Podcasts about Biobank

This week on Health Matters, as we continue to observe Heart Month, we will explore the role that genetics play in heart health.Understanding your family history of cardiovascular health is essential. In fact, about 30% of heart disease can be linked to family history. We speak with Dr. Jessica Hennessy, a clinical cardiac electrophysiologist and cardiogenetics expert at NewYork-Presbyterian and Columbia to help break down which heart conditions and risk factors may be inherited. She provides valuable insight on effectively managing heart health, including the importance of lifestyle modifications in preventing heart disease, including for individuals with a genetic predisposition. She also explains who should get genetic testing and what that process looks like.___ Dr. Jessica Hennessey specializes in Cardiac Electrophysiology, with a special focus on Sports & Exercise Cardiology. She practices primarily in New York, NY, and is affiliated with NewYork-Presbyterian/Columbia University Irving Medical Center. Dr. Hennessey graduated from Duke University School of Medicine in 2014, and completed her training at Massachusetts General Hospital, NewYork-Presbyterian/Columbia University Irving Medical Center and NewYork-Presbyterian/Columbia University Irving Medical Center. She is board certified in Internal Medicine, Cardiovascular Disease and Cardiac Electrophysiology. ___ Health Matters is your weekly dose of health and wellness information, from the leading experts. Join host Courtney Allison to get news you can use in your own life. New episodes drop each Wednesday. If you are looking for practical health tips and trustworthy information from world-class doctors and medical experts you will enjoy listening to Health Matters. Health Matters was created to share stories of science, care, and wellness that are happening every day at NewYork-Presbyterian, one of the nation's most comprehensive, integrated academic healthcare systems. In keeping with NewYork-Presbyterian's long legacy of medical breakthroughs and innovation, Health Matters features the latest news, insights, and health tips from our trusted experts; inspiring first-hand accounts from patients and caregivers; and updates on the latest research and innovations in patient care, all in collaboration with our renowned medical schools, Columbia and Weill Cornell Medicine. To learn more visit: https://healthmatters.nyp.org

In this episode, our guests discuss the potential of large-scale health datasets to transform research and improve patient outcomes and healthcare systems. Our guests also delve into the ethical, logistical, and technical challenges that come with these programmes. We hear how organisations such as UK Biobank, Our Future Health, and All of Us are collecting rich, diverse datasets, collaborating and actively working to ensure that these resources are accessible to researchers worldwide. Hosting this episode is Dr Natalie Banner, Director of Ethics at Genomics England. She is joined by Dr Raghib Ali, Chief Medical Officer and Chief Investigator at Our Future Health, Professor Naomi Allen, Professor of Epidemiology at the Nuffield Department of Population Health, University of Oxford, and Chief Scientist for UK Biobank, and Dr Andrea Ramírez, Chief Data Officer at the All of Us Research Program in the United States. "There are areas where academia and the NHS are very strong, and areas where industry is very strong, and by working together as we saw very good examples during the pandemic with the vaccine and diagnostic tests etc, that collaboration between the NHS and academia industry leads to much more rapid and wider benefits for our patients and hopefully in the future for the population as a whole in terms of early detection and prevention of disease." You can download the transcript or read it below.  Natalie: Welcome to Behind the Genes   Naomi: So, we talked to each other quite regularly. We have tried to learn from each other about the efficiencies of what to do and what not to do in how to run these large-scale studies efficiently. When you are trying to recruit and engage hundreds of thousands of participants, you need to do things very cost effectively. How to send out web-based questionnaires to individuals, how to collect biological samples, how the make the data easily accessible to researchers so they know exactly what data they are using.   All of that we are learning from each other. You know, it is a work in progress all the time. In particular you know, how can we standardise our data so that researchers who are using all of us can then try and replicate their findings in a different population in the UK by using UK Biobank or Our Future Health.    Natalie: My name is Natalie Banner, and I am Director of Ethics at Genomics England. On today's episode we will be discussing how we can unlock the potential of large health datasets. By that I mean bringing together data on a massive scale, including for example genomic, clinical, biometric, imaging, and other health information from hundreds and thousands of participants, and making it available in a secure way for a wide range of research purposes over a long time period.   Through collaboration and industry partnerships, these programmes have the potential to transform research and deliver real world benefits for patients and health systems. But they also come with challenges ranging from issues in equity and ethics through to logistics, funding, and considerable technical complexities. If you enjoy today's episode, we would love your support. Please like, share, and rate us on wherever you listen to your podcasts.     I'm delighted to be joined today by 3 fantastic experts to explore this topic. Dr Raghib Ali, Chief Medical Officer and Chief Investigator at Our Future Health. Professor Naomi Allen, Professor of Epidemiology at the Nuffield Department of Population Health, University of Oxford, and Chief Scientist for UK Biobank, and Dr Andrea Ramírez, Chief Data Officer at the All of Us Research Program in the United States.   Andrea, if I could start with you. It would be really great to hear about All of Us, an incredibly ambitious programme in the US, and maybe some of the successes it has achieved so far.   Andrea: Absolutely. Wonderful to be here with you and thank for you for the invitation. The All of Us Research Program started in 2016 from the Precision Medicine Initiative and was funded with the goal of recruiting 1 million or more participants into a health database. That includes information not only from things like biospecimens including their whole genome sequence, but also surveys that participants provide, and importantly linking electronic health record information and other public data that is available, to create a large database that researchers that access and use to study precision health.   We have recruited over 830,000 participants to date and are currently sharing available data on over 600,000. So, we're excited to be with your audience, and I hope we can learn more and contribute to educating people listening about precision medicine.   Natalie: Thank you, Andrea. And not that this is competitive at all, but Raghib, as we are recording this, I understand the Our Future Health programme is marking quite a phenomenal milestone of 1 million participants. Would you mind telling us a little bit about the programme and something that you see as the benefits of working at scale for health research.   Raghib: Thank you very much. So, Our Future Health is a relatively new project. It was launched in 2020 with the aim of understanding better ways to detect disease as early as possible, predict disease, and intervene early to prevent common chronic diseases. Similar to All of Us, we are creating a very large database of participants who contribute their questionnaire data, physical data, genetic data, and linkage to healthcare records, with the aim as I said, to really improve our understanding of how best to prevent common chronic diseases.   So, we launched recruitment in October 2022. Our aim is to recruit 5 million participants altogether, and in the last 2 years about 1.85 million people have now consented to join the project. But you are right, as of last week we have what we call 1 million full participants, so people that have donated a blood sample, completed the questionnaire, and consented to link to their healthcare records. In our trusted research environment, we now have data on over 1million people available for researchers to use.   Of course, we have learnt a lot from the approach of UK Biobank, which we are going to hear about shortly, but the resource is open to researchers across the world, from academia, from the NHS, from industry, so that will hopefully maximise the benefits of that data to researchers, but as I say with a particular focus on early detection, early intervention, and prevention research.   Natalie: Thank you Raghib. Great to have you with us. Naomi, Raghib mentioned that UK Biobank has been running for a long time, since 2006.  It is a real success story in terms of driving a huge range of valuable research efforts.  Could you talk to us a little bit about the study and its history and what you have learned so far about the sort of benefits and some of the challenges of being able to bring lots of different datatypes together for research purposes?   Naomi: Yeah, sure. So, UK Biobank started recruiting 0.5 million participants in 2006 to 2010 from all across the UK with a view to generating a very deep dataset. So, we have collected information on their lifestyle, a whole range of physical measures. We collected biological samples, so we have data on their genomics and other biomarkers. Crucially because they recruited 15+ years ago, we have been able to follow up their health over time to find out what happens to their health by linkage to electronic healthcare records. So, we already have 8,000 women with breast cancer in the resource, cardiovascular disease, diabetes, and so on.   But perhaps most importantly, not only does it have great data depth, and data breadth, and the longitudinal aspect, is the data is easily accessible to researchers both from academia and industry, and we already have 18,000 researchers actively using the data as we speak, and over 12,000 publications already generating scientific discoveries from the resource.      Natalie: So, we have got 3 quite different approaches. Recruiting in different ways, different scale, different depth of data collection and analysis, but all very much around this ethos of bringing lots of different datatypes together for research purposes. I wonder if you could talk a little bit about how you might be sort of working together, even though you have got slightly different approaches. Are there things that you are learning from one another, from these different data infrastructures, or how might you be looking in the future to work together to address some of the challenges that might come up from working at scale?      Naomi: So, we talk to each other quite regularly. We have tried to learn from each other about the efficiencies of what to do and what not to do in how to run these large-scale studies efficiently. When you are trying to recruit and engage hundreds of thousands of participants, you need to do things very cost effectively. How to send out web-based questionnaires to individuals, how to collect biological samples, how to make the data easily accessible to researchers so they know exactly what data they are using.   All of that we are learning from each other, and you know it is a work in progress all the time. In particular, how can we standardise our data so that researchers who say are using All of Us can then try and replicate their findings in a different population in the UK by using UK Biobank or Our Future Health. So, can we come up with common standards so that researchers can better directly compare the data that they are using? So, we are in close contact with each other.   Natalie: Fantastic, thank you. And Andrea, from your perspective obviously you are collecting data in the US. Are you finding ways of working internationally and with other infrastructures like Biobank and Our Future Health around things like data standards? It sounds like something simple, but I can imagine it is quite complex in practice.   Andrea: Absolutely, and that dialogue and understanding and learning from each other both informally in meetings and talking as well through the published literature. So, all of these datasets are actively widely used, and seeing what is coming out in publications helps us know what researchers are doing with the data. And when you see different researchers either generating hypotheses from our datasets in a different way, or testing hypotheses differently, that helps us understand where some benefit might be added to our dataset or where we really may need to grow in a different direction to meet some other research needs.   I think that every study design always struggles with that balance between knowing exactly what we want to study and therefore building very specific questions and very specific protocols, but also allowing for the knowledge that we don't really know all of the discovery we need to make and bringing in datapoints that will really generate those new hypotheses for the future.     I think for our study in particular, UK Biobank has been so remarkable in this way, helping structure All of Us to be able to contact our participants like UK Biobank and say, “Hey, we didn't really know what we were going to get, but we have put all this wonderful data together and now we need to do a deeper dive.”   So, the engagement and long-term return of those UK Biobank participants has really enriched our data, and we have learnt from UK Biobank a lot there, and hope through growing our partnerships programme that we can continue to create partnered research opportunities to strengthen that data as well. That is a new thing coming out of our group. You may have heard of it previously as ancillary studies, but we recognise the partnership that is important for those research opportunities. So, we are reporting here that we are hoping to rebrand it to reach a larger audience, and that is led by Dr. Shelley, as partnered research opportunities that will allow us to re-contact, bring our participants back, and really deepen that dataset.   Natalie: Thank you. And Raghib, I know that it is a really important part of the Our Future Health model about going back to participants, but you are in quite early stages of working out what those opportunities might look like.   Raghib: Yes, very much early stages. Just to reiterate the point for me personally, having started my research in the UK about 20 years ago, I have certainly learnt a lot personally, but we have all learnt a lot from the model that UK Biobank established in terms of collecting data and providing it to researchers, and I see these 3 studies as very much complimentary.   All of Us again have done a lot more work in terms of providing feedback to participants about their risk of disease and genetic information, and as you say Our Future Health was set up deliberately to not just be a purely observational study, but to give participants feedback about their risk of different chronic diseases as well as the opportunity to take part in not just studies to collect data, but also interventional studies to see if we can change the natural history of disease and prevent diseases in our participants.   So, that has never really been done at scale before, and that is certainly a big challenge for us to do, not just in the UK, but anywhere, including the US and working with health systems as to how best to do that. So, you know we have spent the last 2 years really trying to understand how best to recruit participants and to provide data to researchers for the next couple of years, and long beyond that we will be looking really as to how we can maximise the benefits of providing feedback to participants and taking part in interventional studies.   Naomi: I think one way in which we can all learn from each other actually, is we know how to recruit hundreds of thousands of people, the general population, into research study, and the next challenge is how do you keep engaging them, telling them what you are doing. You can't collect everything when they first join the study, or they would be with you for days. So, what UK Biobank has been doing is sending out web-based questionnaires, a couple a year, to find out extra information about health outcomes, lifestyle factors. Inviting them back to specific assessment centres.   So, we are inviting 100,000 participants back for imaging, and then again over the next few years for a second scan. So, I think the real challenge here is once you have recruited them, how to find that right cadence of engaging those participants to keep contributing their data and their biological samples to really maximise the value of the dataset for research. That is an ongoing challenge for all of us. But I have to say, the UK Biobank participants, they are an amazing group of individuals, very altruistic.   Our Future Health and All of Us, we don't give feedback, so there is nothing in it for our participants other than knowing that their data may help the future health of their children, and their grandchildren, and the rest of the world. So, that is very humbling, to know that the data that they have generated, and we have collected on them, is being used in that way.   Natalie: That's a really interesting point, Naomi, about the difference between a research study that is designed for answering a particular question. You gather specific data for a specific purpose, and when it comes to recruiting participants into that you can be very clear about what it is you are trying to do.   But of course, for all of these programmes, the whole nature of them is that you are collecting a lot of data over a long period of time, and it could be used for all sorts of different purposes. You can't say at the outset exactly what those purposes might be and what those outcomes might be. So, there is a really interesting question, and of course I would say this with my ethics hat on, a really interesting question around sort of participant trust and confidence in those programmes.   Naomi, you spoke just then about one way of retaining engagement and retaining people's interest, but I wonder Raghib and Andrea, if you have got thoughts on those sort of questions of how you can create that environment where participants can trust what you are doing with data over a long period of time, when you can't at the point at which they consent, say exactly how that data might be used? You have got a sense of the kinds of purposes, but you can't be too specific         Andrea: Sure. We know, and I have learnt from my own peers in this role, that enrolment in the study isn't the end point of engagement. All of Us's approach on engagement has been communicating with the entire community and really being there in the community, and that has been very powerful.   One effort over the last year we are proud of has been what we are dubbing participant driven enquiry, and that is where we say, “Thank you participants. We have gotten a ton of data out there for use, and funded researchers to use it all the time, but what do you, the participants, really want?” We were able to then take papers that researchers write and help tell participants and explain it in lay language, so the participants can say, “Hey, I have a question. Could you answer that for me?” Maybe we can, maybe we can't, but it has been very interesting to hear what participants want to know, and that participant driven enquiry project has turned out to be a big opportunity there.    The question they came to was not easy. Certainly, we didn't expect an easy question, but they came to us asking, “Why is my diabetes worse than someone else's? Is it the environment? Is it my genome? Is it my access to care? Why can't my diabetes be as well controlled as someone else's?”  So, that has been huge, to interact directly with our participants and help really close the loop by answering questions in the language of research and show them how their data is contributing back.    Natalie: Thank you. And Raghib, how are you sort of grappling with these questions, particularly because you are recruiting so very heavily at the moment?   Raghib: So, as you say it is a challenge, and people do join the programme primarily based on trust that we will use their data for public health benefit and for the benefit of the whole population, but they also join on the basis that they will get back information about their own health and their risk of disease. To do both of those is not straightforward. I mean, the first of those, it has been well established by UK Biobank, and about 80% of our participants also say they are doing it primarily for to altruistic reasons, which is great. But 80% also said they would like to receive feedback about their own health, which is also understandable, and so we need to find ways to provide that in a timely way, but also in a way that the health service can manage. That is going to be one of our key challenges going forward.    But to echo what Naomi and Andrea have said, I mean to maintain participant's engagement with the programme is not easy. We need to make sure that they are receiving information regularly, are kept up to date with what we are doing with their data, with the work that we are doing with academia, with the NHS, with industry etc. It is easier now than it was before because Our Future Health has been set up as a digital cohort, so we have means of communicating much more easily with our participants. But yeah, as you say we are at early stages. Over time that does get harder, to maintain that engagement. So, we know in the next one to 2 years we need to step up our work on feedback and recontact.   Natalie: Fantastic. I really love the idea of like the participant-led enquiry. That is something that I think our participant panel at Genomics England would really like to hear more about.   So, speaking about sort of ongoing engagement with participants, one of the challenges we know around recruiting into large-scale studies like this is that many research datasets don't have equal representation from all communities. That might have an impact on the quality, the representativeness of the scientific outputs that you can generate, and potentially the benefits back to patients and participants.   How are you addressing this challenge in recruitment where you may have some communities that are not as engaged with scientific research. You may have elements of distrust or people being marginalised, having difficulty accessing research and these sorts of opportunities. Do you have any examples of what has worked really well? Raghib, if I could come to you first.   Raghib: Sure. So, I mentioned I worked on UK Biobank about 20 years ago. One of the things I was looking at then was how we could maximise participation, particularly of people from ethnic minorities into the project. Because of the age group that was chosen by UK Biobank for very good reasons, age 40 to 69, the proportion of people from ethnic minorities was relatively small. So, although it was representative for that age group, I think it was about 6%, or 34,000 out of the 500,000, that were from non-white ethnic minorities.   So, when Our Future Health was set up, we knew that the population has changed anyway. You know, the UK has become a much more ethnically diverse society. But also, because it is a cohort from 18+ and I think minorities tend to be younger on average than the white population, we knew we had an opportunity to really have a big step change in the number of people that could take part in a study like this. So, our aim is actually to get 10% of the whole cohort from ethnic minorities, so 500,000 out of the 5 million from ethnic minorities. Actually, so far we are pretty much on track. So, of the 1.8 million that have consented, about 180,000 are from non-white ethnic minorities.   That is extremely important, particularly for genetic research where non-European populations are very much underrepresented in nearly all genetic databases. Secondly, from a UK context, although it applies of course in all countries, is that people from more deprived backgrounds are also less likely to take part in this type of research. So again, we have made a very deliberate attempt to try and ensure we have adequate numbers from the most deprived quintile. Again, about 10% of the cohort so far, nearly 200,000 are from that most deprived quintile who both are underrepresented in research, but also have the worst outcomes. So, this is really our first study that has been big enough in the UK to look at that group properly and understand some of the factors at an individual level that we haven't been able to in the past.   Finally, geographically, so the first time again because it is a digital cohort, we were able to recruit people from all over the UK. So, every single part of the UK is now represented in Our Future Health, particularly coastal communities and rural areas that haven't been able to take part in this type of study before, as well as Northern Ireland. You know, for the first time we have got that full geographical coverage.   Natalie: Fantastic. I suppose a lot of that recruitment approach has very much been about going to where people are, rather than expecting them to come to you. Is that right?     Raghib: That is right and thank you for reminding me. So yeah, we have had a different approach. So, we have opened up many, many more clinics than previous studies through a combination of mobile units, shopping centres, community pharmacy. Community pharmacy in particular has been very important. So, to date we have had about 400 different venues that we have been able to recruit. That is over 1 million people that have given blood samples, and that has really enabled people from every part of the country to take part. Secondly, we have kept clinics open in areas of greater deprivation and ethnic diversity much longer than in other areas, to maximise the opportunity for them to join. Thirdly, we do provide reimbursement for people with expenses to ensure they aren't excluded because of financial reasons, and again that has helped.    Natalie: So, really making those efforts is evidently paying off. Andrea, have you had similar experiences as All of Us? What has your approach been to try and ensure that you are getting a wider representation from different communities?    Andrea: It has really been a focus on the programme from the start to engage those who have not been included in research in the past and make sure the opportunity is there to participate. Our Engagement Division, led by Dr. Corrine Watson has really pioneered reaching those communities here in the US.   I think one other thing I will mention that we think about when we think about how to engage participants and reach people to return value back to those communities, is to make sure the people who are accessing the data also represent them, and we can build diversity within that researcher workforce. So, since our data was first released in 2020, we have recognised that the biomedical workforce also has a huge group of underrepresented individuals, and a lot of our researcher engagement and researcher outreach has focused on reaching those of diverse backgrounds and career paths.   To that end we have reached out and engaged historically black colleges as well as other minority serving institutions, really looking to make sure that their students and researchers can have the same access as more traditional research-based institutions in the US system.    That has been important because our system is built on cloud-based architecture and shared data that doesn't require a huge cluster on campus, and that helps remove a barrier that some of those institutions and researchers may have had. We also know they haven't been able to participate in the past, and we think that cloud architecture again can make the data much more feasible and be a huge support to diversifying the researcher workforce as we go forward. That circling back, helping them be the voices speaking to their community, helps build out that diverse participant community base as well.    Natalie: That's such an important point, because it is not just about the participants and the data you can collect, but also who is able to look at it? Who is actually able to undertake the research?    Naomi, can I bring you in here? I know that UK Biobank has been thinking a lot about researcher access to data and trying to ensure that the data that you hold, the really rich datasets you hold in UK Biobank, are more accessible to researchers from different backgrounds who may not have the same level of resources. Can you tell us a little bit about the work you have been doing on that?   Naomi: Yeah. So, just following on from what Andrea said, it is really important to get as diverse ideas as possible from across the global research community to really move public health forward.   So, what UK Biobank has done is we are putting mechanisms in place so that early career students, and career researchers, and researchers at all levels of their career from lower income countries, can access the data at a much lower fee. So, currently for most researchers it costs about £9,000 to access all of the data. So, that is 40 petabytes of genomic data, biomarkers, clinical outcomes, lifestyle factors and so on. So, early career researchers and those in lower income countries, it is about £500.   On top of that a group of big pharmaceutical companies have got together to create a global researcher access fund, which essentially covers this reduced fee so that all researchers no matter where they are from have exactly the same opportunity to access the data to advanced scientific discoveries. So, on top of that all our researchers now use our online secure research analysis platform. While there is no charge to access the platform, there are costs associated with compute needed to analyse and store the results.    So, AWS have donated research credits for early career researchers and those from lower income countries up to a total of about $500,000 per year, to use the research platform. So, researchers can apply to use these research credits to offset the costs of compute and storage. So, that means that we are trying to democratise access to researchers from all around the world.   I think actually our biggest challenge is not so much … we have largely dealt with you know subsidising the cost. It is actually making researchers from lower income countries aware that these resources exist, and that are applicable to them.   So, sometimes we hear from say researchers in Africa or South America, “Well, there is no point accessing UK Biobank because it is not relevant to our population.” You know, a third of our researchers are from China. So, even if UK Biobank hasn't got coverage of those racial ethnic populations, that doesn't mean that the associations that you find between risk factors and disease risk are not applicable to other different populations. And that is also why having different resources like UK Biobank, like Our Future Health, like All of Us, in different populations around the world, is so important in order to replicate those findings.    Natalie: Absolutely, and fantastic just to hear the attention that is being paid to trying to ensure that diversity of different types of researchers who will just bring different questions to the table, different perspectives on the data, different priorities, different types of questions.    So, speaking about that diversity of researchers, one really important part of his ecosystem that we haven't really touched on so far is around the role of industry. There are a lot of really important research questions being addressed by industry. Some that can only really come from, maybe it is pharmaceuticals, maybe it is tech.   From your perspectives, what kind of role can and should industry and commercial partners play in supporting the kinds of long-term research studies that you have set up, and ultimately trying to get to that point of sort of generating benefits back to patients and health systems. Naomi, can I start with you, for that sort of longer-term perspective for Biobank?   Naomi: So, industry are great partners for long-term studies like ours because they can bring additional funding, expertise, and technology. So, for UK Biobank, because it is so easily accessible to industry and academics alike on exactly the same terms, what it has meant is that industry, particularly big pharma and also now big tech, they can access the data, they see the value of the data for their own research purposes, and then they have invested into UK Biobank to do whole-exome sequencing, whole genome sequencing, proteomics at scale to increase the value of the dataset for their own drug discovery pipelines.   But of course, it means that the data that they have generated, which cost millions of dollars to generate, when you need deep pockets to do these kinds of study enhancements, then become available to all researchers. So, having access to these large-scale resources that have deep data on genomics, physical measures, other biomarkers, and clinical outcomes enables pharma to rapidly increase their drug discovery pipelines in generating new drugs and treatments for patients, and also those data are then shared with the rest of the global research community.     So, we found it to be a really exciting win/win in which industry get what they need to help move forward new drug targets and discovery, but also other researchers get what they need in order to make other scientific discoveries in different fields of research.        Natalie: Thank you. And Raghib, I know that for Our Future Health, that industry relationship is a really important part of the founding model. Will you tell us a little bit about how you are engaging and working with industry partners?   Raghib: Sure. So, as you said Our Future Health was set up in a different way, as a very public private partnership. Although the largest funder is the UK Government, more than half of our funding has come from a combination of life science companies, so pharmaceutical, diagnostic companies, as well as the medical charities, so the larger medical charities in the UK. That partnership is deliberate for all the reasons that Naomi has outlined. There are areas where academia and the NHS are very strong, and areas where industry is very strong, and by working together as we saw very good examples during the pandemic with the vaccine and diagnostic tests etc, that collaboration between the NHS and academia industry leads to much more rapid and wider benefits for our patients and hopefully in the future for the population as a whole in terms of early detection and prevention of disease. So, we have 16 life sciences companies that have joined as founding partners with Our Future Health who have contributed financially to the programme.    Equally importantly they have also contributed scientifically, so there is a huge amount of scientific expertise in industry, and they work with us with our Scientific Advisory Board with our scientists internally to think about the best use of the resource for drug discovery, diagnostics, new medical technologies, and new targets etc.    So, that is the vision, and so far, it is working well. It is a relatively new model to have set up a project like this in this way, but it has been a very collaborative approach, and we all recognise, all have similar aims, so recognise what we are working towards. You know, we meet regularly. We have a Joint Founders Board where as I say academia, NHS, industry, and the charities come together to decide on the priorities for the coming years.   Natalie: Fantastic. And Andrea, I suppose in the US it might be slightly different culturally from the UK, but the role of industry with All of Us, how are you engaging with those pharmaceutical, technology bodies, and partners as well?     Andrea: Absolutely, and maybe this goes back a bit to your first question. We at All of Us love learning from UK Biobank and have really seen them forge a lot of wonderful partnerships that have enriched and developed their dataset. We at All of Us have started with academia and working through partnership opportunities really intramurally at intramural centres that make up parts of the National Institute of Health. We believe that building on those close friends and family relationships we have both in the government and academia get us through our first step to be able to interface with commercial organisations. That really started with taking the first step this year to ensure broad availability of data that can maximise both use of the data available, as well as look forward to our partnership opportunities in the future.   So, commercial organisations as of 2024 have also been able to access the All of Us dataset that is that first step in thinking about what a partnership would be, and we are glad to build on the access that international organisations and academic organisations already have.   Natalie: A lot to look forward to here. We are going to have to wrap up in a moment, so I'd just like to leave you all with a final question before we have to end the podcast. There is huge ambition in all of the research programmes that you are leading and involved in, but what are you most excited about coming down the line in the next few years? What do you think is going to be feasible? What really gets you excited about the work that you are doing and where you see the potential benefits really landing in the next few years? Andrea, would you like to start?   Andrea: Thanks. There is a lot we are really excited about. I haven't had a chance yet to mention our paediatric cohort, and that in addition to expanding access for international research, in 2024 we were able to enrol our first paediatric participants. That really sets up the potential to observe participants across the lifespan. That is a huge advance for All of Us and we are excited about the paediatric work going forward.    Natalie: I love that, how do you come into the future with us? That is fantastic. Naomi.   Naomi: Yeah, if I had to choose one would be the possibility of being able to measure circulating proteins on all half a million participants. We have done this on about 55,000 participants, and just that subset alone is already generating fascinating insights for early biomarkers for disease through protein profiles and risk prediction of disease. I think having that on all half a million coupled with their genomics data and health outcomes, will bring a sea change in how we diagnose disease earlier. So, I think that is a really exciting avenue for us to go into over the next couple of years.   Natalie: Really enriching. That data sounds like a very exciting set of possibilities. Raghib.   Raghib: Thank you. There are so many opportunities here, but I will just maybe mention 3. So, the first, in terms of being able to combine the genetic data that we are collecting and all the other information about risk factors, and particularly the fact that we have this on a lot of young people, will enable us to identify people at high risk of diseases in the presymptomatic phase and then to be able to offer them both feedback about their risk of disease but also interventions that can change their natural incidences. That has never really been possible before. That is extremely important for all diseases for people, but also it is very important for our healthcare system.   So, those of you listening in the UK, I know the NHS is under a huge amount of pressure, and the current model of healthcare which has been in place really since the inception of the NHS, is to treat late-stage disease when people have already developed symptoms and signs. You know, it wasn't really possible to identify people earlier, but it is now, and Our Future Health will provide the evidence base to show that prevention really is better than cure, and to show that these approaches both lead to better clinical outcomes, but also are cost effective and a good use of resources. Of course, the new government is very much committed to this as well, you know moving from acute care to prevention, from hospitals to community, and from analogue to digital.     Finally, because our cohort has now become so large and does cover every part of the UK, and this wasn't something I necessarily thought about when we started Our Future Health, we are able to have unique insights into the health of the population across every age group, across every ethnic group, across every geographical area, and by deprivation, and to understand not just observationally in terms of risk factors, but also the impact of interventions on those different populations.   We can look at that, as I said at an individual level on millions of people to gain intelligence about what is going on in terms of public health, but also to see what will hopefully improve their health in the future. So, there are really, you know I have described transformational opportunities to improve health through both biomedical research and populational health insights now through the resource, and I look forward to working with colleagues across the UK and globally to deliver them.   Natalie: We will wrap up there. Thank you so much to our guests, Dr Raghib Ali, Professor Naomi Allen, and Dr Andrea Ramírez for joining me today as we discussed how collaboration, scale, ongoing engagement, can really unlock the potential of large-scale health datasets to drive brilliant new research and ultimately improve the lives of patients and the population.   If you would like to hear more like this, please subscribe to Behind the Genes on your favourite podcast app. Thank you for listening. I have been your host, Natalie Banner. This podcast was edited by Bill Griffin at Ventoux Digital and produced by Naimah Callachand.

