Podcasts about MRC

Cette semaine, découvrez Le Domaine Deslandes dans la chronique Radio-Acton sur la route des cultivateurs. Une collaboration avec la MRC d'Acton. See omnystudio.com/listener for privacy information.

After copping weeks of brutal Match Review Committee decisions that left Dylan Brown, Ryley Smith, Will Penisini and Kelma Tuilagi sidelined for a collective 9 games, the MRC has found a way to outdo itself after slapping Izack Tago with an embarrassingly weak 1 game suspension for a hip drop tackle that has rubbed Kitione Kautoga out for 8 weeks. It is a damning indictment on both the post-game process and the match officials as the wild inequities of the NRL rise to the surface. Sixties and Forty20 unload on the broken system and the maddening inconsistency of the NRL after the Eels find themselves on the wrong side of the ledger yet again. Jack De Belin's signing was confirmed by the club and the boys do a quick once over with other Tuesday staples on the docket including Team List Tuesday and the weekend recap. Newcastle dominate the NRL headlines this week with the axe rumoured to be coming for Adam O'Brien while Kalyn Ponga could be looking for the exit with speculation swirling his manager is shopping the star fullback around. The Dogs pull another switcheroo while Cody Walker is done for the year as a calf injury shuts him down.

MRC finishes off January 1968 with returning special guest Jeff Ryan, featuring Fantastic Four #70, Strange Tales #164 with Dr Strange and SHIELD, Tales of Suspense #97 with Iron Man and Captain America, and Avengers #48! The Menta-Wave Unit! Flames of the Faltine! Hyperdimensional Space! Uni-directional explosives! Irma Kruhl! Ant-covered roulette tables! Check it out!

MRC welcomes special guest Jeff Ryan, author of “Father and Son Issues: The Secret History of Spider-Man” to talk about John Romita and the books of January 1968, featuring Amazing Spider-Man 56, Daredevil 36, Thor 148, Tales to Astonish 99 with Hulk and Namor, and X-Men 140! Check it out!

Aujourd'hui dans le podcast, on reçoit en entrevue Luce Daneau, mairesse de la municipalité de Wickham et ancienne collaboratrice du podcast, avec qui on discute de l'orientation gouvernementale poussée par le gouvernement du Québec vers les MRC, puis des MRC vers les municipalités, intitulée Accélérer la transition climatique locale. On demande entre autres aux municipalités de calculer les émissions de GES sur leur territoire dans l'objectif de les réduire selon le Plan Climat 2030 du gouvernement du Québec — et ce, sans ressources supplémentaires.DANS LA PARTIE PATREON, on commence en commentant un exemple parfait de biais médiatique de la part du Journal de Québec à propos d'une étude sur la mobilité routière et celle du transport en commun dans la grande région de Québec. Suivant ce sujet, Frank explique, cartes à l'appui, pourquoi Québec a besoin d'un troisième lien, en prenant exemple sur Montréal. Ensuite, on revient rapidement sur le conflit en Iran, où le président américain Donald Trump semble se préparer pour une attaque du pays, mais hésite. Joey termine le show en présentant sur le vif une vidéo du jeu vidéo Call of Duty: Advanced Warfare et en poursuivant l'écoute de son montage des interventions de Paul Saint-Pierre Plamondon aux podcasts de Pantelis et de Stéphane Bureau.0:00 Intro0:46 Accélérer la transition climatique6:39 L'impact financier de cette politique13:22 Le concret de cette orientation18:54 Calculer les GES des municipalités22:33 0,17% des GES mondiaux27:35 L'UMQ et la FMQ32:20 Mot de la fin

MRC finishes off December of 1967 with Fantastic Four 69, Strange Tales 163 with SHIELD and Dr. Strange, Tales of Suspense 96 with Iron Man and Captain America, Avengers 47, and a bonus fifth book: Marvel Super-Heroes 12 introducing Captain Marvel! (No, not that one. Or that one. The other one.) The Id-Receptor of the Psionic-Revelation Eavesdropper! Goobers! 180 degree manspreading! Check it out!

MRC plows into December 1967 with Amazing Spider-Man 55, Daredevil 35, Thor 147, Tales to Astonish 98 with Namor and Hulk, and X-Men 39! Hoary amnesia tropes! Trapster self-esteem building! Buff Loki! Orca punching! Angel suspenders! Check it out!

