Podcasts about mrc laboratory

In this episode of the Epigenetics Podcast, we talked with Petra Hajkova from the MRC Laboratory of Medical Sciences about her work on epigenetics research on mammalian development, highlighting DNA methylation, histone modifications, and TET enzymes, along with her journey in molecular genetics and future research on epigenetic maintenance. Dr. Hajkova's early work focused on DNA methylation and resulted in innovative collaboration that allowed her to develop bisulfide sequencing techniques. We discuss her transition to the UK, where she began working in Azim Surani's lab at the University of Cambridge. Dr. Hajkova describes the excitement of researching chromatin dynamics in the mouse germline, leading to significant findings published in Nature. Her story highlights the intense yet rewarding nature of postdoctoral research as she navigated the complexities of working with embryos for the first time. As her research progressed, Dr. Hajkova established her own lab at the MRC London Institute of Medical Sciences, where she became a professor in 2017. We delve into her investigations on the differences between embryonic stem cells and embryonic germ cells regarding their distinct developmental origins. Dr. Hajkova outlines the challenges she faced in understanding the mechanisms behind global DNA demethylation in germline cells and the role of hydroxymethylation during early development. The discussion further covers her exciting findings regarding the specific functions of TET enzymes and their regulatory roles in maintaining epigenetic states. We explore her recent research published in Nature, which provides insights into the transition from primordial germ cells to gonocytes, emphasizing the significance of various epigenetic mechanisms in germline development.   References Hajkova P, Ancelin K, Waldmann T, Lacoste N, Lange UC, Cesari F, Lee C, Almouzni G, Schneider R, Surani MA. Chromatin dynamics during epigenetic reprogramming in the mouse germ line. Nature. 2008 Apr 17;452(7189):877-81. doi: 10.1038/nature06714. Epub 2008 Mar 19. PMID: 18354397; PMCID: PMC3847605. Hajkova P, Jeffries SJ, Lee C, Miller N, Jackson SP, Surani MA. Genome-wide reprogramming in the mouse germ line entails the base excision repair pathway. Science. 2010 Jul 2;329(5987):78-82. doi: 10.1126/science.1187945. PMID: 20595612; PMCID: PMC3863715. Hill PWS, Leitch HG, Requena CE, Sun Z, Amouroux R, Roman-Trufero M, Borkowska M, Terragni J, Vaisvila R, Linnett S, Bagci H, Dharmalingham G, Haberle V, Lenhard B, Zheng Y, Pradhan S, Hajkova P. Epigenetic reprogramming enables the transition from primordial germ cell to gonocyte. Nature. 2018 Mar 15;555(7696):392-396. doi: 10.1038/nature25964. Epub 2018 Mar 7. PMID: 29513657; PMCID: PMC5856367. Huang TC, Wang YF, Vazquez-Ferrer E, Theofel I, Requena CE, Hanna CW, Kelsey G, Hajkova P. Sex-specific chromatin remodelling safeguards transcription in germ cells. Nature. 2021 Dec;600(7890):737-742. doi: 10.1038/s41586-021-04208-5. Epub 2021 Dec 8. PMID: 34880491.   Related Episodes Epigenetic Mechanisms of Mammalian Germ Cell Development (Mitinori Saitou) Epigenetic Reprogramming During Mammalian Development (Wolf Reik) DNA Methylation and Mammalian Development (Déborah Bourc'his)   Contact Epigenetics Podcast on Mastodon Epigenetics Podcast on Bluesky Dr. Stefan Dillinger on LinkedIn Active Motif on LinkedIn Active Motif on Bluesky Email: podcast@activemotif.com

 Scientists are using the secrets of biology to unlock living well past current human life spans. Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. A member of the National Academy of Sciences, Venki runs a research group at the MRC Laboratory of Molecular Biology in Cambridge, England. He joins host Krys Boyd to discuss the quest to live forever, if that's even ethical, and what it looks like to alter our physiology. His book is “Why We Die: The New Science of Aging and the Quest for Immortality.”  Learn about your ad choices: dovetail.prx.org/ad-choices

Transcript with time code:  https://cuttingedgehealth.com/wp-content/uploads/2025/02/Transcript-47-Dr-Venki-Ramakrishnan.pdf   In this episode, Jane interviews Nobel Prize winner Venki Ramakrishnan, a molecular biologist who offers a balanced perspective on the anti-aging field.   Ramakrishnan discusses various promising areas of anti-aging research, including caloric restriction drugs like rapamycin, senolytics to target senescent cells, and stem cell therapies. He emphasizes the importance of clinical trials and cautions against rushing into unproven treatments. The conversation covers lifestyle factors that can promote healthy aging, such as regular exercise, proper nutrition, and maintaining social connections.   Ramakrishnan shares personal insights, including his father's experience of maintaining an active lifestyle until age 99. He also touches on his own career journey and winning the Nobel Prize. Throughout the interview, he stresses the need for a scientific approach to anti-aging research while acknowledging the urgency felt by many to combat aging. The podcast provides a thoughtful exploration of the current state of anti-aging science, balancing excitement for potential breakthroughs with the need for rigorous scientific validation.   *****   Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. A National Academy of Sciences member, Venki runs his research group at the MRC Laboratory of Molecular Biology in Cambridge, England. From 2015 to 2020, he served as president of the Royal Society, one of the world's oldest scientific organizations. He is the author of the frank scientific memoir Gene Machine: The Race to Decipher the Secrets of the Ribosome and Amazon bestselling book Why We Die: The New Science of Aging and the Quest for Immortality.   *****   Cutting Edge Health podcast website: https://cuttingedgehealth.com/   Cutting Edge Health Social and YouTube:   YouTube channel: youtube.com/@cuttingedgehealthpodcast   Instagram - https://instagram.com/cuttingedgehealthpodcast   Facebook - https://www.facebook.com/Cutting-Edge-Health-Podcast-with-Jane-Rogers-101036902255756   Please note that the information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Cutting Edge Health podcast, its employees, guests and affiliates assume no liability for the application of the information discussed.   Special thanks to Alan and Maria on the Cutting Edge Health team!    

Aging and death happen to the best of us, but there are increasing efforts to do something about it. That effort requires that we have some reasonable understanding of why aging happens, and what processes are involved. You will be unsurprised to learn that it's complicated. Venki Ramakrishnan, who won the Nobel Prize for his work on the ribosome, investigates what we know about aging in his book Why We Die: The New Science of Aging and the Quest for Immortality. We talk about aging and death, and manage to get some thoughts in about ribosomes. Venki and many other great communicators will be speaking at New Scientist Live, which takes place at ExCeL London between 12 - 14 October 2024, and is also streamed live as well as on-demand.Support Mindscape on Patreon.Blog post with transcript: https://www.preposterousuniverse.com/podcast/2024/09/30/291-venki-ramakrishnan-on-the-biology-of-death-and-aging/Venkatraman (Venki) Ramakrishnan received his Ph.D. in physics from Ohio University. He is currently Group Leader at the MRC Laboratory of Molecular Biology, Cambridge, England, and is a Fellow of Trinity College. He previously served as President of the Royal Society of London. He shared the Nobel Prize in Chemistry for his work uncovering the structure of the ribosome.Lab web pageNobel citationGoogle scholar publicationsWikipediaAmazon author pageSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Una nuova speranza per i malati di Alzheimer. Si tratta di una proteina, la Trim21, modificata in laboratorio che riesce a legarsi e poi a rimuovere gli accumuli nel cervello di proteina Tau, che provocano la malattia. Uno studio promettente nato nel MRC Laboratory of Molecular Biology di Cambridge e pubblicato sulla rivista Cell. Co-autore l'italiano Guido Papa, biotecnologo medico specialista in virologia molecolare. E' lui l'ospite di questa puntata di Science, Please

Send us a Text Message.Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. He runs a lab at the MRC Laboratory of Molecular Biology in Cambridge, England. In this episode, Venki emphasizes the importance of enjoying the scientific process itself, not just aiming for major discoveries. He describes his creativity as a result of mulling over a problem and of talking with people. Venki also highlights the need for scientists to make daily judgment calls about their approach and the future of the project. And he encourages openness and collaboration, viewing the ability to seek help as a strength rather than a weakness.This episode was supported by Research Theory (researchtheory.org). For more information about Night Science, visit https://www.biomedcentral.com/collections/night-science .

The super-rich are trialling innumerable whacky theories to radically extend their lives, from not eating after 11pm to taking hundreds of supplements a day and even blood transfusions from their children. But what does the science tell us? Could some of these ideas actually prove effective? And why are we still so obsessed with the quest that is as old as mankind itself: immortality?This podcast was brought to you thanks to the support of readers of The Times and The Sunday Times. Subscribe today: http://thetimes.com/thestoryGuest: Dr. Venki Ramakrishnan, scientist at the MRC Laboratory of Molecular Biology at Cambridge and author of Why We Die: The New Science of Ageing and the Quest for Immortality.Host: Luke Jones.Clips: WIRED UK, Valuetainment Clips, Diary of a CEO, TalkTV. Find out more about our bonus series for Times subscribers: 'Inside the newsroom'Get in touch: thestory@thetimes.co.uk Hosted on Acast. See acast.com/privacy for more information.