In this episode of The Health Fix Podcast, Dr. Jannine Krause interviews Hannah Went, co-founder of TruDiagnostic, to discuss the revolutionary role of epigenetics in health and aging. Learn how TruDiagnostic's TruAge test analyzes DNA methylation to calculate biological age, empowering you to make personalized lifestyle changes. Discover how tools like the Biobank/Harvard's OMICm Age Algorithm, Yale Symphony AGE, and DunedinPACE analysis can predict and prevent chronic diseases while improving longevity. If you're looking to take control of your aging process and improve overall well-being, this episode is packed with actionable insights. What You'll Learn In This Episode: TruDiagnostic's TruAge Test: How it measures biological age and why it's a game-changer for personalized health. Dr. Krause's Results: Comparing her 2022 and 2024 test results and what they reveal about health and aging. The Biobank and OMICm Age Algorithm: Insights from Harvard's cutting-edge research. Yale Symphony AGE: A closer look at what this metric can teach us about aging. DunedinPACE Analysis: How researchers from Duke and other institutions are predicting the risk of chronic disease and mortality through epigenetic markers. Takeaways for Listeners: Genetics isn't destiny—your choices and environment play a pivotal role in health outcomes. How tracking your biological age with TruAge can empower you to make data-driven lifestyle changes. The potential of epigenetics to predict and prevent chronic diseases, giving you tools to live a longer, healthier life. Resources Mentioned: TruAge + TruHealth Testing - TruDiagnostic Website Hannah Went's Podcast: Everything Epigenetics Podcast Tune In and Take Control: Join Dr. Jannine Krause and Hannah Went for an inspiring conversation that reveals how epigenetics can help you age gracefully and reclaim control over your health journey.  

Dr. Prakash Narayan is a distinguished biotech executive with over 20 years of experience in leading IND- and BLA-enabling programs from concept through clinical trials for heart, lung, kidney, and liver indications. As a founding member of a startup biotech that became a publicly traded company, Dr. Narayan has demonstrated exceptional leadership skills and a proven track record in nonclinical and translational R&D, attracting approximately $30 million in non-dilutive funding as a Principal Investigator from various organizations including NIH, NSF, DoD, and BARDA 00:00 Introduction to the Life Science Success Podcast 00:37 Sponsor Message: D3 Digital Media Marketing 01:10 Guest Introduction: Dr. Prakash Narayan 01:51 Journey from Academia to Biotech Executive 04:34 Growing a Startup into a Publicly Traded Company 06:49 Drug Development Process: From Discovery to FDA Filings 12:53 Challenges and Future of Cell-Based Therapies 16:10 Predictive Analytics in Biomedical Science 19:10 Adapting Approaches Across Disease Areas 22:56 Precision Medicine in Clinical Trials 24:40 Understanding Fatty Liver Disease 25:00 Precision Medicine: A Tailored Approach 25:25 Repurposing Drugs for Kidney Disease 27:10 The Role of Biobanks and Electronic Health Records 28:26 Non-Dilutive Funding: Pros and Cons 32:56 Exploring Transcriptomics and Functionomics 36:55 The Impact of Technology and AI in Medicine 40:53 Inspiration and Concerns for the Future 47:42 Final Thoughts and Advice for Entrepreneurs  

BioCertica is Africa's first digital biobank, combining advanced genetic testing and encryption technology to empower individuals with secure, actionable genetic insights. Pioneers in polygenic risk scoring for direct-to-consumer testing. Arno is the Co-founder and Chief Product Officer with expertise in product management, marketplaces, and HealthTech innovation. Jamie is a Business Development Manager and MSc candidate in functional genetics, driving BioCertica's local and global growth.

We explore the cutting-edge of healthcare digitalisation through the lens of genomics, artificial intelligence, and e-health strategies. Liis Leitsalu, researcher at the Estonian Genome Center and the University of Tartu, will guide us through the evolving world of genomics. She shares her expert insights on how genetic research is revolutionising personalised medicine, the role of Estonia's pioneering Biobank, and the ethical considerations surrounding genetic data.Professor Kristjan Port, a sports biologist with deep roots in academic research, discusses the diverse applications of AI in healthcare, from diagnostics and treatment to managing patient data and the ethical dilemmas posed by AI technology. His insights will illuminate how AI is not just a tool of the future but a present reality shaping our medical landscape.Jaanika Merilo, Head of Digital Health at the Estonian Ministry of Social Affairs, talks about Estonia's new e-health strategy. She outlines how digital tools are enhancing patient care, supporting healthcare professionals, and ensuring data-driven decision-making. She will explain how Estonia is leveraging technology to streamline healthcare services and improve patient outcomes, setting a benchmark for digital health globally.

The annual meeting of the American Society of Human Genetics (ASHG) is about to start. Here's a sneak-peek of the meeting with Dr. Bruce Gelb who is the current president of ASHG, he is also a researcher at the Icahn School of Medicine in New York City. My co-host --Dr. Mike Fletcher senior editor at Nature Genetics-- and I, asked Bruce Gelb about the meeting but also about some trends such as genetics and inclusion, biobanks, sequencing of the genomes of newborns, exposomics and more. 

Roswell Park receives federal funding for State-of-the-Art Biobank full 286 Wed, 09 Oct 2024 15:46:59 +0000 bER1Sj6fzwS9vAqxYJqyYZi7hYGrLwcH news & politics,news WBEN Extras news & politics,news Roswell Park receives federal funding for State-of-the-Art Biobank Archive of various reports and news events 2024 © 2021 Audacy, Inc. News & Politics News False https://player.amperwavepo

Roswell Park receives federal funding for a new State-of-the-Art Biobank full 286 Wed, 09 Oct 2024 15:55:11 +0000 EaJNwVnwLPO4PBNvS55YW39IDjWETJPZ news & politics,news WBEN Extras news & politics,news Roswell Park receives federal funding for a new State-of-the-Art Biobank Archive of various reports and news events 2024 © 2021 Audacy, Inc. News & Politics News False https://player.ampe

South Asians are four times more likely to have heart attacks and six times more likely to have diabetes at a younger age, with fewer symptoms. It's a ticking time bomb that's gone largely unnoticed—until now.Dr. Romit Bhattacharya, a Harvard-trained cardiologist, is on a mission to change that. He's spearheading the first-of-its-kind "Our Health Study" to uncover the complex interplay of genetics and lifestyle that puts South Asians at such high risk.By recruiting participants from all across the U.S., Dr. Bhattacharya hopes to build one of the largest genetic cohorts of South Asians in the world. The goal? To identify genetic targets for personalized prevention and treatment strategies that could save countless lives.Join Dr. Vikram Raya as together they explore the groundbreaking research that aims to rewrite the future of heart health for South Asians everywhere."Once we can identify the genetic target that we want to inhibit or block or augment, then we can go after it specifically, and we can learn."- Dr. Romit BhattacharyaIn This Episode:- Dr. Bhattacharya's journey into researching South Asian heart health- Debunking myths - are South Asians just "lazy and gluttonous"?- Key findings from previous studies like INTER-HEART and MASALA- The U.K. Biobank study and the persistent risk despite lifestyle changes- OurHealth Study - the fastest recruiting genetic cohort of South Asians- How genetic insights can lead to targeted therapies and personalized interventions- The importance of South Asian representation in clinical trials- How to get involved with OurHealth Study and support its missionResources:➡️ Free community of high-performing physicians: the Physician Wealth Accelerator - https://limitless-md.mn.co/ ➡️ Check out my programs - https://vikramraya.com/coaching-tab-revamp/ ➡️ Join our Mastermind - www.i8mastermind.com ➡️ Learn Small Multifamily Real Estate - www.MDTycoon.com Mentioned In the Episode:➡️ OURHEALTH Study: https://ourhealthstudy.org/ ➡️ INTER-HEART Study: https://pubmed.ncbi.nlm.nih.gov/11320357/ ➡️ MASALA Study: https://www.masalastudy.org/ Connect with Dr. Romit Bhattacharya

Estonia is working on becoming the first country to implement personalized health at scale through the Estonian National Biobank.The biobank uses genetic data to create a picture of the Estonian population, leading to the potential adaptation of public health systems. The Estonian Biobank has samples from 20% of the adult population; in comparison, UK biobanks only represent 0.7% of the population. With so much data, Estonia can determine risk factors for cancer, cardiovascular disease, mental and reproductive health, informing health investments to improves patient outcomes.The project seeks to predict patients' responses to certain medications based on their genetic makeup. As well as better patient outcomes, this approach could save health systems millions on ineffective prescriptions in the long run. It could also be a blueprint for other national health systems, including the NHS, to personalize healthcare at scale.Earlier this year, the Estonian Biobank announced the next phase of its European Commission funded project in collaboration with sequencing firm PacBio. On the podcast this week, we have Professor Lili Milani, head of the Estonian National Biobank, and Neil Ward, VP of EMEA at PacBio.01:27-04:06: What is the Estonian National Biobank?04:06-05:15: Background on PacBio05:15-06:43: What are the benefits of using genetic data to create a picture of the Estonian population?06:43-08:24: What data is collected, and how is it used?08:24-09:54: Protecting individual privacy09:54-11:24: Is the databank used regularly by Estonian citizens?11:24-12:35: Can the biobank help address disease earlier?12:35-16:30: Are there economic savings?16:30-17:16: How to expand the biobank program17:16-19:44: How does the biobank help personalize medicine?19:44-20:26: Are there regional differences?20:26-21:57: How can Estonia's system be applied to other countries?21:57-22:57: Has there been international interest in the biobank?22:27-22:52: Are pharma companies interested in the biobank?22:52-24:05: The partnership with PacBio24:05-26:15: Is AI being used in conjunction with the biobank?26:15-27:26: Is the biobank project similar to other PacBio work?27:26-29:00: What is the future for the biobank relationship with PacBio?29:00-31:30: What is the future for the biobank?Interested in being a sponsor of an episode of our podcast? Discover how you can get involved here! Stay updated by subscribing to our newsletter

2024. augusztus 5., hétfő 9-10 óra HEURÉKA EXTRA: Mi az a biobank? Érdekes, hogy a “biobank” és a “biobankolás” kifejezések már 1996-tól kezdve meg-megjelentek publikációkban, de akkoriban még nem igazán figyelt fel rájuk a szélesebb közönség. Az áttörést 2001 hozta el, amikor a Gazdasági Együttműködési és Fejlesztési Szervezet (röviden és közismerten: OECD) felismerte a majdani biobankok gazdasági potenciálját, illetve a biotechnológiai ipar fejlődésében játszott jövőbemutató szerepüket és “Biological Resource Centers” névvel publikálta az első hivatalos definíciót. Prof. Dr. Széll Márta stratégiai rektorhelyettes, az SZTE Biobank vezetője. Tőzsdenyitás Varga Zoltán, senior elemzővel (Equilor Zrt.) HEURÉKA-ÉLMÉNY: Itt a hullócsillag szezon! A Perseidák raja július 14-től szeptember 1-ig lesz látható, a maximum idén augusztus 11-12-én lesz. Hol és hogyan lehet őket látni? Perseidák meteorraj és Csillagok Alatt Kárpát-medencei csillagászati rendezvénysorozat. 2 új üstököst talált egy hét alatt egy magyar csillagász. Már lassan 1,6 milliárd dollárnál jár a Boeing vesztesége az űrhajója miatt. Mikor is robban az a bizonyos csillag az égen? Szabó Norton, a Svábhegyi Csillagvizsgáló, bemutató csillagásza.

Join Fred Bodimer as he delves into the latest health-related issues. This episode covers President Biden's COVID-19 diagnosis and subsequent recovery, insights from a biobank containing genetic information of half a million US veterans, and the pros and cons of paleo diets. Fred also discusses the surprising risks of injuries while cutting avocados and offers safety tips. Learn about the benefits of three minutes of exercise before bed for improving sleep quality, and get expert opinions on food safety, including the risks associated with moldy bread. 

In einigen Museen stehen im Keller riesige Gefrierschränke. Hier wird DNA-Material von Menschen, Tieren oder Pflanzen aufbewahrt. Wie uns das in Zukunft helfen kann.

Episode Highlights: Introduction Overview of functional medicine for women. Importance of addressing root causes of health issues. Focus on brain health and aging in this episode. Key Study Discussion Recent large-scale study involving Biobank participants over age 45. Examination of 15 categories for dementia risk factors. Relevance of study findings to listeners. Top 3 Risk Factors for Dementia Diabetes Impact of high blood sugar on brain health. Connection between diabetes and brain changes related to dementia. Tips for managing diabetes: balanced diet, low sugar, regular exercise. Traffic-Related Air Pollution Effect of polluted air on brain inflammation. Study findings on air pollution and increased dementia risk. Strategies to reduce exposure: avoiding busy roads, using air purifiers, incorporating houseplants for better air quality. Alcohol Consumption The link between excessive alcohol intake and brain health. Effects of alcohol on memory, cognition, and overall brain function Recommendations for moderate alcohol consumption: guidelines and tips for reducing intake. Additional Insights on Brain Health The importance of lifestyle choices in mitigating dementia risk. Role of diet, exercise, and stress management in maintaining brain health. Practical tips for incorporating brain-healthy habits into daily routines. Listener Q&A Segment Addressing common questions from listeners about brain health and aging. Personalized advice and strategies for improving cognitive function. Encouragement for listeners to seek personalized health assessments. Actionable Tips for Listeners Monitoring and managing blood sugar levels. Reducing exposure to air pollution. Moderating alcohol intake. Incorporating regular physical activity and a balanced diet. Prioritizing mental health and stress reduction. Call to Action Encouraging listeners to evaluate their own risk factors. Inviting listeners to join the Functional Medicine for Women community. Providing links to resources and further reading on brain health and dementia prevention. Links and Resources: Study on Dementia Risk Factors Tips for Managing Diabetes Reducing Exposure to Air Pollution Guidelines for Moderate Alcohol Consumption Brain-Healthy Diet and Exercise Plans Connect with Lacy: Social Profiles: Follow Lacy Lain on Instagram for daily tips and updates on functional health and holistic wellness. Join the FREE Holistic Health Hub Membership here. Disclaimer: Our life and health coaches do not diagnose, treat, prevent, or cure any disease or condition. Nothing we share with our clients is intended to substitute for the advice, treatment, or diagnosis of a qualified licensed physician. Lacy Lain, FMCHC may not make any medical diagnoses or claim, nor substitute for your personal physician's care. It is the role of Lacy Lain and her Practitioners to partner with their clients to provide ongoing support and accountability in an opt-in model of self-care and should be done under the supervision of a licensed physician. These platforms share personal experiences and provides education. Interaction on these platforms does not constitute a doctor/patient relationship. Subscribe & Review: Don't miss out on our upcoming episodes! Subscribe to our podcast on Apple Podcasts, Spotify, or your favorite podcast platform. If you enjoyed this episode, please leave a review to help others find our show. Thank you for listening!

The Perpetual Notion Machine speaks with UW Professor Francisco Pelegri about his research and how it is advancing work within the Gaylord Nelson Institute for Environmental Studies and the Great […] The post The Great Lakes Biobank: DNA preservation to save threatened species appeared first on WORT-FM 89.9.

Episode Description: Today's interview is with Joe Landolina, the CEO and Co-founder of Cresilon, Inc. Karl, Erum, and Joe discuss the untapped potential of animal health markets and innovative cancer treatments. Joe shares his entrepreneurial journey from founding Cresilon, Inc. in his NYU dorm to developing Vetigel, a revolutionary product designed to rapidly halt bleeding in both animals and potentially humans. Their conversation not only highlights the critical role of biotech innovations in improving health outcomes but also underscores the vibrant ecosystem of investment and research propelling these advances forward. This episode is a must-listen if you're  interested in the cutting-edge intersections of technology, healthcare, and venture capital! Grow Everything brings the bioeconomy to life. Hosts Karl Schmieder and Erum Azeez Khan share stories and interview the leaders and influencers changing the world by growing everything. Biology is the oldest technology. And it can be engineered. What are we growing? Learn more at ⁠⁠⁠⁠⁠⁠www.messaginglab.com/groweverything⁠⁠⁠⁠⁠⁠ Chapters: 00:00:00 - Meet: Julie Wolf & The "Grow Everything" Podcast 00:00:42 - Julie Unpacks: UK's Thriving Tech Ecosystem 00:02:30 - Innovation Spotlight: Neon Therapeutics' SynBio Breakthrough 00:03:28 - Cancer Care Revolution: The Next-Gen Therapeutics 00:04:11 - Inside the Biotech Studio: Pioneering Startup Growth 00:07:16 - Deep Dive: The Lucrative World of Animal Health 00:09:14 - Introducing Joe Landolina: A Visionary in Biotech Innovation 00:11:36 - The Genesis of Cresilon  and the Groundbreaking Vetigel 00:16:40 - Vetigel's Origin: From Idea to Impact in the Veterinary Market 00:19:07 - Veterinary Breakthroughs: Cresilon's Entry into Animal Health 00:24:03 - Cresilon's Pioneering Approaches to Animal Surgery 00:26:01 - Human Applications: Cresilon's Cross-Species Breakthroughs 00:28:38 - The Path to Human Healthcare: Expanding Cresilon's Reach 00:29:23 - Vetigel's Global Impact: Saving Lives Across Continents 00:31:01 - Future Focused: Advancing R&D at Cresilon 00:35:03 - Biotech in Brooklyn: Cultivating a Local Innovation Hub 00:42:56 - Beyond Biotech: New Frontiers in Science and Technology 00:45:56 - The Cutting Edge: AI, Biobanks, and the Future of Biotech Episode Links: Joe Landolina on LinkedIn Cresilon, Inc. Vetigel Forbes 30 Under 30 Julie Wolf on LinkedIn 2048 Ventures BioNTech Neon Therapeutics Get $300 off ⁠⁠⁠⁠⁠⁠⁠⁠⁠Synbiobeta tickets⁠⁠⁠⁠⁠⁠⁠⁠⁠ (May 6-9 in San Jose, CA) using promo code: Grow Everything Topics Covered:  biomaterials, sustainability, biodegradablility, compostibility Have a question or comment? Message us here: Text or Call (804) 505-5553 ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Instagram⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ / ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠TikTok⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ / ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Twitter⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ / ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠LinkedIn⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ / ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Youtube⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ / ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠GrowEverything website⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Email: groweverything@messaginglab.com Support here: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Patreon⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Music by: Nihilore Production by: Amplafy Media --- Send in a voice message: https://podcasters.spotify.com/pod/show/messaginglab/message

3 millioner danskers blod bliver opbevaret i Staten Serum Instituts Biobank, men i mange tilfælde har blodets ejermænds hverken fået besked eller givet samtykke. Er det i orden, eller skal borgerne først give samtykke, inden deres blod bliver brugt til forskning? Det vender vi i dagens program. Vi spørger også, om det er respektløst at tage billeder i kirken under begivenheder som vielser, konfirmationer og dåb? Medvirkende: Mette Kathrine Grosbøll, præst i Sions kirke på Østerbro. Annemette Voss Fridthjof, blogger, forfatter og influencer. Anne Marie Vangsted, faglig direktør på Statens Serum Institut for Biobank, Digital Infrastruktur & Højkapacitetsdiagnostik. Anders Kjærulff, journalist og tech-kritiker. Thomas Ploug, professor i dataetik på Aalborg Universitet.See omnystudio.com/listener for privacy information.