In healthcare, some of the most meaningful innovations happen when the right people are brought together in the right place. True progress depends on systems and infrastructure designed to connect ideas, people, and expertise across sectors. Citylabs 4.0, now open in the heart of Manchester's Knowledge Quarter on the Oxford Road Corridor, was built with exactly that goal in mind. Bringing the NHS, academia, and life sciences organisations into close, purposeful proximity, providing a structural foundation for collaboration at scale. In this special live recording of the pharmaphorum podcast, developed in association with Bruntwood SciTech, Bruntwood SciTech's CSO Dr Kath Mackay, Manchester University NHS Foundation Trust T's Dr Katherine Boylan, and Dr Gillian Dalgliesh from QIAGEN join Deep Dive editor Eloise McLennan onstage at the opening of Citylabs 4.0 to discuss innovation in life sciences and the role of Greater Manchester in accelerating research, industry collaboration, and real-world evidence generation. Join us as we examine how this deliberate integration of healthcare stakeholders in Manchester is establishing new standards for collaboration and advancing patient outcomes through structured knowledge exchange. About the interviewees Dr Kath Mackay Kath Mackay is Chief Scientific Officer of Bruntwood SciTech - a JV between leading property developer Bruntwood, Legal & General, and Greater Manchester Pension Fund - the UK's leading creator and developer of innovation districts driving growth of the UK science and technology sector.  She has a keen interest in growing businesses and infrastructure within the sector, ensuring the UK is the best place to establish and scale a science and tech organisation.   Dr Mackay joined Bruntwood SciTech from the executive board of Innovate UK where she led the team responsible for growing businesses working in the biomedical, health, agriculture, and food sectors, creating and delivering a £800m portfolio of infrastructure, Catapults, grant and loan investments. She is also non-executive director of the Northern Health Science Alliance, the North of England's health partnership, and an elected fellow of the Royal Society of Biology. Dr Katherine Boylan Katherine is Director of Innovation at Manchester University NHS Foundation Trust (MFT), a position she has held since April 2020. This role involves overseeing innovation activities within MFT, as part of the wider Research and Innovation function. Innovation at MFT supports the whole pipeline from ideation, through to evidence generation, and ultimate implementation. She has been a member of the NICE Medical Technologies Advisory Committee since September 2020. Prior to this position, Dr Boylan worked in the University of Manchester for a number of years, most recently as Operations Director for the MRC funded Molecular Pathology Node, and the Trust-funded Diagnostics and Technology Accelerator. Dr Gillian L Dalgliesh, PhD Global Technical lead, Precision Diagnostics Gillian Dalgliesh has worked for QIAGEN for nine years and is based at their Manchester site, which is the global centre of excellence for molecular diagnostic development. QIAGEN partner with many drug companies to develop companion diagnostic (CDx) tests that enable clinical trials and subsequently launches of novel precision medicines. In recent years they have seen a real move beyond oncology into other disease areas such as immune, neurological and metabolic disorders. Dr Dalgliesh's role as global technical lead allows her to leverage her oncology precision medicine experience across the portfolio to bring precision diagnostic products to more patients. She has built her experience in precision medicine/oncology through not only her QIAGEN role but also through seven years working in precision medicine in AstraZeneca and prior to that working as part of the cancer genome project at the Sanger institute. Dr Dalgliesh is also an honorary senior lecturer at University of Manchester where she coordinates and delivers lectures for a QIAGEN sponsored BSc final year elective module ‘The Role of Diagnostics in Medicine'. This is part of a wider outreach role with the University and our NHS hospital. Through these roles she is keen to impact the local UK science community. About Bruntwood SciTech Bruntwood SciTech is the UK's largest dedicated property platform serving the growth of the nation's knowledge economy to become a global science and technology superpower. It is also the leading developer of city-wide innovation ecosystems and specialist environments, helping companies - particularly those in the science and technology sectors - to form, scale and grow A joint venture between Bruntwood, Legal & General and the Greater Manchester Pension Fund (GMPF), Bruntwood SciTech provides high quality office and laboratory space and tailored business support, offering unrivalled access to finance, talent and markets, an extensive clinical, academic and public partner network and a sector-specialist community of more than 1100 companies. Bruntwood SciTech is experienced in creating and developing strategic partnerships with UK regional cities, universities and NHS Trusts to drive economic growth. Its unique structure and funding vehicle more easily deploys long-term patient capital in innovation infrastructure, ensuring local economic benefit and growth. Valued at £1.5bn, Bruntwood SciTech has a portfolio of 5.2m sq ft across 11 campus locations and 31 city centre innovation hubs in Manchester, Cheshire, Birmingham, Leeds, Liverpool, Cambridge and London. It has plans to create a £5bn portfolio by 2033 and has a 2.3m sq ft secured development pipeline. Its campus locations include Alderley Park in Cheshire; West Village in Leeds; Innovation Birmingham; Birmingham Health Innovation Campus in partnership with the University of Birmingham; Melbourn Science Park in Cambridgeshire; Liverpool Science Park as a shareholder in Sciontec Liverpool; White City Deep Tech Campus in partnership with Imperial College London; and a cluster in the heart of Manchester's Oxford Road Corridor knowledge quarter - Manchester Science Park, Citylabs in partnership with Manchester University NHS Foundation Trust (MFT), Circle Square - a joint venture with Vita Group; and the £1.7bn JV partnership with The University of Manchester - Sister, formerly known as IDManchester. Its city centre innovation hubs include Bloc, Bond, 111 Piccadilly, Pall Mall and Manchester One in Manchester; Platform in Leeds; Cornerblock and Centre City in Birmingham; and The Plaza in Liverpool. Website / Twitter / LinkedIn / Instagram

Michel Lafrance a reçu ce matin Mathis Chouinard, un jeune comédien d’Acton Vale, qui a reçu une une bourse de 1000$ lors de la toute première édition de Bourses en arts de la MRC d'Acton.See omnystudio.com/listener for privacy information.

10:05 – 10:22 (17mins) Weekly: Tim Jones @SpeakerTimJones “The Tim Jones and Chris Arps Show” weekdays 4p-6p on NewstalkSTL Building New Football Stadiums Is NOT The Government’s Job 10:25 – 10:37 (17mins) 10:41 – 10:56 (15mins)See omnystudio.com/listener for privacy information.

11:05 – 11:22 (17mins) Weekly: Mark Harder, St. Louis County Council Host: St. Louis County Insider with Mark Harder, Sundays at 5pm 11:25 – 11:37 (17mins) Vic and Ken talk about Comey and his ability to look and act stupid no matter what Is happening. 11:41 – 11:56 (15mins) Weekly Feature: "CHAT BOX!!"See omnystudio.com/listener for privacy information.

9:05 – 9:22 (15mins) Bill D'Agostino, MRC Senior Research Analyst A new study by the Media Research Center reveals that during the 24 hours following Wednesday night’s shooting of two Israeli embassy employees in Washington, D.C., none of the major broadcast networks—ABC, CBS, NBC, or PBS—reported that the alleged shooter was affiliated with the radical left-wing Party for Socialism and Liberation (PSL).From 6:00 a.m. ET Thursday to 8:59 a.m. ET Friday, MRC analysts monitored every broadcast and transcript across ABC, CBS, NBC, PBS, CNN, and MSNBC. The findings: 0 mentions of “left-wing,” “far-left,” “socialist,” or “liberal” to describe the shooter on ABC, CBS, NBC, PBS, or MSNBC. 1 mention of “far-left,” from CNN’s Jake Tapper. CNN was the only network to reference the shooter’s PSL affiliation at all, and even then only in passing. Commentary across CBS and MSNBC instead shifted blame to right-wing Israeli leadership or pushed a “both sides” narrative.The Legacy Media Lies By Omission Every Single Day 9:25 – 9:37 (12mins) Weekly Feature: “FAKE NEWS!!” 9:41 – 9:56 (15mins) Melanie Collette -Policy Analyst for the Committee for a Constructive Tomorrow. CFACT.org @CFACTSee omnystudio.com/listener for privacy information.

9:05 – 9:22 (15mins) Bill D'Agostino, MRC Senior Research Analyst A new study by the Media Research Center reveals that during the 24 hours following Wednesday night’s shooting of two Israeli embassy employees in Washington, D.C., none of the major broadcast networks—ABC, CBS, NBC, or PBS—reported that the alleged shooter was affiliated with the radical left-wing Party for Socialism and Liberation (PSL).From 6:00 a.m. ET Thursday to 8:59 a.m. ET Friday, MRC analysts monitored every broadcast and transcript across ABC, CBS, NBC, PBS, CNN, and MSNBC. The findings: 0 mentions of “left-wing,” “far-left,” “socialist,” or “liberal” to describe the shooter on ABC, CBS, NBC, PBS, or MSNBC. 1 mention of “far-left,” from CNN’s Jake Tapper. CNN was the only network to reference the shooter’s PSL affiliation at all, and even then only in passing. Commentary across CBS and MSNBC instead shifted blame to right-wing Israeli leadership or pushed a “both sides” narrative.The Legacy Media Lies By Omission Every Single Day 9:25 – 9:37 (12mins) Weekly Feature: “FAKE NEWS!!” 9:41 – 9:56 (15mins) Melanie Collette -Policy Analyst for the Committee for a Constructive Tomorrow. CFACT.org @CFACTSee omnystudio.com/listener for privacy information.

