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Race and Antiracism in Science and the Humanities Michell Chresfield and Josie Gill discuss the ways – lareviewofbooks
Posted: August 14, 2021 at 1:05 am
THE FOLLOWING CONVERSATION, adapted from an event at the University of Marylands Center for Literary and Comparative Studies, is part of the Los Angeles Review of Books special series, Antiracism in the Contemporary University, edited by Tita Chico. Click here for the full series.
JOSIE GILL: Thank you for that question, Michell. The question is how, as humanities scholars, can we approach race and science today, at a moment when certain biological ideas about race seem to be reappearing. There are white supremacist groups discussing (and misinterpreting) genetic studies on internet forums. The New York Times reported that white supremacists were chugging milk because they thought a genetic study was saying that white people were better able to digest milk than others. Trump has often talked about his belief in good genes both his own and those of his followers as a way of signaling the purported superiority of whiteness. So there are seemingly casual but also very prominent ideas about genetics entering public discourse. In relation to COVID-19, recently the home secretary in the UK, Priti Patel, was trying to explain the different impact [of the disease] on Black and Asian communities in the UK. She implied that they are just somehow more susceptible to COVID-19, that theres some kind of biological difference. Whether these ideas represent a return, or whether they have been there all along, there is no doubt that we are in a political moment where these discourses are gaining traction and theres a return to a biological understanding of race.
Approaching this situation as a literary scholar can be quite tricky. There has been an attack on scientific expertise [from the right], and so literary scholars can be under some pressure not to do anything that might undermine science. This is particularly the case for the understanding of race that was confirmed by the Human Genome Project; that race is not biological and has no genetic meaning. That is the established and predominant scientific view. In the main, literary approaches tend to adhere to this view, to support it, and many literary scholars are influenced by critical race scholarship in this regard. Scholars like Kwame Anthony Appiah, Henry Louis Gates Jr., and Paul Gilroy have in different ways brought genetic science into their work to support their own, preexisting understanding of race; that it is not a genetic reality. You might ask, whats wrong with that? Im not disputing the finding of the HGP or saying that it is wrong, but what I find interesting in their usage of science, is that it marks a departure from how these scholars talk about science in the past.
When these scholars discuss the historical construction of race in the 18th and 19th centuries, they acknowledge that it was an interdisciplinary idea a construct created from many discourses including science, philosophy, and literature. In these analyses, science is understood as a product of its time, and the colonial context in particular. Theres an understanding that science was influenced by everything that was going on politically and socially at the time. However, when you turn to literary analyses of 21st-century science, you can see theres a tendency to revert to a different stance toward science, treating it as an objective, neutral authority on race, and not as complicated or imbricated in culture as it was historically.
I was interested to see how I could approach contemporary science by maintaining a focus on the political, social, and cultural contexts which have made certain ideas about race possible in 21st century. Im drawing on the work of STS scholar Jenny Reardon, in doing this, and trying to expand her analysis and include the literary and cultural, to think about how that context enables certain ideas about race to emerge narratively. Im not trying to undo the scientific finding that race isnt genetic; Im not saying thats not true; I just want to understand the conditions that enabled this idea to gain traction. I dont think its a coincidence that that idea came about at the same time as the rise of post-racial discourse at the beginning of this century. It seems strange to think of it now, post-BLM, but with Obama, there really was a widespread belief in the US and UK that we were entering a post-racial period and that racism was no longer an issue, that people of color had gained a certain level of equality and that we were moving beyond race. The science of race was feeding into that political climate.
You touched on it toward the end of your response, but Im interested in what scientific studies of race have to learn from literary studies. Your book talks about how the literary contributes to science. Can you speak more on that?
Im not saying theres one particular relationship that literature has to science; that simply wouldnt be possible given that there is so much diversity in scientific perspectives on race in the 21st century. That said, I think there are two main ways in which literature speaks to some of the absences of genetic discourse. First, the novels that I look at in Biofictions all make connections to the history of race and science and try to position the developments happening now within the context of what has happened before. I think that works against what scientific discourse often does, which is to create a very deliberate separation between eugenics, the racial science of the past, and genetic science today.
I think literature can help us to see how older racial ideas seep into the present. Related to this, the other thing literature does is draw attention to ways in which we cant easily separate science from the imaginary or the fictional. Genetic discourses on race continually try to separate the social and cultural from the scientific; they position race and racism as largely a social problem that no longer has anything to do with science. The novels that I look at in Biofictions demonstrate that it isnt really possible to do that. They are very alive to the ways in which the fictional, the made-up, comes to be incorporated into science; how the imaginary shapes the development, expression, and transmission of scientific ideas and the public understanding of science. They show how genetic science functions narratively, rather than objectively, within the racialized contexts in which it is embedded. To say these things might be to align oneself with people who want to undermine science, but thats not what Im trying to do.
Its necessary that we do this work because often racial configurations emerge when we appear to move beyond race and when science appears to move us beyond race. I think literature is good at revealing how older racial thinking is always latent in the new. To deny this would be as regressive as the attack on science itself. I can give an example on how that happens in one of the novels I discuss in my book. Apex Hides the Hurt by Colson Whitehead was published in 2006. Its the story of an unnamed African American protagonist who works in marketing, and his job is to name products. He becomes famous for naming a range of plasters (band-aids) that are designed to match the skin tone of their wearers so its a kind of multicultural plaster that he calls Apex. The protagonist wears one of these plasters after he stubs his toe; it obscures a serious wound, and, in the end, his toe has to be amputated. The novel is about his recovery from this incident and I think its really a satire on the ways in which race is often invoked in medicine for commercial ends.
It seems to be referencing a real-life example of this BiDil, a drug that was approved by the FDA in 2005, exclusively for the treatment of African Americans with congestive heart failure. BiDil was supported on the basis that it would help a population which really needed the help, but there was no genetic basis for it whatsoever. The makers of the drug admitted that they used race as a proxy for an unknown genetic marker and that the drug might have been effective in nonAfrican American populations. Race was a way of marketing the drug and even though it was a commercial failure, it had a big impact on how Americans (including African Americans) understand race; the drug appeared to signal that, contrary to the findings of the Human Genome Project, there is some genetic basis for race and people were being medicated on that basis.
To go back to the novel, I think Whitehead is interested in exposing the superficiality of the ways in which race is sometimes being invoked in medicine, and the novel is something of a warning about the uncritical adoption of racial categories in that context. He creates a subtle historical comparison to make this point. The amputation of the toe is an echo of a cure sometimes given to enslaved people who were diagnosed with Drapetomania. This was the disease that made enslaved people want to run away, a supposed condition named by Samuel Cartwright, a doctor and major figure in the South in the 19th century. Its obviously an absurd attempt to pathologize enslaved people, and I think what Whitehead shows is how the fictionalization of race and medicine is still happening today with drugs like BiDil, which seems to make race the problem to be treated to make race into the disease.
Id like to ask you some questions now, Michell! Youre working on a period about 100 years before that which Im looking at, but I wonder: Could say something about how your work connects to contemporary social justice movements like Black Lives Matter, and how it speaks to some of the issues which COVID-19 has brought about?
As you said, Im working in an earlier part of history, focusing on the Jim Crow era, specifically on communities of Tri-racial identity for example, those having white, Indigenous, and Black ancestry. Ive been interested in how these communities use scientific technologies in order to make their own identity claims. For example, disease has been one avenue through which these communities make certain racial claims. We know that Black and Indigenous populations experienced a high incidence of diabetes and so this becomes, for some, a way to make certain racial claims.
However, in terms of thinking about BLM and differential health outcomes, with my family being originally from Alabama, I was struck by how the idea that Black people were possibly immune to COVID-19 received a lot of attention throughout the South during the first weeks of COVID-19. It made clear to me that the ideas linking race and disease are not only part of our history but persist into the present day.
Even as we saw Black communities being decimated by COVID-19, it took so long to highlight the narratives surrounding the systemic issues that lead to these health outcomes, rather than some biological innateness specific to black people. It reminded me of the early 20th century and medical discourses which claimed that African Americans were more susceptible to diseases like tuberculosis and syphilis. When we highlight that Black populations are being disproportionately impacted by a disease, we must be vigilant to ensure this calling out isnt misinterpreted as affirming a belief in innate Black difference. BLM is doing important work in terms of combating that narrative.