Transcript with audio and relevant external links, recorded on 6 Feb 2024Eric Topol (00:05):Hello, this is Eric Topol with Ground Truths, and I have a remarkable guest with me today, Professor Michelle Monje, who is from Stanford, a physician-scientist there and is really a leader in neuro-oncology, the big field of cancer neuroscience, neuroinflammation, and she has just been rocking it recently with major papers on these fields, no less her work that's been on a particular cancer, brain cancer in kids that we'll talk about. I just want to give you a bit of background about Michelle. She is a National Academy of Medicine member, no less actually a National Academy of Medicine awardee with the French Academy for the Richard Lounsbery Award, which is incredibly prestigious. She received a Genius grant from the MacArthur Foundation and is a Howard Hughes Medical Institute (HHMI) scholar, so she is just an amazing person who I'm meeting for the first time. Michelle, welcome.Michelle Monje (01:16):Thank you. So nice to join you.Long Covid and the BrainEric Topol (01:18):Well, I just am blown away by the work that you and your colleagues have been doing and it transcends many different areas that are of utmost importance. Maybe we can start with Long Covid because that's obviously such a big area. Not only have you done work on that, but you published an amazing review with Akiko Iwasaki, a friend of mine, that really went through all the features of Long Covid. Can you summarize your thoughts about that?Michelle Monje (01:49):Yeah, and specifically we focused on the neurobiology of Long Covid focusing on the really common syndrome of cognitive impairment so-called brain fog after Covid even after relatively mild Covid. There has been this, I think really important and exciting, really explosion of work in the last few years internationally trying to understand this in ways that I am hopeful will be beneficial to many other diseases of cognition that occur in the context of other kinds of infections and other kinds of immune challenges. But what is emerging from our work and from others is that inflammation, even if it doesn't directly initially involve the nervous system, can very profoundly affect the nervous system and the mechanisms by which that can happen are diverse. One common mechanism appears to be immune challenge induced reactivity of an innate immune cell in the nervous system called microglia. These microglia, they populate the nervous system very early in embryonic development.(02:58):And their job is to protect the nervous system from infection, but also to respond to other kinds of toxic and infectious and immune challenges. They also play in healthy conditions, really important roles in neurodevelopment and in neuroplasticity and so they're multifaceted cells and this is some population of those cells, particularly in the white matter in the axon tracks that are exquisitely sensitive it seems to various kinds of immune challenges. So even if there's not a direct nervous system insult, they can react and when they react, they stop doing their normal helpful jobs and can dysregulate really important interactions between other kinds of cells in the brain like neurons and support cells for those neurons like oligodendrocytes and astrocytes. One common emerging principle is that microglial reactivity triggered by even relatively mild Covid occurring in the respiratory system, not directly infecting the brain or other kinds of immune challenges can trigger this reactivity of microglia and consequently dysregulate the normal interactions between cells and the brain.(04:13):So important for well-tuned and optimal nervous system function. The end product of that is dysfunction and cognition and kind of a brain fog impairment, attention, memory, ability to multitask, impaired speed of information processing, but there are other ways that Covid can influence the nervous system. Of course there can be direct infection. We don't think that that happens in every case. It may not happen even commonly, but it certainly can happen. There is a clear dysregulation of the vasculature, the immune response, and the reaction to the spike protein of Covid in particular can have very important effects on the vessels in the nervous system and that can trigger a cascade of effects that can cause nervous system dysregulation and may feed directly into that reactivity of the microglia. There also can be reactivation of other infections previous, for example, herpes virus infections. EBV for example, can be reactivated and trigger a new immune challenge in the context of the immune dysregulation that Covid can induce.(05:21):There also can be autoimmunity. There are many, we're learning all the different ways Covid can affect the nervous system, but autoimmunity, there can be mimicry of some of the antigens that Covid presents and unfortunate autoimmunity against nervous system targets. Then finally in severe Covid where there is cardiopulmonary compromise, where there is hypoxia and multi-organ damage, there can be multifaceted effects on the nervous system in severe disease. So many different ways, and probably that is not a comprehensive list. It is certainly not a mutually exclusive list. Many of these interactions can happen at the same time in the same individual and in different combinations but we're beginning to wrap our arms around all the different ways that Covid can influence the nervous system and cause this fairly consistent syndrome of impaired attention, memory, multitasking, and executive functions.Homology with Chemo BrainEric Topol (06:23):Yeah, well there's a lot there that you just summarized and particularly you highlighted the type of glia, the microglia that appear to be potentially central at least a part of the story. You also made analogy to what you've seen with chemotherapy, chemo brain. Maybe you could elaborate on that.Michelle Monje (06:42):Yeah, absolutely. So I've been studying the cognitive impairment that can happen after cancer therapies including chemotherapy, but also radiation and immunotherapy. Each time we develop a new model and dig in to understand what's going on and how these cancer therapies influence the nervous system, microglia emerge as sort of the unifying principle, microglial reactivity, and the consequences of that reactivity on other cell types within the nervous system. And so, understanding that microglia and their reactive state to toxic or immune challenges was central to chemotherapy induced cognitive impairment, at least in preclinical models in the laboratory and confirm by human tissue studies. I worried at the very beginning of the pandemic that we might begin to see something that looks a lot like chemotherapy induced cognitive impairment, this syndrome that is characterized by impaired attention, memory, executive function, speed of information processing and multitasking. When just a few months into the pandemic, people began to flood neurologists' office complaining of exactly this syndrome. I felt that we needed to study it and so that was the beginning of what has become a really wonderful collaboration with Akiko Iwasaki. I reached out to her, kind of cold called her in the midst of the deep Covid shutdown and in 2020 and said, hey, I have this idea, would you like to work with me? She's as you know, just a thought leader in Covid biology and she's been an incredibly wonderful and valuable collaborator along the way in this.Eric Topol (08:19):Well, the two of you pairing up is kind of, wow, that's a powerful combination, no question. Now, I guess the other thing I wanted to get at is there've been many other studies that have been looking at Long Covid, how it affects the brain. The one that's frequently cited of course is the UK Biobank where they had CT or MRI scans before in people fortunately, and then once they had Covid or didn't get Covid and it had a lot of worrisome findings including atrophy and then there are others that in terms of this niche of where immune cells can be in the meninges, in the bone marrow or the skull of the brain. Could you comment on both those issues because they've been kind of coming back to haunt us in terms of the more serious potential effects of Covid on the brain?Michelle Monje (09:20):Yeah, absolutely and I will say that I think all of the studies are actually quite parsimonious. They all really kind of point towards the same biology, examining it at different levels. And so that UK Biobank study was so powerful because in what other context would someone have MRI scans across the population and cognitive testing prior to the Covid pandemic and then have paired same individual tests after a range of severity of Covid infection so it was just an incredibly important data set with control individuals in the same cohort of people. This longitudinal study has continued to inform us in such important ways and that study found that there were multiple findings. One is that there appears to be a small but significant atrophy in the neocortex. Two that there are also abnormalities in major white matter tracts, and three, that there is particular pathology within the olfactory system.(10:30):And we know that Covid induces as a very common early symptom, this loss of smell. Then together with those structural findings on MRI scans that individuals even with relatively mild acute disease, exhibited long-term deficits in cognitive function. That fits with some beautiful epidemiological studies that have been done across many thousands of individuals in multiple different geographic populations. Underscoring this consistent finding that Covid can induce lasting cognitive changes and as we begin to understand that biology, it fits with those structural changes that are observed. We do know that the olfactory system is particularly affected and so it makes sense that the olfactory system, which show those structural changes, the neocortical and white matter changes evident on MRI fit with what we found microscopically at the cellular and molecular level that highlighted a loss of myelinating oligodendrocytes, a loss of myelinated axons, a deficit in hippocampal new neuron production. All of those findings fit together with the structural changes that the UK Biobank study highlighted. So clearly this is a disease that has lasting impacts, and the challenge is to understand those better so that we can develop effective interventions for the many, many millions of people who are still struggling with decreases in their cognitive function long after Covid exposure affecting the world population.The Brain's Immune SystemEric Topol (12:17):Yeah, that's a great summary of how the Biobank data UK aligned with the work that you've done and I guess the other question just to round this out is for years we didn't think the brain had an immune response system, right? Then there's been a wakeup call about that, and maybe you could summarize what we know there.Michelle Monje (12:41):Absolutely. Yes, the brain is not, we used to call the nervous system an immuno privilege site, and it is not hidden from the immune system. It has its own and distinct immune system properties, but it's very clear from work by Jony Kipnis and others that there are in fact lymphatics in the nervous system. These are in the meninges. It's also become increasingly clear that there is a unique bone marrow niche in the skull from which many of the lymphocytes and other kinds of immune cells that survey and surveil the brain and spinal cord, that's where they come from. That's where they develop and that's where they return and the lymphatic drainage of the nervous system goes to distinct places like the posterior cervical lymph nodes. We are now understanding the sort of trafficking in and out of the nervous system of cells, and certainly understanding how that changes in the context of Covid, how those cells may be particularly responsive to the immune challenge initiated in the respiratory system is something that is an area of deep importance and active exploration. In fact, some of my ongoing collaborations and ongoing lab work focuses on exactly this question, how does the trafficking from the brain borders into the nervous system change after Covid? And how does potentially cellular surveillance of immune cells contribute of the nervous system contribute to the persistent microglial reactivity that we observe?Eric Topol (14:22):And do you have any hunch on what might be a successful worthwhile therapy to a candidate to test prospectively for this?Michelle Monje (14:30):I think it's too early to nominate candidates, but I think that the biology, the molecular and cellular biology is underscoring a role for particular cytokines and chemokines that are initiated by the immune response in the lung. And clear cellular targets, the goal I think the central goal being to normalize the neurovasculature and normalize microglial reactivity and so the question in this disease context and in others becomes, how can we kind of molecularly coach these reactive cells to go back to doing their normal jobs to being homeostatic? That's the challenge, but it's a surmountable challenge. It's one that I think that the scientific community can figure out, and it will be relevant not only to Covid, but also to many other consequences of immune challenges, including other post-infectious syndromes. It's not only Covid that causes long-term cognitive and other kinds of neurological and neuropsychiatric consequences. We saw this after the influenza pandemic in 1918. We've seen it after many other kinds of infectious challenges and it's important as we prepare for the next pandemic for the next global health challenge that we understand how the long-term consequences of an immune response to a particular pathogen play out.Eric Topol (15:58):No question and that I guess also would include myalgic encephalomyelitis and all the other post-infectious post viral syndromes that overlap with this. Now to switch gears, because that work is just by itself extraordinary but now there's this other field that you are a principal driver, leader, and that is cancer neuroscience. I didn't even know they had boards in neuro-oncology. I thought neurology was enough, but you got board certified in that too. This field is just exploding of interest because of the ability for cancer to cells to hijack neurons and neural circuits, which I guess the initial work goes way back but more recently, the fact that gliomas were just electrically charged. And so maybe you can frame this because this has not just amazing biology, but it's also introducing all sorts of therapeutic opportunities, including many ongoing trials.The Neuroscience of CancerMichelle Monje (17:08):Yes, yes and thank you for asking me about it. It's certainly one of my favorite things to think about, and perhaps as a bridge between the cognitive impairment that occurs after Covid and other inflammatory challenges and the neuroscience of cancer. I'll just highlight that maybe the common theme is it's important to understand the way cells talk to each other and that these sort of molecular conversations are happening on multiple scales and in unexpected ways, and they shape pathophysiology in a very important way. So continuing on that theme, we've known for many, many years, for decades in fact, that the nervous system and its activity shapes the development of the nervous system and actually it doesn't just shape the development of the nervous system where perhaps it's intuitive that the activity within the nervous system might sculpt the way that it forms, but it turns out that innervation is critical for development broadly, that innervation is necessary for organogenesis and that this is becoming clear in every organ that's been studied.(18:15):And so it stands to reason given that kind of perspective on the role that neuronal activity plays in normal development, plasticity, homeostasis, and regeneration of many different tissues, that the activity of the nervous system and those principles can be hijacked in the context of cancer, which is in many ways a disease of dysregulated development and regeneration. And so, I'm a neuro oncologist, I take care of children with a very terrible form of brain cancer called high-grade glioma and the most common form of high-grade glioma in kids occurs in the brain stem, it's called diffuse intrinsic pontine glioma (DIPG). It's really the worst disease you can imagine and understanding it has been the need to understand and treat it has been a guiding principle for me. And so, taking a big step back and trying to wrap my arms around the biology of these terrible high-grade gliomas like glioblastoma, like diffuse intrinsic pontine glioma, I wondered whether nervous system activity might influence cancer the way that it influences normal development and plasticity.(19:23):And as soon as we started to leverage tools of modern neuroscience like optogenetics to ask those questions to modulate the activity of neurons in a particular circuit and see how that influences cancer proliferation and growth, it was clear how very important this was, that active neurons and various subtypes very robustly drives the growth of these brain cancers. And so trying to understand the mechanisms by which that occurs so that we can target them therapeutically, it's become clear that the tumors don't just respond to activity regulated growth signals. They do. There are those paracrine factors, but that in brain cancer, the cancers actually integrate into the neural circuits themselves. That there are bonafide electrophysiological functional synapses that form between various types of neurons and high-grade glioma cells. We're discovering the same can occur in brain metastases from different organs, and that this principle by which neuronal activity drives the cancer is playing out in other tissues.(20:32):So right when we made these discoveries about glioma within this few years, discoveries were made in prostate cancer, in gastric cancer, colon cancer, skin cancer, pancreatic cancer. It seems that innervation is critically important for those tumor, and not just for their growth, but also for invasion metastasis, even initiation in diseases that are driven by particular oncogenes. There's an intersection between the power of those oncogenes to cause the cancer and the necessary environment for the cancer to form and that appears to also be regulated by the nervous system in very powerful ways. So, the exciting thing about recognizing this relatively unsettling feature of cancers is that as we understand it, the neuroscience of cancer becomes an entirely new pillar for therapy to combine with immunotherapy and more traditional cytotoxic therapies and we've been missing it until now. And so the opportunity exists now to leverage medicines that were developed for other reasons, for indications in neurology and cardiology and psychiatry medicines that target neurotransmitter receptors and ion channels that it turns out have a role in some forms of cancer. Now, each cancer has its own biology, so different types of neurons, different neurotransmitters, different neuropeptides play specific roles in that tissue context, but the principle is the same and so as we understand each cancer, we can start to understand what neuroscience inspired medicines we might leverage to better treat these tumors.Rewriting the Hallmarks of CancerEric Topol (22:17):Yeah, I mean it's amazing as a cardiologist to think that beta blockers could be used to help people with cancer and of course there are trials and some studies and particular cancers in that. One of the things that people maybe not outside of oncology don't follow these papers about hallmarks of cancer. There's been two editions, major editions of the hallmarks of cancer, and recently in the journal of cancer Cell, Douglas Hanahan and you wrote a classic about that the hallmarks need to be revised to include neuroscience. Maybe you could elaborate on that because it seems like this is a missing frontier that isn't acknowledged by some of the traditional views of cancer.Michelle Monje (23:08):Absolutely. So I think number one, I want to just give a shout out to Doug Hanahan and the role that the hallmarks of cancer, which is a review article that he wrote and has become sort of the Bible, if you will, of cancer biology really laying out common principles across cancer types that have provided a framework for us to understand this complex and diverse heterogeneous set of diseases. And so it was very exciting when he reached out and asked if I wanted to write this perspective, culminating nervous system interactions, neuroscience interactions as an emerging hallmark of cancer and as we examine them from that, we examine the neuroscience of cancer from that heuristic set of principles, this framework of principles of cancer biology, it's clear that there is a neural influence on the vast majority of them. We now understand from this exciting and burgeoning field that the nervous system can regulate cancer unregulated proliferation.(24:17):It promotes proliferation and growth. It promotes invasion and metastasis. It alters the immune microenvironment. It can both promote pro-tumour inflammation through neurotransmitter signaling. It can also help to modulate anti-tumor immunity. The crosstalk between immune cells, cancer cells and the nervous system are complex, profound, and I would argue incredibly important for immunotherapeutic approaches for cancer. At the same time that there are these diverse effects of the nervous system on cancer, cancer also influences the nervous system. And so, there's really this bidirectional crosstalk happening by which neurons in an activity dependent way, either in short range local neurons or in long range down a nerve or across a circuit, promote the pathophysiology of the cancer and you kind of know it's beneficial because the cancer does many different active things to increase innervation of the tumor. There is in a variety of different tissue context and disease states, elaboration of nervous system interactions through cancer derived either axonogenic or synaptogenic factors secretion, the nervous system remodels the nerves. It remodels the neural circuits to increase the connectivity of the nervous system with the cancer, and also to increase the activity of the nerves to increase the excitability of a neuron. And this contributes to not only driving the cancer, but to many of the really important symptoms that patients face with cancer, including tumor associated seizures as well as cancer associated pain.Eric Topol (26:07):Yeah, I mean this is actually so unusual to see a whole another look at what cancer is about. I mean, this is about as big a revision of thinking as I've seen at least in many, many years. The fact that you pulled this together about the new hallmarks also made me wonder because a number of years ago we went through this angiogenesis story whereby like this cancer can hijack blood vessels and promote it to growth. As you know very well, a lot of these anti-angiogenic efforts didn't go that well. That is they maybe had a small impact overall, but they didn't change the field in terms of success of therapy. I wonder if this is going to play out very differently. What are your thoughts about that? There's lots of shots on goal here and the trials have sprouted out very quickly to go after this.Michelle Monje (27:12):Yeah. I think it's important to recognize various microenvironmental effects on a cancer, including the nervous system effects as one piece of a puzzle that we need to put together in order to effectively treat the disease and I think to effectively treat a particularly very aggressive cancers, we need to hit this from multiple angles. Effective strategies will need to include targeting cell intrinsic vulnerabilities of the cancers as most traditional and targeted therapies are focused on doing right now together with decreasing the strong growth and metastasis influencing effects of the nervous system. I think that's one pillar of therapy that we really have been missing and that represents an important opportunity as well as leveraging the power of the immune system, which perhaps will only work optimally, particularly for solid tumors if you also address the nervous system influences on immune cells. And so I think that it's part of a holistic approach to effective therapy for tumors.(28:21):We have so far failed to treat with single agent or one dimensional kinds of approaches. We need to target not only the cell intrinsic vulnerabilities, the immunotherapeutic opportunities, and the nervous system mechanisms that are influencing all of that in really important ways. So I think it's important to design clinical research in the context of cancer neuroscience with that holistic view in mind. We don't think one strategy is going to be curative for difficult to treat tumors. I don't think that blocking neuron to glioma synapses in glioblastoma and DIPG will alone be sufficient but I do think it may be necessary for other therapies to work.Eric Topol (29:01):Yeah, I think that a perspective of in combination is extremely important. Now the overall, this a big fixation, if you will, about revving up immunotherapies various ways to do that. We'll talk about that in a moment, but without attention to the neurogenic side of this, that might be a problem. Now that gets me to the tumor type that you have put dedicated effort, which is this pediatric pontine tumor, which is horrendous, invading the brainstem and you've even done work with engineering T cells go after that. So you cover all the bases here. Can you tell us about where that stands? Because if you can prevail over that, perhaps that's one of the most challenging tumors of people there is.Diffuse Intrinsic Pontine GliomaMichelle Monje (29:54):Yeah, absolutely. So just a few words about this tumor, for those who don't know, diffuse intrinsic pontine glioma and other related tumors that happen in the thalamus and the spinal cord are the leading cause of brain tumor related death in kids. This is a universally fatal tumor type that tends to strike school age children and it's the worst thing I've ever seen in medicine. I mean, it really has been something that since I saw in medical school, I just have not been able to turn away from. And so studying it from many different perspectives, both the cell intrinsic vulnerabilities, the microenvironmental opportunities for therapy, and also the immunotherapeutic opportunities, it became clear to me that for a cancer that diffusely infiltrates the nervous system forms synapses with a circuit that it is invading and integrates into those circuits in the brainstem and spinal cord, that the only way to really effectively treat it would be a very precise and powerful targeted approach.(30:55):So immunotherapy was a very attractive set of approaches because in the best case, you have an engineered T cell or other immune cell that can go in and kind of like a special forces agent just find the T cells and disintegrate them from this synaptically integrated circuit that has formed. And so I began to search for cell surface targets on this particular type of cancer and found that one of the antigens for which many immunotherapy tools had already been made because it's prevalent in other kinds of cancer, was very highly expressed on diffuse midline gliomas, including diffuse intrinsic pontine glioma. And so this target, which is a sugar, actually it's a disialoganglioside called GD2, is extraordinarily highly and uniformly expressed on DIPG because the oncogene that drives DIPG and other related tumors, which is actually a mutation in genes encoding histone H3, which causes broad epigenetic dysregulation, strongly upregulates the synthesis genes for GD2.(32:05):And so it's a really ideal immunotherapeutic target on every cell, and it's at extraordinarily high levels. Again, speaking to the importance of collaboration, right when we made this discovery, one of the leaders in chimeric antigen receptor T cell therapy, CAR-T cell therapy named Crystal Mackall at Stanford and her offices is in my building, so I walked over and knocked on the door and said, do you want to work on this together? And so, we've been working together ever since and found that indeed CAR-T cells targeting GD2 cure our mice models, which is something I have never seen. I develop these models and have never seen anything that's effective, but it's always easier to help a mouse than to help a person and so we knew that the clinical translation would be challenging. We also knew that it would require intentionally causing inflammation in the brainstem that's already compromised neurocritical care.(33:07):I'm going to not use the word nightmare, but it's a set of challenges that we had to think about really carefully. We spent a lot of time and collaborated with our neurocritical care colleagues, our neurosurgical colleagues, and developed a protocol that had many, we anticipated this neurotoxicity of causing inflammation in the brain stem and we had many safety measures built in an anticipatory way, gave the therapy only in the intensive care unit and had many safeguards in place to treat anticipated hydrocephalus and other consequences of inducing inflammation in this particular region of the nervous system. Over the last four years, we began this trial at the beginning of the pandemic in June 2020 so that was its own unique set of challenges. We've seen some really incredibly exciting promising results we've presented. We've published some of our early experience, we're getting ready to present the larger experience.(34:14):And we've presented this at meetings. We've seen some kids go from wheelchair bound to walking in a matter of weeks. It's been just incredible and reduced to nearly nothing. Other kids have had less robust responses the therapy has really helped some kids, and it's failed others. And so we're working very hard right now to understand what factors affect this heterogeneity and response so that we can achieve durable and complete responses for every kid. I will tell you that my leading hypothesis right now is that it is the intersection of the immuno-oncology with the neuroscience that is modulating the response. Certainly, there are immune suppressive mechanisms, but there's also, I think, really important influences of neurotransmitters and neuropeptides on the immune response against central nervous system cancers in the central nervous system and so we're working hard to understand that crosstalk and develop strategies to optimize this promising therapy.(35:19):But it really has been one of the highlights of my professional life to see kids with DIPG and spinal cord diffuse midline gliomas get better even for a while, something I hoped at some point in my career to ever see and having seen it now so frequently in our trial patients, I'm really hopeful that this approach will be part of the answer. I'm hopeful for the future of immuno-oncology for solid tumors in general. I think when we understand the tumor microenvironment, we will be able to leverage these really powerful therapies in a better way.A Couple of Notable Neuroscientists!Eric Topol (35:58):Wow. Yeah, I mean, if anybody was to try to crack the case of one of the most challenging cancers ever seen, you would be that person. Now, speaking of collaboration, I didn't know this until I was getting ready to have the conversation with you, but your husband, Karl Deisseroth is like the optogenetics father. He is another exceptional rarefied leader in neuroscience. So, do you collaborate with him?Michelle Monje (36:35):We do collaborate, and in fact, so I met Karl when I was a medical student, and he was an intern in psychiatry so we go back a fair ways. We're both MD PhD students at Stanford, and we've been collaborating for many, many years in many different ways both in the clinic, I met him when I was a sub in neurology, and he was the psychiatry intern on neurology. We collaborated when he was a postdoc, and I was a graduate student on some neurobiological studies. We have four children. I have one stepson and four children that I can take full credit for and so we collaborated on five kids. For a while I really wanted, because he is such an amazing scientist, he's such a thought leader in neuroscience, as I started my own independent laboratory, I wanted to not be entirely in his shadow and so I did make it a point to do, I used optogenetics, but I took the course and bought the tools and did it all myself. I did the last questions at the dinner, but I really wanted to be kind of independent in the beginning. Now that my career and my laboratory is a bit more established, we are formally collaborating on some studies because he's a brilliant guy.Eric Topol (38:01):I think that you fit into that category too, and a bit more established is maybe the biggest understatement I've heard in a long time. The body of work you've done already at a young age is just beyond belief and you're on a tear to have big impact and many across the board. As you said, many things that you're learning about the brain with all of its challenges will apply to cancer, generally will apply to hopefully someday a treatment that's effective for Long Covid affects the brain and so many other things. So Michelle, I'm so grateful to have had this conversation. You are an inspirational force. You've covered a lot of ground in a short time and between you and your husband, I don't know that that's got to be the most dynamic duo of neuroscience that exists on the planet, in the human species, I guess. I just can't imagine what those kids of yours are going to do when they grow up.Michelle Monje (39:07):I'm biased, but they're pretty great kids.Eric Topol (39:10):Well, thank you for this and I think the folks that I get to listen to this will certainly get charged up. They'll realize the work that you're doing and the people you collaborate with and making cold calls to people. That's another story in itself that how you can get transdisciplinary efforts when you just approach somebody who's doing some good work. Another lesson just kind of hidden in our discussion. Thanks very much.Michelle Monje (39:40):Oh, thank you. It's wonderful to talk with you, Eric.*******************************************************Please share if your found this podcast informative Get full access to Ground Truths at erictopol.substack.com/subscribe

BUFFALO, NY- February 19, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on February 5, 2024, entitled, “Neurotrophic-tyrosine receptor kinase gene fusion in papillary thyroid cancer: A clinicogenomic biobank and record linkage study from Finland.” Selective tropomyosin receptor kinase (TRK) inhibitors are approved targeted therapies for patients with solid tumors harboring a neurotrophic tyrosine receptor kinase (NTRK) gene fusion. Country-specific estimates of NTRK gene fusion frequency, and knowledge on the characteristics of affected patients, are limited. In this new study, researchers Wei Zhang, Arndt A. Schmitz, Roosa E. Kallionpää, Merja Perälä, Niina Pitkänen, Mikko Tukiainen, Erika Alanne, Korinna Jöhrens, Renate Schulze-Rath, Bahman Farahmand, and Jihong Zong from Bayer HealthCare Pharmaceuticals Inc., University of Turku, Turku University Hospital, Technical University Dresden, and Western Finland Cancer Centre identified patients with histologically-confirmed papillary thyroid cancer (PTC) from Finland's Auria Biobank. “The study objectives were to determine the frequency of NTRK gene fusion in patients with PTC in Finland, and to describe co-occurring genetic alternations, clinical characteristics, disease progression, and treatment pathways in NTRK gene fusion positive patients.” TRK protein expression was determined by pan-TRK immunohistochemistry. Immuno-stained tumor samples were scored by a certified pathologist. Gene fusions and other co-occurring gene alterations were identified by next generation sequencing. Patient characteristics and vital status were determined from linked hospital electronic health records (EHRs). Patients were followed from 1 year before PTC diagnosis until death. 6/389 (1.5%) PTC patients had an NTRK gene fusion (all NTRK3); mean age 43.8 years (and none had comorbidities) at PTC diagnosis. Gene fusion partners were EML4 (n = 3), ETV6 (n = 2), and RBPMS (n = 1). Of 3/6 patients with complete EHRs, all received radioactive iodine ablation only and were alive at end of follow-up (median observation, 9.12 years). “In conclusion, NTRK gene fusion is infrequent in patients with PTC. Linkage of biobank samples to EHRs is feasible in describing the characteristics and outcomes of patients with PTC and potentially other cancer types.” DOI - https://doi.org/10.18632/oncotarget.28555 Correspondence to - Jihong Zong - jihong.zong@bayer.com Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28555 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, NTRK gene fusion, papillary thyroid cancer, clinicogenomic, epidemiology, biobank About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Experts from Indivumed Services answer questions from webinar where they describe the role of longitudinal plasma samples for cancer research.