11:05 – 11:22 (17mins) Weekly: Mark Harder, St. Louis County Council Host: St. Louis County Insider with Mark Harder, Sundays at 5pm 11:25 – 11:37 (17mins) Vic and Ken talk about Comey and his ability to look and act stupid no matter what Is happening. 11:41 – 11:56 (15mins) Weekly Feature: "CHAT BOX!!"See omnystudio.com/listener for privacy information.

Learn about a more intelligent way to fight disputes at www.disputed.ai!   A special thank you to them for making this video possible!   "Now you spend $3,600 total on a conference, including hotel room and registration and food to save a million dollars a year, it's worth every single penny."   In this episode of Payments Corner, Jordan and Jacqueline discuss their experiences at the MRC conference, highlighting the importance of networking, vendor relationships, and peer validation in the payments and fraud prevention industry. They share insights on contract negotiations, data ownership, and the supportive nature of the fraud community. VAMP updates since the recording of this episode: Podbean: https://www.podbean.com/ew/pb-b68fe-1883a94 Apple: https://podcasts.apple.com/us/podcast/bonus-vamp-updates-live-stream-with-rick-lynch-from/id1631865080?i=1000703927192   --------------------------------------------   ➡️ Tired of losing all your chargebacks because your responses are outdated? Checkout out our sponsor Disputed to level your response game up and start recovering your revenue today: https://www.disputed.ai   --------------------------------------------   "It just makes no sense to be overly protective of the trends in the outside world of what fraudsters are trying these days, because the more people block them, the better off we all are."   --------------------------------------------   Sponsorship or live booking inquiries: sponsorships@fraudboxer.com 

MRC and special guest Mike Collins finish up the books of November 1967, including Fantastic Four 68, Strange Tales 162 with SHIELD and Dr. Strange, Tales of Suspense 95 with Iron Man and Captain America, and Avengers 46. A bad Kirby cover! Making Bond Jealous! All swipe-pages! Sitwell! Agent Thirteen! Whirlwind! Check it out!