Professor Venki Ramakrishnan, a Nobel laureate for his work on unraveling the structure of function of the ribosome, has written a new book WHY WE DIE which is outstanding. Among many posts and recognitions for his extraordinary work in molecular biology, Venki has been President of the Royal Society, knighted in 2012, and was made a Member of the Order of Merit in 2022. He is a group leader at the MRC Laboratory of Molecular Biology research institute in Cambridge, UK.A brief video snippet of our conversation below. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are available on Apple and Spotify.Transcript with links to audio and external linksEric Topol (00:06):Hello, this is Eric Topol with Ground Truths, and I have a really special guest today, Professor Venki Ramakrishnan from Cambridge who heads up the MRC Laboratory of Molecular Biology, and I think as you know a Nobel laureate for his seminal work on ribosomes. So thank you, welcome.Venki Ramakrishnan (00:29):Thank you. I just want to say that I'm not the head of the lab. I'm simply a staff member here.Eric Topol (00:38):Right. No, I don't want to give you more authority than you have, so that was certainly not implied. But today we're here to talk about this amazing book, Why We Die, which is a very provocative title and it mainly gets into the biology of aging, which Venki is especially well suited to be giving us a guided tour and his interpretations and views. And I read this book with fascination, Venki. I have three pages of typed notes from your book.The Compression of MorbidityEric Topol (01:13):And we could talk obviously for hours, but this is fascinating delving into this hot area, as you know, very hot area of aging. So I thought I'd start off more towards the end of the book where you kind of get philosophical into the ethics. And there this famous concept by James Fries of compression of morbidity that's been circulating for well over two decades. That's really the big question about all this aging effort. So maybe you could give us, do you think there is evidence for compression of morbidity so that you can just extend healthy aging and then you just fall off the cliff?Venki Ramakrishnan (02:00):I think that's the goal of most of the sort of what I call the saner end of the aging research community is to improve our health span. That is the number of years we have healthy lives, not so much to extend lifespan, which is how long we live. And the idea is that you take those years that we now spend in poor health or decrepitude and compress them down to just very short time, so you're healthy almost your entire life, and then suddenly go into a rapid decline and die. Now Fries who actually coined that term compression or morbidity compares this to the One-Hoss Shay after poem by Oliver Wendell Holmes from the 19th century, which is about this horse carriage that was designed so perfectly that all its parts wore out equally. And so, a farmer was riding along in this carriage one minute, and the next minute he found himself on the ground surrounded by a heap of dust, which was the entire carriage that had disintegrated.Venki Ramakrishnan (03:09):So the question I would ask is, if you are healthy and everything about you is healthy, why would you suddenly go into decline? And it's a fair question. And every advance we've made that has kept us healthier in one respect or another. For example, tackling diabetes or tackling heart disease has also extended our lifespan. So people are not living a bigger fraction of their lives healthily now, even though we're living longer. So the result is we're spending the same or even more number of years with one or more health problems in our old age. And you can see that in the explosion of nursing homes and care homes in almost all western countries. And as you know, they were big factors in Covid deaths. So I'm not sure it can be accomplished. I think that if we push forward with health, we're also going to extend our lifespan.Venki Ramakrishnan (04:17):Now the argument against that comes from studies of these, so-called super centenarians and semi super centenarians. These are people who live to be over 105 or 110. And Tom Perls who runs the New England study of centenarians has published findings which show that these supercentenarians live extraordinarily healthy lives for most of their life and undergo rapid decline and then die. So that's almost exactly what we would want. So they have somehow accomplished compression of morbidity. Now, I would say there are two problems with that. One is, I don't know about the data sample size. The number of people who live over 110 is very, very small. The other is they may be benefiting from their own unique genetics. So they may have a particular combination of genetics against a broad genetic background that's unique to each person. So I'm not sure it's a generally translatable thing, and it also may have to do with their particular life history and lifestyle. So I don't know how much of what we learned from these centenarians is going to be applicable to the population as a whole. And otherwise, I don't even know how this would be accomplished. Although some people feel there's a natural limit to our biology, which restricts our lifespan to about 115 or 120 years. Nobody has lived more than 122. And so, as we improve our health, we may come up against that natural limit. And so, you might get a compression of morbidity. I'm skeptical. I think it's an unsolved problem.Eric Topol (06:14):I think I'm with you about this, but there's a lot of conflation of the two concepts. One is to suppress age related diseases, and the other is to actually somehow modulate control the biologic aging process. And we lump it all together as you're getting at, which is one of the things I loved about your book is you really give a balanced view. You present the contrarians and the different perspectives, the perspective about people having age limits potentially much greater than 120, even though as you say, we haven't seen anyone live past 122 since 1997, so it's quite a long time. So this, I think, conflation of what we do today as far as things that will reduce heart disease or diabetes, that's age related diseases, that's very different than controlling the biologic aging process. Now getting into that, one of the things that's particularly alluring right now, my friend here in San Diego, Juan Carlos Belmonte, who went over from Salk, which surprised me to the Altos Labs, as you pointed on in the book.Venki Ramakrishnan (07:38):I'm not surprised. I mean, you have a huge salary and all the resources you want to carry out the same kind of research. I wouldn't blame any of these guys.Rejuvenating Animals With Yamanaka FactorsEric Topol (07:50):No, I understand. I understand. It's kind of like the LIV Golf tournament versus the PGA. It's pretty wild. At any rate, he's a good friend of mine, and I visited with him recently, and as you mentioned, he has over a hundred people working on this partial epigenetic reprogramming. And just so reviewing this for the uninitiated is giving the four Yamanaka transcription factors here to the whole animal or the mouse and rejuvenating old mice, essentially at least those with progeria. And then others have, as you point out in the book, done this with just old mice. So one of the things that strikes me about this, and in talking with him recently is it's going to be pretty hard to give these Yamanaka factors to a person, an intravenous infusion. So what are your thoughts about this rejuvenation of a whole person? What do you think?Venki Ramakrishnan (08:52):If I hadn't seen some of these papers would've been even more skeptical. But the data from, well, Belmonte's work was done initially on progeria mice. These are mice that age prematurely. And then people thought, well, they may not represent natural aging, and what you're doing is simply helping with some abnormal form of aging. But he and other groups have now done it with normal mice and observed similar effects. Now, I would say reprogramming is one way. It's a very exciting and powerful way to almost try to reverse aging because you're trying to take cells back developmentally. You're taking possibly fully differentiated cells back to stem cells and then helping regenerate tissue, which one of the problems as we age is we start losing stem cells. So we have stem cell depletion, so we can no longer replace our tissues as we do when we're younger. And I think anyone who knows who's had a scrape or been hurt in a fall or something knows this because if I fall and scrape my elbow and get a big bruise and my grandson falls, we repair our tissues at very, very different rates. It takes me days or weeks to recover, and my grandson's fine in two or three days. You can hardly see he had a scrape at all. So I think that's the thing that these guys want to do.Venki Ramakrishnan (10:48):And the problem is Yamanaka factors are cancer. Two of them are oncogenic factors, right? If you give Yamanaka factors to cells, you can take them all the way back to what are called pluripotent cells, which are the cells that are capable of forming any tissue in the body. So for example, a fertilized egg or an early embryo cells from the early embryo are pluripotent. They could form anything in the body. Now, if you do that to cells with Yamanaka factors, they often form teratomas, which are these unusual forms of cancer tumors. And so, I think there's a real risk. And so, what these guys say is, well, we'll give these factors transiently, so we'll only take the cells back a little ways and not all the way back to pluripotency. And that way if you start with skin cells, you'll get the progenitor stem cells for skin cells. And the problem with that is when you do it with a population, you're getting a distribution. Some of them will go back just a little, some of them may go back much more. And I don't know how to control all this. So I think it's very exciting research. And of course, if I were one of these guys, I would certainly want to carry on doing that research. But I don't think it's anywhere near ready for primetime in terms of giving it to human beings as a sort of anti-aging therapeutic.Aging and Cancer Shared HallmarksEric Topol (12:31):Yeah. Well, I couldn't agree more on that because this is a company that's raised billions of dollars to go into clinical trials. And the question that comes up here, which is a theme in the book and a theme with the aging process to try to artificially, if you will affect it, is this risk of cancer. And as we know, the hallmarks of aging overlap considerably with the hallmarks of cancer. And this is just one example, as you mentioned, where these transcription factors could result in generating cancer. But as you also point out in the book at many places, methylation changes, DNA, repair, and telomeres.Venki Ramakrishnan (13:21):And telomeres.Venki Ramakrishnan (13:24):All of those are related to cancer as well. And this was first pointed out to me by Titia de Lange, who's a world expert on telomeres at Rockefeller, and she was pointing out to me the intimate connection between cancer and aging and many mechanisms that have evolved to prevent cancer early in life tend to cause aging later in life, including a lot of DNA damage response, which sends cells into senescence and therefore causes aging. Buildup of senescence cells is a problem later in life with aging, but it has a role which is to prevent cancer early in life. And so, I think it's going to be the same problem with stem cell therapy. I think very targeted stem cell therapy, which is involved in replacing certain tissues, the kind of regenerative medicine that stem cells have been trying to address for a very long time, and only now we're beginning to see some of the successes of that. So it's been very slow, even when the goal and target is very specific and well-defined, and there you are using that stem cell to treat a pretty bad disease or some really serious problem. I think with aging, the idea that somebody might take this so they can live an extra 10 years, it's a much higher bar in terms of safety and long-term safety and efficacy. So I don't think that this is going to happen anytime soon, but it's not to say it'll never happen. There is some serious biology underlying it.Eric Topol (15:13):Right. Well, you just touched on this, but of course the other, there's several big areas that are being explored, and one of them is trying to deal with these senescent cells and trying to get rid of them from the body because they can secrete evil humors, if you will. And the problem with that, it seems that these senescent cells are sort of protective. They stop dividing, they're not going to become cancerous, although perhaps they could contribute to that in some way. So like you say, with telomeres and so many things that are trying to be manipulated here, there's this downside risk and it seems like this is what we're going to have to confront this. We have seen Venki with the CAR-T, the T-cell engineering, there's this small risk of engendering cancer while you're trying to deal with the immune system.SenolyticsVenki Ramakrishnan (16:07):Yeah, I think with senescent cells, the early in life senescent cells have an important role in biology. They're essentially signaling to the immune system that there's a site that's subject to viral infection or wounds or things like that. So it's a signal to send other kinds of cells there to come and repair the damage. Now, of course, that evolved to help us early in life. And also many senescent cells were a response to DNA damage. And that's again, a way for the body that if your DNA is damaged, you don't want that cell to be able to divide indefinitely because it could become cancerous. And so, you send it into senescence and get it out of harm's way. So early life, we were able to get rid of these senescent cells, we were able to come to the site and then clean up the damage and eventually destroy the senescent cells themselves.Venki Ramakrishnan (17:08):But as we get older, the response mechanisms also deteriorate with age. Our immune system deteriorates with age, all the natural signaling mechanisms deteriorate with age. And so, we get this buildup of senescent cells. And there people have asked, well, these senescent cells don't just sit there, they secrete inflammatory compounds, which originally was a feature, not a bug, but then it becomes a problem later in life. And so, people have found that if you target senescent cells in older animals, those animals improve their symptoms of aging improved dramatically or significantly anyway. And so, this has led to this whole field called senolytics, which is being able to specifically target senescent cells. Now there the problem is how would you design compounds that are highly specific for senescent cells and don't damage your other cells and don't have other long-term side effects? So again, I think it's a promising area, but a lot of work needs to be done to establish long-term safety and efficacy.Eric Topol (18:23):Right. No, in fact, just today in Nature, there's a feature on killing the zombie cells, and it discusses just what you're pointing out, which is it's not so easy to tag these specifically and target them, even though as you know, there's some early trials and things like diabetic macular edema. And we'll see how that plays out. Now, one of the things that comes up is the young blood story. So in the young blood, whether it's this parabiosis or however you want to get at it, and I guess it even applies to the young microbiome of a gut, but there's this consistent report that there's something special going on there. And of course the reciprocal relationship of giving the old blood to the young mice, whatever, but no one can find the factor, whether it's platelet factor 4, GDF11, or what are your thoughts about this young blood story?Venki Ramakrishnan (19:25):I think there's no question that the experiments work because they were reproduced and they were reproduced over quite a long period, and which is that when you connect an old mouse or rat with a young equivalent, then the old mouse or old rat benefits from the young blood from the younger animal. And conversely, the younger animal suffers from the blood from the older animal. And then people were wondering whether this is simply that the young animal has better detoxification and things like that, or whether it's actually the blood. And they gave it just as transfusion without connecting the animals and showed that it really was the blood. And so, this of course then leads to the question, well, what is it about young blood that's beneficial and what is it about old blood that is bad? But the problem is blood has hundreds of factors. And so, they have to look at which factors are significantly different, and they might be in such small quantities that you might not be able to detect those differences very easily.Venki Ramakrishnan (20:40):And then once you've detected differences, then you have to establish their mechanism of action. And first of all, you have to establish that the factor really is beneficial. Then you have to figure out how it works and what its potential side effects could be. And so again, this is a promising area where there's a lot of research, but it has not prevented people from jumping the gun. So in the United States, and I should say a lot of them in your state, California somehow seems to attract all these immortality types. Well, anyway, a lot of companies set up to take blood from young donors, extract the plasma and then give it to rich old recipients for a fee for a healthy fee. And I think the FDA actually shut down one of them on the grounds that they were not following approved procedure. And then they tried to start up under a different name. And then eventually, I don't know what happened, but at one point the CEO said something I thought was very amusing. He said, well, the problem with clinical trials is that they take too long. I'm afraid that's characteristic of some portion of this sort of anti-aging therapeutics community. There's a very mainstream rigorous side to it, but there's also at the other end of the spectrum, kind of the wild west where people just sell whatever they can. And I think this exploits people's fear of getting old and being disabled or things like that and then dying. And I think the fear seems to be stronger in California where people like their lives and don't want to age.Eric Topol (22:49):You may be right about that. I like your term in the book immortality merchants, and of course we'll get into a bit, I hope the chapter on the crackpots and prophets that you called it was great. But that quote, by the way, which was precious from, I think it was Ambrosia, the name of the company and the CEO, but there's another quote in the book I want to ask you about. Most scientists working on aging agree that dietary restriction can extend both healthy life and overall life in mice and also lead to reductions in cancer, diabetes, and overall mortality in humans. Is that true? Most scientists think that you can really change these age-related diseases.Caloric Restriction and Related PathwaysVenki Ramakrishnan (23:38):I think if you had to pick one area in which there's broad agreement, it is caloric restriction. But I wouldn't say the consensus is complete. And the reason I say that is that most of the comparisons are between animals that can eat as much as they want, called ad libitum diet and mice that are calorically restricted or same with other animals even yeast. You either compared with an extremely rich medium or in a calorically restricted medium. And this is not a great comparison. And people, there's one discrepancy, and that was in monkeys where an NIH study didn't find huge differences, whereas a Wisconsin study found rather dramatic differences between the control group and the calorically restricted group. And so, what was the difference? Well, the difference was that the NIH study, the controlled group didn't have a calorically restricted diet, but still had a pretty reasonable diet.Venki Ramakrishnan (24:50):It wasn't given a unhealthy rich diet of all you can eat. And then they tried to somehow reconcile their findings in a later study. But it leads to the question of whether what you can conclude is that a rich all you can eat diet, in other words, gorging on an all you can eat buffet is definitely bad for you. So that's why you could draw that conclusion rather than saying it's actually the caloric restriction. So I think people need to do a little more careful study. There was also a study on mice which took different strains of mice and showed that in some strains, caloric restriction actually shortened lifespan didn't increase lifespan. Now, much of the aging community says, ah, that's just one study. But nobody's actually shown whether there was anything wrong with that study or even tried to reproduce it. So I think that study still stands.Venki Ramakrishnan (25:51):So I think it's not completely clear, but the fact is that there's some calorie dependence that's widely been observed across species. So between the control group and the experimental group, whatever you may, however, you may define it as there's been some effective calories intake. And the other interesting thing is that one of the pathways affected by caloric restriction is the so-called TOR pathway and one of the inhibitors of the TOR pathways is rapamycin. And rapamycin in studies has also shown some of these beneficial effects against the symptoms of aging and in lifespan. Although rapamycin has the same issue as with many other remedies, it's an immunosuppressive drug and that means it makes you more prone to infection and wound healing and many other things. I believe one of them was there's a question of whether it affects your libido, but nevertheless, that has not prevented rapamycin clinics from opening up, did I say in California? So I do think that there's often serious science, which leads to sort of promising avenues. But then there are of course people who jump the gun and want to go ahead anyway because they figure by the time trials are done, they'll be dead and they'd rather try act now.Eric Topol (27:36):Right. And you make a good, I mean the rapamycin and mTOR pathway, you really developed that quite a bit in the book. It's really quite complex. I mean, this is a pleotropic intervention, whether it's a rapalogs or rapamycin, it's just not so simple at all.Venki Ramakrishnan (27:53):Right. It's not at all simple because the TOR pathway has so many consequences. It affects so many different processes in the cell from including my own field of protein synthesis. It's one of the things it does is shut down global protein synthesis, and that's one of the effects of inhibiting TOR. So, and it turns up autophagy, which is this recycling of defective proteins and entirely defective entire organelles. So I think the TOR pathway is like a hub in a very large network. And so, when you start playing with that, you're going to have multiple consequences.Eric Topol (28:37):Yeah, no. And another thing that you develop so well is about this garbage disposal waste disposal system, which is remarkably elaborate in the cell, whether it's the proteasome for the proteins and the autophagosome for the autophagy with the lysosomes and the mitochondria mitophagy. Do you want to comment about that? Because this is something I think a lot of people don't appreciate, that waste management in the cell is just, it's a big deal.Venki Ramakrishnan (29:10):So we always think of producing things in the cell as being important, making proteins and so on. But the fact is destroying proteins is equally important because sometimes you need proteins for a short time, then they've done their job and you need to get rid of them, or proteins become dysfunctional, they stop working, or even worse, they start clumping together and causing diseases for example you could think of Alzheimer's as a disease, which involves protein tangles. Of course, the relationship between the tangles and the disease is still being worked out, but it's a characteristic of Alzheimer's that you have these protein tangles and the cell has evolved very elaborate mechanisms to constantly turn over defective proteins. Well, for example, it senses when proteins are unfolded and essentially the chain has unraveled and is now sticking to all sorts of things and causing problems. So I think in all of these cases, the cells evolved very elaborate mechanisms to recycle defective products, to have proper turnover of proteins. And in fact, recycling of entire organelles like mitochondria, when they become defective, the whole mitochondria can be recycled. So these systems also break down with aging. And so, as we age, we have more of a tendency to accumulate unfolded proteins or to accumulate defective mitochondria. And it's one of the more serious problems with aging.Eric Topol (30:59):Yeah, there's quite a few of them. Unfortunately, quite a few problems. Each of them are being addressed. So there's many different shots on goal here. And as you also aptly point out, they're interconnected. So many of these things are not just standalone strategies. I do want to get your sense about another popular thing, especially here out in California, are the clocks, epigenetic clocks in particular. And these people are paying a few hundred dollars and getting their biologic age, which what is that? And they're also thinking that I can change my future by getting clocks. Some of these companies offer every few months to get a new clock. This is actually remarkable, and I wonder what your thoughts are about it.Venki Ramakrishnan (31:48):Well, again, this is an example of some serious biology and then people jumping the gun to use it. So the serious biology comes from the fact that we age at different rates individuals. So anyone who's been to a high school reunion knows this. You'll have classmates who are unrecognizable because they've aged so much and others who've hardly changed since you knew them in high school. So of course at my age, that's getting rarer and rarer. But anyway, but you know what I mean. So the thing is that, is there a way that we can ask on an individual level how much has that individual aged? And there are markers that people have identified, some of them are markers on our DNA, which you mentioned in California. Horvath is a very famous scientist who has a clock named after him actually, which has to do with methylation of our DNA and the patterns of methylation affect the pattern of gene expression.Venki Ramakrishnan (33:01):And that pattern changes as we age. And they've shown that those patterns are a better predictor of many of the factors of aging. For example, mortality or symptoms of aging. They're a better predictor of that than chronological age. And then of course there are blood markers, for example, levels of various blood enzymes or blood factors, and there are dozens of these factors. So there are many different tests of many different kinds of markers which look at aging. Now the problem is these all work on a population level and they also work on an individual level for time comparison. That is to say, if you want to ask is some intervention working? You could ask, how fast are these markers changing in this person without the intervention and how fast are they changing with the intervention? So for these kind of carefully controlled experiments, they work, but another case is, for example, glycosylation of proteins, especially proteins of your immune system.Venki Ramakrishnan (34:15):It turns out that adding sugar groups to your immune system changes with age and causes an immune system to misfire. And that's a symptom of aging. It's called inflammaging. So people have used different markers. Now the problem is these markers are not always consistent with each other because you may be perfectly fine in many respects, but by some particular marker you may be considered old just because they're comparing you to a population average. But how would you say one person said, look, we all lose height as we age, but that doesn't mean if you take a short person, you can consider them old. So it's a difference between an individual versus a population, and it's a difference between what happens to an individual by following that individual over time versus just taking an individual and comparing it to some population average. So that's one problem.Organ ClocksVenki Ramakrishnan (35:28):The other problem is that our aging is not homogeneous. So there's a recent paper from I believe Tony Wyss-Coray group, which talks about the age of different organs in the same person. And it turns out that our organs, and this is not just one paper, there are other papers as well. Our organs don't necessarily age at the same rate. So giving a single person, giving a person a single number saying, this is your biological age, it's not clear what that means. And I would say, alright, even if you do it, what are you going to do about it? What can you do about it knowing your biological, the so-called number of a biological age. So I'm not a big fan. I'm a big fan of using these markers as a tool in research to understand what interventions work because otherwise it would take too long. You'd have to wait 20 years to see some large scale symptoms. And certainly, if you want to look at mortality, you'd have to wait possibly even longer. But if you were to be able to follow track these interventions and see that these markers slowed down with intervention, then you could say, well, your interventions having an effect on something related to aging. So I would say these are very useful research tools, but they're not meant to be used at $500 a pop in your age.Venki Ramakrishnan (37:02):But of course that hasn't stopped lots of companies from doing it.Eric Topol (37:07):No, it's just amazing actually. And by the way, we interviewed Tony Wyss-Coray about the organ clock, the paper. I thought it really was quite a great contribution, again, on a research level.Venki Ramakrishnan (37:19):He's a very serious scientist. He actually spoke here at the LMB as well. He gave a very nice talk here.Is Aging A Disease?Eric Topol (37:26):He's the real deal. And I think that's going to help us to have that organ specific type of tracking is another edge here to understand the effects. Well, before we wrap up, I want to ask you a question that you asked in the book. Is aging a disease?Venki Ramakrishnan (37:49):That's again, a controversial subject. So the WHO, and I believe the FDA decided that aging was not a disease on the grounds that it's inevitable and ubiquitous. It happens to everybody and it's inevitable. So how could something that happens to everybody and inevitable be considered a disease? A disease is an abnormal situation. This is a normal situation, but the anti-aging researchers and especially the anti-aging therapeutics people don't like that because if it's not a disease, how can they run a clinical trial? So they want aging to be considered a disease. And their argument is that if you look at almost every condition of old age, every disease of old age like cancer, diabetes, heart disease, dementia, the biggest risk factor in all of these diseases is age. That's the strongest risk factor. And so, they say, well, actually, you could think of these diseases as secondary diseases, the primary disease being age, and then that results in these other diseases.Venki Ramakrishnan (39:07):I am a little skeptical of that idea. I tend to agree with the WHO and the FDA, but I can see both sides of the argument. And as you know, I've laid them both out. My view is that it should be possible to do trials that help with aging regardless of whether you consider aging a disease or not. But that will require the community to agree on what set of markers to use to characterize success. And that's people, for example, Tony Wyss-Coray has his proteome, blood proteome markers, Horvath has his DNA methylation clock. There are a whole bunch of these. And then there are people with glycation or glycosylation of various proteins as markers. These people need to all come together. Maybe we need to organize a nice conference for them in some place like Southern California or Hawaii or somewhere, put them together in a locked room for a week so that they can thrash out a common set of markers and at least agree on what experiments they need to do to even come to that agreement and then use that to evaluate anti-aging therapies. I think that would be a way forward.Eric Topol (40:35):Yeah, I think you're bringing up a really valuable point because at the moment, they're kind of competing with one another, whether it's the glycosylated proteins or the transcriptomics or the epigenetics. And we don't know whether these are additive or what they're really measuring.Venki Ramakrishnan (40:53):Some of them may be highly correlated, and that's okay, but I think they need to know that. And they also need to come up with some criteria of how do we define age in an individual. It's not one number, just like we have many things that characterize our health. Cholesterol is one, blood pressures another, various other lipids. They're all blood enzymes, liver enzymes. All these things are factors in defining our so-called biological health. So I don't think there's some single number that's going to say this is your age. Just like there isn't one single thing that says you're healthy, you're not healthy.DNA RepairEric Topol (41:38):Right, that's well put. Last topic on aging is on about DNA repair, which is an area that you know very well. And one of the quotes in your book, I think is important for people to take in. “Nevertheless, they will make an error once every million or so letters in a genome with a few billion letters. That means several thousand mistakes occur each time a cell divides. So the DNA repair enzyme, as you point out the sentinels of our genome, the better we repair, the better we age.” Can we fix the DNA repair problem?Venki Ramakrishnan (42:20):I think maybe, again, I'm not sure what the consequences would be and how much it would take. There's one curious fact, and that is that there was a paradox called Peto's paradox after the scientist who discovered it, which is why don't big animals get cancer much more frequently than say a mouse? In fact, a mouse gets cancer far more readily than an elephant does, and in reality, the elephant should actually get cancer more because it has many orders of magnitude more cells, and all it takes is for one cell to become cancerous for the animal to get cancer and die. So the chances that one cell would become cancer would be larger if there are many, many more cells. And it turns out that elephants have many copies of DNA repair proteins or DNA damage response proteins, not so much DNA repair, but the response to DNA damage and in particular, a protein called p53. And so, this leads to the question that if you had very good DNA repair or very good DNA damage response, would you then live longer or solve this problem? I'm not entirely sure because it may have other consequences because for example, you don't want to send cells into senescence too easily. So I think these things are all carefully balanced, evolutionarily, depending on what's optimized to optimize fitness for each species.Venki Ramakrishnan (44:13):For a mouse, the equation's different than for a large animal because a mouse can get eaten by predators and so on. So there, it doesn't pay for evolution to spend too much select for too much spending of resources in maintenance and repair, for larger animals the equation is different. So I just don't know enough about what the consequences would be.Eric Topol (44:40):No, it's really interesting to speculate because as you point out in the book, the elephant has 20 copies of p53, and we have two as humans. And the question is that protection from cancer is very intriguing, especially with the concerns that we've been talking about.Venki Ramakrishnan (44:57):And it was also true, I believe they did some analysis of genomics of these whales that live very long, and they found sorts of genes that are probably involved in DNA repair or DNA damage response.Eric Topol (45:14):Well, this is a masterful book. Congratulations, Venki. I thoroughly enjoyed it. It's very stimulating. I know a lot of the people that will listen or read the transcript will be grabbed by it.Crackpots and ProphetsVenki Ramakrishnan (45:28):I think what I've tried to do is give the general reader a real understanding of the biology of aging so that even a complete non-scientist can get an understanding of the processes, which in turn empowers them to take action to do the sort of things that will actually really help. And also it'll guard them against excessive hype, of which there's a lot in this business. And so, I think that was the goal, and to try and present a balanced view of the field. I'm merely trying to be a realist. I'm not being a pessimist about it, but I also think this excessively optimistic hype is actually bad for the field and bad for science and bad for the public as well.Eric Topol (46:16):Well, and you actually were very kind in the chapter you have on crackpots and prophets. You could have been even tougher on some of these guys. You were very relatively diplomatic and gentle, I thought, I don't know if you were holding back.Venki Ramakrishnan (46:28):I had two lawyers looked at it, so.Eric Topol (46:33):I believe it. And now one thing, apart from what we've been talking about because of your extraordinary contribution on the structural delineation of the ribosome back in the early 2000s and 2009 Nobel Prize. Now, the world of AI now with AlphaFold 3 and all these other large language models, would that have changed your efforts? Would that have accelerated things or is it not really?Venki Ramakrishnan (47:09):Well, it would've helped, but you would still need the experimental data to solve something like the ribosome, a large complex like the ribosome. And the other thing that would really change well has changed our world is the advent of cryo-electron microscopy of which Scripps is one of the leading places for it. And that has really changed it so that now nobody would bother to crystallize a ribosome and try to get an X-ray structure out of it. You would just throw it into an EM grid, collect your data and be off to the races. So new ribosome structures are being solved all the time at a fraction, a tiny fraction of the time it took to solve the first one.Eric Topol (48:02):Wow, that's fascinating. This has been a real joy for Venki to discuss your book and your work, and thanks so much for what you're doing to enlighten us and keep the balance. And it may not be as popular as the immortality merchants, but it's really important stuff.Venki Ramakrishnan (48:19):Yeah, no, I hope actually, I found that many of the public want to read about the biology of aging. They're curious. Humans have been curious ever since we knew about mortality, about why some species live so short lives and other species live such a long time and why we actually have to age and die. So there's natural curiosity and then it also empowers the public once they understand the basis of aging, to take action, to live healthy lives and do that. It's an empowering book rather than a recipe book.Venki Ramakrishnan (49:01):I think a lot of the public actually does appreciate that. And of course, scientists will like the sort of more balanced and tone.Eric Topol (49:13):Well, you do it so well. All throughout you have metaphors to help people really understand and the concepts, and I really applaud you for doing this. In fact, a couple of people who we both know, Max and John Brockman, apparently were influential for you to get to do it. So I think it's great that you took it on and all the power to you. So thank you, and I hope that we'll get a chance to visit further as we go forward.******************Headshot photo credits by Kate Joyce and Santa Fe InstituteThe Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informativeVoluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff tor audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in.A Poll on Anti-Aging Get full access to Ground Truths at erictopol.substack.com/subscribe