The UK Biobank has been tracking the medical outcomes of people since 2006. Inside this giant freezing unit, a robot can access samples provided by half a million people in the UK. The samples include blood and saliva while computers have whole-body scans and medical updates from participants going back almost two decades. The Biobank says tens of thousands of scientists have already benefited from the data stored here, adding to knowledge that can be used to fight disease. This too will be released to researchers aiming to find effective treatments for so far, incurable diseases like dementia, Parkinson's, and soft tissue cancers. According to UK Biobank, the result comes after a £200 million (GBP) investment. Naomi Allen, Professor of Epidemiology at the University of Oxford and the Chief Scientist at the UK Biobank says the information being made available to medical professionals is unprecedented. “We're releasing the most ambitious project ever, which is the single largest tranche of whole genome sequencing data on half a million people. [...] So whole genome sequencing data consists of measuring all of the genetic variation across your entire genome, which has not been done before at this scale,” says Allen. Importantly, the Biobank will be able to offer new insights into how particular diseases can be more prevalent in certain populations, such as Black, Asian, and Hispanic people as well as White people. But the aim of UK Biobank is not just to treat disease and tackle it early but to prevent it too which would be a hugely progressive step for public health. Having information from the whole genome could help anticipate which drugs would work better on a person and which are likely to have severe side effects. According to UK Biobank, the genome bank could also accelerate understanding of illnesses that aren't properly understood such as Parkinson's, Alzheimer's, and autoimmune diseases. Allen believes the dataset can reveal how our genetics affect proteins, metabolites, and other physiological factors that could contribute to these illnesses. According to Allen, the dataset could also accelerate the application of new medical technologies such as gene editing. This article was provided by The Associated Press.

 Staying sane during theholidays: understanding our limitations, using a holy no, & being willing to disappoint people (& why this seems to be so difficult for women, if Kath would agree)... GUEST Dorothy Littell Greco ... writer & photographer who lives outside Boston ... The author of "Making Marriage," and most recently, “Marriage in the Middle: Embracing Midlife Surprises, Challenges & Joys. Pgh's Milk Bank … GUEST Denise O'Connor … Executive Dir Mid Atlantic Mothers' Milk Bank and co-director Human Milk Science Institute and Biobank. Instagram Addicted Your Teenager Because She's Worth $270 to Them ... GUEST Chris Martin ... author of “Terms of Service: The Real Cost of Social Media” … also a content marketing editor at Moody Publishers and a social media, marketing, & communications consultant. Antidote to the Christmas Blues (& EduNations Christmas concert ) ... GUESTRev Dr Dean Weaver ... Stated Clerk of the Evangelical Presbyterian Church ... cofounder and former president of EduNations.See omnystudio.com/listener for privacy information.

 Staying sane during theholidays: understanding our limitations, using a holy no, & being willing to disappoint people (& why this seems to be so difficult for women, if Kath would agree)... GUEST Dorothy Littell Greco ... writer & photographer who lives outside Boston ... The author of "Making Marriage," and most recently, “Marriage in the Middle: Embracing Midlife Surprises, Challenges & Joys. Pgh's Milk Bank … GUEST Denise O'Connor … Executive Dir Mid Atlantic Mothers' Milk Bank and co-director Human Milk Science Institute and Biobank. Instagram Addicted Your Teenager Because She's Worth $270 to Them ... GUEST Chris Martin ... author of “Terms of Service: The Real Cost of Social Media” … also a content marketing editor at Moody Publishers and a social media, marketing, & communications consultant. Antidote to the Christmas Blues (& EduNations Christmas concert ) ... GUESTRev Dr Dean Weaver ... Stated Clerk of the Evangelical Presbyterian Church ... cofounder and former president of EduNations.See omnystudio.com/listener for privacy information.

Die UK Biobank veröffentlicht die gesamten genetischen Daten ihrer 500'000 Studienteilnehmer. Zudem: Mit Ariane 6 und private Raketen will Europa den Zugang zum All zurückgewinnen. Und: Langschnabeligel und Co. - ausgestorben geglaubte und neue Arten entdeckt. (00:49) Quantensprung für die Gen-Forschung: Die UK Biobank veröffentlicht die gesamten genetischen Daten ihrer 500'000 Studienteilnehmer. Es ist der weltweit grösste Datensatz menschlicher Genome, der damit für Forschende aus aller Welt verfügbar wird. Das ist ein grosses Versprechen vor allem für die personalisierte Medizin: Künftig könnte es einfacher werden, Therapien auf das genetische Profil einzelner Patientinnen und Patienten abzustimmen. In der Schweiz bestehen ebenfalls Pläne, eine Biobank mit 100000 Freiwilligen aufzubauen. (00:42) Ariane 6 soll doch noch starten und Europa wieder die Tür zum All öffnen: Nach der Ausmusterung der Ariane-5-Raketen und Verspätung der Ariane 6 hat Europa zurzeit viel zu wenige Transportkapazitäten ins All. Doch nach einem geglückten wichtigen Bodentest soll die Neuentwicklung nun definitiv Mitte nächsten Sommer abheben. Zusätzlich sollen nach dem Vorbild der USA auch in Europa künftig privat entwickelte Raketen starten. (13:47) Meldungen: Workoholics sind suchtkrank. Stadtbienen haben grössere Gehirne als Landbienen. Stierkäfer zum Insekt 2024 gekürt. (19:37) Biodiversität mal positiv: Er sieht aus wie eine Kreuzung aus dem Vogel Kiwi und einem Maulwurf: der Langschnabeligel. Diese ausgestorben geglaubte Tierart hat eine Forschungsexpedition im noch weitgehend intakten Regenwald von Neuguinea entdeckt. Auch eine ganze Reihe neuer Arten wurden entdeckt.

Er du allerede “indsamlet”, og hvad bliver du i så fald brugt til? Dét får vi svar på, når vi går på opdagelse i en af landets mest kuriøse og makabre samlinger, der huser fostre, skeletter, celler og DNA, fra 1700-tallet og frem til i dag. For forskerne har altid gemt hele - eller mindre dele - af os danskere, i forsøget på at forstå mennesket, og ved at undersøge denne samling bliver vi klogere på udviklingen af lægevidenskaben og synet på kroppen gennem de seneste århundreder. Vi stiller herigennem særligt skarpt på de etiske dilemmaer, der er opstået gennem tiden, men også dem vi står overfor i dag, når vi skal indsamle mennesker og menneskedele i videnskabens navn. Medvirkende: Malthe Kouassi Bjerregaard, kurator på Medicisk Museion. Vært: Emma Elisabeth Holtet See omnystudio.com/listener for privacy information.

Amerikaanse onderzoekers waarschuwen na het bestuderen van de data van 50.000 mensen boven de 60 jaar voor een link tussen overmatig zitgedrag en een verhoogd risico op dementie.  De resultaten sluiten aan bij bevindingen in andere studies, al is meer onderzoek wel nodig om een causaal verband aan te kunnen tonen.  De gemiddelde Amerikaan brengt ongeveer 9,5 uur per dag zittend door. Achter een bureau, op de bank voor de televisie, of rijdend in een auto: het telt allemaal mee. Uit dit onderzoek zou blijken dat volwassenen boven de 60, een groep die waarschijnlijk hoger uitkomt dan die 9,5 uur, daardoor mogelijk een verhoogd risico loopt op dementie.   Ze baseren dit op een analyse van gegevens uit de U.K. Biobank. Specifiek op die van een groep van 50.000 mensen boven de 60, die aan het begin van de meting geen dementie hadden en die een week lang een bewegingsmeter droegen.   Vervolgens vergeleken ze deze metingen met data van zes jaar later van dezelfde groep, waarbij ze keken naar dementie diagnoses. Dat ging om 414 mensen. Aan de hand daarvan denken ze aan te kunnen tonen dat bij een gemiddelde zittijd van 10 uur of langer, het risico op dementie flink oploopt. En niet onbelangrijk: daarbij is de totale zittijd veel belangrijker dan de verdeling over de dag.    Zoals gezegd: meer onderzoek om dit te bevestigen is nodig. Ook om te kijken of het omgekeerde – minder zittijd en meer bewegen – het risico in deze groep juist verlaagt. Lees hier meer over het onderzoek: Large amounts of sedentary time linked with higher risk of dementia in older adults, study showsSee omnystudio.com/listener for privacy information.

Prof. Swapnil Rane is a Pathologist by training, and currently a professor in Tata Memorial Center, Mumbai, India. He is instrumental in bringing forward the AI and digital pathology research from India, especially the ongoing project of Indian Image BioBank.

Bioinformatics is a relatively new field of science that is very interdisciplinary in nature. Its practitioners use a mixture of biology, chemistry, physics, statistics, and computer science to develop methods and software aimed at helping integrate and understand biological and other data.  Our guest for this episode is Nikhil Ram Mohan, Staff Scientist at the Stanford University School of Medicine. He describes bioinformatics as the bridge to understanding biology. We learn about his international studies and path that brought him to this current role and field of study, and then dive into some of his recent work. Here he and his team analyze biobank samples using digital PCR (dPCR) and quantitative PCR (qPCR) and compare results from the two while correlating results with additional data available for each sample to determine if SARS-CoV-2 RNA detection and quantification in blood can serve to help predict potential for patient coinfection. Their work found that dPCR was able to detect SARS-CoV-2 in samples that were negative when evaluated by qPCR and that a series of biomarkers can help predict coinfection.   We also get to hear a bit of Nikhil's interesting personal story, which includes his undergraduate engineering studies in India and leaving his native country for the first time when he moved to the U.S. for graduate school.  We learn how he managed changes in culture, what he loves about teaching, and about him being a new father.  Visit the Absolute Gene-ius page to learn more about the guest, the hosts, and the Applied Biosystems QuantStudio Absolute Q Digital PCR System. 

Dr. Bartha Maria Knoppers is a world-renowned expert and pioneer in the field of health law and bioethics, with particular focus on genomics. Her groundbreaking work has fundamentally changed our understanding of the complex intersection between science law, technology and ethics. She currently serves as the Director of the Centre for Genomics and Policy at McGill University, collaborating with international organizations, governments and policymakers to help shape ethical guidelines that safeguard human rights while supporting the health and well-being of individuals and communities.Genetic exceptionalism [03:46]Use of genetic information in healthcare [05:50]Genome sequencing and predicting health outcomes [6:23]Parental consent for newborn screening [10:45]Privacy considerations for genomic sequencing for health research [12:39]Biobanks and the use of data for health research [14:45]Governance, transparency, and accountability in health research [18:40]Considerations for data sharing among academic and commercial researchers [20:41]P3G public population project in Genomics and Society [24:05]The Global Alliance for Genomics and Health (Canada) [26:58]Canadian Health Data Strategy [29:11]Canada Health Data Charter [33:10]Advice on promoting trust in digital health [35:07]Resources:Centre for Genomics and Policy (CGP)McGill Genome CentreThe Public Population Project in Genomics (P3G)The Global Alliance for Genomics and Health (GA4GH) meeting (September 2023)Digital Health under PHIPA: Selected OverviewIPC Strategic Priorities 2021-2025Trust in Digital Health(IPC resources)Info Matters is a podcast about people, privacy, and access to information hosted by Patricia Kosseim, Information and Privacy Commissioner of Ontario. We dive into conversations with people from all walks of life and hear stories about the access and privacy issues that matter most to them. If you enjoyed the podcast, leave us a rating or a review. Have an access to information or privacy topic you want to learn more about? Interested in being a guest on the show? Send us a tweet @IPCinfoprivacy or email us at podcast@ipc.on.ca.  The information, opinions, and recommendations presented in this podcast are for general information only. It should not be relied upon as a substitute for legal advice. Unless specifically stated otherwise, the IPC does not endorse, approve, recommend, or certify any information, product, process, service, or organization presented or mentioned in this podcast, and information from this podcast should not be used or reproduced in any way to imply such approval or endorsement. None of the information, opinions and recommendations presented in this podcast bind the IPC's Tribunal that may be called upon to independently investigate and decide upon an individual complaint or appeal based on the specific facts and unique circumstances of a given case.

Sweltering temperatures wreak havoc across Europe and North America, so what needs to be done to bring them down? We hear from the Cambridge scientist who wants to create the largest ever DNA and health research programme for children and young people. And, did aliens crash-land on Mars? Strange pictures resembling a crash site have been circulating but is there a more mundane explanation? Like this podcast? Please help us by supporting the Naked Scientists

In September 2022, two New Zealand patients became the first in the world to participate in a phase 1 clinical trial testing a new therapy for a rare neurogenetic condition called myotonic dystrophy. Claire Concannon learns about the trial, and how a new Neurogenetic Registry and Biobank covering 70 conditions is helping to connect New Zealand patients with international research.

How The Forever Reef Project aims to establish a global coral biobank, the family of cattle ranchers-turned-conservationists revegetating the Amazon, storing green energy in abandoned coal mines, & more! These are some of the stories I go over in this week's episode of The fairly lame. Podcast, your home of good environmental news!   Head over to Instagram for daily good news stories that I don't cover in the podcasts!   All fairly lame.'s links: https://linktr.ee/fairlylame   4ocean Green Sea Turtle Spotlight: Use Code “FAIRLYLAME” For 20% Off! https://www.4ocean.com/blogs/cause-of-the-month/cotm-green-sea-turtles?rfsn=6871293.82d94d8&utm_source=refersion&utm_medium=affiliate&utm_campaign=6871293.82d94d8   This Week's Topics (0:00) Rats Successfully Eradicated From Another Island! (2:30) Powernest, A Rooftop Unit Combining Solar With Wind Turbines! (4:09) Turning Abandoned Coal Mines Into Clean Energy Batteries! (5:57) Family Of Cattle Ranchers Sell Their Herd And Regenerate Their 40 Hectares Of The Amazon! (7:19) Yumi The Tree Planting Robot Speeding Up Revegetation Projects! (8:54) The Forever Reef Project's Coral Biobank! (10:08)   Rats Successfully Eradicated From Another Island! https://www.scientificamerican.com/article/rats-are-finally-gone-from-this-vulnerable-island/ https://www.islandconservation.org/press-release-marshall-islands-increases-climate-change-resilience-by-tackling-invasive-species-on-irooj-island/   Rooftop Unit Combining Solar With Wind Turbines! https://www.designboom.com/technology/powernest-wind-turbine-solar-panels-01-30-2023/ https://www.youtube.com/watch?v=1vJuKxAIMuA&t=344s   Turning Abandoned Coal Mines Into Clean Energy Batteries! https://www.bbc.com/future/article/20220511-can-gravity-batteries-solve-our-energy-storage-problems https://www.popularmechanics.com/science/energy/a42613216/scientists-turn-abandoned-mines-into-gravity-batteries/   Family Of Cattle Ranchers Sell Their Herd And Regenerate Their 40 Hectares Of The Amazon! https://www.euronews.com/green/2023/06/17/meet-the-cattle-breeders-turned-conservationists-protecting-colombias-amazon-wildlife https://wwf.panda.org/discover/knowledge_hub/where_we_work/amazon/amazon_threats/unsustainable_cattle_ranching/   YuMi The Tree Planting Robot Speeding Up Revegetation Projects! https://futurism.com/the-byte/amazon-reforestation-robot   The Forever Reef Project's Coral Biobank! https://www.foreverreef.org/#top

Sebastian Brunemeier, Building Puerto Rico, Puerto Rico Money, ImmuneAGE Locations, Switzerland Benefits, Distributed Biotech, ChatGPT, vitaDAO, DAOs, Non-profit, Accredited Investors, Mental Energy, Ageism, Hopelessness, Downhill After 18, Psychometrics, Healthspan Capital, Mouse Bottleneck, Business Opportunity, Mouse Models, Synthetic Models, Age-related Diseases, Human vs Mice, Cloning, Reverse Yamanaka Factors, Progeria Cells, IP, Investing, Contracting Out, Matthew "Oki" O'Connor, Cyclarity, Cholesterol, Brain Aging, Bone Marrow Transplant, ImmuneAge Special Sauce, Competitors, Biobank, Missing Team Members, Books, Longevity Biotech Fellowship, The post Immune System Rejuvenation, Startups, & Investing – Sebastian Brunemeier -Learning with Lowell 175 first appeared on Learning with Lowell.

 For the full show notes of this episode visit website https://treesmendus.comVerla's new book Optimize Your Heart Rate: BalanceYour Mind and Body With Green Space. Verla's previous book Take Back Your Outside Mindset: Live Longer, Stress Less, and Control Your Chronic IllnessDr. Tselios is an Assistant Professor of Medicine with the Division of Rheumatology at McMaster University since 2021. He completed his basic training and PhD in Greece and came to Canada in 2014 where he worked as a post-doc fellow with the University of Toronto Lupus Clinic. His main clinical and research interest is the field of autoimmunity and systemic lupus erythematosus, particularly the cardiovascular complications of the disease. He has published more than 70 peer-reviewed articles and book chapters. He is currently developing the McMaster Lupus Clinic and Lupus Ontario/Anne Matheson Lupus Biobank in Hamilton.Time Stamps in minutes of our conversation:2:00 I started looking after lupus patients in 2008 in Greece, and was offered an opportunity to do a PhD in lupus to become the medical director the lupus clinic ...and there, I fell in love with lupus patients and the process of the lupus disease. 4:21 My published research caught the attention of the Toronto Lupus Clinic run by  doctors Touma   and  Gladman who were collecting data on lupus patients since 1971. This clinic at the Toronto Western Hospital at the University Health Network is one of the largest lupus clinic in the world, was a great environment for me to gain expertise in lupus. I worked there since  2014 and it was a great experience. I stayed there for 6  years. 5:00 I stayed there for 6  years as a post doc. Then I was hired at McMaster University in the Division of Rheumatology at Hamilton Health Sciences. My main goal is to develop a new Lupus Clinic for south western Ontario and this Biobank, if we want to talk about it further is about collecting samples for further lupus research. 6:00 Heart involvement and lupus: In the past lupus has been so agressive that it leads to often leads to death. But most people do significantly better now. So our patients will survive but the arteries can stiffen as the years go by (atherosclerosis) and as we get older.8:00  Lupus patients are 50% more likely to have a heart attack than people without lupus. 8:22 I started investigating this in my research with the Toronto Lupus Clinic cohort. As you dig deeper into research sometimes you find things that you would never expect. 8:60 The heart conduction system is about the heart pumping blood to every part ofFor peer reviewed research on how your time spent in green space can change your mindset, balance your nervous system and your heart rate please go to my website https://treesmendus.com and check out my books Take Back Your Outside Mindset: Live Longer, Stress Less, and Control Your Chronic Illness and Optimize Your Heart Rate: Balance Your Mind and Body With Green Space

Biobanks that house data from electronic health records or collect samples directly from participants are precious resources for researchers looking to understand health and disease and translate these discoveries into recommendations and treatments for patients. In this episode, we talk to Nancy Cox, professor and director of the Vanderbilt Genetics Institute, about Vanderbilt's DNA biobank, BioVU. Nancy and her fellow researchers use computational genetics to study the de-identified patient DNA stored in the bank along with corresponding electronic health records in order to discover links between genes and disease. To dive further into this topic, please join Amgen scientists at the Human Data Era Q&A webinar discussion on November 16, 2022. Register for the event here.   Welcome to The Human Data Era, a special edition podcast series produced by The Scientist's Creative Services Team. This series is brought to you by Amgen, a pioneer in the science of using living cells to make biologic medicines. They helped invent the processes and tools that built the global biotech industry, and have since reached millions of patients suffering from serious illnesses around the world with their medicines.   By studying human genetics, scientists discovered mechanisms that, when defective, cause disease. While this type of data is powerful, additional information can provide more insight on the human condition. Researchers and clinicians can now go beyond genetics, combining proteomics, metabolomics, transcriptomics, and environmental factors into a broad category of human data. In this series, Ray Deshaies, senior vice president of Global Research at Amgen, explores the potential of human data and the important transition scientists and clinicians are making to incorporate this wealth of information into drug research and development. 

Diabetes Core Update is a monthly podcast that presents and discusses the latest clinically relevant articles from the American Diabetes Association's four science and medical journals – Diabetes, Diabetes Care, Clinical Diabetes, and Diabetes Spectrum. Each episode is approximately 20 minutes long and presents 5-6 recently published articles from ADA journals. Intended for practicing physicians and health care professionals, Diabetes Core Update discusses how the latest research and information published in journals of the American Diabetes Association are relevant to clinical practice and can be applied in a treatment setting. This issue will review: Management and Outcomes of Severe Hypoglycemia Treated by Emergency Medical Services in the U.S. Upper Midwest T2DM Diabetes Microvascular Disease Diagnosis and Treatment After High-Deductible Health Plan Enrollment Historic Residential Redlining and Present-day Diabetes Mortality and Years of Life Lost: The Persistence of Structural Racism Model for Integration of Monogenic Diabetes Diagnosis Into Routine Care: The Personalized Diabetes Medicine Program Once-Weekly Dulaglutide for the Treatment of Youths with Type 2 Diabetes Dietary Protein Sources, Mediating Biomarkers, and Incidence of Type 2 Diabetes: Findings From the Women's Health Initiative and the U.K. Biobank   For more information about each of ADA's science and medical journals, please visit www.diabetesjournals.org. Presented by: Neil Skolnik, M.D., Professor of Family and Community Medicine, Sidney Kimmel Medical College, Thomas Jefferson University; Associate Director, Family Medicine Residency Program, Abington Jefferson Health John J. Russell, M.D., Professor of Family and Community Medicine, Sidney Kimmel Medical College, Thomas Jefferson University; Director, Family Medicine Residency Program, Chair-Department of Family Medicine, Abington Jefferson Health

Rappin' With ReefBum is a LIVE talk show with host Keith Berkelhamer and guests from the reef keeping community. In this episode I chat with Dr. Dean Miller from the Living Coral Biobank. Dr. Miller is a marine biologist, film maker, photographer and the managing director and project coordinator of Great Barrier Reef Legacy, a non-profit organization based in Port Douglas Australia dedicated to conservation of coral reefs around the world with an array of innovative projects.