Audio FileGround Truths can also be found on Apple Podcasts, Spotify and YouTube.The UK is the world leader in human genomics, and laid the foundation for advancing medicine with the UK Biobank, Genomes England and now Our Future Health (w/ 5 million participants). Sir John Bell is a major force in driving and advising these and many other initiatives. After 22 years as the Regius Professor of Medicine at the University of Oxford he left in 2024 to be President of the Ellison Institute of Technology. Professor Bell has been duly recognized in the UK: knighted in 2015 and appointed Companion of Honor in 2023. In our conversation, you will get a sense for how EIT will be transformational for using A.I. and life science for promoting human health.Transcript with audio links Eric Topol (00:06):Hello, this is Eric Topol from Ground Truths. And I'm really delighted to welcome today, Sir John Bell who had an extraordinary career as a geneticist, immunologist, we'll talk about several initiatives he's been involved with during his long tenure at University of Oxford, recently became head of the Ellison Institute of Technology (EIT) in the UK. So welcome, John.Sir John Bell (00:30):Thanks, Eric. Thanks very much for having me.Eric Topol (00:34):Well, I think it's just extraordinary the contributions that you have made and continue to make to advance medicine, and I thought what we could do is get into that. I mean, what's interesting, you have had some notable migrations over your career, I think starting in Canada, at Stanford, then over as Rhodes Scholar in Oxford. And then you of course had a couple of decades in a very prestigious position, which as I understand was started in 1546 by King Henry VII, and served as the Regius Professor of Medicine at the University of Oxford. Do I have that right?Sir John Bell (01:11):It was actually Henry VIII, but you were close.Eric Topol (01:14):Henry VIII, that's great. Yeah. Okay, good. Well, that's a pretty notable professorship. And then of course in recent times you left to head up this pretty formidable new institute, which is something that's a big trend going on around the world, particularly in the US and we'll talk about. So maybe we can start with the new thing. Tell us more about the Ellison Institute of Technology (EIT), if you will.Sir John Bell (01:47):Yeah. So as you know, Larry Ellison has been one of the great tech entrepreneurs focused really on developing terrific databases over his career and through Oracle, which is the company that he founded. And Larry is really keen to try and give back something substantial to the world, which is based on science and technology. So he and I did quite a bit together over the Covid pandemic. He and I talked a lot about what we're doing and so on. He came to visit afterwards and he had, I think he decided that the right way to make his contributions would be to set up an institute that would be using the state-of-the-art science and technology with a lot of AI and machine learning, but also some of the other modern tools to address the major problems in healthcare, in food security, in green energy and climate change and in global governance.Sir John Bell (02:49):So anyway, he launched this about 18 months ago. He approached me to ask whether I would run it. He wanted to set it up outside Oxford, and he wanted to do something which is a bit different than others. And that is his view was that we needed to try and create solutions to these problems which are commercially viable and not all the solutions are going to be commercially viable, but where you can create those, you make them sustainable. So the idea is to make sure that we create solutions that people want to buy, and then if they buy them, you can create a sustainable solution to those issues. So we are actually a company, but we are addressing many of the same problems that the big foundations are addressing. And the big issues that you and I talk about in health, for example, are all on our list. So we're kind of optimistic as to where this will go and Larry's supporting the project and we're going to build out an institute here which will have about 5,000 people in it, and we'll be, I think a pretty exciting new addition to the science and technology ecosystem globally.Eric Topol (04:02):Well, I know the reverberations and the excitement is palpable and some of the colleagues I've spoken to, not just in England, but of course all over the world. So congratulations on that. It was a big move for you to leave the hardcore academics. And the other thing I wanted to ask you, John, is you had distinguished your career in immunology, in genetics, type 1 diabetes and other conditions, autoimmune conditions, and now you've really diversified, as you described with these different areas of emphasis at the new institute. Is that more fun to do it or do you have deputies that you can assign to things like climate change in other areas?Sir John Bell (04:50):Trust me, Eric, I'm not making any definitive decisions about areas I know nothing about, but part of this is about how do you set up leadership, run a team, get the right people in. And I have to say one of the really interesting things about the institute is we've been able to recruit some outstanding people across all those domains. And as you know, success is almost all dependent on people. So we're really pretty optimistic we're going to have a significant impact. And of course, we also want to take risks because not a lot of point in us doing stuff that everybody else is doing. So we're going to be doing some things that are pretty way out there and some of them will fail, so we are just going to get used to trying to make sure we get a few of them across the finish line. But the other thing is that, and you've experienced this too, you never get too old to learn. I mean, I'm sucking up stuff that I never thought I would ever learn about, which is fun actually, and really marvel.Eric Topol (05:55):It's fantastic. I mean, you've really broadened and it's great that you have the runway to get these people on board and I think you're having a big building that's under construction?Sir John Bell (06:07):Yeah, we've got the original building that Larry committed to is about 330,000 square feet of space. I mean, this is completely amazing, but we are of course to accommodate up to 5,000 people, we're going to need more than that. So we are looking at a much wider campus here that'll involve more than just that building. I think we'll end up with several million square feet of space by the time we're finished. So mean, it's a really big project, but we've already made progress in some domains to try and get projects and the beginnings of companies on the road to try and solve some of the big problems. So we're quite excited about it.Eric Topol (06:49):Now you, I assume it's pretty close to Oxford, and will you have some kind of inter interactions that are substantial?Sir John Bell (06:58):Yeah, so the university's been terrific about this actually, because of course most universities would say, well, why don't you do it inside the university and just give us the money and it'll all be fine. So of course Larry. Larry wasn't born yesterday, so I said, well, thank you very much, but I think we'll probably do this nearby. But the university also realized this is a really exciting opportunity for them and we've got a really good relationship with them. We've signed an agreement with them as to who will work where. We've agreed not to steal a lot of their staff. We're going to be bringing new people into the ecosystem. Some of the university people will spend some time with us and sometime in the university, so that will help. But we're also bringing quite a few new people into the setting. So the university has been really positive. And I think one of the things that's attractive to the university, and you'll be familiar with this problem in the UK, is that we're quite good. The discovery science here is pretty good.Sir John Bell (08:06):And we do startups now at scale. So Oxford does lots of little startup companies in the biotech space and all the rest of it, but we never scale any of these companies because there isn't the depth of capital for scaling capital to get these things scaled. And so, in a way what we're trying to do here at Ellison actually avoids that problem because Larry knows how to scale companies, and we've got the financial support now. If we have things that are really successful, we can build the full stack solution to some of these problems. So I think the university is really intrigued as to how we might do that. We're going to have to bring some people in that know how to do that and build billion dollar companies, but it's sufficiently attractive. We've already started to recruit some really outstanding people. So as a way to change the UK system broadly, it's actually quite a good disruptive influence on the way the thing works to try and fix some of the fundamental problems.Eric Topol (09:07):I love that model and the ability that you can go from small startups to really transformative companies have any impact. It fits in well with the overall objectives, I can see that. The thing that also is intriguing regarding this whole effort is that in parallel we've learned your influence. The UK is a genomics world leader without any question and no coincidence that that's been your area of emphasis in your career. So we've watched these three initiatives that I think you were involved in the UK Biobank, which has had more impact than any cohort ever assembled. Every day there's another paper using that data that's coming out. There's Genomes England, and then now Our Future Health, which a lot of people don't know about here, which is well into the 5 million people enrollment. Can you tell us about, this is now 15 years ago plus when these were started, and of course now with a new one that's the biggest ever. What was your thinking and involvement and how you built the UK to be a world leader in this space?Sir John Bell (10:26):So if you turn the clock back 20 years, or actually slightly more than 25 years ago, it was clear that genomics was going to have a play. And I think many of us believed that there was going to be a genetic element to most of the major common disease turn out to be true. But at the time, there were a few skeptics, but it seemed to us that there was going to be a genetic story that underpinned an awful lot of human disease and medicine. And we were fortunate because in Oxford as you know, one of my predecessors in the Regius job was Richard Doll, and he built up this fantastic epidemiology capability in Oxford around Richard Peto, Rory Collins, and those folks, and they really knew how to do large scale epidemiology. And one of the things that they'd observed, which is it turns out to be true with genetics as well, is a lot of the effects are relatively small, but they're still quite significant. So you do need large scale cohorts to understand what you're doing. And it was really Richard that pioneered the whole thinking behind that. So when we had another element in the formula, which was the ability to detect genetic variation and put that into the formula, it seemed to me that we could move into an era where you could set up, again, large cohorts, but build into the ability to have DNA, interrogate the DNA, and also ultimately interrogate things like proteomics and metabolomics, which were just in their infancy at that stage.Sir John Bell (12:04):Very early on I got together because I was at that stage at the Nuffield Chair of Medicine, and I got together, Rory and Richard and a couple of others, and we talked a little bit about what it would look like, and we agreed that a half a million people late to middle age, 45 and above would probably over time when you did the power calculations, give you a pretty good insight in most of the major diseases. And then it was really a question of collecting them and storing the samples. So in order to get it funded at the time I was on the council of the MRC and George Radda, who you may remember, was quite a distinguished NMR physiologist here. He was the chief executive of the MRC. So I approached him and I said, look, George, this would be a great thing for us to do in the UK because we have all the clinical records of these people going back for a decade, and will continue to do that.Sir John Bell (13:01):Of course, we immediately sent it out to a peer review committee in the MRC who completely trashed the idea and said, you got to be joking. So I thought, okay, that's how that lasted. And I did say to George, I said, that must mean this is a really good idea because if it had gone straight through peer review, you would've known you were toast. So anyway, I think we had one more swing at peer review and decided in the end that wasn't going to work. In the end, George to his credit, took it to MRC council and we pitched it and everybody thought, what a great idea, let's just get on and do it. And then the Wellcome came in. Mark Walport was at the Wellcome at the time, great guy, and did a really good job at bringing the Wellcome on board.Sir John Bell (13:45):And people forget the quantum of money we had to do this at the time was about 60 million pounds. I mean, it wasn't astonishly small. And then of course we had a couple of wise people who came in to give us advice, and the first thing they said, well, if you ever thought you were really going to be able to do genetics on 500,000 people, forget it. That'll never work. So I thought, okay, I'll just mark that one out. And then they said, and by the way, you shouldn't assume you can get any data from the health service because you'll never be able to collect clinical data on any of these people. So I said, yeah, yeah, okay, I get it. Just give us the money and let us get on. So anyway, it's quite an interesting story. It does show how conservative the community actually is for new ideas.Sir John Bell (14:39):Then I chaired the first science committee, and we decided about a year into it that we really needed the chief executive. So we got Rory Collins to lead it and done it. I sat on the board then for the next 10 years, but well look, it was a great success. And as you say, it is kind of the paradigm for now, large genetic epidemiology cohorts. So then, as you know, I advise government for many years, and David Cameron had just been elected as Prime Minister. This was in about 2010. And at the time I'd been tracking because we had quite a strong genomics program in the Wellcome Trust center, which I'd set up in the university, and we were really interested in the genetics of common disease. It became clear that the price of sequencing and Illumina was now the clear leader in the sequencing space.Sir John Bell (15:39):But it was also clear that Illumina was making significant advances in the price of sequencing because as you remember, the days when it cost $5,000 to do a genome. Anyway, it became clear that they actually had technology that gets you down to a much more sensible price, something like $500 a genome. So I approached David and I said, we are now pretty sure that for many of the rare diseases that you see in clinical practice, there is a genetic answer that can be detected if you sequenced a whole genome. So why don't we set something up in the NHS to provide what was essentially the beginnings of a clinical service to help the parents of kids with various disabilities work out what's going on, what's wrong with their children. And David had had a child with Ohtahara syndrome, which as you know is again, and so David