In that sense, they are doing what genetic science isnt, which is focusing on racism, rather than on the idea of race itself as being the problem. It is structural inequality and racism which is causing inequalities in the COVID-19 pandemic. This relates to my next question: how do you work through the relationship between race and racism, something that is often elided in genetic science?
That question is so important, and its one that I engage students on quite a lot. One of the things I tell them, and this is borrowed from Ta-Nehisi Coates, is to understand, Race is the child, not the father. Meaning that race is the child of racism, not the father. And this for me is a productive way to think about the relationship between the two.
We can have good debates about the etymology or genealogy of these terms, but it is important to remember that race and racism are not always engaged in the same ideological and political projects. They can converge and diverge in all sorts of ways. When we focus on race as the cause or equivalent to racism we can miss the ways in which critical engagement with race and its construction allows us to engage biases and prejudices that can help us combat racism.
Also, because Im an intellectual historian and I study ideas, Im attached in weird ways to the idea of race, because it matters so much for the communities I study. One community I study has been marginalized because of how they racially classify, and there are dozens of communities like that in the United States. We can say were beyond race, but race continues to matter, as do the categories that are part of it.
Is there a tension between the more popular uses of genetics the way certain communities are buying into a biological idea of race and the way academics think about race and science. How does this play out in your work?
There are tensions, particularly when we think about some of the racial politics of the present. The communities that I study want to be recognized as Native peoples. To that end, they are often very invested in the need for outside recognition of inward feeling of identity. This is how the acknowledgment process has worked for much of the 20th century. It has depended on how outsiders view you rather than on how you see yourselves.
There is also tension because when scholars come to communities and they ask questions about lived experiences and identities, were not always cognizant of how these questions will impact the political projects these communities have underway. In my work, Im trying to be sensitive to not repeating the violence of treating my research interests like they dont have real-world consequences. I want to be sensitive to the political projects of the communities and individuals involved. The same should hold for scientists and humanists.
Turning back to the academy, do you see potential synergies in the way scientists and humanists approach race and antiracism?
Im interested in interdisciplinary conversations between the sciences and humanities, whether there can be more dialogue between our disciplines and how that can happen not just at an intellectual level but at a practical level within universities. The most immediate way to tackle the issues of race in science and racism would be to have more face-to-face conversations across our disciplines.
The work Im doing is as much concerned with how humanities scholars approach race, as it is with how scientists approach the concept. I would like to see a renewed focus on talking about race across both the humanities and sciences. I don't know the situation in the US but in the UK, many people are afraid to talk about race and it is avoided because people are afraid of saying the wrong thing, or they are afraid of the decolonization debates, seeing them as too radical. When we talk about race and genetics, that cant be separated from broader discussions of racial issues as they play out in a university, and all the different facets of racism and peoples experiences of it.
These conversations are good. In my own work, I find that scientists are often very earnest about the limitations of their own work, however, the people impacted arent always acknowledging those limitations. For those reasons, having conversations with multiple stakeholders is key. As is thinking about the ways that our work translates outside of the scholarly bubble.
I work in communities that have been victimized by both the academy and the members of the scientific discipline who have been interested in their lived experience. I want to investigate this process and highlight the injustices that have occurred as a result. However, Im also very much interested in how communities have combated these efforts. Both sides of this story highlight the fact that race-making doesnt just happen from the top-down. It happens from bottom-up as well, as individuals and communities push back against notions of scientific expertise. My scholarly position is to highlight that co-production as a way of challenging the hegemony of scientific knowledge and by extension that of the academy.
In the broadest sense, my work is interested in how academic disciplines have marshaled their power and expertise when they have produced studies of racial identity. In terms of my own position, I know that I am within the academy, but it remains an important part of my practice to ensure that this work doesnt stay here, but that I engage with the communities impacted by it.
How has your position within the university informed your work on race and specifically the evolution of academic constructions of and attitudes toward race?
Im a founding member and former director of the Centre for Black Humanities at the University of Bristol. Its an interdisciplinary research center in the Faculty of Arts that we established four years ago. It came together because there was a group of us working on a wide range of topics relating to Black life in Britain, Africa, the Americas, and the Caribbean. So the remit is quite wide, but thats good because there arent many research centers in the UK that explicitly foreground Blackness as a topic of study. There are many reasons for that. Black as a term has a different history in the UK, to the US. In the 1970s and 80s, it was a term used by and to describe people of color but thats now changed. It now refers to people of African descent. It was a bold move to establish the Centre because when we were trying to set it up, some people were saying race isnt real, so why are you talking about Blackness and why would you single out Blackness from other ethnicities?
But for us, as a group of researchers, it made a lot of sense because we are situated in Bristol where there is a large, historic Black community, an activist community that has for years been trying to address the legacies of slavery in the city. These legacies were addressed very publicly in June 2020 when the statue of slave trader Edward Colston was pulled down during a BLM demonstration. Creating the Centre for Black Humanities was one way in which we could expand the involvement of that community with the university, creating a space where Black people and Black staff and students could feel that they have a place to have these discussions. Weve developed an MA program, and theres now a bursary for Black teachers wishing to take it. With regard to science, what I have found interesting is that Ive started to have PhD students from the sciences coming to me wanting to talk about racism and Black Lives Matter. Science faculty are beginning these conversations now, but I think that creating the Centre did a lot of work within the university. It immediately had an institutional visibility that meant we could support students and staff from across the disciplines, even though we are only focused on the arts and the humanities in an intellectual sense. In a broader activist sense, were engaging with a much wider constituency of academics and people within Bristol.
We began our conversation today by discussing the return of explicit, biological racism to the public sphere. How might we relate this to the relationship between fact and fiction and the loaded question of truth and post-truth in contemporary society? In your book, Josie, youre thinking about the negotiation of fact and fiction in the development of scientific knowledge.
Scientific facts change all the time. One of the things I havent mentioned yet is epigenetics, which is a recent development within genetics. It overturns what was previously understood about genetics which is broadly that you have genes that are inherited and passed on through generations and apart from a few mutations here and there, they remain largely fixed and stable. Epigenetics has come along and now scientists are looking at how genes have these epigenetic marks that are switched on and off depending on the environment in which someone (or a body) is located. Its still an emerging area, but some studies suggest that those marks, those changes, can also be passed down through generations. This is an interesting example of how we have to be open to the nature of scientific discovery.
To bring fiction into the conversation, for me, the finding of epigenetics that genes can carry a memory of past environments and experiences (that is the metaphor which is often used) is really interesting. It speaks to the way that race has already been imagined in fiction. Im thinking of Octavia Butlers novel, Kindred, which is about a woman, Dana, living in the 1970s who gets pulled back in time to the 19th century to the plantation of her ancestors, who are both white enslavers and enslaved Black people. Dana is in a very dynamic relationship with the past: her body is mutilated through whipping and torture when shes on the plantation, and she ends up having to live in the (1970s) present without an arm and is disabled by this experience and encounter with history. This is an interesting representation of how bodies come to be raced, of how raced bodies are created through racist environments. Im interested in the ways in which we can think about fiction and the kinds of fictional models that are already there for thinking about race not as genetically real, but as the result of certain fictional (i.e., racist) beliefs. The idea that some people are inferior to others because of their race is fiction; but this fiction through racism has real consequences for the body. There are all kinds of interesting and productive ways to think about fact and fiction. We shouldnt limit how we think about this relationship just because some people want to question the validity of science and scientific fact. Theyre going to do that anyway.
Josie Gill is senior lecturer in Black British Writing at the University of Bristol. Her book Biofictions: Race, Genetics and the Contemporary Novel was published by Bloomsbury in 2020 and won the British Society for Literature and Science Book Prize for 2020. She is principal investigator of the Wellcome Trust funded project Black Health and the Humanities (20202022) located at the Centre for Black Humanities.
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Race and Antiracism in Science and the Humanities Michell Chresfield and Josie Gill discuss the ways - lareviewofbooks
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Prehistoric Graves: Why They Are Time Capsules Of Early Britain – BBC History Magazine
Posted: at 1:05 am
As well as the objects we find in graves, were able to extract ever more information from the bones themselves. For me, as a biological anthropologist, its been astonishing how the science around this has developed over the past 20 to 30 years.
If Im presented with a skeleton, I can tell quite a lot just by looking at the bones with the naked eye. I have a background as a medical doctor and before I started learning the business of osteoarchaeology, I would have thought: Its just a skeleton. How much can you really tell? You cant ask it about symptoms, you cant do blood tests. But I was astonished at how much you could work out. First, bone responds to disease. Some infections, such as syphilis and tuberculosis, affect bone in very distinctive ways. Osteoarthritis is also easy to identify from tiny holes on the surface of a joint.