Why is hibernation something that bears and squirrels do, but humans don't? Even more interesting, what's going on inside a hibernating animal, on a physiological and genetic level, that allows them to survive the winter in a near-comatose state without freezing to death and without ingesting any food or water? And what can we learn about that process that might inform human medicine?Those are the big questions being investigated right now by a four-year-old startup in California called Fauna Bio. And Harry's guests today are two of Fauna Bio's three founding scientists: Ashley Zehnder and Linda Goodman. They explain how they got interested in hibernation as a possible model for how humans could protect themselves from disease, and how progress in comparative genomics over the last few years has made it possible to start to answer that question at the level of gene and protein interactions. The work is shedding light on a previously neglected area of animal behavior that could yield new insights for treating everything from neurodegenerative diseases to cancer.Please rate and review The Harry Glorikian Show on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:1. Open the Podcasts app on your iPhone, iPad, or Mac. 2. Navigate to The Harry Glorikian Show podcast. You can find it by searching for it or selecting it from your library. Just note that you'll have to go to the series page which shows all the episodes, not just the page for a single episode.3. Scroll down to find the subhead titled "Ratings & Reviews."4. Under one of the highlighted reviews, select "Write a Review."5. Next, select a star rating at the top — you have the option of choosing between one and five stars. 6. Using the text box at the top, write a title for your review. Then, in the lower text box, write your review. Your review can be up to 300 words long.7. Once you've finished, select "Send" or "Save" in the top-right corner. 8. If you've never left a podcast review before, enter a nickname. Your nickname will be displayed next to any reviews you leave from here on out. 9. After selecting a nickname, tap OK. Your review may not be immediately visible.That's it! Thanks so much.TranscriptHarry Glorikian: Hello. I'm Harry Glorikian, and this is The Harry Glorikian Show, where we explore how technology is changing everything we know about healthcare.It's April and spring is well underway, even though it's been a pretty cold one so far here in New England.It's the kind of weather that makes you want to pull the covers over your head in the morning and just sleep in. Or maybe just hibernate like a bear until summer is really here.But when you think about it, what is hibernation? Why is it something that bears and squirrels do, but humans don't?Even more interesting, what's going on inside a hibernating animal, physiologically, that allows them to survive all winter without freezing to death and without ingesting any food or water?And what can we learn about that process that might inform human medicine?Those are the big questions being investigated right now by a four-year-old startup in California called Fauna BioAnd my guests today are two of Fauna Bio's three founding scientists: Ashley Zehnder and Linda Goodman. I asked them to explain how they got interested in hibernation as a possible model for how humans could protect themselves from disease.…And how progress in comparative genomics over the last few years has made it possible to start to answer that question at the level of gene and protein interactions.We've always looked to the natural world, especially the world of plants, for insights into biochemistry that could inspire new drugs. But what's exciting to me about Fauna Bio is that they're shining a light on a previously neglected area of animal behavior that could yield new insights for treating everything from neurodegenerative diseases to cancer.So, here's my conversation with Ashley Zehnder and Linda Goodman.Harry Glorikian: Ashley. Linda, welcome to the show.Ashley Zehnder: Thanks, Harry, we're excited to be here today. It's going to be fun.Linda Goodman: Yeah, thanks for having us.Harry Glorikian: Yeah, I mean, well, you guys are someplace sunny and warm, and I'm actually I shouldn't say that it's actually sunny right now on the East Coast. So I'm not I'm not.Linda Goodman: Don't jinx yourself.Harry Glorikian: But the temperature is going to drop. Like to I think they said 18. So everything will freeze tonight for sure. So it'll, you know, it's one of those days, but. I want to jump right into this because we've got a lot of ground to cover. Like there's so many questions that I have after sort of looking into the company and sort of digging in and, you know, but even before we jump into what you're working on. Right, I really want to talk about hibernation. Maybe because I'm jealous and I'd like to be able to hibernate. I have sleep apnea. So sleep is a problem. But humans don't hibernate. But there's a ton of other mammalian species that that do. And sometimes I do feel, though, that my teenager hibernates, but that's a different issue. So, but, what what is interesting to you about hibernation from a physiological point of view. What what goes on with metabolism or gene expression during hibernation, that's that's not found in humans, but that could be relevant to human health?Ashley Zehnder: Yeah, I think this is a great question, Harry, because I think both Linda and I came to fauna from different backgrounds. I came from veterinary science, Linda from comparative genomics. We can go into our details later, but neither of us really appreciated the amazing physiology of these species. There are some of the most extreme mammals on the planet, and there are hibernating bears and literally every group of mammals. Right. This is something Linda specializes in. But there are primates in Madagascar that hibernate very similar to the 39 ground squirrels that we tend to work with. So it's this really deeply conserved trait in mammals, including primates. And, you know, it kind of highlights for us what our genes can do when they're adapted for extreme environments. And so that's kind of the lens that we take when we look at hibernation. It's how do these species protect their own tissues from being nearly frozen for six, seven months out of the year, having to protect their brains, their hearts, all their vital organs? They're not eating, they're not drinking. They're not moving for these really deep bodied hibernaters. When you think of 100 kilogram animal that's not eating for seven months, how do they survive that? Right. And it has to do with metabolic rates that change 200- to 300-fold over the course of a couple of hours. It has to do with oxygenation changes and protection from oxidative stress and ischemia reperfusion. And so if you look at a tissue by tissue level, you can start to see how these animals are finally adapted to protecting themselves from from damage. And then we can start to say, well, this is similar damage to what we see in human diseases. And that's why this is such an interesting system, because it's so dynamic and because it happens across so many groups of mammals, it really lends itself to this comparative genomics approach that we take to drug discovery.Harry Glorikian: Yeah. Because I was wondering sort of like what ways of healing from different sort of traumas and conditions do hibernating animals have that that humans don't, that we sort of maybe wish we did? It's sort of like, you know, almost Marvel or one of those things where you like go to sleep, you wake up, you've totally healed again, which kind of be kind of be cool. Yeah. So, you know. But when did scientists first begin to think about whether having a better understanding of hibernation might help us solve? Some of these riddles that we have in human health. I mean, it surely it can't be like a new concept. It has to go further back. I mean, what has changed recently to make it more actionable? I mean, is it, you know, omics, costs coming down that are making it easier, computational capabilities that are, you know, making all these come together? I mean, those. What do you guys. What's. What's the answer? You guys know the answer better than I do.Ashley Zehnder: I'll comment on a little bit on the physiology, and I will let Linda talk about the data revolution, because that's that's really what she knows very intimately. So from a physiology standpoint, these are species and not just hibernaters, but a lot of other species that we've been studying since the early 1900s, 1950s. I mean, these are some of our earliest biological experiments and our earliest understandings of biology. We're not necessarily done by studying humans. A lot of that was done by studying natural disease models, right? How did we figure out that genes cause cancer? So it's a little bit of a tangent, but bear with me, it was not by studying human cancer, it was by studying Rous Sarcoma Virus and how that virus picked up bird genes and then turn them on. Right and other in other individuals. So but then kind of this almost the same year in 1976 that we figured out that genes cause cancer by studying chickens. 1974 we figured out how to genetically modified mice. And we sort of figured out that like, okay, maybe we don't need to study natural biology anymore. And so I feel like we sort of lost a lot of those skills and figured out we had humans and we had model organisms and we were done. And I think now we're kind of in this renaissance where people are realizing that actually there's still a lot of natural biology that we can learn from. But it's being powered now by this data revolution and the decrease in cost and sequencing and availability of omics data like RNA. Seq and then I will pitch that over to Linda because that's really what she knows best.Linda Goodman: Yeah, yes, absolutely. You know, Ashley's right. And I think just to add on to that, that there was this issue in which there were a lot of field biologists out there working with these really fascinating hibernating animals. They knew a lot about what these animals could do, the extreme environments they were exposed to, that they could overcome, they could protect all of their tissues. And there was so there was a group of field biologists who knew all that information. And then on the other side, you have all of these geneticists who are studying the genomes of probably humans and mouse and rat. And they weren't really talking to each other for a long time. And I've been in the genomics field for at least a decade, and not until very recently did I even hear about all these amazing adaptations that these hibernating mammals have. So I think some of it was just a big communication gap. And now that the genomics field is starting to become a little more aware that all these exciting adaptations are out there that we can learn from, I think that's going to be huge. And yes, of course, it certainly does not hurt that there's been a dramatic drop in sequencing costs. We can now sequence a reference genome for around $10,000. That was unheard of years ago. And so a lot of these species that people would previously consider untouchables because they were not model organisms with a pristine reference genome, we can now start to approach these and thoroughly study their biology and genomics in a way that was not possible several years ago.Harry Glorikian: Yeah. I was thinking I was, you know, I was laughing when you said $10,000, because I remember when we did the genome at Applied Biosystems and it was not $10,000.Ashley Zehnder: Yeah.Harry Glorikian: Yeah. And it took I remember Celera, we had an entire floor of sequencers working 24/7 I mean, it was an amazing sight. And now we can do all that, you know, on a.Ashley Zehnder: Benchtop. Benchtop. Exactly. On a benchtop.Harry Glorikian: So. But, you know, it's interesting, like in a way, studying animals to learn more about disease mechanisms seems like a no brainer. I mean, we share a, what, about 99% of our DNA with chimpanzees. And for those listening. Yes, we do. You know, I'm sure there's people out there that, like, bristle when I say that. But what is it, 97.5% of our DNA with rats and mice. That's why we use all these things for sort of safety and effectiveness of drugs meant for humans. But. Still, I'm not used to drug hunters starting out by looking at animals, you know? Why do you think it's taken the drug industry, although I'm I say that very loosely, [so long] to wake up to that idea?Ashley Zehnder: Yeah. I think it's I think it's again, this almost reversal of the paradigm that exists today, which is let's take a human disease that we want to make a new drug for. Let's take a mouse and let's try to genetically manipulate that mouse to mimic as closely as possible what we see in the human disease. And those are always imperfect. I mean, I did a cancer biology PhD at Stanford, and there's that trope of like, Oh, if I had a dollar for every time you occurred mouse in a human right, it would need to work anymore. That's replicated across many fields, right? They're not good models. And so we're saying like obviously that doesn't really work for discovery. It's fine for preclinical and safety and you have to use those models. But for pure discovery, that's not where you want to be, right? Instead, you want to take the approach of saying, where has nature created a path for you? Where is it already solved this problem? And I think there are companies like Varian Bio who are doing this in human populations. We're saying, let's look at humans that have unique physiologies and a unique disease adaptations. And of course then you have to find those niche pockets of human populations.Ashley Zehnder: So that's not a not a simple problem either. But the approach is very analogous. What we're saying is we can use that rare disease discovery approach and just expand that scope of discovery. Look at highly conserved genes, look at how other species are using them to reverse how phosphorylation in the brain to repair their hearts after damage, to reverse insulin dependence. To heal, we'll heal their tissues or regenerate stem cells. Let's just see how nature did it right and just mimic that instead of trying to fix something that we artificially created. So it's literally reversing that paradigm of how we think about animals and drug discovery. But you have to know how to do that. You have to know which models are correct. You have to know how to analyze 415 genomes together in an alignment which is really complicated. Linda knows how to do that, so you have to know how to do it correctly, although you could screw it up very badly. So there's a lot of expertise that goes into these analyses and also again, the data availability, which wasn't there nearly a decade ago. So.Harry Glorikian: So I asked this question out of pure naivete, because I'm not sure that I could sort of draw a straight line. But, you know, which drugs were have been discovered through research on genetic mechanisms of disease in animals. Is there, are there?Ashley Zehnder: You know, I think directly it's a new field. Right. So I think, Linda, you and I have looked at some examples of looking at drugs for narcolepsy, looking at dog genetics and studies, looking at muscle disorders in certain species of cattle that have naturally beefed up muscles and translating those into therapies. I mean, there are examples of looking at animals for things like genotype, right, came from Gila monster venom, although that's not strictly a genetic program. Right? So I think this idea of looking at natural animal models is a source of innovation. It's just that, again, the data wasn't really available until fairly recently, but we know the strategy works by what's been done on things like PCSK9 inhibitors in humans, right? It's a very similar approach to that. It's just expanding that scope of discovery.Harry Glorikian: So because you guys raised money and you guys are moving this forward, sort of and I don't want you to tell me anything that's confidential, but. So what was the pitch when you when you put that in front of everybody?Ashley Zehnder: It was really that, look, drug discovery right now is really been hampered by a lack of innovation. And we're really stuck in looking at these very kind of currently limited data sources, which is humans and again, these handful of really imperfect animal models. But we can take what we've learned from working with human genomics and really greatly expand the opportunities for a number of diseases that still don't have good therapies. Right. We've had the human genome for really close to 20 years now. We spent a lot of money sequencing it. And still, if you go back and look at the FDA approvals in the last two years, which I did by hand a while ago, or more than three quarters of those are not new targets. They're new drugs for a new indication or new drugs, same drugs before a new indication or they're kind of meta pathway drugs or they're drugs for which we still don't know the mechanism. It's some small molecule. It's been around since fifties. And so like where is the innovation in the top ten diseases of people still have it changed? So like where I pulled these two headlines right not too long ago, one from 2003, which is like the era of the genomics revolution. Right? And then one from 2019, which was the genomics revolution question mark. Right. Like we're still sort of waiting for it. And so what is that missing piece of data that's really going to allow us to really leverage the power that's in the human genome? And to do that, we have to put our own genes in an evolutionary context to understand what's important. That's been that third dimension of genomics that's been missing. So it's really not necessarily about any particular species that we work on, all of which are amazing. It's really about using that data to shine a better light on what's important in our own genome. And so that's a lot of the pitches, like how are we going to use our own genome better and find better treatments?Harry Glorikian: Yep. Understood. So. You have a third founder, Katie Grabek. Right. So. Tell me about yourselves. I mean, did the three of you get interested in comparative genomics and hibernation? How did you come together? How did you decide like, oh, hey, let's do a startup and get this thing going in this area? So tell tell me the origin story.Ashley Zehnder: Linda, do you want to kick off?Linda Goodman: Sure. I think it all really started, Ashley and I initially started batting a few ideas around. We both had this understanding that that drug discovery today did not look outside of human mouse rat very much. And we both understood there was this wealth of animal data that's just waiting to be used and no one was doing it and we couldn't really figure out why. And we were having trouble figuring out exactly which animal we wanted to study and which diseases we wanted to study. And it just so happened that we lucked out. There was another woman in our lab at Stanford, Grabek, who had the perfect study system for what we were thinking about. She had these amazing hibernates our animals that have exquisite abilities in terms of disease, resistance and repair. And once she started talking about all the amazing phenotypes these animals have, we thought, wow, that would make a great study system to make the next human therapeutic. Yeah. And I think it's interesting that both Katie and Linda have human genetics PhDs. Right. So I think both of them and Linda can expound on this. But from Katie perspective. Right, she she went in to do a human genetics Ph.D. trying to understand how genes can be used to improve human health and shouldn't be rotating the lab of somebody who studied the 39 ground squirrel and said this physiology is way more extreme than anything we see in humans, but they're doing it using the same genes.Linda Goodman: What are those genes doing in these animals that we can adapt for human therapeutics? And so she brought that work with her to Stanford and was really one of the preeminent researchers studying the genetics and genomics of these species. My background is I'm of Marion, so my clinical training is in exotic species. So as a clinician, I treated birds, mammals, reptiles and saw that they all presented with different kinds of diseases or in some cases didn't present with diseases like cancer that were super interesting. And then coming to a place like Stanford to do a PhD, it was working with a bunch of human researchers, human focused researchers. They're all generally human researchers, but you know what I mean? It's a little bit tricky with the nomenclature. Generally, I have my doubts about, you know, maybe there's some chimpanzees doing research somewhere, people studying human diseases, right from a human lens who are completely ignorant of the fact that animals often also had these disease traits or in some cases were resistant to them. So there was this huge disconnect there of of biologists and veterinarians and physiologists who understood all these traits across different species and the people who knew the molecular mechanisms, even though a lot of those are shared.Linda Goodman: And so one of the things that I found really interesting just from a cancer perspective was that a lot of our major oncogenes are highly conserved because these are core biological genes that if you screw them up, will give you cancer. But there's an evolutionary pressure to maintain these genes. And so there's a reason why they're conservative, because they're really important biologically, and that's true across many other diseases as well. So from that perspective, I was really interested in this intersection of human and animal health. I always wanted to do more genomics myself and just never had had the training. Linda had always been interested in veterinary science, and so we kind of immediately started collaborating and saying, Look, look, there's a huge opportunity in this, again, third space, third dimension of genomics that people are not looking at. What do we do trying to start a comparative genomics company? I'm using air quotes here for the podcast listeners is a little bit broad. Where do you start? And I think Katie really gave us that start in saying, here's a model. We have a biobank of samples that are proprietary to fauna. We have an expert in this field. We have a model that's good for so many different diseases. Let's prove that the process works here and then we can expand into multiple disease areas.Harry Glorikian: You know, you got to love, people I think, underestimate that magic that happens when the right people get together and the spark happens, right? I mean, I'll take that. Any day. I mean, I love coming up with a plan and then, you know, working to the plan. But when it happens, when the right people in the room and they're all get excited, those are those are the most incredible start ups, in my opinion. Yeah. So you're starting off with targets in heart disease, stroke, Alzheimer's, diabetes, very different areas, right? Cardiovascular, neurodegenerative and metabolic. So. Why start with those areas in particular?Linda Goodman: So I think for us it was really again showing showing what we can translate from this model. So some of the phenotypes that we see, the traits that we see in the ground squirrel, which is predominantly one of the species we use for our work, is that they're exquisitely resistant to ischemia, reperfusion injury. So the kind of injury that gets, if you have a heart attack and you go and get the heart attack on block, you get this rush of warm, oxygenated blood back into your heart that can actually be damaging. And that's a lot of what causes damage after a heart attack, what these animals happen, they do this 25 times over the course of a 6 to 7 month hibernation cycle. And if you look at their hearts in the peak of one of these periods, there is an upregulation of collagen, which is cause of fibrosis. There's an upregulation, there's histologically, there's a little bit of damage. It's less than you would I would have, but there's a little bit there. But if you get to the end of that whole cycle and look at their hearts, they look normal and they do it again next year. Right. So you and I could not survive 25 of these attacks over six or seven month period, right? Obviously not. So let's pick the strongest phenotypes we have in these animals and let's show that we can use information from that and come up with genes and compounds that are protective in our more standard models of these diseases.Linda Goodman: And that's what we did really with the first round of data that we had is we generated four genetic targets and two compounds that came out of the heart data that we had from hibernating and that we tested them in human cardiomyocytes in a dish and said if we take oxygen and glucose away from these cells, they get really unhappy and die and we could double survival of human heart cells in a dish. And then we said, okay, great, let's actually move this into animals. And so we used AAV or some of these viral vectors to then knock down genes in vivo in hearts of rats. So we literally tied off a coronary artery and then let the blood come back in and saw that we could almost fully protect these hearts from damage by knocking down genes that we found in the hibernating data. So it was really closing that loop and saying, where are the strongest traits? Can we show that this works? And then it was really figuring out where are the really large areas of unmet need. And so in terms of metabolism, we end up connecting with Novo Nordisk, which is a publicly disclosed partnership. They are very focused on obesity. We have a model that increases this metabolism, 235 fold over an hour. Name another model that can do that, right?Harry Glorikian: I need that. I need that. I need like, because...Ashley Zehnder: We all need that!Harry Glorikian: I could get rid of a few pounds right around here.Linda Goodman: Exactly. So then it's really just figuring out where are the unmet needs, who is really interested in these areas we're looking at and do we have unique data that speaks to those models? And that's really we just try to be guided by the biology and saying, where do we have unique data sets that can answer high unmet needs?Harry Glorikian: Okay. Well, all I mean, all sounds super exciting if we can make the translation, you know, in the right way and find those targets. But. You guys have built up a significant biobank, right? I understand you have a huge database of genomic readout from various hibernating animals. Can you tell us a little more about the extent of that biobank? How did you collect the data and how unique is that database in the industry?Ashley Zehnder: Yeah. Linda, do you want to talk a little bit about the data sources that we're currently using at Fauna?Linda Goodman: Yeah. So maybe, you might be the best person to talk about the Biobank and then I can talk about all the other data sources layering on top of that.Ashley Zehnder: Yeah, I'll talk a little about the BiobanK. So we have yeah, we have a number of different data sources. The Biobank is one of them and probably one of the main ones that we use. So Katie, during her PhD, built a really unique biobank of very precisely time tissue samples from 39 ground squirrels across the whole hibernation cycle. And the reason why that timing is so important is because the cycle is so dynamic. If you don't have really precise sample timing, you end up with a big kind of smush of data that you can't tease apart by having really precisely timed data points, you can separate these genes into clusters and know exactly kind of where you are in time. And that timing relates to the physiological injuries that we study. So we know what time points their hearts are protected because those physiological studies have been done. We've looked at those time points very specifically. So we have that biobank of samples that we in licensed as founding IP at Fauna CANI literally drove it across the country in a U-Haul because we didn't trust anybody to move it. So that's that's now in our freezers and Emeryville with a cadre of backup batteries to protect it.Ashley Zehnder: So that's the founding data that we have. And that's been really crucial because I look at other companies trying to use data for drug discovery, particularly in the early stage. A lot of it is kind of publicly available data or cell lines or kind of shared data sources. And part of what is unique about font, as we literally have truly novel data sources that we're starting with that are wholly owned that we control and we know the quality of those. So that's really the Biobank that we have is and it's 22 different tissues. I mean, it's brain, it's kidney, it's lung, it's hard. It's liver or skeletal muscle. Right? Pretty much every kind of tissue you would want in that founding biobank. But then on top of that, I think what we've done with the other data is super important. Yeah. And so we layer on top of that all sorts of publicly available data and also data we've been able to source, such as human data from the UK Biobank. But I really want to hit on the point of, of why the model species hibernate or data is so different. All of the other data that most people work with is trying to compare animals that are healthy to animals that are diseased, or people that are healthy to people who are have disease. What's really unique about the model species that we're working with is we're trying to figure out why they have these superpowers in terms of disease, resistance and repair.Ashley Zehnder: So it's kind of the other end of the spectrum that we're making this comparison between a normal, normal hibernate or during, say, the summer months and then a hibernate or that has gene expression patterns that mean that it's resistant to many diseases and it can repair tissues when it gets damaged. So it's actually quite different from the normal types of comparisons that others would make. But yes, and then we integrate publicly available data from sources like Open Targets Reactance. And one of the other data sets that we work with that's that's valuable is that we go back through literature that is relevant to the disease, indications that we're going after. And we have a team of curators that mines these papers that where the biology is relevant and we integrate those transcriptomic studies generally into our database. And that that really helps with our comparisons. And I can kind of give you an example of the way that we would do this type of cross-species analysis compared to what other what others in the industry might do if they were just looking at humans or say, just looking at mouse and rat is that, you know, if you're if you're just looking at at a human study and you're trying to say, look, for what genes do we think are involved in heart failure? You would look at, say, transcriptomic, differences between healthy human hearts and failing human hearts.Ashley Zehnder: And then you would have some type of gene list where you'd see the genes that have differential regulation between those two groups. And it fa not we we look at that type of data and then we also look at hibernate or data and then we can compare that. And that's really where the magic happens because we can look at hibernate hours when their hearts are protected during the winter months. So we have an example of these are genes that are involved in protection and then compare that to the summer months where they're not protected. And then we can integrate both of those to analyses so we can say what's really different about a human heart when it is failing to a hibernating heart when it is protected. And we do very fancy types of network analyses and then we layer on all of these data from external sources and the really exciting moments where we see these networks light up with the exact regulation patterns we are expecting that is relevant to our biology. Those are really fun. And I would say the other data source, Linda, that would be good to touch on is the genomic data, right? I think the comparative genomics data. So maybe give a little context on that. I think that really broadens the the views point of what we work with.Linda Goodman: Yeah, absolutely. So that's another data source that we work with. We have a collaboration with the Broad Institute that is one of the leaders of the Zoonomia Project that has in the neighborhood of 250 mammals in a in a big alignment. So we can do comparative genomics across all of these animals. And what we like to look for are comparing the genomes of animals that have a specific phenotype to others that don't. So for example, what is different in the genomes of hibernaters compared to the mammals that cannot hibernate? And we typically do this with how fast or slow evolving genes are, right? So if a gene doesn't accumulate very many mutations in hibernate hours, then it's probably pretty important for hibernation because there's a lot of purifying selection on that versus say, in other mammals that are not hibernaters, like like a human or a rat. It got a lot of mutations in it because it didn't matter as much for those animals. So that's another way of pinpointing the genes that are really important to hibernation. And we know, of course, that some of those might relate to the overall hibernation trait, but many of them are going to be disease relevant because they've had to evolve these genes in a way to protect their hearts and their other organs from these extreme environments they're in during hibernation.Harry Glorikian: So that, if I'm not mistaken, so did the Zoonomia Consortium, there was a big white paper about comparative genomics published in Nature.Ashley Zehnder: Nature last year? Yep. Two years ago. Yeah. A little bit.Harry Glorikian: Yes. Time seems to blur under COVID.Ashley Zehnder: Yeah.Harry Glorikian: How long have I been in this room? Wait. No.Harry Glorikian: But. Can you guys I mean, because doing comparative genomics is not, you know. It's not new necessarily, but can you guys summarize sort of the. Arguments or the principles of that paper, you know, quickly. And then, you know, my next question is going to be like, do you feel that Fauna Bio is part of a larger movement in science and drug discovery that sort of gaining momentum? So I'll, I'll I'll let you guys riff on that launch.Ashley Zehnder: Linda, you're you're the best one to do a perspective on that paper for sure.Linda Goodman: Sure. Yeah. You know, I think this is really born out of the concept that in order to identify the most important genes in the human genome, we need to be looking at other animals and more precisely, other mammals to see their pattern of evolution. Because if you see a gene that looks nearly identical across all other mammals, that means that it's really important. It means that it has been evolving for somewhere in the neighborhood of 100 million years, not accumulating mutations, which really translates to if you got damaging mutations in that gene, you were a dead mammal. Those have been selected out. And that's really how you can tell these are the key genes that are important to to your physiology, the difference between life and death. And you can't understand those things as well by just looking within humans and human populations. We're all too similar to each other. But it's really when you get to these long time scales that the statistics work out where you can see, okay, this has been this mutation has not happened in 100 million years. We don't see it in anybody's genome. So that is obviously very important. And that's just this other way of looking at our own human genome that helps highlight the genes that are going to be important to diseases. And I think, you know, another side to this paper related to conservation and the fact that a lot of these animals with really exciting genomes, the ones that are exciting to people like us, are those that have these really long branch lengths where they're they're kind of an ancient lineage. And that's really where the gold is, because that helps us even more understand how quickly or slowly some of these genes are evolving, and it related to trying to conserve some of these species as well.[musical interlude]Harry Glorikian: Let's pause the conversation for a minute to talk about one small but important thing you can do, to help keep the podcast going. And that's leave a rating and a review for the show on Apple Podcasts.All you have to do is open the Apple Podcasts app on your smartphone, search for The Harry Glorikian Show, and scroll down to the Ratings & Reviews section. Tap the stars to rate the show, and then tap the link that says Write a Review to leave your comments. It'll only take a minute, but you'll be doing a lot to help other listeners discover the show.And one more thing. If you like the interviews we do here on the show I know you'll like my new book, The Future You: How Artificial Intelligence Can Help You Get Healthier, Stress Less, and Live Longer.It's a friendly and accessible tour of all the ways today's information technologies are helping us diagnose diseases faster, treat them more precisely, and create personalized diet and exercise programs to prevent them in the first place.The book is now available in print and ebook formats. Just go to Amazon or Barnes & Noble and search for The Future You by Harry Glorikian.And now, back to the show.[musical interlude]Harry Glorikian: I should say congratulations because you guys did raise a $9 million seed round last fall from a group of venture funds, some in life sciences, some more general. Right. What does that funding do? What is it? What does that unlock next?Ashley Zehnder: You. I will answer that question. I do want to jump back to your other question that was kind of is this part of a larger movement and comparative genomics? Right. I think that's an important question. I think you sort of hit the nail on the head there. We were invited to a symposium in August of 2019 called Perspective and Comparative Genomics that was held at NHGRI in Bethesda. And I think there's a recognition and actually some of our grant funding is also through NHGRI. And I think there's a recognition from the folks who sequenced the human genome, that they don't have all those answers. And so it's an interesting time where we realize that there is this kind of other data out there that can help us really understand that better. And it does feel a little bit like a rising tide. And so that's that's something that I think is important to recognize. But in terms of the seed round, really, that was meant to expand the platform and the pipeline that we built with our initial funding back from Laura Deming and Age One and True Ventures, who led around for us in early 2019. It's really saying like that initial $3 million or so is really to say like, does this work or is this crazy, right? Can we it's just a crazy idea.Ashley Zehnder: And that's what we really started to generate those first few animal studies that said, yes, actually we can find genes and compounds from this data that meaningfully affect not only human cells, but animal models of human disease. And now we're really expanding into new disease areas. We're looking at areas like fibrosis. We're looking at areas like pulmonary disease. We've got some really interesting data coming out of animal models of pulmonary hypertension with a compound that we found on our platform. We've got the collaboration with Novo Nordisk, which of the five genes that they tested in animals? We have one that has a significant obesity phenotype. So I mean, 20% hit rate on a novel target discovery in vivo is not bad, right? So we've gotten to the point now where repeatedly over multiple disease areas, we've seen that between 20 and 30% of our either compounds or genes are hits, which shows us that this is not only kind of a we got lucky in cardiac disease, but actually this is a process for enriching for important drug targets. And now it's a matter of really expanding the pipeline. We brought on a really experienced head of Therapeutics Discovery, Brian Burke, who spent 20 years at NIBR running very early discovery programs and then seeing programs go into the clinic.Ashley Zehnder: He worked on drugs like Entresto and then worked on a couple of startups after that. So he's kind of gotten both big pharma and startup experience, and his job at Fauna is to really look at the menu of things that we're presenting him from an early research and discovery phase and picking the winners and really figuring out how to take them forward and also killing the programs that are less exciting to him for a number of technical or practical reasons. So that's been really, really helpful to have someone come in truly from the outside and take a look at the science at Fauna and say this is as good or better as anything that I've worked on before. I'm really excited to work on this, and that's been kind of a nice external perspective on on the science and the pipeline at Fauna. So that's really what the $9 million is for. It's really expanding a lot of the computational expertise and and progress and Linda can talk a little bit about that, but also just expanding into new disease areas as well.Harry Glorikian: Understood. So, you know, on this show, like, I talk a lot about, you know, technology, data, and how it's all affecting health care, which this all fits into. But one of the things we talk about a lot is how crappy, terrible, I should use, you know, terrible, right, electronic health records are in the lack of interoperability between them. And Ashley, you actually wrote a paper.Ashley Zehnder: I did, yeah, veterinary medical records are just as bad, actually, veterinary medical records are probably a little bit worse, if it's possible.Harry Glorikian: And to be quite honest, I'm sorry, I just hadn't thought about Fifi or Rover and their...Ashley Zehnder: Their medical records.Harry Glorikian: EHR. Is like is the problem bigger, even, when it comes to functional genomics? I'm trying to think of like obtaining and storing and analyzing 'omics of different species. I mean, who's working on this? Is that part of the Zoonomia consortium? Right. I'm just trying to think it through, like, how do you get all this information and then look at it across all these different species. And at some point, you know, look looking at it against humans also.Ashley Zehnder: Yeah. I'll let Linda talk about the genomics side. I'll comment on sort of some of the validation, some of the externally curated data that Linda talked about. I think this is actually becoming a really important data set. It was a little bit of a slow burn to figure out how to get it and to curate it. But there are a lot of studies now coming out and not just your traditional model organisms, but naked mole rats and long lived rock fishes and primate studies and bats and all kinds of people looking at genomics and RNA seek metabolomics and proteomics across these species that have interesting phenotypes. The problem is, every one of those researchers really heads down on their own species of interest, right? Nobody's saying, oh, well, actually, we're seeing the same genetic signature in these bats that we're seeing in the naked mole rats that we're seeing in some of these long lived fish. Right. But that data is not in a very friendly format. So we were like originally we were like, okay, we're going to write some scripts, we're going to try to pull some of the stuff out of supplemental tables. It's going to be awesome. No, no, no. We have very highly trained curators who work on this data and bring it in. And we have a very standard pipeline and a process and a way to normalize the data across different studies and standard ontologies and ways to clean up this data in a way that it can be integrated with the genomics coming out of the platform. And that is a tedious and painful and ongoing effort to bring in all this data.Ashley Zehnder: Now, we have data from well over 330 individual studies, over 30 species. I think Linda, you told me it was like more than 800,000 gene entries at this point that's curated and that's kind of growing month over month. So now that's becoming part of our defensible moat, is that we've taken the last two or three years, again, slow burn, pulling all this data together in a way that it can be reused. And now we can turn a paper around and put it on a platform in a week or two. So we're kind of always scanning for these studies. But yeah, it's, it's, it's out there, but it's not always in a usable format without a lot of pain and effort. And so we've kind of put that pain and effort into getting that data in a place that we can use it. And then, of course, the comparative genomics is like a whole 'nother level of complexity.Linda Goodman: Yeah, so I can talk a little bit about how we do that within the comparative genomics community and how we've done that for Zoonomia. Because I referenced before that we like to do these sorts of studies to examine the genomes of hibernate ers and non hibernate and figure out what's different. And you'd think it would be a trivial question who is a hybrid nature amongst mammals? But it's actually not. And so along with our collaborators Alison Hindle and Cornelia Santer, as part of the Genome Project, Fauna tried to go through and categorize every every genome that was in Zoonomia. So we're talking about around 250 mammals for is it a hibernater, or is it not? And you'd be surprised how often it was digging through literature from the 1970s and someone would say, this animal is not often seen during the winter. So we think it hibernates and it's not always the most satisfying. And so it is an extremely tedious effort, but well worthwhile to go through and say this animal, I'm very sure, hibernates. This one, I'm very sure does not. And then there's this third category of animals that were unsure about we're going to remove those. And it's tedious, but you have to do that part, right? Because if you do the analysis with bad data, you're never going to find the genes that you want. And Linda, I remember you telling me when you were going through this very painful process, I think your threshold for being a perpetrator, quote unquote, was that you could drop your metabolism like 50%. Correct me if I'm wrong, and humans could go down to like 40 like in certain instances, like humans are almost there. You know, it's it's hard to know when there is only one paper about it, but certainly there are some really deep meditative states and humans and low oxygen environments where, you know, we're getting kind of close to the area where we might say that that's a hibernated, but certainly not the duration that you get out of hibernation. But it's it's it surprised me to see how close how much how much metabolic flexibility there really is when you start to look at it. Yeah.Harry Glorikian: Yeah. We've got to go talk to the monks.Linda Goodman: Absolutely. Absolutely. You know, we have that in mind. It sounds like an interesting travel experience. Yeah.Harry Glorikian: So I want to jump back for a second because. You guys don't necessarily have from what I have pieced together, the normal sort of like startup story. Right. First of all, you're an all female founding team, right? Highly unusual, right? Not something I see every day. You guys started at an accelerator program in San Francisco called Age One.Ashley Zehnder: Age One.Harry Glorikian: And then you moved to QB3 and the East Bay Innovation Center.Ashley Zehnder: Yep.Harry Glorikian: And then I think they helped you with some paid interns.Ashley Zehnder: Well, we got some from Berkeley. Yep, we did.Harry Glorikian: Yeah. And then you went through a SBIR grant.Ashley Zehnder: A couple of them.Harry Glorikian: From the Small Business Administration. And then a small business technology transfer grant from the Human Genome Research Initiative at NIH. Right.Ashley Zehnder: Yep.Harry Glorikian: I'm hopeful, hopefully my notes are all correct. Talk a little bit about the on ramp or infrastructure today for sort of seed stage startups like you. I mean, what were the most important resources?Ashley Zehnder: This is such an important conversation. I'm really glad you're asking this question. We had a call with a reporter from Business Insider yesterday who was talking to all three of us about this early founder ecosystems in biotech and sort of East Coast versus West Coast ways of starting biotechnology companies. Right. And that is a whole do a whole podcast on that, let me tell you. But I will say that there are a lot of resources for, let's call them founder led bio. Right. In the West Coast, which is kind of the buzzword these days, but people really supporting the scientists who originate the concepts and training them to be founders as opposed to assuming that you need to bring in an experienced CEO to run a company at this stage. Right. So I think we were very fortunate to meet Laura Deming at Stanford, who is one of the founding VCs. And longevity before that was a buzz word, right? She was one of the first longevity funds, literally Longevity Fund, and is really been a champion of founders, starting companies and really training founders to start companies who are deep science founders. So we started in age one. It was the first batch of age one. We're still very close to that cohort of companies doing interesting things from machine learning and image analysis through pure therapeutics development. And then Laura really helped us, her, her. We asked her later, like, why did you end up investing in us? She said, Well, the science was amazing.Ashley Zehnder: This is totally a field with so much promise. I just needed to teach you guys how to pitch. The science was there, right? So she helped me just how to pitch and how to use less science words in our pitches, which we're still working on to some extent. But then it was this balanced approach of taking in some venture money to really support the growth of the company, but balance with some of this non-dilutive funding for specific projects where it made sense and some of that was some of that in the early stage is validation, right? Having having funding through groups like NHGRI, having an early partnership with a company like Novo Nordisk, which provided also some non-dilutive funding for the company, really validated all of the science that we were doing because we were first time founders, because we're a little bit outside of the normal profile. For me, I don't feel weird being a female founder only because 80% of veterinarians are female. Like, I'm used to being in a room with all women. You go to a bio conference, it's not the same thing, right? So for us, we're just we are who we are. Right. But it's helpful, I think, to get some of that external validation and then really be able to use that to to start to build on programs and show progress.Ashley Zehnder: And then it becomes more about the data and the progress and what you can do with it. So that's a lot of how we started the company. There's I said there's a lot of support in the West Coast for this kind of thing. There's great programs like Berkeley Foreman Fund Talks, which I worked, which I was in as well, just about logistics around starting companies. There's a lot of good startup accelerators. I've got a really amazing all of us, how amazing a network of founders who we can reach out to on different. I got four or five different Slack channels of founders that I could reach out to for all kinds of advice. And usually it's always good to have a company that's one or two stages ahead of you, like talking to folks who IPO'd or something last year is is not as helpful as folks who recently raised a series B, right. And figuring out what those milestones look like and then particularly those that have taken mostly money from tech investors like we have all the lifeforce capital who led our last round is also has funded some very good therapeutics companies, Sonoma Therapeutics and Second Genome and other therapeutics companies as well. So I think it's it's helpful to see how people balance the needs of the companies at different stages in what you need.Harry Glorikian: But so do you guys think that you could have started Fauna ten years ago? I mean, did the support systems exist for starting a company like this?Ashley Zehnder: Well, no, for two reasons. We couldn't have started Fauna ten years ago. One is the data just simply wasn't in a place that the company was a tractable strategy. Everything was still too expensive and we had really shitty genomes for a few species at that point. And B, I think there really wasn't the kind of groundswell of support for deeply scientific technical founders to start their own companies and train them to be the kind of leaders they need to be to run those companies for a longer term. So I think it's a confluence of those things and being in an environment like Stanford that really encourages people to to try startups, it's not a crazy idea. Like people don't look at you like you're your heads backwards. If you start to start a company at Stanford, it's like, okay, cool. Like, when are you launching? You know.Harry Glorikian: I think it's the opposite.Ashley Zehnder: Yeah, exactly. Exactly. Like, why aren't you have a company yet? Whereas you know, a lot, many, many, many, many other places like that is seen as a very strange thing to do. So I think the environment plays a huge role. Yeah, for sure.Harry Glorikian: Yeah. I think between East Coast and West Coast too, there's.Ashley Zehnder: That's a whole, we should have a whole 'nother podcast on that.Harry Glorikian: Yeah. Yeah, exactly. Well, I live here and I was I was born and raised on the West and I remember there and I came here and I was like, Oh, this is where you are not in Kansas anymore. Like, this place is different. So, I mean, I'm hoping that the East Coast is actually embracing risk a little bit more and sort of stepping out on the edge. But it's really slow. They don't call it New England for nothing. So. But, you know, it was great having you both on the show. I this was great. I we covered a lot of ground. I'm sure people's heads are spinning, thinking about, you know, you know, different animal species and how that's going to play into this. And I mean. It really does sound like I know we have to do the hard work, but there's a lot of computational effort that has to go on here to sort of. Make sense of this and bring it all together and align it so that you can be looking at it properly and make the right decisions going forward.Ashley Zehnder: Yep. Millions of data points coming together to find drug targets for sure.Harry Glorikian: So thanks for being on the show. And you know, I wish you guys incredible luck.Ashley Zehnder: Thanks, Harry, so much. This was fun.Linda Goodman: Thanks for having us.Harry Glorikian: Thanks.Harry Glorikian: That's it for this week's episode. You can find a full transcript of this episode as well as the full archive of episodes of The Harry Glorikian Show and MoneyBall Medicine at our website. Just go to glorikian.com and click on the tab Podcasts.I'd like to thank our listeners for boosting The Harry Glorikian Show into the top three percent of global podcasts.If you want to be sure to get every new episode of the show automatically, be sure to open Apple Podcasts or your favorite podcast player and hit follow or subscribe. Don't forget to leave us a rating and review on Apple Podcasts. And we always love to hear from listeners on Twitter, where you can find me at hglorikian.Thanks for listening, stay healthy, and be sure to tune in two weeks from now for our next interview.