was very, he said, oh God, I'll tell you the story about how awful it was for me and for my wife Samantha.Sir John Bell (16:41):And nobody could tell us anything about what was going on, and we weren't looking for a cure, but it would've really helped if somebody said, we know what it is, we know what the cause is, we'll chip away and maybe there will be something we can do, but at least you know the answer. So anyway, he gave us very strong support and said to the NHS, can you please get on and do it? Again massive resistance, Eric as you can imagine, all the clinical geneticists said, oh my God, what are they doing? It's complete disaster, dah, dah, dah. So anyway, we put on our tin hats and went out and got the thing going. And again, they did a really good job. They got to, their idea was to get a hundred thousand genomes done in a reasonable timeframe. I think five years we set ourselves and the technology advance, people often underestimate the parallel development of technology, which is always going on. And so, that really enabled us to get that done, and it still continues. They're doing a big neonatal program at the moment, which is really exciting. And then I was asked by Theresa May to build a life science strategy because the UK, we do this stuff not as big and broad as America, but for a small country we do life sciences pretty well.Eric Topol (18:02):That's an understatement, by the way. A big understatement.Sir John Bell (18:04):Anyway, so I wrote the strategies in 2017 for Theresa about what we would do as a nation to support life sciences. And it was interesting because I brought a group of pharma companies together to say, look, this is for you guys, so tell us what you want done. We had a series of meetings and what became clear is that they were really interested in where healthcare was going to end up in the next 20 years. And they said, you guys should try and get ahead of that wave. And so, we agreed that one of the domains that really hadn't been explored properly, it was the whole concept of prevention.Sir John Bell (18:45):Early diagnosis and prevention, which they were smart enough to realize that the kind of current paradigm of treating everybody in the last six months of life, you can make money doing that, there's no doubt, but it doesn't really fix the problem. And so, they said, look, we would love it if you created a cohort from the age of 18 that was big enough that we could actually track the trajectories of people with these diseases, identify them at a presymptomatic stage, intervene with preventative therapies, diagnose diseases earlier, and see if we could fundamentally change the whole approach to public health. So we anyway, went back and did the numbers because of course at much wider age group, a lot of people don't get at all sick, but we thought if we collected 5 million people, we would probably have enough. That's 10% of the UK adult population.Sir John Bell (19:37):So anyway, amazingly the government said, off you go. We then had Covid, which as you know, kept you and I busy for a few years before we could get back to it. But then we got at it, and we hired a great guy who had done a bit of this in the UAE, and he came across and we set up a population health recruitment structure, which was community-based. And we rapidly started to recruit people. So we've now got 2.9 million people registered, 2.3 million people consented, and we've got blood in the bank and all the necessary data including questionnaire data for 1.5 million people growing up. So we will get to 5 million and it's amazing.Eric Topol (20:29):It is. It really is, and I'm just blown away by the progress you've made. And what was interesting too, besides you all weren't complacent about, oh, we got this UK Biobank and you just kept forging ahead. And by the way, I really share this importance of finally what has been a fantasy of primary prevention, which never really achieved. It's always, oh, after a heart attack. But that's what I wrote about in the Super Agers book, and I'll get you a copy.Sir John Bell (21:02):No, I know you're a passionate believer in this and we need to do a lot of things. So we need to work out what's the trial protocol for primary prevention. We need to get the regulators on board. We've got to get them to understand that we need diagnostics that define risk, not disease, because that's going to be a key bit of what we're going to try and do. And we need to understand that for a lot of these diseases, you have to intervene quite early to flatten that morbidity curve.Eric Topol (21:32):Yeah, absolutely. What we've learned, for example, from the UK Biobank is not just, of course the genomics that you touched on, but the proteomics, the organ clocks and all these other layers of data. So that gets me to my next topic, which I know you're all over it, which is AI.Eric Topol (21:51):So when I did the NHS review back in 2018, 2019, the group of people which were amazing that I had to work with no doubt why the UK punches well beyond its weight. I had about 50 people, and they just said, you know what? Yeah, we are the world leaders in genomics. We want to be the world leader in AI. Now these days you only hear about US and China, which is ridiculous. And you have perhaps one of the, I would say most formidable groups there with Demis and Google DeepMind, it's just extraordinary. So all the things that the main foci of the Ellison Institute intersect with AI.Sir John Bell (22:36):They do. And we, we've got two underpinning platforms, well actually three underpinning platforms that go across all those domains. Larry was really keen that we became a real leader in AI. So he's funded that with a massive compute capacity. And remember, most universities these days have a hard time competing on compute because it's expensive.Eric Topol (22:57):Oh yeah.Sir John Bell (22:58):So that is a real advantage to us. He's also funded a great team. We've recruited some people from Demis's shop who are obviously outstanding, but also others from around Europe. So we really, we've recruited now about 15 really outstanding machine learning and AI people. And of course, we're now thinking about the other asset that the UK has got, and particularly in the healthcare space is data. So we do have some really unique data sets because those are the three bits of this that you need if you're going to make this work. So we're pretty excited about that as an underpinning bit of the whole Ellison Institute strategy is to fundamentally underpin it with very strong AI. Then the second platform is generative biology or synthetic biology, because this is a field which is sort of, I hesitate to say limped along, but it's lacked a real focus.Sir John Bell (23:59):But we've been able to recruit Jason Chin from the LMB in Cambridge, and he is one of the real dramatic innovators in that space. And we see there's a real opportunity now to synthesize large bits of DNA, introduce them into cells, microbes, use it for a whole variety of different purposes, try and transform plants at a level that people haven't done before. So with AI and synthetic biology, we think we can feed all the main domains above us, and that's another exciting concept to what we're trying to do. But your report on AI was a bit of a turning point for the UK because you did point out to us that we did have a massive opportunity if we got our skates, and we do have talent, but you can't just do it with talent these days, you need compute, and you need data. So we're trying to assemble those things. So we think we'll be a big addition to that globally, hopefully.Eric Topol (25:00):Yeah. Well that's another reason why I am so excited to talk to you and know more about this Ellison Institute just because it's unique. I mean, there are other institutes as like Chan Zuckerberg, the Arc Institute. This is kind of a worldwide trend that we're seeing where great philanthropy investments are being seen outside of government, but none have the computing resources that are being made available nor the ability to recruit the AI scientists that'll help drive this forward. Now, the last topic I want to get into with you today is one that is where you're really grounded in, and that's the immune response.Eric Topol (25:43):So it's pretty darn clear now that, well, in medicine we have nothing. We have the white cell neutrophil to lymphocyte ratio, what a joke. And then on the other hand, we can do T and B cell sequencing repertoires, and we can do all this stuff, autoantibody screens, and the list goes on and on. How are we ever going to make a big dent in health where we know the immune system is such a vital part of this without the ability to check one's immune status at any point in time in a comprehensive way? What are your thoughts about that?Sir John Bell (26:21):Yeah, so you seem to be reading my mind there. We need to recruit you over here because I mean, this is exactly, this is one of our big projects that we've got that we're leaning into, and that is that, and we all experienced in Covid the ins and outs of vaccines, what works, what doesn't work. But what very clear is that we don't really know anything about vaccines. We basically, you put something together and you hope the trial works, you've got no intermediate steps. So we're building a really substantial immunophenotyping capability that will start to interrogate the different arms of the immune response at a molecular level so that we can use a combination of human challenge models. So we've got a big human challenge model facility here, use human challenge models with pathogens and with associated vaccines to try and interrogate which bits of the immune response are responsible for protection or therapy of particular immunologically mediated diseases or infectious diseases.Sir John Bell (27:30):And a crucial bit to that. And one of the reasons people have tried this before, but first of all, the depth at which you can interrogate the immune system has changed a lot recently, you can get a lot more data. But secondly, this is again, where the AI becomes important because it isn't going to be a simple, oh, it's the T-cell, it's going to be, well, it's a bit of the T cells, but it's also a bit of the innate immune response and don't forget mate cells and don't forget a bit of this and that. So we think that if we can assemble the right data set from these structured environments, we can start to predict and anticipate which type of immune response you need to stimulate both for therapy and for protection against disease. And hopefully that will actually create a whole scientific foundation for vaccine development, but also other kinds of immune therapy and things like cancer and potentially autoimmune disease as well. So that's a big push for us. We're just busy. The lab isn't set up. We've got somebody to run the lab now. We've got the human challenge model set up with Andy Pollard and colleagues. So we're building that out. And within six months, I think we'll be starting to collect data. So I'm just kind of hoping we can get the immune system in a bit more structured, because you're absolutely right. It's a bit pin the tail on the donkey at the moment. You have no idea what's actually causing what.Eric Topol (29:02):Yeah. Well, I didn't know about your efforts there, and I applaud that because it seems to me the big miss, the hole and the whole story about how we're going to advanced human health and with the recent breakthroughs in lupus and these various autoimmune diseases by just targeting CD19 B cells and resetting like a Ctrl-Alt-Delete of their immune system.Sir John Bell (29:27):No, it's amazing. And you wouldn't have predicted a lot of this stuff. I think that means that we haven't really got under the skin of the mechanistic events here, and we need to do more to try and get there, but there's steady advance in this field. So I'm pretty optimistic we'll make some headway in this space over the course of the next few years. So we're really excited about that. It's an important piece of the puzzle.Eric Topol (29:53):Yeah. Well, I am really impressed that you got all the bases covered here, and what a really exhilarating chance to kind of peek at what you're doing there. And we're going to be following it. I know I'm going to be following it very closely because I know all the other things that you've been involved with in your colleagues, big impact stuff. You don't take the little swings here. The last thing, maybe to get your comment, we're in a state of profound disruption here where science is getting gutted by a madman and his henchmen, whatever you want to call it, which is really obviously a very serious state. I'm hoping this is a short term hit, but worried that this will have a long, perhaps profound. Any words of encouragement that we're going to get through this from the other side of the pond?Sir John Bell (30:52):Well, I think regardless of the tariffs, the scientific community are a global community. And I think we need to remember that because our mission is a global mission, and we need to lean into that together. First of all, America is such a powerhouse of everything that's been done scientifically in the human health domain. But not only that, but across all the other domains that we work in, we can't really make the kind of progress that we need to without America being part of the agenda. So first of all, a lot of sympathy for you and your colleagues. I know it must be massively destabilizing for you, not be confident that the things that work are there to help you. But I'm pretty confident that this will settle down. Most of the science is for, well, all the science is really for public good, and I think the public recognizes it and they'll notice if it's not being prosecuted in the way that it has to be. And the global science community cannot survive without you. So we're all leaning in behind you, and I hope it will settle. One of my worries is that these things take years to set up and literally hours or minutes to destroy. So we can't afford to take years to set them back up again. So we do need to be a bit careful about that, but I still have huge confidence in what you guys can achieve and we're all behind you.Eric Topol (32:37):Well, that's really helpful getting some words of wisdom from you there, John. So this has been terrific. Thanks so much for joining, getting your perspective on what you're doing, what's important is so essential. And we'll stay tuned for sure.Sir John Bell (32:59):And come and visit us at the EIT, Eric. We'd be glad to see you.*******************************Some of the topics that John and I discussed—immunology, A.I., genomics, and prevention—are emphasized in my new book SUPER AGERS. A quick update: It will have a new cover after making the New York Times Bestseller list and is currently ranked #25 for all books on Amazon. Thanks to so many of you for supporting the book!Here are a few recent podcasts:Dax Shepard: Dr. Mike Sanjay Gupta ***********************Thanks for reading and subscribing to Ground Truths.If you found this interesting please share it!That makes the work involved in putting these together especially worthwhile.All content on Ground Truths— newsletters, analyses, and podcasts—is free, open-access.Paid subscriptions are voluntary and all proceeds from them go to support Scripps Research. They do allow for posting comments and questions, which I do my best to respond to. Please don't hesitate to post comments and give me feedback. Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. Get full access to Ground Truths at erictopol.substack.com/subscribe