Next you can look at teeth. People suffered from dental disease in the past, just as we do today, but most prehistoric people actually had much better teeth than ours because they didnt have such a starchy, sugary diet. They didnt brush their teeth as fastidiously as we do, but their teeth are nevertheless usually in surprisingly good condition.
Employing radiography techniques, such as using X-rays, allows us to uncover more clues hidden features of the bones. And with a micro CT [computed tomography] scanner were able to slice up the bones virtually, allowing us to analyse them without incurring any damage.
Then there are chemical techniques that allow us to analyse the ratios of different elements in bones and teeth. Our bodies are built from what we consume, so we are essentially made out of our surroundings. That means that the signatures of the landscapes in which we grew up are written into our bodies particularly into teeth, because tooth enamel is laid down in childhood.
For instance, your body is constantly incorporating different stable isotopes of oxygen and strontium in various ratios. We can analyse isotopes in ancient human remains, and see how these elemental ratios match those found in the geology of places in Britain or farther afield. This can be really useful for telling where somebody grew up, for instance, or where they spent the last decade of their life.
Finally, we can extract DNA from ancient bones and sequence it. That technology has come on in leaps and bounds in recent years.
Alice Roberts is the author of Ancestors: A Prehistory of Britain in Seven Burials (Simon & Schuster, 2021)
The human genome was fully sequenced in 2003. Since then weve developed the ability to extract DNA from very ancient bones, and to work out how to combine separate fragments of DNA into a complete genome. By doing that, were able to look for rare variants that might give us clues indicating when particular groups of people moved in or out of Britain. Sometimes were able to reconstruct more detailed information about individuals, too. One of the prehistoric skeletons I discuss in the book is known as Cheddar Man, who was discovered in Somerset in 1903, and lived around 10,000 years ago. By analysing his genome, geneticists have revealed that he probably had an unusual combination of dark skin and bright blue eyes. Being able to work that out from just a skeleton is utterly extraordinary.
DNA can also reveal information about kinship and relationships between individuals. Thats been quite profound when it comes to looking at the communal burials found inside Neolithic chamber tombs, for instance. One theory about these chamber tombs is that they were intended to anonymise the dead, and therefore contain people from across the whole community. Another theory is that they effectively acted as family vaults and some recent genetic analyses provide hints that this may indeed have been the case. For example, its been revealed that two bodies buried together in a Neolithic monument at Primrose Grange in County Sligo, Ireland are those of a father and his daughter.
Elsewhere in Ireland, DNA analysis of a man buried at Newgrange Stone Age tomb in the Boyne valley has revealed that he was the son of an incestuous union between either a parent and a child or two siblings. So were finding out some quite extraordinary details, some of which may not even have been public knowledge at the time of those peoples deaths.
Genetic science is not a panacea. Its not as though DNA technology somehow supersedes archaeology in fact, it could actually leave us with more questions than answers. But it does provide important strands of new evidence with the potential to answer some big questions, especially about mobility and migration. We should view it more as a tool for archaeologists to use one that will hopefully help us see the picture more clearly.
Genetics can certainly be disruptive. In fact, its probably as disruptive as radiocarbon dating was when that emerged, from the late 1940s suddenly, archaeologists were able to pin absolute dates on organic material. I think you can see a similar effect playing out with DNA analysis at the moment.
There have been some instances of geneticists treading on archaeologists toes. Theres been a perception by some archaeologists that geneticists have waded into long-standing archaeological debates and simply said: Youve been arguing about this for ages. Well, now weve got the answer. Not surprisingly, archaeologists have responded: Hang on a minute first you need to learn a bit about archaeology and the kinds of questions were asking.
But weve got to capitalise on the power of genetics to help us solve archaeological conundrums. In the book, I talk about a cutting-edge new project called 1,000 Ancient British Genomes, led by Swedish geneticist Pontus Skoglund of the Francis Crick Institute. This is a brilliant example of the power of collaboration between geneticists and archaeologists. Skoglund is engaging with archaeologists up and down the UK, asking them to identify questions that genetics might be able to help solve.
One of the people I became quite obsessed with is Augustus Pitt-Rivers (18271900). Hes best known as a collector, but he also came up with some really interesting ideas about how cultures change and evolve over time, and how these transitions happened. Pitt-Rivers was very influenced by 19th-century evolutionary theory and biology, and wondered how these ideas could apply to culture. He also started to think about whether the origins of new cultures might be linked to the movement of people.
For instance, Bronze Age people in Britain obviously had a different culture from the Neolithic people who preceded them. But where did they pick up this culture from? Pitt-Rivers suggested that there had effectively been a population replacement that Bronze Age culture was actually brought in by a whole load of new people. He tried to back up this theory by measuring skulls, arguing that there were detectable differences between the shapes of Neolithic and Bronze Age skulls. He was trying to use the study of skulls in a similar way to how we would now use DNA studies.
Whats astonishing is that DNA evidence now emerging suggests that Pitt-Rivers may have been right that a lot of people may have arrived in Britain during the Bronze Age, largely replacing Neolithic populations. Those earlier people didnt completely disappear, but there was a really profound turnover of population. Its really interesting to think about the contact between these two groups, and about the ways in which their different cultures may have merged.
Archaeology is a very introspective, self-aware discipline, which I think is extremely useful. Weve long been aware that every archaeologist always has ideas from their own time in the back of their mind whenever they approach a set of observations.
That can impact ideas about gender, for example. Take Iron Age chariot burials: not all of them contain men we know that some, such as the site at Wetwang in East Yorkshire, definitely contain women. I think that in the past antiquarians would have very quickly jumped to a conclusion that the body was male, based on the style of the burial or perhaps artefacts that were buried with the body. This is similar to what Reverend William Buckland (17841856) did when he discovered the oldest skeleton yet found in Britain, on the Gower peninsula in south Wales, which he called the Red Lady of Paviland. The remains are clearly male, but Buckland didnt think it could possibly be a man because the individual was buried with what looked to him like ivory jewellery. As a 19th-century antiquarian, he couldnt stomach the idea that a man might be buried with jewellery.
And these ideas still persist. When we find an Iron Age burial with a sword, theres often an assumption that its a man. Or if a mirror is excavated from a burial, theres an assumption that the remains are that of a woman. In the book, I talk about the need to avoid seeing discoveries through our own current cultural lens to accept that there may have been many more diverse identities in the past than perhaps we understand today, for example. We think that our society and culture is normal in the way that it defines two genders, but perhaps in the past there was a much more diverse approach to identity. Certainly, if you find an Iron Age burial with both a sword and a mirror (and one such site has been excavated), that might be telling us something quite interesting about ancient identities.
I think that new scientific technologies encourage us to move away from our current preconceptions to look at the evidence in isolation to begin with and then to build up a bigger picture.
Its a stunning discovery the most richly furnished Copper Age burial yet found in Britain. This man was buried with almost 100 objects in his timber-lined grave, so he was certainly high status or special in some way. All sorts of things were buried with him: lots of flints and arrowheads, and stone items that we presume are wrist guards for archery hence his name as well as copper knives and five bell-shaped beakers. There were also gold ornaments, thought to be hair wraps or possibly earrings the oldest gold found in Britain.
Because the Amesbury Archer was found only about three miles from Stonehenge, some have suggested that he may have had a link with that site. That may be true, but well never be able to prove it. You can also speculate about who he was his position in that society: are we looking at some kind of Bronze Age shaman or magician? And, connected with that idea, what did people think of those who first developed the ability to extract metal out of stone? It must have been amazing to see a completely new material being produced.
What I find particularly interesting about the Amesbury Archer is that analysis of the stable isotopes in his remains shows that he wasnt a local in fact, he grew up in or near the Alps. Graves such as his show just how far these connections stretched, and the distances that people were travelling. Theres this popular idea that in the ancient past people never travelled farther than the next village, but now we have evidence of some, such as the Amesbury Archer, travelling hundreds of miles in a lifetime.
That burial, found in 2017, is absolutely spectacular. I was lucky enough to visit it with the team that discovered it. We dont see many Iron Age burials across most of Britain, but in Yorkshire several very characteristic chariot burials have been found. These belonged to the Arras culture, which had connections to the near continent and possibly brought this very distinctive funerary style with them.