In Why We Die: The New Science of Ageing and the Quest for Immortality, Venki Ramakrishnan explores the current research on and prospects for human longevity.Ramakrishnan leads a group at the MRC Laboratory of Molecular Biology in Cambridge, England. For his research on the structure and function of ribosomes, he won the 2009 Nobel Prize in Chemistry. From 2015 to 2020, he served as president of the Royal Society. In his new book, Ramakrishnan explains the mechanisms of aging and their potential impacts on life expectancy, health span, and lifespan.Together with Martin Reeves, Chairman of the BCG Henderson Institute, Ramakrishnan discusses the likely social, economic, and ethical implications of increasing longevity as well as the specific efforts researchers are making to prolong healthy life—and how close they are to achieving a breakthrough. He shines a light on a set of technologies which could be every bit as impactful as artificial intelligence, which therefore also deserve our attention.Key topics discussed: 02:28 | Life expectancy vs. health span vs. maximum lifespan08:21 | Mechanisms of aging13:25 | Potential interventions for promoting longevity18:27 | How close are we to a longevity breakthrough?24:02 | Societal and ethical implications28:48 | The art of communicating complex ideaAdditional inspirations from Venki Ramakrishnan:The Most Promising Ways to Stop Ageing (New Scientist Interview, 2024)The Story of Deciphering the Ribosome (The Royal Society Talk, 2020)Gene Machine: The Race to Decipher the Secrets of the Ribosome (Basic Books, 2018)This podcast uses the following third-party services for analysis: Chartable - https://chartable.com/privacy