MRC welcomes the legendary British penciller Mike Collins (who drew the first appearance of Gambit!) to discuss the books of November 1967, featuring Amazing Spider-Man 54, Daredevil 34, Thor 146, Tales to Astonish 97 with Namor and Hulk, and X-Men 38! Roomer has it! Too Dumb to Die! Volstagless-Thor! Swamp Men! Living Lightning! Blobby pupils! Check it out!

In today's MadTech Daily, we cover the IAB and MRC's release of draft guidelines for attention measurement, Frasers Group's launch of retail media network ELEVATE, and new research valuing the global podcast industry at USD$7.3bn, more than double previous estimates.

Entérate de lo que está cambiando el podcasting y el marketing digital:-Interpodcast 2025 arranca con una nueva edición internacional de intercambio podcastero.-IAB y MRC lanzan métricas de atención para audio y medios digitales.-Cómo mujeres afroamericanas están transformando su futuro financiero a través del podcasting.-El futuro de un auto sin radio inquieta a la industria.Patrocinios ¿Estás pensando en anunciar tu negocio, producto o pódcast en México? En RSS.com y RSS.media tenemos la solución. Contamos con un amplio catálogo de pódcast para conectar tu mensaje con millones de oyentes en México y LATAM. Escríbenos a ventas@rss.com y haz crecer tu idea con nosotros.Entérate, en solo cinco minutos, sobre las noticias, herramientas, tips y recursos que te ayudarán a crear un pódcast genial y exitoso. Subscríbete a la “newsletter“ de Via Podcast.

La menace spatiale! Shamelessplug Hackfest Swag Join Hackfest/La French Connection Discord Join Hackfest us on Mastodon Nouvelles La menace spatiale! Explosion d ‘emploi en cybersécurité, une vraie farce CVE will live on DOGE Whistle blower DOGE via NPR SSH exploit Deepfake et ingénierie sociale….seriez-vous différencier le vrai du faux avec vos proches SuperCard X Android Malware Enables Contactless ATM and PoS Fraud via NFC Relay Attacks Piratage et demande de rançon à la MRC de Maskinongé Dossier santé numérique: un conflit d'intérêts comme dans le fiasco SAAQclic? Publier une simple photo peut vous mettre en DANGER Crew Patrick Mathieu Steve Waterhouse Francis Coats Jacques Sauvé Richer Dinelle Crédits Montage audio par Hackfest Communication Music par Ecometric – TransPlants - Beatroots - Sailor (Ecometric Renavigation) Locaux virtuels par Streamyard

MRC finishes up October of 1967 with Fantastic Four 67, Strange Tales 161 with SHIELD and Dr. Strange, Tales of Suspense 94 with Iron Man and Captain America, and Avengers 45. The Creature in Lock 41! The Id-Paralyzer! All-Swipes! Titanium Miniskirts! MODOK vs. Beekeepers! Waffle-Pattern Eyes! Check it out!