That Pocklington grave contains the body of a man buried within a chariot. In other similar burials, the chariots tend to have been dismantled before being put in the grave flatpacked, essentially. This one, though, was standing up and intact, with the man placed inside in a crouching position.
Along with the grave, theres evidence of a funeral feast. You get the impression that this funeral was a great spectacle, intended to show off the status of the deceased individual but also that of the surviving family. There are animal bones in the grave, including a rack of ribs, so it looks as if dishes from the feast were being shared with the deceased individual.
The other utterly extraordinary thing is that two pony skeletons were found standing up in the grave. That was just unbelievable. We spent quite a long time scratching our heads, wondering how on earth they got those ponies in there upright. Did they winch dead animals into the grave and then somehow support them, maybe piling up the soil underneath to hold them in a standing position? Or were the ponies led into the grave and then killed? I dont know if well ever quite get to the bottom of how it was achieved, but obviously it was extremely important to the design of the grave to have the chariot looking as though it was ready to depart, taking the dead man off, possibly to the afterlife. That is, of course, if they believed in the afterlife we dont know!
I think that exploring prehistory shows us just how multicultural Britain has always been. What weve seen is that many different groups of people have crossed the North Sea and the Channel in both directions over time, and that those cultures all enriched the others.
Although I write a lot about the power of genetics, I dont think we should be trying to trace direct genetic links between us and people in the ancient past because, once you get back into prehistory, these connections arent terribly meaningful. You dont need to have a direct genetic link with the Red Lady of Paviland or the Amesbury Archer to think about what the lives of these individuals might have been like. Im aiming for an egalitarian approach to ancestry in the landscape. The ancestors I look at in the book belong to everybody.
Alice Roberts is the author of Ancestors: A Prehistory of Britain in Seven Burials (Simon & Schuster, 2021). Buy it now on Amazon, Waterstones or Bookshop.org
This article was first published in the July 2021 issue of BBC History Magazine
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Accelerated ageing linked to sleep loss in new mothers: Study – Hindustan Times
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According to the University of California Los Angeles (UCLA) researchers, when new mothers complain that all those sleepless nights caring for their newborns are taking years off their life, they just might be right.
UCLA research published this study in the journal Sleep Health.
Scientists studied 33 mothers during their pregnancies and the first year of their babies' lives, analyzing the women's DNA from blood samples to determine their "biological age," which can differ from chronological age. They found that a year after giving birth, the biological age of mothers who slept less than seven hours a night at the six-month mark was three to seven years older than those who logged seven hours or more.
Mothers who slept less than seven hours also had shorter telomeres in their white blood cells. These small pieces of DNA at the ends of chromosomes act as protective caps, like the plastic tips on the ends of shoelaces. Shortened telomeres have been linked to a higher risk of cancers, cardiovascular and other diseases, and earlier death.
"The early months of postpartum sleep deprivation could have a lasting effect on physical health," said the study's first author, Judith Carroll, UCLA's George F. Solomon Professor of Psychobiology. "We know from a large body of research that sleeping less than seven hours a night is detrimental to health and increases the risk of age-related diseases."
While participants' nightly sleep ranged from five to nine hours, more than half were getting less than seven hours, both six months and one year after giving birth, the researchers report.
"We found that with every hour of additional sleep, the mother's biological age was younger," said Carroll, a member of the Cousins Center for Psychoneuroimmunology at UCLA's Jane and Terry Semel Institute for Neuroscience and Human Behavior. "I, and many other sleep scientists, consider sleep health to be just as vital to overall health as diet and exercise."
Carroll urged new mothers to take advantage of opportunities to get a little extra sleep, like taking naps during the day when their baby is asleep, accepting offers of assistance from family and friends, and, when possible, asking their partner to help with the baby during the night or early morning. "Taking care of your sleep needs will help you and your baby in the long run," she said.
Co-author Christine Dunkel Schetter, a distinguished professor of psychology and psychiatry at UCLA, said the study results "and other findings on maternal postpartum mental health provide the impetus for better-supporting mothers of young infants so that they can get sufficient sleep -- possibly through parental leave so that both parents can bear some of the burdens of care, and through programs for families and fathers."
Dunkel Schetter added that while accelerated biological ageing linked to sleep loss may increase women's health risks, it doesn't automatically cause harm to their bodies. "We don't want the message to be that mothers are permanently damaged by infant care and loss of sleep," she emphasized. "We don't know if these effects are long-lasting."
The study used the latest scientific methods of analyzing changes in DNA to assess biological ageing -- also known as epigenetic ageing, Dunkel Schetter said. DNA provides the code for making proteins, which carry out many functions in the cells of our body, and epigenetics focuses on whether regions of this code are "open" or "closed."
"You can think of DNA as a grocery store," Carroll said, "with lots of basic ingredients to build a meal. If there is a spill in one aisle, it may be closed, and you can't get an item from that aisle, which might prevent you from making a recipe. When access to DNA code is 'closed,' then those genes that code for specific proteins cannot be expressed and are therefore turned off."
Because specific sites within DNA are turned on or off with ageing, the process acts as a sort of clock, Carroll said, allowing scientists to estimate individuals' biological age. Greater an individual's biological, or epigenetic, age, the greater their risk of disease and earlier death.
The study's cohort -- which included women who ranged in age from 23 to 45 six months after giving birth -- is not a large representative sample of women, the authors said, and more studies are needed to better understand the long-term impact of sleep loss on new mothers, what other factors might contribute to sleep loss and whether the biological ageing effects are permanent or reversible.
Carroll and Dunkel Schetter reported last year that a mother's stress prior to giving birth may accelerate her child's biological ageing, which is a form of "intergenerational transfer of health risk," Dunkel Schetter said.
Co-authors of the new study included researchers from the department of psychology, the department of psychiatry and biobehavioral sciences, and the department of human genetics and biostatistics at UCLA and from the psychology department at the University of Colorado at Colorado Springs.
Funding sources for the study included the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Institute of Aging, both part of the National Institutes of Health. (ANI)
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Taboo: Why has Africa emerged as the global coronavirus ‘Cold Spot’ and why are we afraid to talk about it? – Genetic Literacy Project
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The first COVID-19 case in Africa was confirmed on February 14th, 2020, in Egypt. The first in sub-Saharan Africa appeared in Nigeria soon after. Health officials were united in a near-panic about how the novel coronavirus would roll through the worlds second most populous continent. By mid-month, the World Health Organization (WHO) listed four sub-Saharan countries on a Top 13 global danger list because of direct air links to China. Writing for the Lancet, two scientists with the Africa Center for Disease Control outlined a catastrophe in the making:
With neither treatment nor vaccines, and without pre-existing immunity, the effect [of COVID-19] might be devastating because of the multiple health challenges the continent already faces: rapid population growth and increased movement of people; existing endemic diseases re-emerging and emerging infectious pathogens and others; and increasing incidence of non-communicable diseases.
Many medical professionals predicted that Africa could spin into a death spiral. My advice to Africa is to prepare for the worst, and we must do everything we can to cut the root problem, Tedros Adhanom Ghebreyesus, the first African director-general of the WHO,warned in March 2020. I think Africa, my continent, must wake up. By spring, theWHO was projecting 44 million or more cases in Africaand the World Bank issued a map of the continent colored in blood red, anticipating that the worst was imminent:
These dire warnings seemed to make sense. After all,two-thirds of the global extreme poor population(63 percent) live in sub-Saharan Africa. According to the World Bank, more than40 percent of the regionlives in extreme poverty and unhygienic environments, conflict, fragmented medical and education systems, and dysfunctional leadershipall factors that was expected to light a match to the tinder of the SARS-CoV-2 outbreak. Scientists say that most African countries lack the capacity and expertise to manage endemic deadly diseases like malaria. Africa seemed ripe for catastrophe.
But disaster never came. Africa has not been affected on anything like the scale of most countries inAsia, Europe, and North and South America.(The major exceptions being China, Taiwan, Australia, and New Zealand, which zealously enforced lockdowns.) In fact, the vast African sub-continent south of the Sahara desert, more than 1.1 billion people, has emerged as the worlds COVID-19 cold spot, as illustrated by anECDC map reproduced by BBC and by graphics like these:
Thelatest statisticsshow about four million cases and 107,000 coronavirus-related deaths, concentrated mostly in the Arab majority countries north of the Sahara. Except for South Africathe most multiracial of the black-majority countriesand Nigeria, sub-Saharan Africa has largely been spared. And these startling low case and death statistics come even asAfrica has the lowest vaccination rate in the worldless than one dose administered per 100 people, and with many countries having given none to the general population.