This week's guest is Nathalie Kingston, Director of the NIHR BioResource. She talks to Patrick about how the scale of the BioResource has grown dramatically over the last nine years, her most exciting moments as Director to date, and how the BioResource is using Sano's technology to accelerate and support its research programmes.

This week's guest is Nathalie Kingston, Director of the NIHR BioResource. She talks to Patrick about how the scale of the BioResource has grown dramatically over the last nine years, her most exciting moments as Director to date, and how the BioResource is using Sano's technology to accelerate and support its research programmes.

Please note this episode was recorded in November 2018 as part of Brain, a CICM Neuro Special Interest Group meeting click here for more info. Oli Flower gives us a preview into the future of traumatic brain injury (TBI) management. It is late in the 21st century and a man suffers a TBI. Oli describes the on scene immediate management of this patient. Drones and closed-circuit cameras combine to provide the closest ever trauma centre, taking tissue samples and patient images. Not only that, but the samples have been analysed and referenced against a huge database, providing the awaiting critical care clinicians with an individualised and effective treatment plan for each patient. But, this future depends on information. To develop the technology that Oli envisages, we need to collect more information in the right way. Ultimately, the future of TBI management requires the development of tools to apply masses of information to the patient in a meaningful way. One such was to achieve this, is by using biobanks. A biobank is a repository of human tissues and samples with the corresponding appropriate and correct annotating data. Specifically, for TBI this primarily means blood and CSF. The tissue is annotated with prognostic information and patient centred long-term outcome data from its donor, allowing a huge pool of information that can be accessed to inform treatment moving forward. Evidently, the potential for a biobank is enormous. Oli describes rapid genomic assessment, proteomic analysis and metabolomic profiling as potentials in the near future. This data would provide a plethora of information per patient. This does however, pose a challenge, and leads to the need for advanced computer processing to interpret the data, whilst being able to factor in the dynamic and evolving processes that define critical care. Artificial intelligence no doubt has a part to play. Biobanks have started to be developed across Australia and the world. However, they requires a massive collaboration that spans across countries. In doing so, we can strive towards the future treatment of TBI. Finally, for more like this, head to our podcast page #CodaPodcast