Scientists are using the secrets of biology to unlock living well past current human life spans. Venki Ramakrishnan shared the 2009 Nobel Prize in Chemistry for uncovering the structure of the ribosome. A member of the National Academy of Sciences, Venki runs a research group at the MRC Laboratory of Molecular Biology in Cambridge, England. He joins host Krys Boyd to discuss the quest to live forever, if that's even ethical, and what it looks like to alter our physiology. His book is “Why We Die: The New Science of Aging and the Quest for Immortality.”

The Nobel prize winning scientist Venki Ramakrishnan considers both why we might live longer and also the dilemmas this raises. In the last few years medical advance had led to treatments that really do offer the potential to tackle life threatening cancers and debilitating diseases such as Parkinson's and Alzheimer's. In discussion with Nuala McGovern, Venki also explores the questions such treatments raise. Initially they will be expensive, we already have a global society in which there is a direct link between life expectancy and affluence, will access to these treatments or lack of it, increase that disparity? And although your incurable disease may now be cured, what about the rest of your quality of life? Can the planet support an increasingly needy older and older generation? Does trying to live longer become a selfish act? Nobel prize-winning molecular biologist Venki Ramakrishnan heads a research group at the MRC Laboratory of Molecular Biology in Cambridge, England. This is the first in a series of four programmes from the Oxford Literary Festival, Presented by Nuala McGovern and produced by Julian Siddle. Recorded in front of an audience at Worcester College Oxford.

Be it biology, psychology or philosophy, ageing and death are undoubtedly two of the most difficult concepts to tackle in any field of research, so where do we even begin? In this episode I speak to Prof Sir Venki Ramakrishnan, a researcher based at Cambridge University's MRC Laboratory of Molecular Biology, a former president of the Royal Society and recipient of the 2009 Nobel Prize in Chemistry. We talk about the fascinating discoveries he outlines in his latest book Why We Die: The New Science of Ageing and the Quest for Immortality. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Making every researcher seek grants is a broken model, published by jasoncrawford on January 26, 2024 on LessWrong. When Galileo wanted to study the heavens through his telescope, he got money from those legendary patrons of the Renaissance, the Medici. To win their favor, when he discovered the moons of Jupiter, he named them the Medicean Stars. Other scientists and inventors offered flashy gifts, such as Cornelis Drebbel's perpetuum mobile (a sort of astronomical clock) given to King James, who made Drebbel court engineer in return. The other way to do research in those days was to be independently wealthy: the Victorian model of the gentleman scientist. Eventually we decided that requiring researchers to seek wealthy patrons or have independent means was not the best way to do science. Today, researchers, in their role as "principal investigators" (PIs), apply to science funders for grants. In the US, the NIH spends nearly $48B annually, and the NSF over $11B, mainly to give such grants. Compared to the Renaissance, it is a rational, objective, democratic system. However, I have come to believe that this principal investigator model is deeply broken and needs to be replaced. That was the thought at the top of my mind coming out of a working group on "Accelerating Science" hosted by the Santa Fe Institute a few months ago. (The thoughts in this essay were inspired by many of the participants, but I take responsibility for any opinions expressed here. My thinking on this was also influenced by a talk given by James Phillips at a previous metascience conference. My own talk at the workshop was written up here earlier.) What should we do instead of the PI model? Funding should go in a single block to a relatively large research organization of, say, hundreds of scientists. This is how some of the most effective, transformative labs in the world have been organized, from Bell Labs to the MRC Laboratory of Molecular Biology. It has been referred to as the "block funding" model. Here's why I think this model works: Specialization A principal investigator has to play multiple roles. They have to do science (researcher), recruit and manage grad students or research assistants (manager), maintain a lab budget (administrator), and write grants (fundraiser). These are different roles, and not everyone has the skill or inclination to do them all. The university model adds teaching, a fifth role. The block organization allows for specialization: researchers can focus on research, managers can manage, and one leader can fundraise for the whole org. This allows each person to do what they are best at and enjoy, and it frees researchers from spending 30-50% of their time writing grants, as is typical for PIs. I suspect it also creates more of an opportunity for leadership in research. Research leadership involves having a vision for an area to explore that will be highly fruitful - semiconductors, molecular biology, etc. - and then recruiting talent and resources to the cause. This seems more effective when done at the block level. Side note: the distinction I'm talking about here, between block funding and PI funding, doesn't say anything about where the funding comes from or how those decisions are made. But today, researchers are often asked to serve on committees that evaluate grants. Making funding decisions is yet another role we add to researchers, and one that also deserves to be its own specialty (especially since having researchers evaluate their own competitors sets up an inherent conflict of interest). Research freedom and time horizons There's nothing inherent to the PI grant model that dictates the size of the grant, the scope of activities it covers, the length of time it is for, or the degree of freedom it allows the researcher. But in practice, PI funding has evol...

Link to original articleWelcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Making every researcher seek grants is a broken model, published by jasoncrawford on January 26, 2024 on LessWrong. When Galileo wanted to study the heavens through his telescope, he got money from those legendary patrons of the Renaissance, the Medici. To win their favor, when he discovered the moons of Jupiter, he named them the Medicean Stars. Other scientists and inventors offered flashy gifts, such as Cornelis Drebbel's perpetuum mobile (a sort of astronomical clock) given to King James, who made Drebbel court engineer in return. The other way to do research in those days was to be independently wealthy: the Victorian model of the gentleman scientist. Eventually we decided that requiring researchers to seek wealthy patrons or have independent means was not the best way to do science. Today, researchers, in their role as "principal investigators" (PIs), apply to science funders for grants. In the US, the NIH spends nearly $48B annually, and the NSF over $11B, mainly to give such grants. Compared to the Renaissance, it is a rational, objective, democratic system. However, I have come to believe that this principal investigator model is deeply broken and needs to be replaced. That was the thought at the top of my mind coming out of a working group on "Accelerating Science" hosted by the Santa Fe Institute a few months ago. (The thoughts in this essay were inspired by many of the participants, but I take responsibility for any opinions expressed here. My thinking on this was also influenced by a talk given by James Phillips at a previous metascience conference. My own talk at the workshop was written up here earlier.) What should we do instead of the PI model? Funding should go in a single block to a relatively large research organization of, say, hundreds of scientists. This is how some of the most effective, transformative labs in the world have been organized, from Bell Labs to the MRC Laboratory of Molecular Biology. It has been referred to as the "block funding" model. Here's why I think this model works: Specialization A principal investigator has to play multiple roles. They have to do science (researcher), recruit and manage grad students or research assistants (manager), maintain a lab budget (administrator), and write grants (fundraiser). These are different roles, and not everyone has the skill or inclination to do them all. The university model adds teaching, a fifth role. The block organization allows for specialization: researchers can focus on research, managers can manage, and one leader can fundraise for the whole org. This allows each person to do what they are best at and enjoy, and it frees researchers from spending 30-50% of their time writing grants, as is typical for PIs. I suspect it also creates more of an opportunity for leadership in research. Research leadership involves having a vision for an area to explore that will be highly fruitful - semiconductors, molecular biology, etc. - and then recruiting talent and resources to the cause. This seems more effective when done at the block level. Side note: the distinction I'm talking about here, between block funding and PI funding, doesn't say anything about where the funding comes from or how those decisions are made. But today, researchers are often asked to serve on committees that evaluate grants. Making funding decisions is yet another role we add to researchers, and one that also deserves to be its own specialty (especially since having researchers evaluate their own competitors sets up an inherent conflict of interest). Research freedom and time horizons There's nothing inherent to the PI grant model that dictates the size of the grant, the scope of activities it covers, the length of time it is for, or the degree of freedom it allows the researcher. But in practice, PI funding has evol...

A Netflix documentary has been raising awareness of and public interest in one of the most fascinating and mysterious groups in the animal kingdom. Neuroscientist Dr Amy Courtney, originally from Dublin and now working at the MRC Laboratory of Molecular Biology in Cambridge, England, admits herself that she has become obsessed with octopuses.

