. Even those who support capitalism understand this distinction if they've done a tiny bit of research outside their partisan echo chambers. You don't get to just change someone else's definition of words to defend your belief system from their criticisms. That's not a thing. By distorting this definition supporters of capitalism can always object to its critics with this isn't real capitalism because trade and finance are regulated by corrupt governments. No it's capitalism. Real capitalism is not just entirely compatible with the corruption of capitalist governments but an unavoidable component of it saying it's not capitalism that's the problem it's crony capitalism or it's not capitalism that's the problem it's corporatism is the same as saying it's not my chain smoking that's the problem it's my emphysema one inevitably leads to the other. Only narrative says I should be able to use my socio economically advantaged position to hire workers who exponentially multiply my wealth for a fraction of what it costs me to pay them. Capitalist narrative created and promulgated for generations by those who benefit from it. Malignant narcissists don't typically seek out therapy partly because they're wired to assume they're perfect and partly because our current systems reward the tendencies of malignant narcissism. We are ruled by untreated malignant narcissists who are elevated by this system. It's a pretty interesting coincidence how western news media just happened to keep discovering reasons why censorship of internet platforms is gravely necessary in a globe-spanning empire that is held together by global narrative control. The most significant political moment in the U.S. since 9-11 and its aftermath was when liberal institutions decided that Trump's 2016 election wasn't a failure of status quo politics but a failure of information control.  This was when the belief among mainstream journalists became widespread that internet censorship is needed and that is their duty to manipulate public opinion. Another 2016 WikiLeaks drop in 2020 would never have been reported on by the mass media as evidenced by their response to the Hunter Biden laptop. Now we're seeing an increased homogenization of online information as the media class cheers on censorship in the name of fighting Russia, fighting white supremacy, fighting COVID misinformation, and in the name of protecting U.S. elections, while the media acts weirder and weirder. The way the entire mass media jumped right on board the Russiagate narrative instead of asking what's true, for example, or the way questionable claims about COVID, which have since been invalidated, were asserted with adamant aggression. This all followed from that moment. And now we're watching Cold War escalations continually ramp up against Russia and China, and the mass media are forcefully and uncritically pumping all U.S. government narratives into public consciousness. The 2016 reshaping of their values lubricated the way for this. You only criticize the U.S. and its allies, not Russia and China, people say. Focusing one's criticisms on the world's most powerful and destructive government requires no defense. It's not weird that I do it, it's weird that more people don't. Those who want to hear criticisms of Russia and China are advised to switch on the nearest television.  Oh, it's so strange and suspicious that you only focus on the worst impulses of the globe-spanning power structure, which is vastly more destructive than any other in existence, instead of yelling about the same governments as every billionaire media outlet throughout the Western world. Duh. Remember when moral panic was a specific thing that would happen once in a while, instead of Western civilization's general, continuous state of existence? Our rulers always have to choose between bread and circuses or accelerationism. They're either choosing to keep the people mollified and distracted while stealing a little, or to risk provoking revolution by stealing a lot. Right now, they're picking the latter. Interesting choice. When you look at it that way, you realize that even when something horrible is happening, it could also be leading to something very healthy. They're walking a delicate tightrope walk while trying to keep their greed from consuming them. They're not really in control here.