If you're a parent, you've probably had this experience many times: Your young child has a high fever, and maybe a sore throat, but you don't know exactly what's wrong. Is it a bacterial infection, in which case an antibiotic might help? Or is it a viral infection, in which case, you just have to wait it out? The symptoms of bacterial and viral infections are often the same, and most of the time, even a doctor can't tell the difference. Viral infections are more common, but sometimes, the doctor will prescribe an antibiotic anyway, if only to help the parents feel like they're doing something to help. But what if doctors didn't have to guess anymore? What if there were a fast, easy blood test that a doctor could run in their own office to look for biomarkers that discriminate between bacterial and viral infections? Well, that's the seemingly simple problem that a company called MeMed has been working on solving for 13 years now. Recently MeMed's first testing product got approval from the FDA, and now the company is finally beginning to roll out it out commercially in the US. And here today to tell us more about how it got built, how artificial intelligence fits into this picture, and how rapid diagnosis could change the practice of medicine, is MeMed's co-founder and CEO, Eran Eden.Please rate and review The Harry Glorikian Show on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:1. Open the Podcasts app on your iPhone, iPad, or Mac. 2. Navigate to The Harry Glorikian Show podcast. You can find it by searching for it or selecting it from your library. Just note that you'll have to go to the series page which shows all the episodes, not just the page for a single episode.3. Scroll down to find the subhead titled "Ratings & Reviews."4. Under one of the highlighted reviews, select "Write a Review."5. Next, select a star rating at the top — you have the option of choosing between one and five stars. 6. Using the text box at the top, write a title for your review. Then, in the lower text box, write your review. Your review can be up to 300 words long.7. Once you've finished, select "Send" or "Save" in the top-right corner. 8. If you've never left a podcast review before, enter a nickname. Your nickname will be displayed next to any reviews you leave from here on out. 9. After selecting a nickname, tap OK. Your review may not be immediately visible.That's it! Thanks so much.TranscriptHarry Glorikian: Hello. I'm Harry Glorikian, and this is The Harry Glorikian Show, where we explore how technology is changing everything we know about healthcare.If you're a parent, you've probably had this experience many times: Your young child has a high fever, and maybe a sore throat, but you don't know exactly what's wrong. Is it a bacterial infection, in which case an antibiotic might help?Or is it a viral infection, in which case, you just have to wait it out?The symptoms of bacterial and viral infections are often the same, and most of the time, even a doctor can't tell the difference.Viral infections are more common, but sometimes, the doctor will prescribe an antibiotic anyway, if only to help the parents feel like they're doing something to help.But what if doctors didn't have to guess anymore? What if there were a fast, easy blood test that a doctor could run in their own office to look for biomarkers that discriminate between bacterial and viral infections?Well, that's the seemingly simple problem that a company called MeMed has been working on solving for 13 years now. Recently MeMed's first testing product got approval from the FDA, and now the company is finally beginning to roll out it out commercially in the US.And here today to tell us more about how it got built, how artificial intelligence fits into this picture, and how rapid diagnosis could change the practice of medicine, is MeMed's co-founder and CEO, Eran Eden.MeMed has a growing office in Boston, but I reached him at the company's first office in Haifa, Israel.Harry Glorikian: Eran, welcome to the show.Eran Eden: Thank you very much for having me.Harry Glorikian: It's great to have you here, I know that there's a significant time difference, so I appreciate like but it still looks like it's really bright and shiny out there right now. So what time is it in in Israel right now?Eran Eden: Five o'clock in the evening,Harry Glorikian: It's five o'clock. All right. Well, you guys have a lot more sun than we do anyway because we're in the middle of winter, but absolutely.Eran Eden: So this, here, is actually full of people as well. So yeah, you don't stop innovation as five o'clock in the evening.Harry Glorikian: So, you know, I was looking at your background and I mean, it's really it's interesting. It's diverse. You have a degree in biology, computer science, systems biology. You were first job was in computer vision data and analysis. But then all of a sudden you wound up starting a company that builds sensors and software for infectious disease. Like, how did you end up down this path, and do you feel like everything that you were doing until you got here was preparing you for it?Eran Eden: Well, I think... A great question. So I think, on the face of it, it obviously the background in data science, as you know, in molecular biology, obviously all of that relates to what we're doing is part of our day to day and it is a good starting point. But in reality, there's a very big gap between what I was trained to do and today, my every day, day to day activity. I would say that probably the most important training that I got during my days at the Weizmann Institute has got less to do with differential equations or molecular biology, and it was more about a story that my mentor, Professor Uri Alon, told me when I was three years into the PhD, about three years into the PhD, he asked me, Am I already in the cloud? He said what? And he said, are you in the cloud? I said, Well, what is the cloud? He said, Well, every PhD, every scientist, when you start your PhD, you know, you have you go you go and read the latest papers in Science and in Nature and you see how somebody starts at Point A, makes a hypothesis about point B and then take the straight line from A to B, and then you say, OK, I'm going to do the same thing and you start at Point A, the known. You shoot for the unknown and you start going and suddenly you hit a roadblock. And then you hit another one and another one. At a certain point, you'd really lose direction, which he called the cloud. You're in the cloud. And then if you have enough perseverance and luck, you find a point C which is not exactly where you thought you're going to end. You go there with, you know, your last energy. And if you're lucky enough, then you publish another paper about how you started at point A, went to point C and connected between the two dots with a straight line. And then you have another generation of PhDs that are asking themselves, Well, why am I the only one that's struggling? And that lesson about how to be in the cloud, how to deal with uncertainty, to deal with failure and still move on. That is probably more important in the training that I got to become an entrepreneur and CEO of a company than any specific scientific knowledge.Harry Glorikian: Ok. Yeah, no, I mean, trial and error, dusting yourself off, getting up and moving forward is, you know, my wife calls me crazy when I keep doing it, but I think you have to be a little on the edge to constantly keep repeating and being willing to fail and then stand up and then move on. Maybe it's a, I think I was reading a paper recently that said forgetting quickly is evolutionary, you know, a positive trait so that you forget what happened, that wasn't good and you keep moving forward. So. But let's talk about your company, MeMed, like you started that in, I believe, it was 2009. And what was your founding vision? I mean, if you can talk about what you and your co-founder did when you came up with this idea, I think you were both studying at the Technion at the time?Eran Eden: Yeah, so so he was studying at the Technion, M.D., Ph.D. I was studying at the Weizmann Institute and Data Science and Biology. And frankly, I would love to tell you a story about a vision, but it started with a game. I don't think we had the presumptions to have really something that would grow to what MeMed actually became today. It was playing. We both have had different reasons first of all for doing this. I can say that from my my end, it was probably a pretty big gap between the places, the caliber of where we were able to publish high impact journals. And when I was looking at myself in the mirror and I was asking myself, Is this actually going to have an impact on real patients? I couldn't really see the connection. There's another reason why I decided to found MeMed or co-found MeMed. That's probably off topic for today. We can take this on a beer some time when we meet face to face. But so it's first of all, it didn't start with a vision. It started with a scratch wanting to apply a some of the know how that we had had in converting between molecular immunology and data science, and to try to solve big, ugly problems that don't have a good solution in 21st century medicine and trying to find something pragmatic now rather than having it a eureka moment. You know, some pioneers describe a eureka moment where suddenly you have the best and coolest idea in vision. For us, it was darkness for almost a year rather than the eureka moment. It is was more like an evolutionary process. Trial and error. We tried a bunch of solutions to problems that didn't really exist until eventually we came up with what we want to work with, but again was no, no eureka, and the way that it actually started was again, Kfir was coming from from med school talking about this problem of of AMR, antimicrobial resistance and the problem of distinguishing between bacterial infections and given our different backgrounds, we said that's interesting. How can we apply immunology and then science to try to solve that, and then at that point, we formulated what was to become MeMed's vision. And MeMed is based on a very simple premise, a very simple idea. Our immune systems have evolved to tell us what's going on our bodies and all we do at MeMed is we listen to the immune response with biochemical sensors and machine learning and what have you. And we use that to translate or decode the immune system into insights that can potentially transform the way that we manage patients with acute infections and inflammatory disorders. The first problem we went after, because that's a very lofty goal, was potentially the most prevalent clinical indication on the face of this planet. A child with sniffles. Our elderly patients that coughs. Come to the doc, they have a fever. As a parent, you're many times hysterical, you're asking yourself, is it a bacterial infection or bowel infection. If it's a bacterium, antibiotics. It's a viral infection, chicken soup. And we said, Well, what if we can harness the immune system? What if we could measure or listen to the immune system in real time and use that to try to aid clinicians to tackle this seemingly simple problem? So the vision was listening to the immune response. In the first embodiment of the first problem we went after is this huge intractable problem, B versus V versus. Bacterial versus viral infection. To treat or not to treat.Harry Glorikian: Yeah, I mean, you know, it's funny, you say simple, and I've worked in this area for a long time and now not simple, not simple, but I've been watching dozens of companies over time try and tackle this problem, and everybody always comes at it and says, Yep, we should be able to do it. And I'm like, OK, that's a big hill, you know, to go and try and die on so. But you got FDA approval for your device in the U.S., and I want to talk about that later. But it did take 13 years. Like to, you know which parts of the process turned out to be harder or slower than you thought it would be?Eran Eden: Before I answer that, I just want a minor correction. I didn't say it's simple. I said it's a seemingly simple problem. In reality, it's an extremely difficult problem to go after. I think some of the most the biggest challenges that we have can be phrased in a very simple manner. But as you alluded to, yeah, it's an intractable problem. Bacterial and viral infections are often clinically indistinguishable. And it took us over a decade to take this from my idea on a napkin and grandmother's kitchen. That's where we found with no garage, it was Grandmother's Kitchen to what is considered a landmark FDA clearance that I think many folks did not believe we're going to be able to get this because it required so many innovations, not only on the technological side, but also on the regulatory side. And when you ask why only a decade? I think it's, we're very lucky that it took us only a decade and it sounds there, let's not call them challenge. Let's call it problems. Challenges is something I always envy the people that have challenges. We have problems with immune, and we work every day to solve those problems, right? So. So there's many problems or hurdles you have to go through. So there's first of all, you have to overcome some pretty big research issues, where do you find these hypothetical molecules of the immune response that go after bacteria and viruses. So research, then you learn the hard way.Eran Eden: The research is very different from development, and development is very different than product, and product is very, very, very different than manufacturing, and manufacturing is very different than regular regulation, and regulation is very different than reimbursement in marketing, which is a very different than commercial, et cetera, et cetera. So it's not good, it's not enough to excel in one thing. You have to really reinvent the wheel on several things, and as a company and as a team, reinvent yourself, and that's probably one of the biggest challenge, probably your biggest impediment to progress is yourself and your team because you might be an excellent data scientist, but you have to talk with the clinician. You might be an excellent clinician, but you have to talk the language of the molecular immunology. You might be very versed in all these three, but it's still not product and it's still not the graphical user interface. And how is that connected to manufacturing and really creating a culture or a team that can combine these seemingly very diverse elements within a small company. That is a very, very daunting and big task, and again, we frankly failed on multiple avenues there. We had to go back, we were in the cloud and we had to reinvent point C again and again and again. So, you know, we were in a very far position that we are today that we thought we were going to be at this stage.Harry Glorikian: So I'm going to ask at some point, you know, after this whole interview is I'm going to encourage you to write the next IVD book because everything you said is absolutely the way that I've seen it over time is, you know, having to bring all these pieces together is not trivial in our world. But let's step back here for a second for everybody that's listening, right? Talk a little bit about basic immune system biology and the, you know, technology behind your diagnostic system. So if someone presents with an inflammatory response, why is it so hard for doctors to destroying distinguish between the bacterial and viral infection?Eran Eden: Because bacterial and viral infections are clinically indistinguishable and you don't have to be an M.D. to to understand this. Intuitively, we know our kids so well. But still, you know, when they have a fever or runny nose, you know, we know that it's 80 percent, 85 percent a viral infection. But what if? What if there's a lingering bacterial infection? And it just it turns out that because of the clinical manifestation is very similar. It's really hard to figure it out. Not only children, also adults with suspected LRTI or a fever without sores, and even when we apply modern, I would say diagnostics, there's still a big gap that remains. So for example, when as a scientific community or a clinical community, when we approach this problem, we have tools at our disposal. A rapid strep test. A rapid influenza tests. Multiplex PCR. In today's world, I think everybody, even my grandmother is talking to me about the difference between rapid antigen tests suddenly becomes a really interesting topic over, you know, weekend dinners, culture. So there's technologies out there. And going back to your question, why is it still, why is there still a gap? And we've identified several things. The first one is probably the most trouble is time to results. Many of the clinical encounters, you want to have the solution here and now where whereas that technology that we have often provide solutions in hours and even days, and that's not always good.Eran Eden: That's one hurdle. Not the biggest one. The second one is that many times the infection site is inaccessible. Take, for example, otitis media, an ear infection or sinusitis or bronchitis or pneumonia. It's really hard to reach the infection side and therefore identify the pathogen. It's one in four patients in the most prevalent disease on Earth. That's really hard. Third, even if you use the best, most broad technology diagnostics to try to identify the bug, say a multiplex PCR. In more than 50 percent, five, zero percent of the cases, you're not be able to put your hands on any microorganism, but you still, as a clinician, have to make a decision. And lastly, there's the issue of colonization. So even if you're lucky, the infection that is readily accessible and you do get some sort of a virus, for example, that you detect, say, for example, an influenza or or let's take a rhinovirus, the rhinovirus is very prevalent in children. That's a problem. It's very prevalent in children. Even if you take seemingly healthy children in a very high percentage of those children, they're going to have a rhinovirus. So mere detection does not apply causality. All this complexity is sunk into this few minutes that the clinician basically needs to make a decision, and it's a really hard dilemma because it's hard to know to distinguish between the two and the ramifications could be quite significant.Harry Glorikian: So I know the answer to the question, but I'm going to ask it so you can explain it is: So who cares? I mean, I know that it's ineffective to treat a viral infection with antibiotics and that only you know, that only work against a bacteria, but you know. We've been doing a trial and error, so what's the downside of doing that?Eran Eden: So it's actually a pretty deep, it's a very deep question because there are several layers. You're right, this sometimes people actually say there's several layers to answering because the first one is, well, if you treat erroneously, with antibiotics, antibiotics, because of this uncertainty, there's a lot of antibiotics overuse that one of the consequences of this it drives anti microbial resistance, which basically means that the drugs don't work anymore. And if we continue on that path, we will potentially lose modern medicine because if you lose the potency of antibiotics, you cannot treat infants when they have an infection. Or an oncology patient that would succumb to a parasitic infection, or even yet have your wisdom tooth pulled out, because antibiotics won't be effective. And there's several quite influential studies that came out in the last few years. The last one actually in The Lancet came out two weeks ago portraying a world without antibiotics, which is, you know, we're seeing right now the consequences of COVID SARS-CoV2. Some might argue it's not a smaller problem. So that's and it has both clinical and health economic consequences. According to Jim O'Neill, over $100 billion by 2050 in lost GDP.Eran Eden: And. And it's a big number, right? It's a really, really big number. And maybe, maybe it's overly inflated and maybe it's conservative, but it's a big problem. The issue is that nobody cares. Sometimes the individual doesn't care because the doctor, right now, when he has a patient in front of him, he doesn't think about the masses. He thinks about the patient. So you might ask, well, what the doctor care. Why does the patient care? And it turns out that there is an angle on the personal level as well, not only the societal level. If you give erroneous antibiotics, you can drive anaphylactic responses. You can drive allergies, which have a toll. But then there's another element that people are less aware of. In addition to overuse, there's also simultaneously underuse. One in five patients that have a bacterial infection are not receiving antibiotics in time. There's much less publication on that. But it is a reality. And that also has consequences, including prolonged disease, duration and sometimes even morbidity and mortality. So it's a really delicate equation, right? You don't treat. And you don't want to get ... some countries overtreat, some undertreat. And again, at the end of the day, the day to day, it does have ramifications both from the patient and on the doctor.Harry Glorikian: You know, if we could accurately treat people right, I think there would be a whole host of issues that could get solved and a whole host of issues that wouldn't emerge because of overtreatment or treating the wrong people that you know, we could spend hours over a beer discussing the microbiome and allergies and all sorts of other consequences of doing this. [musical interlude]Harry Glorikian: Let's pause the conversation for a minute to talk about one small but important thing you can do, to help keep the podcast going. And that's leave a rating and a review for the show on Apple Podcasts.All you have to do is open the Apple Podcasts app on your smartphone, search for The Harry Glorikian Show, and scroll down to the Ratings & Reviews section. Tap the stars to rate the show, and then tap the link that says Write a Review to leave your comments. It'll only take a minute, but you'll be doing a lot to help other listeners discover the show.And one more thing. If you like the interviews we do here on the show I know you'll like my new book, The Future You: How Artificial Intelligence Can Help You Get Healthier, Stress Less, and Live Longer.It's a friendly and accessible tour of all the ways today's information technologies are helping us diagnose diseases faster, treat them more precisely, and create personalized diet and exercise programs to prevent them in the first place.The book is now available in print and ebook formats. Just go to Amazon or Barnes & Noble and search for The Future You by Harry Glorikian.And now, back to the show.[musical interlude]Harry Glorikian: So your system, which is, I love, is a basic blood test, right? So the MeMed BV looks at three immune system proteins in the blood: TRAIL, IP 10 and CRP. So how are these proteins related to infection and how can measuring their levels tell you about the nature of the infection?Eran Eden: Ok, so. Each one of those proteins that you just mentioned plays a critical role in the immune response to different invaders, bacteria and viruses. What's special about this particular trio, is that they work really well as a team. Maybe if you take a step backward to identify them, we had to run for about four years what is arguably the largest prospective proteomic study ever to be conducted of the human response to acute infections. And start with a host of multiple tens of thousand proteins bioinfomatically and then down-select this eventually to three. And these three, while none of them is perfect in itself, they cover one another's blind spots. So let's go one level deeper. When we went on this, one of the things where we were surprised to find out that is a clinical community, we've been obsessed with the bacterial side of the equation. Every biomarker that you have in 21st century medicine, 20th and 21st century medicine, has been mostly predominantly upregulated in bacterial infection. Procalcitonin: bacterial infections, CRP: bacterial infections, white blood count: bacterial infections, absolute neutrophil count, which we use as part of routine day to day care: bacterial infections. What about the viral side of the equation? We couldn't find one that was used or cleared by FDA as part of 21st century medicine. The last. The reason the FDA cleared us, we actually just cleared the first viral protein ever to be cleared by FDA. And so we went on this fishing expedition and four years into the process, again, this was 2009-2013. We identified this trio. TRAIL Is a protein that shoots up in your bloodstream when you have a viral infection, whether it's a common influenza A, influenza B, parainfluenza or corona, and it has this very unique property that it goes down when you have a bacterial infection, why nobody really understands the reason. But it really creates a very dramatic full change because of this up and down type of a response. And the story there, there's a lot of interesting stories around TRAIL, but one of the ways mechanisms by which it does that it causes the cells that are infected by viruses to commit apoptosis. Cells suicide. And by that, protect the brethren cells. So that's one of the mechanisms that the body is using.Eran Eden: The second one is called IP 10, which is an interferon. This protein basically shoots up in your bloodstream if you have a general infection, and more so if you have a viral infection. It recently got a lot of headlines in the context of SARS-CoV-2 and hyperactivity of the immune response. It's also associated with lung injury, but a really interesting biomarker that plays a critical role there in clearance of infections. The third one is called C-reactive protein, that's been around for about 40 years. Goes up in bacterial. And the nice thing about them? They work as a team. So as I said, they're not perfect. So take, for example, CRP. It's reasonably OK after 48 hours. But because it takes it to about 48 hours to reach maximum level, but in the early phases, you have a blind spot. Whereas TRAIL, at time of symptom onset, it's already differentiated, so they cover one another. By the way, we didn't identify this. The computer identified that. This is a lot of insights that we had in hindsight when we were looking.Harry Glorikian: Yeah, that was going to be my next question, which is. You know, the the heart of the show is always like, you know, artificial intelligence and its whole basket of tools and biology. So how does machine learning come into this process? Is there some corpus of training data that shows that certain levels of these three proteins correlate? Or can you tell us, you know, how you developed that part of the system?Eran Eden: Absolutely. And I think again, I was teaching a machine learning at the Weizmann Institute over a decade ago before it was a sexy topic. You know, people are using the term machine learning and data science so often so frequent. I think what's important to say is that machine learning is part of the component technology, but there's hardcore immunology and molecular biology. So it's not just one technology that we're, you know, it's a it's a very high entry barrier because of that and adds to the complexity. So that's one thing, just to put machine learning in context. Where machine learning plays an important role here is two places: in the development and in the final product. In the development, there's a process of how do you find the optimal team of biomarkers that would give you the the best performance? And over there, there's a lot of activities around using publicly available data sets and and proprietary data sets and data analysis and statistical analysis and feature selection and find the right models, et cetera, et cetera, coming up with what is the right model. Some of these are more conventional tests. Some of these are more cutting edge tests in the final product. It basically uses what's called a supervised learning approach, which basically means the following. Imagine every problem in here, I'm going to be a little bit technical here. Imagine you have, let's say one feature. Say a viral biomarker. TRAIL. High levels, viruses, low levels, bacteria. You find some sort of cutoff that separates between the two. It was the most informative biomarker that we found.Eran Eden: Is it good? It's reasonably good, but there's no perfect biomarkers out there. We don't have them, nor do we believe they exist. Nor do we believe in unicorns, even though my daughter is trying to continually persuade me that there is one. Then you add another biomarker to that. Imagine that you have right now a two dimensional grid. And now suddenly, every patient is met this two dimensional coordinates and you have a cloud of bacterial and the cloud of viruses. And you find a line that separates the two. And then a third dimension and a fourth and so forth and so on. And eventually, the problem becomes how can I find this type of plane or hyper surface that separates between the cloud of bacteria and the cloud of viruses? This is the essence of the machine learning and the way you go about this. You train give it a lot of patients, a lot of data, and then you train the system. And the more data you have, the smarter it becomes. The same principle applies for doing diagnostics in oncology, span detection, computer vision and what have you. It's the same underlying, often similar underlying principles to try to solve many of these problems. So hopefully I was able to to simplify and somewhat exaggerate how this is actually working and where the AI plays here.Harry Glorikian: So what's that accuracy rate of the diagnosis from your system? And is there are certain things, let's say it's good at in certain things, it's maybe not so good at?Harry Glorikian: Yeah, absolutely. So so if you look at the overarching population, if you look at our pivotal FDA study, the AUC, the area under the operating curve, the entire population was 0.9 to 0.97 across different cohorts, which is considered very high. So that's the short answer. The more we see deeper level, it's there's obviously nuances across different populations. One of the things you have to show is what happens in children versus adults. Upper respiratory tract infections, lower respiratory tract infections, et cetera, et cetera. So we've shown a relatively consistent and robust response. That's how the system was developed. But there are, for example, certain viruses that we know that we perform less accurate. For example, adenoviruses. Adenoviruses are notoriously hard to to treat well. By the way, they're one of the most prevalent, for example, viruses in children, why? Because the immune response looks like a bacterial infection. For many, many reasons. So white blood count is going to be elevated. Procalcitonin is going to be elevated, CRP is going to be elevated and we're often going to overtreat with antibiotics. So if you look at our performance in that particular sub-cohort, our performance drops somewhat from, you know, a 0.90-something to maybe 0.89, but that's actually one of the viruses that we see the most added value because compared to standard of care, it's many times close to flipping a coin.Eran Eden: So even though our performance is eroded in this particular virus. The standard of care in this particular situation is particularly challenged, and it's almost 0.5, 06. so that's one example. There's multiple examples. We can study the immune response to pathogens again for almost a decade now. This is just one interesting anecdote. And I think just connecting this to the who cares question that you had. So here's an interesting case that we had a few weeks ago. A child, young, three years old, coming to a major medical center, not really sure if it's a bacterial or viral. Ran a PCR, came positive for adenoviruses and it looked a little bit bacterial. But yeah, OK. Adenovirus explains everything. Released home. Got a 99 score. 99 probability of bacterial infection. So they start to do additional follow up and then it eventually turned out to be a bacterial axis in the spinal cord of that particular child. It had to be mechanically removed. This is a very dramatic case. This is one of those potentially underused cases that could be very dramatic. This is very rare. It doesn't happen often. But again, it's hard. It's really, really tricky to distinguish between infections and we added this right now, this is how everything maps together to the adenoviruses and and to why we think this could be helpful.Harry Glorikian: So, you know, like I said earlier in the show, you know, you got FDA approval and granted 510K clearance back in September, which congratulations, that's a huge step. But you know, for everybody listening, what Gates does, does that open for you. What's the pathway to getting the device out into the market?Eran Eden: So as you said, first of all, you have to get the clearance, which I think took us almost five years working with FDA. FDA, by the way, we've worked with them extremely collaboratively and they've been instrumental in helping us form and shape, what's the methodology to actually prove something. We didn't talk about this? But how do you prove that absence or presence of bacterial viral infection in the absence of a true gold standard? So let's put that thing aside. We were able to work with FDA and come up with a methodology to do that. So now, what is required to take it to the next step? There's several things. The first one you need, and we didn't talk about this, you need a way to measure those biomarkers. You need a platform. Right, one of the challenges that we had is that in the early days, none of the big strategic players, the Roches, the Abbotts, the DiaSorins of the world were willing to bet on this because the risk were so high, as you alluded to in the beginning, the graveyard. And nobody got FDA clearance, so they basically they wouldn't. They were not willing to bet on us today. Some of them become partners and we're working with them. So it's, you know, there's been great development. But at that time, it was really hard. The platform is also challenged because some of the proteins are picograms, some are nanogram and some are micro per mil, which poses again the challenge from a technological perspective. Again, not going too much into the technology side, but we've been able to come up with a technology or a platform that can actually measure multiple proteins across almost a six to nine order of magnitude range. And so you have to have a platform and can do that in about 15 minutes right now, serum working in whole blood.Eran Eden: The second thing you need, you need obviously manufacturing capability, which is again, a different story, you have to manufacture the cartridge. The third thing you need is building the clinical evidence beyond, I mean, FDA's great, but you have to create what's called a clinical utility, real world evidence, what have you, working with peers. Work with partners or with clinicians working the societies. Publishing. Building a commercial team which we're right now established commercial team in the U.S. So there's multiple things. And probably last but not least, this is too big of a challenge to go at it by yourself. You need to have partners. Whether it's governments, the U.S. Department of Defense, the European Commission have funded this heavily and have been amazing partners, whether it's strategic partners, you can take it by yourself versus vs not one market. It's markets. You have patients in the wards and the EDs and the urgent care physicians' offices, retail clinics. No single player has enough of a presence in one platform that covers it all. So again, we've announced about a year ago, you know, the first partnership with DiasSorin, which has today almost a thousand installed installed across Europe and the US in these large automated immunoassay machines. And that's covering certain parts of the market that are overlapping or, sorry, that are complementary where we're going at. So that's a little bit of what needs to be done. But again, it's changing the boundaries of what what we've been doing so far, and that's always a it's always a challenge, but also an opportunity.Harry Glorikian: So you guys raised I believe it was $93 million, if I remember the number correctly, in new funding, which sort of really adds to the firepower of being able to take that next step, but. You know, can you can you envision a future where we get a solid diagnosis and an appropriate treatment plan, you know, quickly while you're in the doctor's office?Eran Eden: Oh, yeah.Harry Glorikian: That was the shortest answer you've given yet.Eran Eden: I think you can be much more radical. I think there's several things that are happening. There's two major discontinuities. There's a technological discontinuity. There's a regulatory discontinuity. And I'll actually add another one, which is there's a psychological discontinuity. The technology that we can do today that we have today, the tip of our fingers can do can provide so much valuable information that can help make better decisions. The regulatory framework has changed because of COVID, it's basically shattered a lot of things. And from a psychological perspective, I think there's a push to polarization, right? Both decentralization and centralization at the same time. And so I definitely see that happening. I think we can take this several step further. How can we take it from physician's office, also retail clinics and even further? And that will take time, obviously, because we're dealing here with some pretty, pretty deep questions. But I think the world across multiple fields and this is not different than anything else. I think it's definitely going in that direction.Harry Glorikian: Yeah, no, I mean, I was going to, you know, looking at what you've created and, you know, obviously first getting everybody on board, but then seeing how it can be deployed at a CVS or something like that, it could drum, you know, you could have a dramatic impact on how we manage patients. The whole antibiotic dynamic and maybe even relieving stress on the system so that, you know, it doesn't get overwhelmed by what your system may be able to sort of help get to a much faster, much more accurate answer too.Eran Eden: I wanted to say relieving stress from stressed mothers and fathers. But yeah, I agree with you also, relief. And by the way, as you start going from more centralized to decentralized, there's obviously additional workflow challenges. How do you make this simpler? There's regulatory bars that you have to meet. How do you go from a mod complex to a clear waived test that can actually go to those directions so that there's we still have we have work, there's work, work to be done. But I think we've been able to potentially break a glass ceiling in terms of getting the clearance. And now I think with that, there's going to be additional innovation that will come in both by us and others who are entering the space.Harry Glorikian: So. Just slightly moving to one side is like, how has MeMed responded to say, COVID-19? I think you guys have developed a test that runs on your platform and predicts how severe the infection will be. How does that test work? Did your previous work, you know, and also did your previous work like on the platform prep you for this virus? Just curious how it works and how you got there?Eran Eden: Absolutely so. So it always starts with the clinical question. I mean, many of us are technophiles, but at the end of the day it's about solving a real problem. And the problem here is the following. You have see SARS-CoV-2 positive patient presenting to the ED. And one of the questions that we have in mind is whether that patient is going to deteriorate or not. Do we escalate treatment or not? And it's a real question, right? And the more you know, the more stress the system is feeling because, you know, because of the the peak of a pandemic, the more important that is. So we said, Well, how can we harness the technology? Is the framework that we created host response in general, right? The biomarkers we've developed, the platform that we have, the Biobank and what have you. And so and how can we take a process that maybe took 10 years and now collapsed into something maybe that's 10 months? How do you get a 10 X? And and first of all, with amazing partners around the globe, you start running huge clinical studies to basically collect patient samples. We also use again information from the public domains, our own repositories, our own previous data because from many perspectives. Sars-cov-2 is very interesting, but guess what? Similar to SARS and to other types of severe viruses, there's differences, but also commonalities.Eran Eden: So we use a lot of the bioinformatics, the previous data samples. Current data samples. The know how and the platform that's readily available right now. They can measure basically anything to collapse this and develop. This is probably just got clearance in Europe that basically allows to take a snapshot, the main response again in real time. Give you a risk stratification regarding the probability of a patient to experience severe outcome defined as ICU level of care and mortality within two weeks. Again, it's only clear right now in Europe, not cleared in the U.S. and we view this also as a stepping stone going beyond just COVID severity to a general severity signature. So what you do, both B versus V and severity, what if you could do it in the same cartridge or what have you? So I think what's what's really interesting, we build here this core technology. We went after one big problem, B versus V, but now that you have that, you're like a child in a candy store. There's many more things that you can do. And rather than taking you a decade, you can start to collapsing things because there's a lot of there's a lot of. Resources that you can now leverage or platform that you can leverage, so that's a story around MeMed and COVID severity.Harry Glorikian: Yeah, platforms are wonderful in that way, right, that I like a platform more than I like, like a, you know, sharpshooter bullet, from an investment perspective. Thinking about it that way. But so. You recently got COVID. We were supposed to talk like over a week ago, and I, you know, we had to postpone it. Did you use the test on yourself? I mean, if you did, like did it work the way you thought it was going to?Eran Eden: Yeah, so so yeah, I got my I got it from my daughter. We went on a trip and five out of five family members got infected. So yes, it was at least from our small experiment. It was very infectious. We got the Omicron. Actually we didn't have symptoms, apart from the fact that I think it just jacked up the energy level of my kids. So before we talk about running around the house and thank God, you know, my wife didn't didn't kill any one of them. So there's no casualties from this, from this infection. So because we didn't have symptoms, we didn't go to the ED. It was not relevant. You have to have SARS-CoV-2 symptoms. So in that case, no, no, no need. I mean, we were pretty much hunky dory. But what I can tell you is that on the B versus V. Again, it's potentially bacterial and viral infections are potentially the most prevalent indication in children. And my children, those little incubators of bacteria and viruses, are no exception. So I had a chance to use the technology on my kids many, many times, including last time was about a month and a half ago, and my eldest daughter, who is four, before going to a business trip. And my wife is asking, is it a bacterial infection? I said, I don't know. She spits on me. The shoemaker is going barefoot. So we ran it. It was a viral infection. No antibiotics. Went back to school. So and I got a lot of brownie points with my wife and my mother in law, which is obviously always very, very strategic.Harry Glorikian: That's that's a good one. That's always helpful. Exactly.Eran Eden: So we're actually using this quite often in our families as well. And it's very very gratifying.Harry Glorikian: Interesting. Excellent. So now you guys are, you know, I believe you have an office in Haifa, which I remember as being beautiful and hilly and wonderful food, and then you have Boston. You know. What are the strengths of being in these two locations. What happens in Boston that can't happen in Haifa and vice versa?Eran Eden: Well, again, we're going after a global problem and you have to have a global team to have a global perspective. Whatever you have in San Francisco today, you have tomorrow in Shanghai and the day after that in Tel Aviv. So you have to look at this from a global perspective, number one. Number two, since the US is the primary market, as I said, we have to build a very significant presence in the U.S.. Why specifically Boston? Very talented pool of, a pool of talent that's very wide in the domain. There's a big overlap in terms of hours between Boston and Tel Aviv, so you can grow one unified team. And that's basically, that's where we're basically building our U.S. headquarter. And the team is quite complementary. Again, we've we've recruited by now roughly 25 to 30 folks, folks with a very strong background, both IBD, Troy Battelle, formerly Thermo Fisher, who's buying commercial for microbiology in the Americas. Fred, who is running Corp Dev, from bioMérieux. Again, another large multinational, Jim Kathrein was former head of sales for BioFire. Again, not sure if your audience is familiar with but and so forth and so on.Eran Eden: And Will Harris was running our marketing global marketing, is ex-Amazon and then before that, 15 years in IBD. So it's really bring here a blend of, we call this affectionately an anti disciplinary team. We don't care about disciplines, we care about solving big, ugly problems. So you have to bring the IBD experts with the clinicians, with the folks and the big data science side or in the molecular immunology and the manufacturing. And nobody knows, single location has all the know how, no single location has the recipe because frankly, we're doing here something new. There is no real tech like this. And so bringing those this pool of talent, I think has really helped us, propels us moving forward. And it is the bridge to be able to to launch in the U.S., a U.S. very focused, commercially marketing product where a lot of the I would say more of the molecular immunology data science team is more in Israel. I'm simplifying and exaggerating. That's some of the team.Harry Glorikian: So the last funding round, was that the argument to the investors, like we need to hire these types of people to help blow this out? What was what was the rationale for that last round?Eran Eden: So, so basically three things. Number one, commercialization. U.S. Europe, Israel. That's our initial focus and then the rest of the world. Second is product pipeline, so we talked about bacterial versus viral infection and a bit about COVID severity. But what would you do if you had a blank canvas and these platforms to go after the new response to measure the immune response? What additional big problems would you go after? So it turns out that there's some pretty interesting stuff in. We're working on additional activities. So that's the second thing product pipeline. And the third thing is a scaling manufacturing. So as I think people have a new appreciation for manufacturing and supply chain during COVID times, it's a really big topic and critical for success. So this these are the three major elements that we raise the funds for.Harry Glorikian: No sounds I've I've been I've seen this rodeo a few times, so yes, I understand completely. So, well, you know, especially because I come from the diagnostic world and I can't wish you enough success because we need more products like this out on the market to help us manage patients and help give physicians better information so that they can make better decisions, right? More informed decisions than just, you know, looking at a patient and trying to figure out what's going on. So I wish you incredible success and I'm, you know, great. Great to have you on the show.Eran Eden: Thank you so much for for the kind invitation. Enjoyed our discussion.Harry Glorikian: Thanks.Harry Glorikian: That's it for this week's episode. You can find a full transcript of this episode as well as the full archive of episodes of The Harry Glorikian Show and MoneyBall Medicine at our website. Just go to glorikian.com and click on the tab Podcasts.I'd like to thank our listeners for boosting The Harry Glorikian Show into the top three percent of global podcasts.If you want to be sure to get every new episode of the show automatically, be sure to open Apple Podcasts or your favorite podcast player and hit follow or subscribe. Don't forget to leave us a rating and review on Apple Podcasts. And we always love to hear from listeners on Twitter, where you can find me at hglorikian.Thanks for listening, stay healthy, and be sure to tune in two weeks from now for our next interview.