Alojz Ihan, Alenka Zupančič, Marina Dermastia in Tomaž Zwitter o dvomu in kritičnem razumu Zadnja tri leta so nam govorili, naj zaupamo v znanost in izsledke raziskav. Govorili so, naj zaupamo in verjamemo poznavalcem, strokovnjakom, znanstvenikom. Vendar; ali ni prav dvom bistvo znanosti? Ali ni kritični razum tisto, kar najbolj krasi inteligentnega človeka? Vprašanja, ki odpirajo širše dileme. Ali moramo zaupati v znanost? Ali lahko verjamemo znanstvenicam in znanstvenikom? V Intelekti razmišljajo: zdravnik Alojz Ihan, filozofinja Alenka Zupančič, biologinja Marina Dermastia in astrofizik Tomaž Zwitter. Vsi so doktorji znanosti, ugledni predavatelji, vsi pišejo in objavljajo. Na debato v studio Prvega jih je povabil Iztok Konc. Foto, od leve proti desni in od spodaj navzdol: Aristotel, filozof (384-321 pr. n. št) Satyendra Nath Bose, fizik in matematik (1894-1974) Emanuelle Charpentier, genetičarka (1954) Dorothy Hodgkin, kemičarka (1910-1994) Gregor Mendel, genetik (1822-1884) Stephen Hawking, kozmolog (1942-2018) Sigmund Freud, psihoanalitik (1856-1939) Charles Darwin, biolog (1809-1882) Mohamed ibn Musa al Hvarizmi, astronom in matematik (780-847) Ada Lovelace, matematičarka (1815-1852) Niels Bohr, fizik (1885-1962) Tu Youyou, farmakologinja (1930) Nikolaj Kopernik, astronom (1473-1543) Dmitri Mendeleev, kemik (1834-1907) Albert Einstein, fizik (1879-1955) Marie Curie, fizičarka in kemičarka (1867-1934) Jennifer Doudna, biokemičarka (1964) Alan Turing, računalničar (1912-1954) Max Planck, fizik (1858-1947) Konstantin Ciolkovski, raketni znanstvenik (1857-1935) Alessandro Volta, fizik in kemik (1745-1827) Maryam Mirzakhani, matematičarka (1977-2017) Fibonacci, matematik (1170-1250) Nikola Tesla, elektroinženir (1856-1943) Louis Pasteur, mikrobiolog (1822-1895) Ferdinand de Saussure, jezikoslovec (1857-1913) Galileo Galilei, astronom (1564-1642) Rosalind Franklin, kemičarka (1920-1958) Isaac Newton, fizik (1642-1727) Herman Potočnik Noordung, teoretik plovbe po vesolju (1892-1929) Claude Levi-Strauss, antropolog (1908-2009) Vera Rubin, astronomka (1928-2016) Johannes Kepler, astronom (1571-1630) Jane Goodall, primatologinja (1934)   Vse fotografije so na Wikipediji objavljene kot javna last, z izjemo naslednjih: al-Hvarizmi (Wikipedija, Davide Mauro), de Saussure (Wikipedija, Frank-Henri Jullien), Tu (Wikipedija, Bengt Nyman), Franklin (Wikipedija, MRC Laboratory of Molecular Biology), Charpentier (Wikipedija, Bianca Fioretti), Doudna (Wikipedija, Cmichel67), Goodall (Wikipedija, Muhammad Mahdi Karim), Rubin (Wikipedija, NOIRLab), Lévi-Strauss (Wikipedija, UNESCO), Fibonacci (Wikipedija, Hans-Peter Postel), Mirzakhani (Wikipedija, Maryeraud9),

Nobel Prize recipient Frances Arnold joins Tim to talk about winning a Nobel Prize honor for her pioneering work in “directed evolution,” which harnesses the power of evolution to enhance products throughout society – from biofuels and pharmaceuticals, to agriculture, chemicals, paper products and more. Directed evolution was in the news this week tied to Covid jab research. We talk with Frances about her journey and her work that is changing the world for the better. This episode was originally released November 5, 2018. https://traffic.libsyn.com/secure/shapingopinion/Encore_-_Frances_Arnold_Nobel_Recipient_Pioneered_Directed_Evolution.mp3 Since the Nobel Prize in Chemistry was first awarded in 1901, 117 years ago, only four women had won the honor, and in October, American Frances Arnold became the fifth. The professor of chemical engineering, bioengineering and biochemistry at the California Institute of Technology, received the honor for her pioneering work in “directed evolution.” Frances's work centers on the directed evolution of enzymes, proteins that serve as catalysts for chemical reactions that take place in living organisms, animals and people. In its most simple form, the process focuses on harnessing the power of natural evolution to solve problems for society. Frances is the Linus Pauling Professor of Chemical Engineering, Bioengineering and Biochemistry at Caltech. Today, directed evolution is used in research laboratories around the world to create things from laundry detergents to biofuels to pharmaceuticals. Enzymes created with through this process have been able to replace some toxic chemicals traditionally used in industry. Frances shares the prize with George Smith of the University of Missouri, who created a “phage display” process for protein evolution, and Gregory Winter of the MRC Laboratory of Molecular Biology in the United Kingdom, who used phage display for antibody evolution. Arnold was born in Pittsburgh, Pennsylvania. Her undergraduate degree in mechanical and aerospace engineering is from Princeton University. Her graduate degree in chemical engineering is from UC Berkeley. She has been at Caltech since 1986, first as a visiting associate, then as an assistant professor, and progressing to professor in 1996. In 2017, she became the Linus Pauling Professor. She became the director of the Donna and Benjamin M. Rosen Bioengineering Center at Caltech in 2013. Frances is a member of the American Academy of Arts and Sciences and the American Philosophical Society, and is a fellow of the American Association for the Advancement of Science and the Royal Academy of Engineering. How Directed Evolution Works Directed evolution is similar to how animal breeders mate cats or dogs to create hybrids or new breeds of animal. To conduct directed evolution mutations are induced to DNA, or a gene, which “encodes” a particular enzyme. That mutated enzyme, along with other thousands, are produced and tested to what Frances calls a desired trait. The preferred enzymes are selected, and the process continues until the enzymes are working to achieve a desired outcome or solution. “I copy nature's design process. There is tremendous beauty and complexity of the biological world, but it all comes about through this one, simple, beautiful design algorithm.” – Frances Arnold Links Frances Arnold Wins 2018 Nobel Prize in Chemistry, Caltech Frances H. Arnold Group Caltech scientist is among 3 awarded Nobel Prize in chemistry for sparking ‘a revolution in evolution', LA Times The Latest: Nobel chemistry winner credits team at Caltech, Washington Post Nobel winner overcame personal loss, cancer, and being a woman, NBC News

"It's a good conversation starter," says Dr Miriam Ferrer of her job title. "People say 'food supplements? That's just cheap vitamins'. Then I tell them all about it." Dr Ferrer is Head of New Product Development at Cambridge Nutraceuticals, a company that makes health supplements with proven clinical benefits. The company says: "If it isn't supported by data, we won't sell it." In this episode of the Career Conversations podcast series, Dr Ferrer tells us all about her role and how she ended up in the field of nutraceuticals. Her love of science began when she was a teenager and watched a documentary about the double helix.  "I wanted to genetic engineering," she says. "I was told I had to study biology, so I did." She studied at the University of Barcelona before securing a position at the Laboratory of Molecular Biology in Cambridge: "The very first thing you see when you go in is the pictures of all the Nobel Prize winners. So no pressure!" Dr Ferrer decided that she wanted to lay down some roots in Cambridge, something she says is not always easy to do as a scientist. "With science, you end up having to travel, which is great to some extent," she says. "But at some point you might want to start a family and not keep moving from one place to another." She got her current job at Cambridge Nutraceuticals in 2017 and has not looked back since. "The products we develop have a lot of scientific research behind them," she explains. "I am able to read through all of that and say whether or not I agree with the science. "I can also use my expertise to help the marketing team translate the scientific knowledge into layman's terms and communicate that to our customers." Listen to the full episode to find out exactly what a nutraceutical is, why Dr Ferrer thinks it is possible to balance both science and art within your career, and how much you can expect to earn if you follow a career path similar to hers. Dr Miriam Ferrer, Head of New Product Development, Cambridge Nutraceuticals Miriam Ferrer studied Biology at the University of Barcelona (Spain) and later at the Biochemistry Department of Wageningen University (Netherlands). She then moved to the Vrije Universiteit of Amsterdam to start her PhD, which focused on cancer gene therapy. After graduating she took a post-doctoral research position at the prestigious MRC Laboratory of Molecular Biology in Cambridge to work on BRCA1, a DNA repair protein involved in breast cancer. Miriam decided to move into industry and went on to work for nine years at Abcam, a leading supplier of research reagents for life scientists. Her roles included Business Development Associate and Product Manager for biochemical kits. Looking for a change, she took on her current position at Cambridge Nutraceuticals, which commercialises premium supplements under the brand FutureYou Cambridge. Her scientific background helps her to evaluate research data and develop effective supplements that are backed by science.

For more details, visit the #DrGPCR Podcast Episode #75 page https://www.drgpcr.com/episode-75-with-vaithish-velazhahan/ ------------------------------------------- About Vaithish Velazhahan Vaithish obtained dual bachelor's degrees with honors in Medical Biochemistry and Microbiology from Kansas State University, USA. His undergraduate thesis work on studying the biochemical mechanisms of flavonoids in cancer using nuclear magnetic resonance spectroscopy (NMR) led to a Barry M. Goldwater Scholarship. He then received a prestigious Gates Cambridge Scholarship to study for a Ph.D. at the MRC Laboratory of Molecular Biology and the University of Cambridge, where he is currently a final year Ph.D. candidate. His Ph.D. work has been focused on understanding the structure and activation of Class D fungal GPCRs. He has developed novel tools and methodologies to study fungal GPCRs which allowed the determination of the first structures of the prototypical fungal GPCR Ste2. This work has led to two first-authored manuscripts published in the journal Nature. Vaithish has been recognized with the MRC LMB's Max Perutz Prize for outstanding Ph.D. work and has been elected a Research Fellow at Gonville and Caius College, which is one of the most prestigious positions at the University of Cambridge. Vaithish Velazhahan on the web Twitter GatesCambridge PubMed ------------------------------------------- Become a #DrGPCR Ecosystem Member ------------------------------------------- Imagine a world in which the vast majority of us are healthy. The #DrGPCR Ecosystem is all about dynamic interactions between us who are working towards exploiting the druggability of #GPCR's. We aspire to provide opportunities to connect, share, form trusting partnerships, grow, and thrive together. To build our #GPCR Ecosystem, we created various enabling outlets. Individuals Organizations ------------------------------------------- Are you a #GPCR professional? Subscribe to #DrGPCR Monthly Newsletter Listen and subscribe to #DrGPCR Podcasts Listen and watch GPCR focused scientific talks at #VirtualCafe

#40 — Brad Amos, Emeritus Scientist at the MRC Laboratory of Molecular Biology, joins Peter O'Toole in this episode of The Microscopists to discuss his varied career, from zoologist to confocal microscope designer to amateur artist. We'll discover how Brad developed the confocal microscope taken up by Bio-Rad, as well as the Mesolens microscope, which he is using in his work as Visiting Professor at the University of Strathclyde. We'll hear how Brad has never fully retired and how his artwork ended up on a stamp for the Ascension Islands. Brad also reveals how he has played Robin Hood, the Pope, and Boris Johnson is his legendary lab skits and where to put your hands when scuba diving with sharks! Tune in now to learn more about Brad's inspiring career. Watch or Listen to all episodes of The Microscopists here: http://bit.ly/the-microscopists-yt #TheMicroscopists #microscopy #imageanalysis

#40 — Brad Amos, Emeritus Scientist at the MRC Laboratory of Molecular Biology, joins Peter O'Toole in this episode of The Microscopists to discuss his varied career, from zoologist to confocal microscope designer to amateur artist. We'll discover how Brad developed the confocal microscope taken up by Bio-Rad, as well as the Mesolens microscope, which he is using in his work as Visiting Professor at the University of Strathclyde. We'll hear how Brad has never fully retired and how his artwork ended up on a stamp for the Ascension Islands. Brad also reveals how he has played Robin Hood, the Pope, and Boris Johnson is his legendary lab skits and where to put your hands when scuba diving with sharks!Tune in now to learn more about Brad's inspiring career.Watch or Listen to all episodes of The Microscopists here: https://themicroscopists.bitesizebio.com/

Dr. Maximina Yun, Ph.D. (https://tu-dresden.de/cmcb/crtd/forschungsgruppen/crtd-forschungsgruppen/yun/group-leader) is Research Group Leader at the Center for Regenerative Therapies Dresden (CRTD), Technical University Dresden, jointly affiliated with Max Planck Institute for Molecular Cell Biology and Genetics (MPI-CBG). Dr. Yun and her group (https://tu-dresden.de/cmcb/crtd/forschungsgruppen/crtd-forschungsgruppen/yun) study the cellular and molecular basis of regeneration of complex structures with the help of salamanders (like newts and axolotls) and these vertebrates exceptional regenerative abilities, which in contrast to humans, are capable of regenerating complex tissues, and even entire organs, to a remarkable extent. Therefore, they offer unique insights into what molecular mechanisms must be in place for achieving quasi-perfect regeneration. Research in the Yun group focuses on three main areas: describing cellular and molecular mechanisms driving regeneration (Mechanisms underlying the plasticity of the differentiated state), their connection with cellular aging (Role and regulation of senescence in regeneration), and the role that the immune system plays in regenerative context. The research in the Yun group combines advanced molecular biology methods with state-of-the-art microscopy. Most recently the group has established Salamander-Eci, a novel method that enables the three-dimensional visualization of salamander tissues for a more comprehensive understanding of regenerative processes. Dr. Yun received her Ph.D. in Biological Sciences from MRC-Laboratory of Molecular Biology of Cambridge / Cambridge University, UK, and did her Postdoctoral Research at the Institute of Structural and Molecular Biology, University College London, UK; Dr. Yun also has a BSc in Biological Sciences from University of Buenos Aires, Argentina.