Europe has less than two-thirds of the population of Africa, but by late-March it had41 million casesand more than 900,000 deaths900 percent more. The US, with less than a third of the population of Africa, has approximately 30.4 million cases and 551,00 deaths as of March 31, thousands of percent more on a per capita basis than Africa. In other words, the US, Europe, and parts of South America are experiencing far more than 1,000 deaths per million while most of sub-Saharan Africa has between 0.5 and 25 deaths per million, according to stats updated regularly byWikipedia.
Journalistsand even somescientistshave beentwisting themselvesinto speculative pretzels trying to explain this phenomenon. Theories range from sub-Saharan Africas quick response (no); favorable climate (which has not protected tropical sections of Brazil, Peru, and other warmer climes in South America); and good community health systems (directly contradicted by WHO and Africa CDC). In each of the articles acknowledging these puzzling statistics, journalists were sure to suggest that Armageddon might be right around the corner.
Experts fear a more devastating second surge,warnedNational Geographicin late December, although there was no first surge and just two weeks before Africas tiny December uptick (driven almost entirely by the mutant variant in South Africa) turned back downward,according to Reuters:
So whats going on here? And why are the media and most scientists so unwilling to engage one of the most plausible science-based factors: that black Africans appear to be protected, at least in part, by their ancestry? Combined with the fact that sub-Saharan Africa is the youngest region in the worldyouth brings fewer co-morbidities and age is the most significant factor in contracting and dying from COVID-19ancestry is likely a significant contributing factor to sub-Saharan Africas comparatively modest case and death count.
With the notable exception of a research project in Hawaii, scientists tend to shy away from exploring the population genetics angle, almost certainly fearful of stirring the embers of race science.It is really mind boggling why Africa is doing so well, while in US and UK, the people of African ancestry are doing so poorly,Maarit Tiirikainen, a cancer and bioinformatics researcher at the University of Hawaii Cancer Center, told us in an email.
Dr. Tiirikainen is a lead researcher in a joint project at the University of Hawaii and LifeDNA in what some believe is a controversial undertaking considering the taboos on race research. They areattempting to identifythose that are most vulnerable to the current and future SARS attacks and COVID based on their genetics.
Blacks (along with other ethnic minorities) in the US and Great Britain who have contracted COVID-19 have generally fared worse than Whites. For the latter, it seems the Western socioeconomics may play a major role, Dr. Tiirikainen wrote. Each individuals risk of dying from a particular disease tends to reflect access to adequate healthcare and underlying health conditions (co-morbidities). Those factors have proved a lethal mix in poorer communities in theUS, UK, and other countries, with lower income groupsoften ethnic and racial minoritiesdying at disproportionately high rates.
But Africa has proven unique. Dr. Tiirikainen, like many candid researchers in this field, is skeptical that social and environmental factors alone can account for the extraordinarily low COVID-19 African infection and death rates. It is not because Africa took extraordinary steps to insulate itself as the pandemic spread. Healthcare remains fragmented at best and COVID information outreach has been limited by scant resources.There may also be genetic differences in immune and other important genes, she said.
At the end of March, 2020, when much was still to be learned about the science of COVID-19, the co-authors of this articlethe Genetic Literacy Projects Jon Entine and contributing science journalist Patrick Whittlediscussed some of the potential reasons in the article Whats race got to do with it? Following discussions with many experts, we decided not to reflexively exclude genetic explanations, which are a taboo subject. Rather, we examined the panoply of likely causes, rejecting thea prioriWestern prejudice that often excludes evidence that might be linked to population-level genetics and group differences for fear of racializing the analysis. We are obviously aware that skin color isnot a recognized science-based population concept. Given theracist historyof biological beliefs about human differences, addressing the fact of ancestrally-based genetic differences must be pursued carefully.
Why even discuss possible genetic factors? Because biases among researchers and public policy officials could undermine the development and deployment of treatments and antiviral vaccines for all of us, but particularly for more vulnerable populations in Africa and in the African diaspora. Blacks and other racial minorities in the US, Latin America, and the UK are more likely to suffer chronic health problems. For example, in the US, blacks aremore than 50 percent likelier to report having poor health as compared to whites, and more than two-thirds of black adult women are overweight. Developing therapies for at-risk populations is critical. Those with genetic resistance to infection or who may be genetically protected in some degree from developing symptoms could help scientists develop treatments for all. Lives are at stake.
So lets dip into these murky waters. Could our ancestry, which defines our genetic make-up, play a role in susceptibility to COVID or other viruses?
. . .
The rest of this article can be read at Quillette. Quillette can be found on Twitter @Quillette
A version of this article originally appeared on the GLP as a two part series. Read those articles here:
Jon Entineis the founding editor of the Genetic Literacy Project, and winner of 19 major journalism awards. He has written extensively in the popular and academic press on population genetics, including two best-sellers,Taboo: Why Black Athletes Dominate Sports and Why Were Afraid to Talk About It,andAbrahams Children: Race, Genetics, and the DNA of The Chosen People. You can follow him on Twitter@JonEntine
Patrick Whittle has a PhD in philosophy and is a New Zealand-based freelance writer with a particular interest in the social and political implications of biological science. You can find him at his websitepatrickmichaelwhittle.comor follow him on Twitter @WhittlePM
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Research to explore how genes, other factors affect cardiometabolic disease risk Washington University School of Medicine in St. Louis – Washington…
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$8.8 million to fund research into interaction of specific genes with demographic, lifestyle factors
With an $8.8 million grant from the National Institutes of Health (NIH), researchers at Washington University School of Medicine in St. Louis will study how an individuals risks of cardiometabolic diseases are influenced by the interaction of specific genes with demographic and lifestyle factors.
Researchers at Washington University School of Medicine in St. Louis have received a four-year, $8.8 million grant to ramp up research aimed at unraveling how an individuals risks of cardiometabolic diseases, such as heart disease and Type 2 diabetes, are influenced by the interaction of specific genes with demographic and lifestyle factors.
Going beyond the small percentage of disease risk explained by genes alone, this study will explore how an individuals gender, race, ethnicity, smoking, alcohol use, diet and exercise levels may combine with genetic risks to trigger the metabolic processes that underlie heart disease.
By investigating genomic and lifestyle contributors to cardiometabolic health through their interactions across genders and diverse populations, our research can help advance the emerging field of precision medicine, said principal investigator D.C. Rao, PhD, professor of biostatistics, of genetics, of psychiatry and of mathematics.
Raos key co-investigators at the School of Medicine include cardiologist Lisa de las Fuentes, MD, professor of medicine and of biostatistics, and statistical geneticist C. Charles Gu, PhD, associate professor of biostatistics and of genetics.
Precision medicine uses information about a persons genetic makeup, metabolism and other biological and lifestyle factors to optimize strategies that potentially can prevent or treat a health condition. Such personalized approaches to treatment are more likely to be successful for individual patients, rather than a one-size-fits-all approach.
Funded by the National Institutes of Health (NIH), this new investigation will be the third in a series of similar studies in which Rao and his team use statistical analysis to identify gene-lifestyle interactions associated with cardiovascular and cardiometabolic diseases the leading causes of death in the United States and worldwide.
Their original study identified promising gene-lifestyle interactions, including several tied to African ancestry, but the study lacked the sample size necessary to robustly validate the interactions as statistically significant.
The current study, involving investigators from within and outside the U.S., will overcome that hurdle by expanding the sample size tenfold to include data from more than 1 million individuals, including people from several countries outside the United States. With a sample of 912,000 people of European ancestry, 231,000 of Asian ancestry, 91,000 of African ancestry and 33,000 of Hispanic ancestry, it will be the largest, most diverse investigation of gene-lifestyle interactions attempted.
By focusing heavily on gene-lifestyle interactions, Raos study represents a shift from traditional genomewide association studies (GWAS), which rapidly scan the genomes of many people to find genetic variations associated with a particular disease. His approach, known as a genomewide interaction study (GWIS), adds the potential to show how smoking, alcohol consumption, physical activity, obesity, sleep duration and other lifestyle factors interact with genes to influence high blood pressure, diabetes, cholesterol levels and other metabolic traits that may increase the risk of a heart attack or stroke.