Hello and welcome to the Alcohol Alert, brought to you by The Institute of Alcohol Studies.In this edition:IAS seminar on Alcohol and the United Nations’ Sustainable Development GoalsExtensive OECD publication details the investment case for alcohol control policies 🎵 Podcast feature 🎵New minimum unit pricing studies in Scotland bolster the argument for its implementation 🎵 Podcast feature 🎵Confusion over WHO global alcohol action plan 🎵 Podcast feature 🎵Brain imaging study suggests there is no safe level of alcohol consumption for brain health Study highlights the prevalence of alcohol advertising in the Rugby Six Nations Parliament debates labelling and the Misuse of Drugs ActWe hope you enjoy our roundup of stories below: please feel free to share. Thank you.Alcohol and the United Nations’ Sustainable Development GoalsIAS sustainability series, seminar 1. Seminar speakers: Chair: Kristina Sperkova, Movendi InternationalDudley Tarlton, United Nations Development ProgrammeProfessor Jeff Collin, University of EdinburghAadielah Maker Diedericks, South African Alcohol Policy AllianceThe Institute of Alcohol Studies hosted the first seminar in its four-part series on alcohol and sustainability, 10 June 2021. The seminar focused on the impact of alcohol on the United Nations’ (UN) Sustainable Development Goals (SDGs) and the opportunities for improved alcohol policy arising from the Goals.Goal 3.5 explicitly targets alcohol, with the commitment to ‘Strengthen the prevention of treatment of substance abuse, including…harmful use of alcohol’. Beyond that, alcohol has been identified as an obstacle to achieving 14 of the 17 SDGs, which can be seen as social, environmental, and economic. Social goals such as ending poverty, hunger, achieving gender equality and maintaining peace and justice, are all affected by alcohol harm. Kristina Sperkova, President of Movendi International, highlighted that alcohol pushes people into poverty and keeps many there, and consumes spending that would otherwise be used on education and food. There are many studies that demonstrate the link between alcohol use and violence, particularly between young men and relating to domestic violence. Ms Sperkova detailed the high environmental cost of alcohol production. Land required to grow crops for alcohol reduces biodiversity. Huge amounts of water are used for alcohol production, with 870 litres of water needed to produce one litre of wine. She pointed out that alcohol is often produced in places that have scarce water supplies, to serve the desires of higher income countries that have an abundance of water.The economic burden of alcohol use across the world is enormous, with high-income countries seeing annual losses of between 1.4% and 1.7% of GDP due to alcohol harm. Much of this is due to the loss of productivity. In England in 2015, 167,000 working years were lost due to alcohol. It was suggested that more effective alcohol control policies would not only reduce the harm but would also help finance sustainable development. The investment case Dudley Tarlton, Programme Specialist at the United Nations Development Programme (UNDP), introduced the work UNDP is doing in collaboration with the World Health Organization (WHO), to present the case for improving and implementing effective alcohol policies, with economic rationale being the main driver.WHO’s SAFER initiative details the five most cost-effective interventions to reduce harm. Mr Tarlton stated that these five interventions would give a 5.8% return on investment.  Modelling by UNDP across 12 countries including Russia, Turkey, and Ethiopia, shows that investing in WHO’s recommended prevention measures would generate 19 billion USD over the next 15 years – mainly due to productivity gain – and 865,000 deaths would be averted. UNDP is also looking into investment cases relating to alcohol-attributable deaths from causes such as liver cirrhosis, road injuries, tuberculosis, and HIV. They are drafting toolkits for countries to take up these policies and could be instrumental in getting revenue to help close covid-related fiscal gaps. As lower socioeconomic groups would disproportionately benefit from the health benefits of increased alcohol taxes, Mr Tarlton highlighted that part of Goal 10 on reducing health inequalities would be targeted by such taxes. The obstacle of the alcohol industryProfessor Jeff Collin, Edinburgh University, posited how the alcohol industry has positioned itself as aligned with the SDGs and as engines of development. The International Alliance for Responsible Drinking (IARD) has a toolkit for governments on how to build partnerships with the alcohol industry. Diageo’s ‘Business Avengers’ coalition highlights their role in aiming to achieve the SDGs. Namibian Breweries (NBL) has listed out which SDGs it is helping, including SDG 3: “NBL has a responsibility to minimise harmful alcohol consumption.”Prof Collin explained that the industry is using the commitment of governments and organisations to SDG 17 – ‘Partnerships for the Goals’ – to push their own strategic agenda, particularly during the Covid-19 pandemic. Pre-pandemic, Diageo collaborated with CARE to address barriers to gender inclusion in the alcohol giant’s supply chain. Following the outbreak of the pandemic, Diageo supported CARE’s emergency response, giving clean water supplies, hygiene kits, and food. According to Prof Collin’s work, the alcohol industry is using corporate social investment (CSI) and philanthropy to shape policy and pursue partnerships, to further its strategic interests. This is especially true in its targeting of women in developing countries, who are seen as a key emerging market. Pernod Ricard India launched an initiative around women entrepreneurs, which aptly shows the two faces of alcohol philanthropy, with the company’s CMO Kartik Mohindra stating: “It is quintessential for brands to create products that appeal to them [women]. And if they don’t have more women in senior leadership roles, they are not likely to have the significant insights needed to tap into the highly sensitive minds of their ever-growing numbers of female consumers.”In Southern Africa – as Aadielah Maker Diedericks of the Southern African Alcohol Policy Alliance (SAAPA) discussed – there are particularly striking examples of industry-government partnerships and conflicts of interest, with civil society in the region perceiving Big Alcohol’s involvement in the region as a form of neo-colonisation. Ms Diedericks explained that policy makers are often on the boards of alcohol companies in the region, that governments hold shares in the industry, and the industry’s agenda is often successfully pushed through. Very few Southern African countries are taking on issues of marketing, pricing, and availability, instead focusing on road safety and underage drinking. Both Prof Collin and Ms Diedericks said that SDG 17 has confused countries, with governments thinking the only relationship with the alcohol industry is one of partnership, ignoring potential conflicts of interest. South Africa case studySouth Africa has seen intense lobbying by the industry in recent months, with Ms Diedericks saying that they are using the narrative of job promotion to demonstrate their value. This is despite R246billion being spent on alcohol harm compared to R97billion in revenue. The industry has campaigned extensively around the idea of economic loss associated with alcohol control policies, using dubious research to back up their claims. This comes at a time of high unemployment rate in South Africa and therefore gets a lot of media attention. Ms Diedericks described the relationship between industry and South Africa’s government as “abusive” due to the industry threatening disinvestment in the country if there were controls to alcohol availability. What next? The speakers argued that the SDGs need to be used better as a rallying point for alcohol control measures. SDG 17 in particular should be used to develop policy coherence and that the building of coordinated approaches across other unhealthy commodities, such as junk food, should be considered. There needs to be clear rationale for why enacting alcohol control policies would help achieve the SDGs, and taxation has a lot to offer towards sustainable financing. Please watch the full seminar below, or click here for a 30minute edited version. Join us in September for seminar two in our four-part series. New OECD report models economic effect of alcohol policies  🎵 Podcast feature 🎵The Organisation for Economic Co-operation and Development (OECD) published a book entitled ‘Preventing Harmful Alcohol Use’, 19 May 2021. It analyses the cost of alcohol consumption in 52 countries (OECD, EU and G20 countries), due to reduced life expectancy, increased healthcare costs, decreased productivity, and lower GDP. As with the IAS seminar on alcohol and sustainability, this report provides clear economic rationale for why countries should consider implementing alcohol control policies. The report looks at trends and patterns in alcohol consumption in the 52 countries, as well as looking at the regional differences across Europe. The following statistics and modelling relate to the 52 countries, unless otherwise stated. Health and economic burden of alcoholHealth care costs for alcohol as percentage of total health care expenditureChildren’s education and bullyingPolicies for reducing consumption The report looked at which alcohol control policies countries currently implement and those that they should consider. It mentions the World Health Organization’s Global Strategy and Global Action Plan in reducing the harmful use of alcohol, referring to these as the best practice policy responses. The report states that:“policies to reduce the harmful consumption of alcohol and associated harms cannot be addressed through one policy intervention – rather, a suite of interventions is needed within a comprehensive strategy”. This will “require a multi-sectoral approach, including health, law enforcement and social services sectors”.How would policies affect health and the economy?  Simulation modelling shows varying degrees of impact of alcohol control policies across the countries. Across the 48 countries analysed by OECD it was found that savings in healthcare costs are greater than the costs of running interventions.How has minimum unit pricing affected Scotland and Wales so far? 🎵 Podcast feature 🎵Since Scotland implemented minimum unit pricing for alcohol (MUP) in May 2018 and Wales in March 2020, initial studies have shown a substantial shift in alcohol purchases and consumption. On 28 May 2021, The Lancet published a study, by Professor Peter Anderson and colleagues, that analysed the purchasing habits of over 35,000 British households, in order to assess the impact of MUP in Scotland and Wales. Purchases in northern England were compared with Scottish purchases, and western England purchases with Wales. The measured changes associated with MUP were: price paid per gram of alcohol, grams of alcohol purchased, and amount of money spent on alcohol.The results of the study were:In Scotland the price per gram saw a 7.6% increase and a purchase decrease of 7.7%In Wales the price increased by 8.2% and purchasing decreased by 8.6%The biggest changes were in households that generally bought the most alcohol. Little change was seen in households that bought small amounts of alcohol and those with low incomesFollowing The Lancet report, on 17 June 2021 Public Health Scotland released its report Monitoring and Evaluating Scotland’s Alcohol Strategy. The report looked at alcohol purchasing, affordability and consumption in Scotland in 2020. The report found that:The report also shows a reduction in alcohol-specific deaths in Scotland from 2018-2019, with the rate for men being the lowest since 1996. However, rates are still higher in Scotland than in both England and Wales. Alison Douglas of Alcohol Focus Scotland (AFS) said:“We're really pleased to see that as a nation we are drinking less for the third year running and that alcohol consumption is at a 25-year low - this is a good indication that minimum unit pricing is having the intended effect. But given nearly a quarter of Scots are still regularly drinking over the chief medical officers' low-risk drinking guidelines, we can't afford to take our eye off the ball where preventing alcohol harm is concerned.” AFS has called on the government to raise the level at which MUP is set from 50p to 65p per unit, arguing that inflation has made it less effective since the legislation was passed eight years ago. Following the success Scotland has seen, Baroness Finlay of Llandaff, Chair of the Alcohol Harm Commission, and Dr Katherine Severi, Chief executive of IAS, called on the UK Government to introduce MUP in England. They argued that there is now sufficient evidence of MUP’s effectiveness and that it is now more urgent than ever due to increases in high-risk drinking and alcohol-specific deaths in England. Public Health Scotland released an interim report at the end of June, which suggests that there is little evidence that MUP has led to people substituting cheap alcohol with other substances or illicit alcohol. Confusion over WHO’s global action plan on alcohol 🎵 Podcast feature 🎵In mid-June, the World Health Organization (WHO) published the first draft of its ‘Global alcohol action plan 2022-2030’. The action plan’s aim is to aid in the implementation of WHO’s Global strategy to reduce the harmful use of alcohol, which in turn aims to reduce morbidity and mortality due to harmful alcohol use and the ensuing social consequences. The strategy aims to “promote and support local, regional and global actions”, giving guidance and support on policy options, national circumstances, religious and cultural contexts, public health priorities, as well as resources and capabilities. In response to the draft action plan, media across the UK focused on a statement included that said:“Appropriate attention should be given to prevention of the initiation of drinking among children and adolescents, prevention of drinking among pregnant women and women of childbearing age.”Most news reports lambasted the wording that women of childbearing age should be prevented from drinking. Two prominent commentators quoted in press reports were Christopher Snowdon of the Institute of Economic Affairs, and Matt Lambert of the Portman Group, who said it was “unscientific, patronising and absurd” and “sexist and paternalistic” respectively. Responding to the media furore, Professor Niamh Fitzgerald, University of Stirling, spoke on BBC Radio 4’s Woman’s Hour: “It is striking that the commentators in the reports are from the alcohol industry. It is clearly an attempt to discredit WHO…before a WHO forum next week [week-commencing 21 June], which is looking at empowering governments against industry marketing. This is a first draft and that mention, which is ill-advised, doesn’t appear in the actions, so we shouldn’t worry that WHO is trying to stop women of childbearing age from drinking.”Dr Sadie Boniface, the Institute of Alcohol Studies’ Head of Research, said “It is a shame that this one phrase in the report has hoovered up attention. This is the launch of an ambitious plan to address alcohol harm, and alcohol is the top risk factor globally for mortality among 15–49 year olds.”According to the Sydney Morning Herald, Dag Rekve, Alcohol Policy Advisor at WHO, said:“It was just meant as the period where you are potentially carrying children and this is not generalising to all women in that age. It can be interpreted that we are saying that women of childbearing age should not drink alcohol and is a completely wrong interpretation and we will make sure that it’s not interpreted like that. If the media also can pick up on the incredible harm from alcohol in the world in the same way they picked up on this poorly formulated phrase, then perhaps we could really achieve something.”No safe level of alcohol for brain health A yet to be peer-reviewed study suggests that all levels of drinking are associated with adverse effects on the brain.Researchers at Oxford University, led by Dr Anya Topiwala, used brain imaging data from 25,000 participants of the UK Biobank study and looked at the relationship between this and moderate alcohol consumption. The results found that higher consumption of alcohol was associated with lower grey matter density and that alcohol made a larger contribution than any other modifiable risk factor, including smoking. Negative associations were also found between alcohol and white matter integrity. Particular damage was seen to the anterior corpus callosum, which connects the frontal lobes of the left and right hemispheres of the brain and ensures both sides of the brain can communicate with each other. Dr Topiwala, said “There’s no threshold drinking for harm – any alcohol is worse. Pretty much the whole brain seems to be affected – not just specific areas, as previously thought.”In response to the study, Dr Sadie Boniface, IAS Head of Research, said:“While we can’t yet say for sure whether there is ‘no safe level’ of alcohol regarding brain health at the moment, it has been known for decades that heavy drinking is bad for brain health. We also shouldn’t forget alcohol affects all parts of the body and there are multiple health risks. For example, it is already known there is ‘no safe level’ of alcohol consumption for the seven types of cancer caused by alcohol, as identified by the UK Chief Medical Officers.”The authors highlighted that one of the limitations of the study was the use of the Biobank data: that the sample is healthier, better educated, less deprived, and with less ethnic diversity than the general population. Dr Rebecca Dewey of the University of Nottingham responded to this, saying that “Therefore some caution is needed, but the extremely large sample size makes it pretty compelling”. The study argues that current drinking guidelines could be amended to reflect the evidence about brain health rather than solely about cardiovascular disease and cancer risk. Professor Paul M. Matthews, Head of the Department of Brain Sciences, Imperial College London, supported this suggestion. Alcohol, rugby and adolescent drinking A study by Dr Alex Barker and colleagues that looked at the prevalence of Guinness advertising in the 2019 Rugby Six Nations Championship, found the following across the 15 games:Two weeks after this study was published it was announced that the National Football League (NFL) in the US was to get its first spirits sponsor, with Diageo signing a multiyear deal. Until four years ago advertising of spirits was banned in the NFL, with beer advertising dominating. Why is this important? Dr Barker’s research states that exposure to alcohol advertising is associated with adolescent initiation of drinking and heavier drinking among existing young drinkers. It goes on to explain that the Advertising Standards Authority in the UK does not regulate footage of imagery from sporting events and although this should be covered by Ofcom it is not. Sports sponsorship is self-regulated by the Portman Group, whose code states that it “seeks to ensure that alcohol is promoted in a socially responsible manner and only to those over 18” and that “drinks companies must use their reasonable endeavours to obtain data on the expected participants, audience or spectator profile to ensure that at least the aggregate of 75% are aged over 18”. The study authors point out that even if 75% of the audience are adults, as sporting programmes are very popular with children they are still being exposed to regular alcohol advertising. If the remaining 25% are children, with huge sporting events there will still be millions of children seeing such advertising. The England versus Croatia Euros 2020 game had a UK audience of 11.6 million, which would potentially mean 2.9 million children seeing alcohol advertising during that game alone – a number acceptable under the self-regulatory rules.  The researchers argue that this weak regulatory approach should be reviewed and “Restrictions on, and enforcement of, alcohol advertising during sporting events are needed to protect children and adolescents from this avenue of alcohol advertising.” They go on to say that future studies should look at if this increased exposure leads to increased sales for alcohol brands. The conversation around advertising of unhealthy commodities in sport has picked up in June, due to the actions of footballers at the European Football Championship.Portugal’s Cristiano Ronaldo removed bottles of Coca-Cola from a press conference and held up a bottle of water declaring “Agua. Coca-Cola, ugh”. A few days later Paul Pogba removed a bottle of Heineken from his conference. This led to the launching of a Muslim athletes’ charter, which seeks to "challenge organisations" to make progress in supporting Muslim sportsmen and women. There are 10 points in the charter, such as “non-consumption of alcohol, including during celebrations, the provision of appropriate places to pray, halal food, and being allowed to fast in Ramadan”. UEFA, the governing body of the Euros, then threatened to fine teams if players continued to snub sponsors. England’s manager Gareth Southgate came out in support of sponsors, saying “the impact of their money at all levels helps sport to function, particularly grassroots sport…we are mindful in our country of obesity and health but everything can be done in moderation”.What happened in Parliament? Obesity strategyThe House of Commons debated the implementation of the 2020 Obesity Strategy on 27 May. Minister Jo Churchill (Department of Health and Social Care) brought up the topic of alcohol labelling. She highlighted the number of calories some people in the UK consume via alcohol: “each year around 3.4 million adults consume an additional day’s worth of calories each week from alcohol”. She went on to state that the Government will be publishing a consultation shortly on the introduction of mandatory calorie labelling on pre-packed alcohol and alcohol sold in the on-trade sector. Churchill said that the main aim was to ensure people were fully informed so that they can make educated choices on what they consume. Labour MP Dan Carden’s contribution focused solely on alcohol labelling. He brought attention to the fact that non-alcoholic drinks have to display far more nutritional information than alcoholic drinks. He also pushed the UK government for a national alcohol strategy, as “We had the highest rate of deaths from alcohol on record this year. Alcohol-specific deaths are at an all-time high at a moment when drug and alcohol services are underfunded and mental health services are overstretched.” During the debate, Alex Norris MP (Labour) and Jim Shannon MP (Democratic Unionist Party) agreed that there needs to be a stronger alcohol strategy. Carden also spoke of the importance of bringing together strategies to combat obesity, drugs, gambling and alcohol.Food and drink regulationsThe House of Lords debated the Food and Drink Regulations 2021 on 19 May. Baroness Finlay of Llandaff discussed alcohol labelling, saying that people had the right to information in order to take control of their health and make informed choices. She argued that alcoholic drink labelling should form part of an obesity strategy and a comprehensive alcohol strategy. “If the role of food labelling is to inform, to empower people to protect themselves from harm and to allow regulation to support that duty to protect our citizens from harm, updating the labelling becomes a moral imperative.”Baroness Bennett of Manor Castle of the Green Party agreed with Baroness Finlay that alcohol labelling is currently inadequate.Baroness Bloomfield of Hinton Waldrist (Conservative) responded to Baroness Finlay “The Department of Health is planning to issue a consultation on calorie labelling for alcohol in the near future with a view to making it a requirement from perhaps 2024.”Misuse of Drugs ActThe Commons debated the 1971 Misuse of Drugs Act on 17 June. MPs agreed that the UK’s current drug policy is not working. Labour MP Jeff Smith argued that it should be liberalised to reduce harm, advocating the legalising of cannabis. He stated that alcohol is more harmful than many illegal drugs and yet it is legal. “We mitigate the harm from alcohol use by legalising it, regulating it, making sure that it is not poisonous and making it safe, and we can invest the tax raised from its sale in the NHS and public messaging.”Labour, Conservative and SNP MPs agreed with Smith, with Allan Dorans of the SNP saying that “Advice, support and education should be provided in the same way as they are for other health issues, including alcohol and tobacco.” The UK Alcohol Alert (incorporating Alliance News) is designed and produced by The Institute of Alcohol Studies. Please click the image below to visit our website and find out more about us and what we do, or the ‘Contact us’ button. Thank you. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit instalcstud.substack.com

Welcome to the BC Platforms Podcast!  BC Platforms is the global leader in providing a powerful data discovery and analytics platform, as well as data science solutions for personalized health care. BC Platforms enables cross-functional collaboration with our global federated network of data partners. This episode is an open discussion with three key leaders in the healthcare data industry.   Tõnu Esko is the Professor of Human Genomics at the University of Tartu, and the longtime leader and member of the Senior Management Board for the Estonian Biobank.  Sirpa Soini is the Director of The Finnish Institute for Health and Welfare Biobank (THL Biobank). She has been collaborating with BBMRI-ERIC, and BBMRI-ERIC.fi in Finland, and with a background as a lawyer, she has also been involved in legal and ethical compliance work.  Outi Törnwall is Data Partnership Director at BC Platforms, driving forward and building a data partnership network that enables sharing of data and collaboration, particularly in industry driven research. What is Covered:  - Overview of the work of Estonian Biobank, THL Biobank and Data Partnership at BC Platforms - The increase of real-world data and the challenges of creating meaningful databases across different industries and countries - What positive results have been achieved so far within global data partnerships and networks  - How to bridge the gaps between academic research, industry needs and policy makers  - Advice for researchers and industry stakeholders for a more effective collaboration that benefits patients and the society as a whole Links and Resources Mentioned in This Episode:  - BC|RQUEST - Global Data Partner Network https://bcrquest.com/  - Estonian Biobank https://genomics.ut.ee/en  - THL Biobank https://thl.fi/en/web/thlfi-en   - Fingen Research Project https://www.finngen.fi/en  - Europe Biobank Week https://europebiobankweek.eu/  Connect with Sirpa Soini: -  https://www.linkedin.com/in/sirpasoini/  Connect with Outi Törnwall:  -  https://www.linkedin.com/in/outitornwall/  Connect with Dr. Tõnu Esko:  - https://www.linkedin.com/in/tõnu-esko-24511524/  Connect with BC Platforms:  - https://www.bcplatforms.com  - https://www.linkedin.com/company/bc-platforms/  - sales@bcplatforms.com  

Show NotesFebruary 17, 2021IntroductionMany thanks to Jennifer Frontera, MD, Professor of Neurology at NYU Grossman School of Medicine, New York, New York, for discussing the new Neuro Databank-Biobank for COVID-19. Dr. Frontera is a neurocritical care specialist and has been caring for COVID-19 patients in New York City since the start of the pandemic. She has contributed to several important research publications on this topic found at www.pubmed.gov.“Disaster Medicine” in NYCDr. Frontera described the challenges of practicing “disaster medicine” at the onset of the pandemic. The high numbers of COVID-19 infected patients required impromptu field hospitals and the recruitment of all available medically trained personnel. New York City physicians are now applying lessons learned to the current “second surge” of the disease.Neuro Databank-BiobankTo better understand the neurologic complications of COVID-19, NYU collected information on approximately 5,000 patients last spring. With the help of a grant from the National Institutes of Health (NIH) and the National Institute of Neurological Disorders and Stroke (NINDS), the program now accepts data and specimens from physicians treating COVID-19-infected patients anywhere in the country. The registry also welcomes information and samples from outpatients with “Long-COVID.” Reimbursement is available to compensate for the time required to complete the data entry form.Dr. Frontera encouraged both academic and community neurologists to contact the databank to submit their experience with COVID-19 patients. https://med.nyu.edu/departments-institutes/population-health/divisions-sections-centers/biostatistics/research/nih-neurodatabank-neurobiobankConclusionsAs much as the Neuro Databank and Biobank welcomes COVID-19 samples, Dr. Frontera and I agree that vaccination is a low-risk and highly effective way to prevent the disease and the neurologic complications that may result. The registry will gladly settle for fewer contributions if it means a healthier population!

Professor Sir Rory Collins, Founder and Chief Executive of the UK Biobank, talks to us this week about the origins of this world-changing project that has catalysed a wave of new discoveries in large part by levelling playing field in data access. In this inspiring conversation Professor Sir Rory Collins describes the 'if you build it, they will come' attitude of the UKBiobank, and how he believes the biggest impact from the UKBiobank is still to come. The conversation finishes with details on their COVID-19 work, which has involved not just members from the original 500,000 strong UKBiobank cohort, but also family members of these participants.

Results were recently published in a study in  the Journal of Clinical Microbiology that show  limitations of currently available diagnostic tests for early-stage Lyme disease, and highlight the need for more research toward improved diagnostics and treatments. Joining me today to discuss the study and the findings is Liz Horn, PhD. Dr Horn is the Principal Investigator with the Lyme Disease Biobank.