Gianluca Petris, MRC Laboratory of Molecular Biology, UK speaks on "CRISPR-Cas9 and beyond: delivery, specificity and therapy".

You're listening to the June 2021 episode of 3 Minute 3Rs The papers behind the pod: Winning paper: Pellegrini L et al. (2020). Human CNS barrier-forming organoids with cerebrospinal fluid production. Science 369(6500): eaaz5626. doi.org/10.1126/science.aaz5626. Highly commended: Ashworth J et al. (2020). Peptide gels of fully-defined composition and mechanics for probing cell-cell and cell-matrix interactions in vitro. Matrix Biology 85-86: 15-33. doi.org/10.1016/j.matbio.2019.06.009. [Transcript]It's the 3rd Thursday of June, and you're listening to 3 Minute 3Rs, your monthly recap of efforts to replace, reduce, and refine the use of animals in research. This month, we've got a special double feature to highlight the results of the 2020 3Rs Prize, awarded by the NC3Rs and sponsored by GSK. Let's start with the winner: Laura Pellegrini at the MRC Laboratory of Molecular Biology, for her animal-replacing organoid work. NA3RsC Deep within each of our brains, there's a vital fluid providing essential nutrients and signaling molecules while protecting the brain from toxic compounds. It's called the cerebrospinal fluid which is produced by the choroid plexus. Our understanding of this fluid and organ is limited due to the difficulty in studying them. In turn, many new drugs developed for the central nervous system have failed because of lack of efficacy, inability to cross the blood-brain barrier, or limited translation from animals. But now, Dr. Pellegrini and her colleagues have developed a human choroid plexus organoid. This organoid has a selective barrier that quantitatively predicts the permeability of small molecules into the brain. It even secretes a liquid very much like cerebrospinal fluid. Overall, this model holds great promise for deeper study into this incredible part of our bodies. To learn more, read the full paper in Science. 2020 also brought us highly commended replacement to mouse-derived Matrigel. NC3Rs A cell's environment has a lot of influence on their behavior so for cells to be the best experimental representative their environment needs to be as similar to in vivo as possible. In many research areas, there is now a move towards 3D culture techniques using biomaterials as a matrix, providing both structure and cell-matrix interactions. Often these matrices are animal-derived, such as Matrigel which is derived from mouse sarcomas. Approximately one hundred mice can be required to produce the Matrigel needed by a single research institute every year. However, the chemical components of Matrigel are not well defined affecting the reproducibility of studies and given the number of different cell types, organs and tissues, a one-size-fits all approach is unlikely to be the best representation of an in vivo situation. Dr Jennifer Ashworth was highly commended in the 2020 3Rs Prize for her work published in Matrix Biology detailing a non-animal derived synthetic hydrogel that can replace the use of Matrigel. The hydrogels are derived from a commercially available precursor peptide. This ‘blank slate' can then be ‘tuned' altering a hydrogel's stiffness and composition by adding proteins and sugars to replicate different in vivo environments. Check out Jenny's paper to learn more. And with... See acast.com/privacy for privacy and opt-out information.

The world is always on the lookout for new drugs - but they're not easy to make. Synthesising them is often an expensive and prolonged process. But what if we could employ a miniature assistant to do it for us? That's what a team from the MRC Laboratory of Molecular Biology have come up with. They're managed to genetically reprogramme living cells to build complex molecules - molecules that no living thing would ever normally produce. Phil Sansom learned how from researcher Jason Chin... Like this podcast? Please help us by supporting the Naked Scientists

The world is always on the lookout for new drugs - but they're not easy to make. Synthesising them is often an expensive and prolonged process. But what if we could employ a miniature assistant to do it for us? That's what a team from the MRC Laboratory of Molecular Biology have come up with. They're managed to genetically reprogramme living cells to build complex molecules - molecules that no living thing would ever normally produce. Phil Sansom learned how from researcher Jason Chin... Like this podcast? Please help us by supporting the Naked Scientists

#22 — In this episode of The Microscopists, we're joined by molecular biologist, biophysicist and Nobel Laureate Richard Henderson from the MRC Laboratory of Molecular Biology. We'll discuss some of his earlier career challenges in biophysics and what attracted him to biology, his pioneering work in the field of electron microscopy, his favorite comic books, and passion for electronics.Watch or Listen to all episodes of The Microscopists here: https://themicroscopists.bitesizebio.com/

#22. In this episode of The Microscopists, we’re joined by molecular biologist, biophysicist and Nobel Laureate Richard Henderson from the MRC Laboratory of Molecular Biology. We’ll discuss some of his earlier career challenges in biophysics and what attracted him to biology, his pioneering work in the field of electron microscopy, his favorite comic books, and passion for electronics. Watch or Listen to all episodes of The Microscopists here: http://bit.ly/the-microscopists-pds

Alexander is currently a postdoc as a member of the personalized medicine cluster in Copenhagen and at the Institute of Biological Psychiatry in Roskilde working with the UK Biobank and other large-scale population cohorts. Alexander has a big interest in the integration of large biomedical data in genomics, structural biology, pharmacology, and pharmacoepidemiology with innovative computational methods to gain novel insights into receptor biology. During his Ph.D. with David Gloriam at the Department of Drug Design and Pharmacology in Copenhagen, he worked on novel analytical methods to identify human signaling systems and thereby discovered endogenous peptides activating several orphan receptors. Alexander had a research sabbatical with Madan Babu at the MRC Laboratory of Molecular Biology in Cambridge, UK, where he was working on the impact of genetic variations on drug response. He received the “HC Ørsted Research talent prize” and “Bayer Pharmaceuticals Ph.D. Award” for his work on GPCRs. ------------------------------------------- Imagine a world in which the vast majority of us are healthy. The #DrGPCR Ecosystem is all about dynamic interactions between us who are working towards exploiting the druggability of #GPCR's. We aspire to provide opportunities to connect, share, form trusting partnerships, grow, and thrive together. To build our #GPCR Ecosystem, we created various enabling outlets. For more details, visit our website http://www.DrGPCR.com/Ecosystem/. Are you a #GPCR professional? - Register to become a Virtual Cafe speaker http://www.drgpcr.com/virtual-cafe/ - Subscribe to our Monthly Newsletter http://www.drgpcr.com/newsletter/ - Listen and subscribe to #DrGPCR Podcasts http://www.drgpcr.com/podcast/ - Support #DrGPCR Ecosystem with your Donation. http://www.drgpcr.com/sponsors/ - Reserve your spots for the next #DrGPCR Virtual Cafe http://www.drgpcr.com/virtual-cafe/ - Watch recorded #DRGPCR Virtual Cafe presentations: https://www.youtube.com/channel/UCJvKL3smMEEXBulKdgT_yCw - Bring in a #GPCR Consultant http://www.drgpcr.com/consulting/ - Share your feedback with us: http://www.drgpcr.com/audience-survey/ - Become a #DrGPCR Ecosystem Member http://www.drgpcr.com/membership/

What governs the shape of organs and tissues in the human body and beyond. Research is being carried out to determine coordinating factors within the body. Press play to learn: The events that have the most significant impact on shaping an organism.  How cell division is oriented in a particular direction. The role mathematic models play in predicting shapes that form within an organism Group leader at MRC Laboratory of Molecular Cell Biology at University College London, Yanlan Mao, shares their research into the formation and growth orientation of organisms.  Cell proliferation determines how organisms grow and divide, and the rate of proliferation can lead to the formation of specific shapes or disorders as development continues. If cells have traits that can orient the direction of the division, shapes can morph from spherical to oblong, and finally into recognizable figures. Fruit flies are invaluable resources in discovering genetic predispositions in cell growth, showing predictable growth for research purposes, and modifiable traits to test independently. By slightly changing characteristics in specific tissue cells, tension can be altered, and regrowth traits in cells can be sped up. To learn more, search for the name Yanlan Mao on your preferred engine. Episode also available on Apple Podcasts: apple.co/30PvU9C

Guido Papa, MRC Laboratory of Molecular Biology, Cambridge, UK speaks on "Role of SARS-CoV-2 Spike cleavage in virus entry and cell-cell fusion". This seminar has been recorded at ICGEB Trieste.

Subscribe and receive the next podcast in you mailboxTell us your thoughts about this episodeLast summer, we were honored to host Magdalena Skipper, Editor of Nature, to share her tips with the community. When Nature announced its new Open Access policy in November 2020, we asked her to come back for another interview in January 2021, to discuss these specific issues. This episode is in two parts: the classic interview with Magdalena sharing her stories with the community and a second part with an extended discussion on the recent announcements made by Nature. As a consequence, this episode is longer than usual, but we believe that it includes enriched content that you will appreciate.In this episode Magdalena Skipper tell us about her role at Nature and her personal thoughts about editing, publishing and communicating scienceMagdalena offers tips to authors, including thinking about why you want to share your story, what the message of the paper is and who the audience isWe discuss a metaphor for the publishing process in which the author feels like a Medieval knight throwing the manuscript over the castle wallMagdalena sees herself more as a facilitator and reminds us that every stakeholder in the process is humanShe stresses that editors and publishers need to work to make the publishing process more transparentShe makes the point that the objective of peer review is to make the paper better and we talk about new models for publishing and sharing dataWe discuss how impact factors can be mis-used and what alternative metrics existMagdalena tells us how she feels as the first woman editor at Nature and about prizes for women scientists. She mentions these journals and institutions :MRC Laboratory of Molecular BiologyCancer Research UKNature journalNature Research Mentoring in Science AwardTo find out more about Magdalena and her journalNature editors150 years of Nature: A century and a half of research and discovery.Magdalena on WikipediaMagdalena on TwitterTo find out more about Renaud :TwitterLinkedInTo find out more about Jonathan :TwitterLinkedIn To learn more about the soundtrack :Music by Amaria - Lovely Swindlerhttps://soundcloud.com/amariamusique/https://twitter.com/amariamusiqueAnd Bab Tista - Text Me Records / GrandBankss

For more on brain organoids and their many applications, check out this episode of Journal Club: "Modeling Mysterious Brain Structures." Host Lauren Richardson talks to Dr. Madeline Lancaster, a Group Leader at the MRC Laboratory of Molecular Biology in Cambridge, about her lab's article in Science describing an organoid model for studying the cerebrospinal fluid and the choroid plexus, and how these organoids can be used to study brain development, evolution, and improve the drug development process.