Guest Bill D'Agostino, Research Analyst with MRC, joins to discuss low ratings and trust in the mainstream media. Discussion of negative coverage of the Trump administration, the changes of media coverage for ratings and profits, and the future of gathering content.  Update on Florida State Shooting and upcoming 2A debate on firearms.  REAL ID coming in May in order to travel? What is the purpose for another federal ID and who will be following the new rule? 

En 2009, une étude menée par le Conseil de Recherche Médicale d'Afrique du Sud (MRC) a révélé que plus d'un quart des hommes sud-africains interrogés ont admis avoir commis un viol. Cette enquête, dirigée par la professeure Rachel Jewkes, a porté sur un échantillon représentatif de 1 738 hommes des provinces du Cap-Oriental et du KwaZulu-Natal. Principaux résultats de l'étude :27,6 % des hommes interrogés ont reconnu avoir violé une femme ou une fille.Parmi eux, 23,2 % ont déclaré avoir violé deux ou trois femmes, 8,4 % entre quatre et cinq, 7,1 % entre six et dix, et 7,7 % plus de dix femmes ou filles. 46,5 % des auteurs de viols ont commis leur premier acte entre 15 et 19 ans, et 9,8 % avant l'âge de 10 ans.Ces chiffres alarmants mettent en lumière une culture de la violence sexuelle profondément enracinée en Afrique du Sud. Les raisons évoquées par les auteurs incluent la recherche de "plaisir", l'ennui, la pression des pairs et des notions de punition envers les femmes. Facteurs contribuant à cette situation :Normes culturelles et sociales : Des idées de masculinité basées sur la hiérarchie de genre et le sentiment d'un droit sexuel des hommes sont répandues. Inégalités socio-économiques : Les disparités économiques et le chômage élevé exacerbent les tensions et la violence.Héritage de l'apartheid : La période de l'apartheid a laissé une société fragmentée avec des structures familiales déstabilisées et une méfiance envers les institutions. Conséquences sur la santé publique :L'étude a également établi un lien entre la violence sexuelle et la prévalence du VIH. Les hommes violents envers leurs partenaires sont deux fois plus susceptibles d'être séropositifs. De plus, une femme violée par un homme de plus de 25 ans a une chance sur quatre que son agresseur soit porteur du VIH. Réactions et mesures prises :Face à ces révélations, des organisations locales et internationales ont intensifié leurs efforts pour lutter contre la violence sexuelle en Afrique du Sud. Des campagnes de sensibilisation ont été lancées pour remettre en question les normes de genre toxiques et promouvoir des relations égalitaires. Cependant, malgré des lois progressistes, leur application reste insuffisante, et la culture de l'impunité persiste. Conclusion :Les résultats de l'étude du MRC ont mis en évidence l'ampleur de la crise de la violence sexuelle en Afrique du Sud. Ils soulignent la nécessité d'une approche multidimensionnelle, combinant des réformes législatives, des programmes éducatifs et des initiatives communautaires pour transformer les attitudes et réduire la prévalence du viol dans le pays. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

MRC launches into October of 1967 with Amazing Spider-Man #53, Daredevil #33, Thor #145, Tales to Astonish #96 with Namor and Hulk, and X-Men #37! Seeds of the clone sagas! A laundry list of things not associated with beetles! T-Shirt Thor! Polar Serpents! The Beginning of the End of Human Evolution! Far Out Helmets! Check it out!

Dan Schneider, Vice President for Free Speech at the Media Research Center, joins me to discuss Big Tech's censorship of conservative voices and the legacy media's unwillingness to reform in the wake of Trump's 2024 election victory. - - -  Today's Sponsor: Helix Sleep - Go to https://helixsleep.com/klavan to get an exclusive offer.

Jerry Giordano, author of Your 7 Words to a Happier You: Unlock the Story Sabotaging Your Relationships? With personal insights and a lot of humor, Jerry will talk about why we do what we do and how it's sabotaging our relationships and ourselves. Jerry has put his 7-word philosophy into practice by interviewing over 200 people from ages thirteen to ninety-four. He can share: How he tried every form of therapy, seminar, retreat, life coach, past-life regression, psychic and self-help book available, but still felt the same His realization that these were all left-brained approaches (logic) to a right-brained problem (emotion)Hitting rock bottom -- in the span of weeks, he lost his mother to cancer and his fiancée broke up with him How his newfound mindfulness practice and meditations helped him discover that his easygoing, people-pleasing persona was fake How he discovered the 7 words approach and how that's led to an in-depth understanding of the unconscious story that was affecting his life “As a psychotherapist, introducing a number of clients to their 7 Words has been an effective tool for uncovering their unconscious stories and circumventing their sabotaging lifelong patterns. The discovery of my own words was the breakthrough I was unknowingly in search of for decades! Jerry's writing exudes an uncommon vulnerability, clarity and authenticity, and this book takes self-help/self-discovery to a transcendent level.”— Melissa D. Borski, MRC, CFRC, LPCBecome a supporter of this podcast: https://www.spreaker.com/podcast/arroe-collins-unplugged-totally-uncut--994165/support.

MRC wraps up September 1967 with Fantastic Four #66, Strange Tales #160 with SHIELD and Dr. Strange, Tales of Suspense #93 with Iron Man and Captain America and Avengers #44! Electroni-Blades! Gravity-Nullifying Belts! The Lost Communion of Evil Intent! MODOK! Deadly belt buckles! Check it out!