The study aims to identify new gene-lifestyle interactions that contribute to cardiometabolic disease risk, and to better understand the molecular mechanics underlying these interactions, Gu said. By detailing associated molecular biomarkers and traits, such as DNA methylation, gene expression and metabolites, the study could reveal new opportunities for disease intervention.
Added de las Fuentes: Our findings could reveal new diagnostic and therapeutic tools, identify targets for novel drug development and serve as the foundation for a more precise, more personalized approach to health care for heart disease, diabetes, and other metabolic diseases. This project has high potential to move the field forward.
Washington University School of Medicines 1,700 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, consistently ranking among the top medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.
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Regenerative Medicine Market Size Worth $57.08 Billion By 2027: Grand View Research, Inc. – Markets Insider
Posted: at 12:55 am
SAN FRANCISCO, Aug. 12, 2021 /PRNewswire/ --The global regenerative medicine marketsize is expectedto reach USD 57.08 billion by 2027, growing at a CAGR of 11.27% over the forecast period, according to a new report by Grand View Research, Inc. Recent advancements in biological therapies have resulted in a gradual shift in preference toward personalized medicinal strategies over the conventional treatment approach. This has resulted in rising R&D activities in the regenerative medicine arena for the development of novel regenerative therapies.
Key Insights & Findings:
Read 273 page research report, "Regenerative Medicine Market Size, Share & Trends Analysis Report By Product (Cell-based Immunotherapies, Gene Therapies), By Therapeutic Category (Cardiovascular, Oncology), And Segment Forecasts, 2021 - 2027", by Grand View Research
Furthermore,advancements in cell biology, genomics research, and gene-editing technology are anticipated to fuel the growth of the industry. Stem cell-based regenerative therapies are in clinical trials, which may help restore damaged specialized cells in many serious and fatal diseases, such as cancer, Alzheimer's, neurodegenerative diseases, and spinal cord injuries. For instance, various research institutes have adopted Human Embryonic Stem Cells (hESCs) to develop a treatment for Age-related Macular Degeneration (AMD).
Constant advancements in molecular medicines have led to the development of gene-based therapy, which utilizes targeted delivery of DNA as a medicine to fight against various disorders. Gene therapy developments are high in oncology due to the rising prevalence and genetically driven pathophysiology of cancer. The steady commercial success of gene therapies is expected to accelerate the growth of the global market over the forecast period.
Grand View Research has segmented the global regenerative medicine market on the basis of product, therapeutic category, and region:
List of Key Players of Regenerative Medicine Market
Check out more studies related to Global Biotechnology Industry, conducted by Grand View Research:
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About Grand View Research
Grand View Research, U.S.-based market research and consulting company, provides syndicated as well as customized research reports and consulting services. Registered in California and headquartered in San Francisco, the company comprises over 425 analysts and consultants, adding more than 1200 market research reports to its vast database each year. These reports offer in-depth analysis on 46 industries across 25 major countries worldwide. With the help of an interactive market intelligence platform, Grand View Research helps Fortune 500 companies and renowned academic institutes understand the global and regional business environment and gauge the opportunities that lie ahead.
Contact:Sherry JamesCorporate Sales Specialist, USAGrand View Research, Inc.Phone: 1-415-349-0058Toll Free: 1-888-202-9519Email: sales@grandviewresearch.comWeb: https://www.grandviewresearch.comFollow Us: LinkedIn| Twitter
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Regenerative Medicine Market Size Worth $57.08 Billion By 2027: Grand View Research, Inc. - Markets Insider
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VTX-801 Receives U.S. FDA Fast Track Designation for the Treatment of Wilson Disease – Yahoo Finance
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VTX-801 Receives U.S. FDA Fast Track Designation for the Treatment of Wilson Disease
Paris, France and New York, NY, August 12, 2021 Vivet Therapeutics (Vivet), a clinical-stage biotechnology company, and Pfizer Inc. (NYSE: PFE) today announced the U.S. Food and Drug Administration (FDA) has granted Fast Track designation to VTX-801, Vivets clinical-stage gene therapy for the treatment of Wilson Disease a rare, genetic disorder that reduces the ability of the liver and other tissues to regulate copper levels, causing severe hepatic damage, neurological symptoms, and potentially death. The FDAs Fast Track program is designed to facilitate the development, and expedite the review of, novel potential therapies that are designed to treat serious conditions and fill unmet medical need.
VTX-801 is a novel investigational gene therapy to be evaluated in a Phase 1/2 clinical trial to determine the safety, tolerability, and pharmacological activity of a single intravenous infusion in adult patients with Wilson Disease. Pfizer is collaborating with Vivet on the clinical supply of VTX-801 for the Phase 1/2 clinical trial.
The FDAs decision to grant VTX-801 Fast Track designation underscores the urgent need for new therapeutic options to address this devastating disease, which, if left untreated, can be fatal, said Seng Cheng, Senior Vice President and Chief Scientific Officer of Pfizers Rare Disease Research Unit. We are pleased to collaborate with Vivet on this important development program, which we believe, if successful, could make a meaningful difference in the lives of patients living with Wilson Disease.
Dr. Michael Schilsky, Principal Investigator at Yale University School of Medicine (Connecticut, United States), said, We are proud to participate in this important clinical trial. If VTX-801 is successfully developed, it has the potential to be a truly innovative medicine with the ability to restore copper metabolism after a single injection, addressing significant unmet medical needs for patients with Wilson Disease.
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With the FDAs authorization of the IND application for VTX-801 combined with Pfizers state-of-the-art gene therapy manufacturing capabilities we are well-positioned to rapidly advance development of this potential therapy, concluded Jean-Philippe Combal, CEO and co-founder of Vivet.
About Fast Track designation
Fast Track is a process designed to facilitate the development, and expedite the review of, drugs to treat serious conditions that address an unmet medical need, by providing a therapy where none exists or providing a therapy which may be potentially better and shows some advantage over available therapy. Fast Track designation includes opportunities for more frequent meetings with the FDA to discuss trial design, development plans, data needed to support drug approval, submission of a New Drug Application (NDA) on a rolling basis, and eligibility for accelerated approval and priority review, if relevant criteria are met.
Visit FDAs website for more information
About VTX-801
VTX-801 is a novel investigational gene therapy for Wilson Disease, which has been granted Orphan Drug Designation (ODD) by the Food and Drug Administration (FDA) and the European Commission (EC) and Fast Track designation by the FDA. Wilson Disease, a rare genetic disorder, is caused by mutations in the gene encoding the ATP7B protein, which reduces the ability of the liver and other tissues to regulate copper levels, causing severe hepatic damage, neurologic symptoms and potentially death.
VTX-801 is a novel, investigational rAAV-based gene therapy vector designed to deliver a miniaturized ATP7B transgene encoding, a functional protein that has been shown to restore copper homeostasis, reverse liver pathology and reduce copper accumulation in the brain of a mouse model of Wilson Disease. VTX-801s rAAV serotype was selected based on its demonstrated tropism for transducing human liver cells.
About GATEWAY - Phase 1/2 Clinical Trial of VTX-801 in Wilson Disease
The GATEWAY trial (NCT04537377) is a multi-center, non-randomized, open-label, Phase 1/2 clinical trial designed to assess the safety, tolerability, and pharmacological activity of a single intravenous infusion of VTX-801 in adult patients with Wilson Disease, prior to and following background WD therapy withdrawal.
Six leading centers in the United States and Europe are expected to participate in the GATEWAY Phase 1/2 trial. The trial is expected to enroll up to sixteen adult patients with Wilson Disease and will evaluate up to three doses of VTX-801. Patients will participate in a pre-dosing observational period and will be administered a prophylactic steroid regimen.
The primary endpoint of the GATEWAY trial is to assess the safety and tolerability of VTX-801 at 52 weeks after a single infusion. Additional endpoints include changes in disease-related biomarkers, including free serum copper and serum ceruloplasmin activity, as well as radiocopper-related parameters and VTX-801 responder status to allow standard-of-care withdrawal.
A list of sites, contact information and more details on the study are available on:https://clinicaltrials.gov/ct2/show/NCT04537377
To learn more about gene therapy on Wilson Disease, visit: https://patienteducation.asgct.org/
About Vivet Therapeutics
Vivet Therapeutics is a clinical-stage emerging biotechnology company developing novel gene therapy treatments for rare, inherited metabolic diseases.