Dr Madeline Lancaster, Group Leader at the Cell Biology Division of the MRC Laboratory of Molecular Biology in Cambridge, is interviewed by PhD student Ella Hubber. Madeline talks about the chance discovery and ongoing development of cerebral organoids and their use in studying human brain development and size differences between human and non-human apes. She also touches on the importance of engaging with the public as a scientist. To learn more about Madeline's work visit the following link: https://www2.mrc-lmb.cam.ac.uk/groups/lancaster/

Consumer trends in wellbeing, healthy ageing and nutrient rich convenience food are creating significant opportunities for nutraceutical manufacturers, with the current market valued at $41.95bn (Market Data Forecast figures). This is expected to continue to grow as conventional pharmaceutical companies also turn their hand to this growing market. In this Table Talk Podcast, recorded back in March at the beginning of the COVID-19 pandemic, we’re joined by a panel of experts who’ll provide their unique insight into this growing category in health and nutrition. Our guests are Nick Bennett, Head of Nutrition and Sustainability at IVc Brunel, Miriam Ferrer, PhD, Head of New Product Development, Cambridge Nutraceuticals, and Cheryl Fallow, MD, Viridian. We’ll focus on how the category is growing, the market accessibility and what it means in terms of product development and new opportunities. We’ll also investigate how regulation could affect manufacturers what significance any proposals in regulation could mean for manufacturers. About our panel Nick Bennett, Head of Nutrition and Sustainability at IVc Brunel Nick Bennett is Head of Nutrition at Brunel Healthcare where he is responsible for Innovation, Communication and Sustainability. Nick has worked in the food supplement industry for more than 21 years specialising in all matters relating to product development, regulations and the support that appropriate nutritional supplementation can provide to health and well-being. Nick qualified in Nutritional Biochemistry from Nottingham University in 1994 and has been a Registered Nutritionist since 2003. During this time he has worked in a variety of food supplement companies of different sizes from very small UK focussed, to very large international, before joining the UK’s number one food supplement manufacturer, IVC Brunel in 2009. Aimee Benbow, Technical Services Manager, Viridian With a degree in nutrition and experience in food law, Aimee is perfectly placed to ensure Quality Control & Quality Assurance at Viridian Nutrition. Aimee is also the hub of education and technical services. Miriam Ferrer, PhD, Head of New Product Development, Cambridge Nutraceuticals Miriam completed her Biology Degree at the University of Barcelona (Barcelona, Spain). She has a PhD from the Vrije Universiteit in Amsterdam (The Netherlands), where she worked on cancer gene therapy. She moved then to Cambridge, as postdoctoral researcher at the prestigious MRC-Laboratory of Molecular Biology, where she further her experience in the DNA repair field working on BRCA1 (Breast cancer type susceptibility protein). She moved out of the research to work for Abcam, one of the leading manufacturers of life-science researchers. Miriam worked at Abcam for 9 years, 7 of them as Product Manager for the cellular assays range. Since 2017, she is Head of New Product Development at Cambridge Nutraceuticals (who commercialises food supplements under the brand FutureYou), where she is responsible for researching ingredients and developing new products. Key areas of expertise: science, role of science in food supplements Food Matters Live On-Demand available now! Food Matters Live brought together five streams of unrivalled unique sessions, more than 50 hours of live webcasts, with the experts shaping the future of food, diet and nutrition. On-demand passes give you access to the complete programme now. Join 5,000 viewers who are already gaining a professional advantage from Food Matters Live On-Demand.

The human brain is endlessly fascinating and mysterious, but the majority of brain research to date has focused on neurons and their functions. While the other types of brain cells, such as astrocytes and glia, are starting to get their due, there is another element of the brain that to this day has gone woefully unstudied: the cerebrospinal fluid (CSF) and the brain structure that produces it, the choroid plexus. The CSF is a clear, colorless fluid found in the brain and spinal cord, and is traditionally thought to protect the brain from injury by acting as a shock absorber. In this episode, Madeline Lancaster, a Group Leader at the MRC Laboratory of Molecular Biology in Cambridge and Lauren Richardson discuss the article "Human CNS barrier-forming organoids with cerebrospinal fluid production" by Laura Pellegrini, Claudia Bonfio, Jessica Chadwick, Farida Begum, Mark Skehel, Madeline A. Lancaster published in Science. The paper describes a new model for studying the CSF and the choroid plexus by creating what’s sometimes called a mini-brain or a brain-in-a-dish, but is more accurately known as a cerebral organoid. With this model, Dr. Lancaster and her team were able to reveal new insights into the composition and function of the choroid plexus, and importantly, how it forms a key barrier between the blood and the brain. We discuss the how these organoids can be used to study brain development, evolution, and improve the drug development process.

Takeaways from today's episode: Research culture requires dialling down on perfectionism which would help to relieve the pressure.People respect it when you say NO, so learn to say NO. politely.Institutions should support mental health support to researchersBe sensitive to different cultural views about mental healthIntersectionality in mental health means that different people experience the pressures of research in different ways.Recognise diversity of individuals in research and use a more individual approach to dealing with mental health. ResourcesBurnout in global health by Madhu Pai: https://www.forbes.com/sites/madhukarpai/2020/07/20/burnout-a-silent-crisis-in-global-health/#56387cab4df8WHO:https://www.who.int/mental_health/evidence/burn-out/en/#:~:text=%E2%80%9CBurn%2Dout%20is%20a%20syndrome,related%20to%20one's%20job%3B%20andSpotting signs of burnout: https://www.priorygroup.com/blog/managing-burnout-for-patients-and-gpsBlog by Beth Thompson: https://blogs.bmj.com/bmj/2020/02/14/beth-thompson-we-need-to-reimagine-the-way-research-works/Wellcome research culture survey:https://wellcome.ac.uk/press-release/largest-survey-research-culture-reveals-high-levels-stress-and-insecurityReducing stigma of mental health by using the Friendship Bench approach https://www.friendshipbenchzimbabwe.org/Chris Denning (Uni of Nottingham blog) has posted his blog on his twitter account: @chrisdenning42 Guest informationDr Beth Thompson leads Wellcome’s UK & EU policy and advocacy work, covering issues including Brexit and research investment, as well as Wellcome’s programme on research culture. Beth was awarded an MBE in 2017 for services to science. She gained her PhD from the MRC Laboratory of Molecular Biology in 2008. @Beth_Thompson@wellcometrust Halle Rubera is a Rwandan who grew up in Kenya. She holds a B.A. in Political Science at Wellesley College, and was one of 6 finalists for the Rhodes Scholarship - East Africa. She is passionate about education in Africa, which is reflected in her podcast "Drained"-- a platform for African students to discuss their mental health. AcknowledgementsEditing by Mariana Vaz, https://www.marianacpvaz.com/Research: Christine BoinettProducers: Christine Boinett (Creator and Executive producer), Alice Matimba (Senior Producer), Isabela Malta (Producer) and Emmanuela Oppong (Producer).Host: Christine BoinettMedia and Marketing: Catherine HolmesMusic: https://freesound.org/s/477388/ Sponsors:Wellcome Genome Campus Advanced Courses and Scientific ConferencesWellcome Sanger InstituteSocial Entrepreneurship to Spur Health

Martin Dougherty, Chief Operating Officer Wellcome Sanger Institute Genome Campus. Core theme of operation leadership in the scientific or research setting.Martin’s career spans four sectors: academic, commercial, charity and public. He had a successful academic research career in tropical medicine. He then formed a company with colleagues working in pharmaceutical medical communications. After capitalising on this experience, he went to go on to lead a healthcare research group, at the Royal College of Obstetricians and Gynaecologists, developing clinical and cost effectiveness guidelines for the National Institute for Health and Clinical Excellence. He went on to become Executive Director at the Royal Statistical Society, a learned and professional body supporting statisticians, developing statistical science and promoting the appropriate use and understanding of statistics. Latterly, Martin held the role of COO at the MRC Laboratory of Molecular Biology during the completion of the new Institute laboratories on the Cambridge Biomedical Campus, successfully lead, and completed the transition programme in to the new facility. Top Tip: Never forget People are at the heart of any operational process #InspiringLeadership #leadership #CEOs #MotivationalSpeaker #teamcoach #Boards See acast.com/privacy for privacy and opt-out information.

This interview is with Dr. Sian Culley (recorded 05/06/20), @SuperResoluSian a postdoctoral researcher at the MRC Laboratory for Molecular Cell Biology at UCL, London with the Henriques Lab #femalewithmicroscope Teledyne Photometrics Web: https://www.photometrics.com/ Twitter: https://twitter.com/Photometrics LinkedIn: https://www.linkedin.com/company/teledynephotometrics/

Dr. Madeline Lancaster is a Group Leader at the MRC Laboratory of Molecular Biology in Cambridge, UK. The Lancaster lab has developed cerebral organoids as a model system to better understand human brain evolution, development, and neurodevelopmental disorders. She joined us to discuss her research presentated at the ISSCR 2020 conference.

You're listening to the June episode of 3 Minute 3Rs.The papers behind the pod:A novel, high-welfare methodology for evaluating poultry red mite interventions in vivo. https://www.sciencedirect.com/science/article/pii/S030440171930041XPluripotent state transitions coordinate morphogenesis in mouse and human embryos. https://www.nature.com/articles/nature24675TranscriptIt's the Third Thursday of June and you're listening to 3 Minute 3Rs, your monthly recap of efforts to replace, reduce, and refine the use of animals in research. Instead of the usual 3 segments this month, we're featuring two, in recognition of the two winners of the 2019 3Rs Prize, awarded by the NC3Rs and sponsored by GlaxoSmithKline. We'll start with a recap of Dr. Francesca Nunn's paper on red mite interventions in poultry. [NA3RsC] Laying hens can be infested with poultry red mites which causes major economic and animal welfare issues. These mites can cause anemia, reduced production, and even death. Current treatments are often inadequate and research methods to find new treatments typically have poor translation to field trials. A recent paper in Veterinary Parasitology describes a novel, high-welfare method for evaluating poultry red mite interventions in vivo. This paper is the winner of 2020 NC3Rs 3Rs Prize award. Nuun and colleagues developed and optimized a sealed mesh device that attaches to a hen's thigh. The depth and width of the mesh is precisely sized to both contain the mites and allow them to feed on the hens. This device will both reduce and refine the use of animals in research by allowing efficient pre-screening of new treatments before they enter large field trials. To learn more, read the full paper online. [NC3Rs] The second winner of the 2019 3Rs Prize award is Dr Marta Shahbazi from the MRC Laboratory of Molecular Biology for her work reducing the number of mice needed for embryonic developmental research. Historically embryos have been difficult to culture beyond the implantation stage of pregnancy. But with up to 40 per cent of pregnancies ending by implantation, it's a critical stage to understand. So researchers typically use extensive breeding programmes to generate transgenic mice and retrieve embryos needed for experiments with invasive surgeries. Now, building upon previous research, Marta and colleagues have established advanced 3D cultures of human and mouse embryonic stem cells to mimic the embryo at implantation. Using these cultures, they've been able to study the cellular events triggering implantation in greater detail than ever before. Not only that, they've also replaced the use of 500 mice. Groups worldwide are now adopting the cultures to answer their own biological questions about embryonic development. Why not join them, and check out Marta's prize-winning research by following the link in the description.With congratulations to Dr. Nunn and Dr. Shahbazi, that'll do it for June! 3 Minute 3Rs is brought to you by the NC3Rs, the North American 3Rs Collaborative, and Lab Animal. Come back in July for three more 3rs papers. See acast.com/privacy for privacy and opt-out information.

Watch the video podcast Dr. Sarah Caddy, (MA VetMB PhD DACVM MRCVS) is a Wellcome Trust Clinical Research Fellow at the MRC-Laboratory of Molecular Biology and the Cambridge Institute for Therapeutic Immunology and Infectious Disease (CITIID). She is also a veterinary surgeon with a Diploma from the American College of Veterinary Microbiology. Dr Caddy's studies focus on the interactions between viruses and antibodies. Full show notes: Dr. CaddyUPDATE|Mind-jam Podcast

Watch the video podcast With massive, non-stop media conflicting headlines, terrible humans are dumping pets into the streets and/or off at their local shelters. If you know of such a person, please be sure to share this podcast before they make those terrible decisions. Dr Sarah Caddy MA VetMB PhD DACVM MRCVS - is a veterinarian surgeon and a Diplomat of the American College of Veterinary Microbiology. A Wellcome Trust Clinical Research Career Development Fellow at the MRC-Laboratory of Molecular Biology and the Cambridge Institute for Therapeutic Immunology and Infectious Disease. Full show notes: Dr. Caddy|Mind-jam Podcast

Sir Venki Ramakrishnan is President of the Royal Society and was awarded the Nobel Prize in 2009 for his research into the ribosome – the mysterious ancient molecule that decodes DNA, what he terms ‘the mother of all molecules’. He’s what you might call a science all-rounder: he gained a PhD in Physics before turning to Biology, and his Nobel Prize was in Chemistry. Born in India, he moved to the US as a postgraduate student, and in 1999 came to Britain to work at the MRC Laboratory of Molecular Biology in Cambridge. Alongside science Venki Ramakrishnan has another passion – for music, and, in particular, chamber music, which grew out of the Indian classical music he heard as a child. His son Raman is the cellist with the Horszowski Trio and we hear their performance of music by Schubert, as well as a Brahms piano quartet and a Beethoven cello sonata, reflecting both Raman's and Venki’s deep engagement with that instrument. Venki's other great love is for the violin, and he chooses music by Mozart alongside Bach's Double Violin Concerto - which Venki himself played whilst learning the violin as a graduate student in the USA. He talks to Michael about the central role of music in his life, about how he would reform the Nobel Prizes in science, and why he swapped the mountains of Utah for the fens of East Anglia. Producer: Jane Greenwood A Loftus production for BBC Radio 3

Nobel Prize recipient Frances Arnold joins Tim to talk about winning a Nobel Prize honor for her pioneering work in “directed evolution,” which harnesses the power of evolution to enhance products throughout society - from biofuels and pharmaceuticals, to agriculture, chemicals, paper products and more. We talk with Frances about her journey and her work that is changing the world for the better. https://traffic.libsyn.com/shapingopinion/The_Nobel_Prize_-_Directed_Evolution_auphonic.mp3 Since the Nobel Prize in Chemistry was first awarded in 1901, 117 years ago, only four women had won the honor, and in October, American Frances Arnold became the fifth. The professor of chemical engineering, bioengineering and biochemistry at the California Institute of Technology, received the honor for her pioneering work in “directed evolution.” Frances’s work centers on the directed evolution of enzymes, proteins that serve as catalysts for chemical reactions that take place in living organisms, animals and people. In its most simple form, the process focuses on harnessing the power of natural evolution to solve problems for society. Frances is the Linus Pauling Professor of Chemical Engineering, Bioengineering and Biochemistry at Caltech. Today, directed evolution is used in research laboratories around the world to create things from laundry detergents to biofuels to pharmaceuticals. Enzymes created with through this process have been able to replace some toxic chemicals traditionally used in industry. Frances shares the prize with George Smith of the University of Missouri, who created a "phage display" process for protein evolution, and Gregory Winter of the MRC Laboratory of Molecular Biology in the United Kingdom, who used phage display for antibody evolution. Arnold was born in Pittsburgh, Pennsylvania. Her undergraduate degree in mechanical and aerospace engineering is from Princeton University. Her graduate degree in chemical engineering is from UC Berkeley. She has been at Caltech since 1986, first as a visiting associate, then as an assistant professor, and progressing to professor in 1996. In 2017, she became the Linus Pauling Professor. She became the director of the Donna and Benjamin M. Rosen Bioengineering Center at Caltech in 2013. Frances is a member of the American Academy of Arts and Sciences and the American Philosophical Society, and is a fellow of the American Association for the Advancement of Science and the Royal Academy of Engineering. How Directed Evolution Works Directed evolution is similar to how animal breeders mate cats or dogs to create hybrids or new breeds of animal. To conduct directed evolution mutations are induced to DNA, or a gene, which “encodes” a particular enzyme. That mutated enzyme, along with other thousands, are produced and tested to what Frances calls a desired trait. The preferred enzymes are selected, and the process continues until the enzymes are working to achieve a desired outcome or solution. “I copy nature’s design process. There is tremendous beauty and complexity of the biological world, but it all comes about through this one, simple, beautiful design algorithm.” - Frances Arnold Links Frances Arnold Wins 2018 Nobel Prize in Chemistry, Caltech Frances H. Arnold Group Caltech scientist is among 3 awarded Nobel Prize in chemistry for sparking ‘a revolution in evolution’, LA Times The Latest: Nobel chemistry winner credits team at Caltech, Washington Post Nobel winner overcame personal loss, cancer, and being a woman, NBC News

This week’s podcast episode, Dr Ines Sequeira interviews Dr Agathe Chaine from the MRC Laboratory for Molecular Cell Biology based at UCL. We hear about her research history, working with “soft cells”, asymmetric division during the development of embryos, and the different types of techniques are being used in her lab… Dr Chaine was awarded her PhD from the CIRB Collége de France where she stayed on to do a Post Doctoral position researching the biophysical properties of embryonic mitosis. She is now a Post-Doctoral Fellow at the MRC Laboratory for Molecular and Cell Biology based at UCL, where she is studying how cells control their shape and size in asymmetric division during embryonic development For more information about her research please click the following link: http://www.ucl.ac.uk/lmcb/users/agathe-chaigne

Seán and Emma talk to Juan Garaycoechea from the MRC Laboratory of Molecular Biology about his work on DNA damage and petrologist Victoria Honour from the Department of Earth Sciences at Cambridge University. They also discuss the curious incident of vanished North American dogs.

Georgina Ferry interviews Matthew Freeman. Matthew Freeman FRS joined the Dunn School as Professor of Pathology and head of department in 2013. He remembers meeting the Nobel-prizewinning immunologist Peter Medawar as a teenager, who told him 'Chemistry is dead, Physics is dying and Biology is the only science that’s worth pursuing.' Inspired by this, Freeman read Biochemistry at Oxford before going to Imperial College London to undertake a PhD in on the genetic control of the cell cycle in fruit flies, in a department that was one of the first to use recombinant DNA methods to clone genes. This led to a post-doc at the University of California at Berkeley, from which he returned in 1992 to set up his own lab at the MRC Laboratory of Molecular Biology in Cambridge, working on receptors that are critical to the development of the Drosophila eye. He remained at LMB for 21 years, for the last six as head of the Cell Biology Division. Since his move to head the Dunn School he has focused on encouraging collaboration between research groups, under an over-arching definition of pathology as ‘the cell biology that underlies human disease’. He is a trustee of the EP Abraham Research Fund.

Georgina Ferry interviews Gillian Griffiths. Gillian Griffiths FRS is Professor of Immunology and Cell Biology and Director of the Cambridge Institute for Medical Research at the University of Cambridge. While an undergraduate at University College London she was encouraged by immunologists Martin Raff and Avrion Mitchison to apply for a PhD with César Milstein at the MRC Laboratory of Molecular Biology in Cambridge. Under Milstein’s guidance she was the first to sequence the complete variable regions of antibodies. She then spent five years as a post-doc at Stanford University in California before moving to the Basel Institute of Immunology in 1990 to work on the cell biology of killer T cells. In 1995 she won a Wellcome Trust Senior Fellowship and two years later came to the Dunn School to set up her lab. Her work revealed the mechanisms by which killer cells neutralise infected or cancerous cells with exquisite precision. In 2001 she was given the title of Professor, the first woman to hold such a title in the department. She moved to Cambridge for family reasons in 2008.

Georgina Ferry interviews Herman Waldmann. Herman Waldmann FRS is Emeritus Professor of Pathology, and was head of the Dunn School from 1994-2013. He read medicine at Cambridge and qualified as a doctor in London before returning to Cambridge to do a PhD in the Department of Pathology. In 1978 he joined César Milstein at the MRC Laboratory of Molecular Biology to learn about monoclonal antibodies. Thereafter he pioneered the development of monoclonals as therapeutic agents, particularly Campath-1 (Alemtuzumab, now used to treat conditions including chronic lymphocytic leukaemia and multiple sclerosis). In 1990 he set up a facility in Cambridge to make these agents (with Geoff Hale), but on his appointment as head of the Dunn School, he moved the Therapeutic Antibody Centre to Oxford. His headship saw a massive development on the Dunn School site, with the building of a new animal house, the Medical Sciences Teaching Centre, the EP Abraham Research Building and the Oxford Molecular Pathology Institute (OMPI). The number of research groups also grew rapidly, and Waldmann's introduction of a central café has ensured that staff and students have a place to interact. Following his retirement he has continued to lead a research group working on mechanisms of immunological tolerance.

Georgina Ferry interviews George Brownlee. George Brownlee FRS is Emeritus Professor of Chemical Pathology in the Dunn School. He obtained his PhD at the MRC Laboratory of Molecular Biology in Cambridge, working with the Nobel prizewinner Fred Sanger on the sequencing of small RNAs. He continued to work at the LMB as an independent scientist, on messenger RNA and the RNA genome of the influenza virus. In 1978 he was invited by Henry Harris to become the inaugural Professor of Chemical Pathology at the Dunn School, where he introduced molecular biological techniques to the department and developed faster methods of sequencing RNA. He also bought the first computer in the department in order to store and analyse nucleic acid sequences. Brownlee continued to work on the influenza virus, work that was critical to developing some influenza vaccines, and also cloned human Factor IX, which is deficient in some forms of haemophilia. With the royalties from these discoveries he has partly endowed the Brownlee Abraham Chair of Molecular Biology in the Dunn School, and he is also a past Chair of the EPA Cephalosporin Fund.

Progress in science depends on a rapid exchange of ideas and exposure to new approaches and viewpoints. Historically, this progress has been accelerated by the movement of people. Scientists have been among the most mobile of people, going where they perceive the action to be. This talk will explore examples from various periods in history on how mobility resulted in scientific development. It will also describe the reasons behind the moves in my own peripatetic life. Biography Venki Ramakrishnan received his bachelor’s degree in physics from Baroda University in India in 1971 and his Ph.D. in physics from Ohio University in 1976. He then studied biology for two years at the University of California, San Diego before beginning his postdoctoral work with Peter Moore at Yale University. After a long career in the US, he moved to England in 1999 to become a group leader at the MRC Laboratory of Molecular Biology in Cambridge. He is also the current president of the Royal Society. Ramakrishnan has a long-standing interest in ribosome structure and function. In 2000, his laboratory determined the atomic structure of the 30S ribosomal subunit and its complexes with ligands and antibiotics. This work has led to insights into how the ribosome “reads” the genetic code, as well as into various aspects of antibiotic function. Ramakrishnan’s lab subsequently determined high-resolution structures of functional complexes of the entire ribosome at various stages along the translational pathway, which has led to insights into its role in protein synthesis during decoding, peptidyl transfer, translocation and termination. More recently his laboratory has been applying cryoelectron microscopy to study eukaryotic and mitochondrial translation.

VENKATRAMAN "VENKI" RAMAKRISHNAN is a Nobel Prize-winning biologist whose many scientific contributions include his work on the atomic structure of the ribosome. He is Group Leader and Former Deputy Director of the MRC Laboratory of Molecular Biology in Cambridge, and the current President of the Royal Society. The Conversation: https://www.edge.org/conversation/venki_ramakrishnan-soul-of-a-molecular-machine

A NASA space capsule, Orion, that could transport humans to Mars is due to make its maiden flight. Given that this is a first outing, there will be no people aboard. The capsule will orbit the earth twice in four and a half hours, before splashing down in the Pacific. BBC correspondent Jonathan Amos is on location at Cape Canaveral and gives Adam the latest news. This is a step towards a crewed mission to Mars. But how do humans cope with being confined for the 8 months it takes to get there? The European Space Agency studied this question in 2010. 6 volunteers were shut up in a replica space shuttle for over a year. Engineer Diego Urbina was one of them. He shares his thoughts on taking part in a fake Mars mission. Philip Holliger from the MRC Laboratory of Molecular Biology in Cambridge heads the team that two years ago built XNA, a set of genetic molecules that behave just like DNA, but are man-made. Like DNA, those XNAs didn't actually do that much, but this week, the team has published a paper where they have got them working. These are the first synthetic enzymes on Earth. Back in 2012, a shallow grave was uncovered underneath a car park in Leicester. Evidence suggested the skeleton in it was King Richard the Third. Finally this week, the DNA confirmation by geneticist Turi King is in. And something is rotten in the state of his lineage. Kevin Schurer, historian, and Richard Buckley, the lead archaeologist on the dig, talk us through the DNA anomaly that hints at infidelity in the royal line.

Sir Aaron Klug grew up in Durban, South Africa on the edge of the Bush, which provided him with enough snakes and monkeys to satisfy his curiosity. A bright child, he read anything that was available and enjoyed an idyllic childhood. He started studying medicine at university level in Johannesburg at the age of fifteen, but soon switched to chemistry, physics and mathematics, which provided more stimulus for his enquiring mind.He began to research at Cape Town University and later Cambridge, where he joined the world-famous Cavendish Laboratory and later the MRC Laboratory of Molecular Biology. His work led to him winning the Nobel prize for Chemistry in 1982 for his work on cell structure. [Taken from the original programme material for this archive edition of Desert Island Discs]Favourite track: The Ode to Joy (Symphony No 9) by Ludwig van Beethoven Book: A set of books on Roman Republican and Imperial coinage Luxury: A set of mixed Greek and Roman coinage

Sir Aaron Klug grew up in Durban, South Africa on the edge of the Bush, which provided him with enough snakes and monkeys to satisfy his curiosity. A bright child, he read anything that was available and enjoyed an idyllic childhood. He started studying medicine at university level in Johannesburg at the age of fifteen, but soon switched to chemistry, physics and mathematics, which provided more stimulus for his enquiring mind. He began to research at Cape Town University and later Cambridge, where he joined the world-famous Cavendish Laboratory and later the MRC Laboratory of Molecular Biology. His work led to him winning the Nobel prize for Chemistry in 1982 for his work on cell structure. [Taken from the original programme material for this archive edition of Desert Island Discs] Favourite track: The Ode to Joy (Symphony No 9) by Ludwig van Beethoven Book: A set of books on Roman Republican and Imperial coinage Luxury: A set of mixed Greek and Roman coinage