Vivet is building a diversified gene therapy pipeline based on novel recombinant adeno-associated virus (rAAV) technologies developed through its partnerships with, and exclusive licenses from, the Fundacin para la Investigacin Mdica Aplicada (FIMA), a not-for-profit foundation at the Centro de Investigacin Medica Aplicada (CIMA), University of Navarra based in Pamplona, Spain.
Vivets lead program, VTX-801, is currently under clinical development.
Vivets second gene therapy product, VTX-803 for PFIC3, received US and European Orphan Drug Designation in May 2020.
Vivet is supported by international life science investors including Novartis Venture Fund, Roche Venture Fund, HealthCap, Pfizer Inc., Columbus Venture Partners, Ysios Capital, Kurma Partners and Idinvest Partners.
Please visit us at http://www.vivet-therapeutics.com and follow us on Twitter at @Vivet_tx, on Facebook at Facebook/Vivet-Therapeutics and LinkedIn.
About Pfizer: Breakthroughs That Change Patients Lives
At Pfizer, we apply science and our global resources to bring therapies to people that extend and significantly improve their lives. We strive to set the standard for quality, safety and value in the discovery, development and manufacture of health care products, including innovative medicines and vaccines. Every day, Pfizer colleagues work across developed and emerging markets to advance wellness, prevention, treatments and cures that challenge the most feared diseases of our time. Consistent with our responsibility as one of the world's premier innovative biopharmaceutical companies, we collaborate with health care providers, governments and local communities to support and expand access to reliable, affordable health care around the world. For more than 170 years, we have worked to make a difference for all who rely on us. We routinely post information that may be important to investors on our website at http://www.Pfizer.com. In addition, to learn more, please visit us on http://www.Pfizer.com and follow us on Twitter at @Pfizer and @Pfizer News, LinkedIn, YouTube and like us on Facebook at Facebook.com/Pfizer.
Pfizer Disclosure Notice
The information contained in this release is as of August 12, 2021. Pfizer assumes no obligation to update forward-looking statements contained in this release as the result of new information or future events or developments.
This release contains forward-looking information about Vivet Therapeutics (Vivet) investigational gene therapy, VTX-801, including its potential benefits, that involves substantial risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. Risks and uncertainties include, among other things, the uncertainties inherent in research and development, including the ability to meet anticipated clinical endpoints, commencement and/or completion dates for our clinical trials, regulatory submission dates, regulatory approval dates and/or launch dates, as well as the possibility of unfavorable new clinical data and further analyses of existing clinical data; the risk that clinical trial data are subject to differing interpretations and assessments by regulatory authorities; whether regulatory authorities will be satisfied with the design of and results from the clinical studies; whether and when any applications may be filed in any jurisdiction for VTX-801; whether and when any such applications may be approved by regulatory authorities, which will depend on myriad factors, including making a determination as to whether the products benefits outweigh its known risks and determination of the products efficacy and, if approved, whether VTX-801 will be commercially successful; decisions by regulatory authorities impacting labeling, manufacturing processes, safety and/or other matters that could affect the availability or commercial potential of VTX-801; uncertainties regarding the impact of COVID-19 on Pfizers business, operations and financial results; and competitive developments.
A further description of risks and uncertainties can be found in Pfizers Annual Report on Form 10-K for the fiscal year ended December 31, 2020 and in its subsequent reports on Form 10-Q, including in the sections thereof captioned Risk Factors and Forward-Looking Information and Factors That May Affect Future Results, as well as in its subsequent reports on Form 8-K, all of which are filed with the U.S. Securities and Exchange Commission and available at http://www.sec.gov and http://www.pfizer.com.
Contacts
Vivet Media Contact: Thomas Daniel-Robintdaniel@vivet-therapeutics.com
Pfizer Media Contact: Jerica Pitts212-733-1226Jerica.Pitts@pfizer.com
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VTX-801 Receives U.S. FDA Fast Track Designation for the Treatment of Wilson Disease - Yahoo Finance
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CU Researcher Awarded NIH Grant to Study Genetics of Bone Density – CU Anschutz Today
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Researchers from the CU School of Medicine Department of Orthopedics have been awarded a $3.4 million National Institutes of Health grant to study the genetics of bone density and to look for therapeutic targets to counter bone loss.
With the grant, Cheryl Ackert-Bicknell, PhD, associate professor of orthopedics at the CU School of Medicine, plans to map the key genes and pathways involved with bone cell activity. Using that information, researchers hope to find targets for more effective treatments to counter bone loss. Ackert-Bicknells fellow principal investigator on the grant is Charles Farber, PhD, associate professor of public health sciences at University of Virginia.
Bone is in a constant state of remodeling, Ackert-Bicknell said, and her study is designed to look at cells known as osteoblasts, which work to build bones. When a healthy body is functioning properly, osteoblasts work in balance with other cells called osteoclasts to maintain sufficient bone mineral density.
In the process of walking from your car to here, you did microcrack damage to your bone, Ackert-Bicknell explained. The osteoclasts job is to home to that site of the microcrack, eat a hole out all the way around that microcrack and the osteoblast comes and fills that in. Thats called normal bone turnover. Thats most of your life. If the osteoclasts go haywire and there is insufficient building of new bone, thats osteoporosis.
Current therapies to cause the body to build the right amount of new bone are limited. These therapies can often only be used for a limited time, and none can be used in children. There is a need for better therapies, Ackert-Bicknell said, but they cannot be developed without improved understanding of how a healthy body gets bone density just right.
Thats where Ackert-Bicknells study comes in. She plans a comprehensive analysis of how the genes influence the process. She will conduct a genome-wide association study that seeks to identify genetic variations that are associated with osteoblast function and bone mineral density.
Osteoblasts build bone. Osteoclasts chew up bone. And thats how I always teach it: Blasts build and clasts chew, Ackert-Bicknell said. Osteoblasts do two things to make bone. They make a protein matrix and then they mineralize that matrix. For that to be accomplished, the osteoblast has to get to the right place, and it has to proliferate. So, it is proliferating, it is migrating, then it is making that bone by making matrix, and it is mineralizing that matrix.
Previous studies of osteoblasts have shown that its characteristics are highly heritable, or transmissible from parents to children. But how osteoblasts form and do their work is not fully understood. What might appear to be a small change on osteoblast behavior can have significant developmental consequences. Ackert-Bicknell cited an example of how knocking out a single gene in one type of bone cell can result in an obese mouse.
You can actually knock out a gene, just in these osteoblast bone cells, and get an obese mouse, she said. In that cell only. It is the only cell in the whole body that makes that gene, and you end up with an obese mouse. This just shows how bone is tied into all of physiology.
To get a better understanding of those connections, Ackert-Bicknells new study will look at the network of all the genes expressed in this cell and their relative expression in different contexts of genetics.
To do this, we must compare bone image after bone image to identify variations that could be meaningful in relation to the genetics, said Douglas Adams, PhD, associate professor of orthopedics, who has worked with Ackert-Bicknell on previous studies that underpin the work in this new award.
Adams is also working with Ackert-Bicknell on another NIH grant studying how the leading treatment for osteoporosis might have variable efficacy because of genetic differences between patients. To conduct such studies, researchers grind through thousands of data points to discover links that have yet to be uncovered. By identifying those unknown connections, the team hopes to discover new ways to treat disorders of bone mineralization.
Its sort of along the lines of looking under the streetlamp for your keys, Ackert-Bicknell said. As long as your keys fell down where the lamp is shining light youve got a good chance of finding them. In our work, we are looking outside of the streetlight for the things we havent studied before.
Lets face it, what we know now isnt giving us enough drug targets, enough information. It isnt helping us. The most unique pathways and the ones that are going to get us drugs are not the ones we have already studied.
Ackert-Bicknells new grant provides funding for a five-year research project. Coupled with the parallel active NIH grant held by both Ackert-Bicknell and Adams, CU Orthopedics is at the forefront of the effort nationally and globally to understand and develop disease modifying approaches to address bone loss in osteoporosis patients. These projects are just part of a growing portfolio of research activity in the Department of Orthopedics, which has seen a greater than 10-fold increase in extramural grant support since the departments leadership committed to expand its research mission in 2018.
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CU Researcher Awarded NIH Grant to Study Genetics of Bone Density - CU Anschutz Today
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Hunting down the mutations that cause cancer drug resistance – UT Southwestern
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LentiMutate identified a mutation that changes an amino acid of KRAS G12C at position 96 from tyrosine (Y) to histidine (H). This change impairs the binding of the novel lung cancer drug LUMAKRAS/AMG 510 (depicted in green) to KRAS G12C (depicted by greyscale). Credit: Kenneth D. Westover
DALLAS Aug. 10, 2021 Using a virus to purposely mutate genes that produce cancer-driving proteins could shed light on the resistance that inevitably develops to cancer drugs that target them, a new study led by UTSouthwestern scientists suggests. The findings, published online in Cancer Research, could help researchers develop drugs that circumvent resistance, validate new drug targets, or better understand the interaction between drugs and their target proteins.
Ralf Kittler, Ph.D.
We believe this approach will be a very useful tool in the fight against cancer therapeutic resistance and could have potential in a variety of other areas of drug development, said study leader Ralf Kittler, Ph.D., Associate Professor of Pharmacology in the Eugene McDermott Center for Human Growth and Development and the Harold C. Simmons Comprehensive Cancer Center. Dr. Kittler co-led the study with John D. Minna, M.D., Professor of Internal Medicine and Pharmacology, Director of the Hamon Center for Therapeutic Oncology Research and member of the Simmons Cancer Center.
Targeted therapies represent a major advance in cancer treatment for multiple tumor types, comprising drugs that specifically alter the function of oncoproteins that drive tumors to grow and spread. They are often oral agents with low toxicity that provide symptom relief and prolong survival. However, explained Dr. Kittler, these drugs have a marked drawback: they lose effectiveness over time as tumors become resistant because the genes responsible for the targeted oncoproteins inevitably mutate, producing proteins that no longer bind the drugs. For example, patients with non-small cell lung cancer are often treated with drugs that inhibit a protein known as the epidermal growth factor receptor (EGFR), providing great clinical benefit; unfortunately, most of these tumors develop resistance to the treatment within about a year. This response has led to second-, third-, and even fourth-generation versions of such EGFR-targeting drugs to try to overcome this resistance.
Although methods exist to predict mutations that will develop in cancer target genes an important step toward developing drugs that can attack the resulting mutant proteins these methods are cumbersome, expensive, time-consuming, or can only predict a limited type of mutation known as a point mutation, Dr. Kittler explained.
Looking for a better way to predict therapeutic resistance, the researchers developed a technique they call LentiMutate. This approach relies on a class of viruses called lentiviruses to cause mutations. In contrast with human cells and many other viruses, lentiviruses take RNA and convert it to DNA while infecting its target cells to eventually produce proteins; however, this process is inherently error-prone, producing mutant mistakes in the resulting DNA.
Working with a lentivirus engineered to make it even more error-prone, Dr. Kittler and his colleagues used the vector to insert EGFR RNA in human cells, causing the cells to produce mutant versions of this protein. They then dosed the cells with a commonly used inhibitor for EGFR called gefitinib to search for resistant cells. By sequencing the introduced single gene in the resistant cells, the researchers were able to identify several mutations that made EGFR resistant to gefitinib, a first-generation anti-EGFR drug, including those previously identified in human patients.
Further experiments showed that LentiMutate was able to identify mutations that conferred resistance to the fourth-generation anti-EGFR drug osimertinib, which is now the standard of care for EGFR mutant non-small cell lung cancer. The approach also identified mutations that cause resistance to imatinib, a drug that targets the BCR-ABL1 protein, which drives chronic myelogenous leukemia, and AMG 510, a drug that targets a specific mutant form of the KRAS protein, which drives non-small cell lung cancer.
Dr. Kittler noted that identifying these mutations through LentiMutate can greatly speed up the process of developing new drugs that can bind to the drug-resistant mutant proteins so that it takes weeks rather than years. LentiMutate could also be used in different ways in drug development: to confirm that new drugs are acting on the target protein and not a different one, to help researchers gain a better understanding of how drugs are interacting with their targets, or to develop new types of drugs for a variety of other diseases beyond cancer.
Precision medicine that comes from sequencing a patients tumor to identify specific proteins to target for therapy has revolutionized cancer treatment. However, we need patients to be cured and not just benefit for 10 to 15 months from such targeted therapy, said Dr. Minna. To do this, we need to deal with drug resistance mutations, including by developing new drugs, and LentiMutate gives us an important new tool in our research armamentarium to help solve this pressing problem.
Other UTSW researchers who contributed to this study include Paul Yenerall, Rahul K. Kollipara, Kimberley Avila, Michael Peyton, Yan Liu, and Kenneth D. Westover.
A patent pending for LentiMutate lists Yenerall, Dr. Minna, and Dr. Kittler as inventors. Dr. Minna receives licensing royalties from the National Cancer Institute and UTSouthwestern for cell lines.
This study was supported by funding from the Simmons Cancer Center at UTSouthwestern (P30CA142543), the Cancer Prevention and Research Institute of Texas (CPRIT) (RP120732-P3, RP160652, RP170373), the National Institutes of Health (NCI SPORE in lung cancer 5P50CA070907, R01CA200787, R01CA244341, and R01CA065823), the Margot Johnson Foundation, and the Howard Hughes Medical Institute.
Dr. Kittler is a John L. Roach Scholar in Biomedical Research and a CPRIT Scholar in Cancer Research. Dr. Minna holds the Sarah M. and Charles E. Seay Distinguished Chair in Cancer Research and the Max L. Thomas Distinguished Chair in Molecular Pulmonary Oncology.
About UTSouthwestern Medical Center
UTSouthwestern, one of the nations premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institutions faculty has received six Nobel Prizes, and includes 25 members of the National Academy of Sciences, 16 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 2,800 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide care in about 80 specialties to more than 117,000 hospitalized patients, more than 360,000 emergency room cases, and oversee nearly 3 million outpatient visits a year.
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Atf3 and Rab7b genes drive regeneration in mature cells – Baylor College of Medicine News
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When an injury occurs, damaged cells need to be replaced. Stem cells, known as the go-to cells when new specialized cells need to be produced, are rare in adult tissues, so the job often falls to differentiated, or mature, cells.
Dr. Jason Mills and his lab have been working on identifying the genes driving mature cells to return to a regenerative state, a process called paligenosis.
My lab has been promoting the idea that given that cells in all organs use similar functions like mitosis and apoptosis, theres likely to be a conserved genetic program for how mature cells become regenerative cells, said Mills, senior author of the study and professor of medicine gastroenterology,pathology and immunologyandmolecular and cellular biologyat Baylor. The research was conducted while his lab was atWashington University School of Medicine in St. Louis.
To begin paligenosis and reenter the cell cycle, mature cells must first go through the process of autodegredation, breaking down larger structures used in specialized cell function. Mills and his team, led by first author Dr. Megan Radyk, a postdoctoral associate at the Washington University School of Medicine in St. Louis at the time of research, found that the genes Atf3 and Rab7b are upregulated in gastric and pancreatic digestive-enzyme-secreting cells of mice during autodegredation, and return to normal expression before mitosis.
The researchers showed that Atf3 activates Rab7b, which directs lysosomes to begin dismantling cell parts not needed for regeneration. But when Atf3 was not present, Rab7b did not trigger autodegredation.
The team also found Atf3 and Rab7b expression were consistent in paligenosis across other organs and organisms. Similar gene expression also appeared in precancerous gastric lesions in humans. According to Mills, the discoveries in this research are foundational to understanding how repetitive injury and paligenosis may impact cancer.
The more tissue damage you have, the more youre calling mature cells back into regeneration duty, said Mills, co-director of theTexas Medical Center Digestive Disease Center. Theres emerging evidence that, when these cells go through paligenosis, they dont check for DNA damage well. The cells are storing DNA mutations when they return to their differentiated function. Over time, they become so damaged that they cant go back to normal function and instead keep replicating.
Its our belief that paligenosis is at the heart of cancer development.
This research also provides groundwork for potential therapeutic targets. Existing drugs like hydroxychloroquine can be used to inhibit autodegredation, therefore stopping paligenosis.
According to Mills, further study is required to determine whether drugs targeting autodegredation can be used in conjunction with cancer treatments to stop cells from replicating.
The complete study is published in EMBO Reports.
For a full list of authors, their contributions to this work and sources of support, see the publication.
By Molly Chiu
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Atf3 and Rab7b genes drive regeneration in mature cells - Baylor College of Medicine News
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