Les recherches en génomique humaine effectuées en Afrique ont été le sujet principal du sommet de la Human Genome Organisation (HUGO) qui s'est tenu pour la première fois sur le continent en mars, dans la ville sud-africaine de Durban. Comme dans le cas de l'intelligence artificielle, le domaine de la génétique est aussi victime d'un biais dans la construction de son modèle de référence, avec très peu de données venues d'Afrique. Et cela peut avoir des conséquences pour le traitement des populations locales et pour la recherche mondiale. De notre envoyée spéciale à Durban,Faute d'infrastructures, de ressources ou de personnel, beaucoup de maladies génétiques restent non détectées sur le continent. En République démocratique du Congo (RDC), Aimé Lumaka, en est régulièrement témoin avec son équipe.« Nous avons, au début de notre carrière, rencontré une famille qui a perdu environ 14 garçons. Leur peau devenait très noire et ils mourraient. Nous avons pensé à une maladie génétique, et nous avons pu la confirmer, explique le chercheur de l'université de Kinshasa. Ce qui était choquant, c'est que c'était une maladie qu'on pouvait traiter facilement avec une supplémentation en cortisol. C'est dans ce genre de situation qu'on voit la force de la génomique : cela peut permettre d'éviter des décès inutiles, des décès évitables. »À lire aussiCes scientifiques qui tentent de faire progresser la recherche génomique en Afrique« La médecine de précision est très importante »Le manque de recherches sur les variations des génomes en Afrique complique aussi les diagnostics, car les bases de données proposent comme référence des séquençages liés à des populations d'origine européenne ou américaine.Segun Fatumo travaille sur la question de la diversité génétique pour l'université Queen Mary de Londres, et le Conseil pour la recherche médicale (MRC) d'Ouganda : « La médecine de précision est très importante. Un traitement qui fonctionne bien sur des personnes qui ont une ascendance spécifique, peut ne pas aussi bien marcher pour d'autres. C'est pour cela que l'on doit étudier les génomes de tout le monde. »Un médicament anti-cholestérol conçu grâce à des études génétiquesL'absence de données freine, de plus, le développement de traitements pour les maladies génétiques qui touchent particulièrement le continent, comme la drépanocytose. Sans compter que la recherche en Afrique et l'identification de mutations peuvent avoir un intérêt pour le reste du monde. La professeure de l'université du Witwatersrand Michèle Ramsay prend l'exemple un médicament anti-cholestérol conçu grâce à des études génétiques.« Cette découverte a été réalisée grâce à l'observation de mutations génétiques qui sont davantage répandues chez des populations d'origine africaine, et on savait que ces populations avaient un taux de cholestérol plus bas que la normale. Il y a encore beaucoup de choses que l'on ignore, sur le plan de la biologie, et la génétique peut nous apporter des indices. S'il y a des variants, en Afrique, qui ne sont pas sortis du continent, et qui ont pu être sélectionnés à cause de facteurs environnementaux, ces variants vont être associés à certaines spécificités. Et si on arrive à comprendre ce lien, cela peut créer des opportunités en termes d'intervention, pour n'importe qui dans le monde. »Mais si des découvertes sont faites à partir de données africaines, les chercheurs sont unanimes : il faut mettre des protocoles en place afin que les populations du continent puissent aussi bénéficier des résultats et des traitements.À lire aussiEn Afrique, développer les connaissances sur les variations du génome [1/3]

MRC goes guestless to tackle the first half of September, 1967, with Amazing Spider-Man 52, Daredevil 32, Thor 144, Tales to Astonish 95 with Namor and the Hulk, and X-Men 36! Penthouse Dungeons! Convenient antidotes! Asgaaard! The resource curse! Vacuum rays! The Quest for Gas Money! Check it out!

RECORDED LIVE from the MRC 2025 Vegas conference, Angela Borden, Fraud Specialist at Little Caesars, and Lisa Meyers, founder of Mastfiv Consulting, join the show recorded in the same room for a change! Angela is fresh off her first-ever speaking panel where she discussed the common "Build vs. Buy" scenario product people face. We discuss some key takeaways from our time so far at the show like the evolving role of AI in fraud management and the industry's future direction in areas like ad fraud, Visa and Mastercard network changes and of course Visa's VAMP program and recent changes We end with some practical advice for conference-goers: capturing actionable insights, justifying attendance costs, and planning follow-ups. Overall, the short episode highlights industry shifts, new fraud prevention trends, and insights into navigating professional growth and networking at major conferences.   Angela Borden: https://www.linkedin.com/in/angelamborden/ Lisa Meyers: https://www.linkedin.com/in/lisakmeyers/  

Buying a car is a big deal. Unless you live in a walkable area, your car is likely the primary method of transportation used to get around. If so, you'll want something reliable as well as affordable. Many factors affect the price of vehicles from inflation, chip shortages, supply chain interruptions, and even the possibility of looming tariffs. At the time of this recording the average new car price is around $48,000 and with a price tag like that, it may be wise to make sure the next car you choose is reliable. But with so many cars to choose from, how do you know which is the best for you? Keep listening to learn what cars should be your next ride.  Links: Check out the Consumer Report for the Most Reliable Cars for 2025 Shop for a new car with Triangle's AutoSmart tool Learn more about Mechanical Repair Coverage Check out TCU University for financial education tips and resources!  Follow us on Facebook, Instagram and Twitter!  Learn more about Triangle Credit Union Transcript: Welcome to Money Tip Tuesday from the Making Money Personal podcast.   A good place to start when looking for a reliable vehicle is Consumer Reports. Consumer Reports is a nonprofit organization that unbiasedly tests products with consumers in mind, to educate and inform potential buyers. For this particular report, they asked their members about the variety of car problems they encountered in the past 12 months. As a result, Consumer Reports gathered information on over 300,000 vehicles with model years ranging from 2000 to 2025.   They then looked at problem areas, from minor inconveniences such as squeaky brakes and broken interior trim to major problems like engine or transmission issues. Consumer Reports then used the results to score the reliability of vehicles in all the different areas, with the major problems being weighted more.  According to Consumer Reports' findings, the top 3 most reliable new car brands for 2025 are Subaru, Lexus, and Toyota. On the other side, the bottom 3 unreliable new car brands turned out to be GMC, Cadillac, and Rivian. For those looking to buy a used car, the top 3 most reliable brands are Lexus, Toyota, and Mazda. The bottom 3 unreliable brands are Dodge, Jeep, and Chrysler.   If you were considering getting an electric vehicle, Consumer Reports found that hybrids are the way to go. Results showed they are incredibly fuel efficient and just as reliable as gas powered cars. It was revealed that pure electric vehicles, on the other hand, have 42% more problems than gas-powered and hybrids and plug-in hybrids have 70% more problems than gas-powered and conventional hybrids. For those thinking of purchasing an electric vehicle it's important to consider how much driving you plan on doing. They don't have as far a range as gas-powered and hybrid vehicles, so make sure the infrastructure around you and wherever you plan to travel supports electric vehicles. Remember to check beforehand to see if there are any charging stations near you.  To explore more information and data on this particular report, visit consumerreports.org or check the link in the show notes.  Another great way to determine a car's reliability is to ask a trusted mechanic. They work constantly on cars and know which ones come in the most and what common issues are. Before buying a car, you can take it to a mechanic for an inspection. Similarly, ask friends and family what kind of car they drive, if they like it, and how dependable it is.  Okay, so what if you're considering a car that maybe wasn't on the Consumer Report's top reliable vehicle list. Maybe you've been eyeing that Jeep, Cadillac or Rivian for quite some time now? That's completely fine! Just do your research beforehand, talk to friends and mechanics to make sure you're fully aware of any long-term costs and maintenance associated with your vehicle. Another great way to make sure your car doesn't end up costing you more than you initially planned, is to consider getting Mechanical Repair Coverage, or MRC for short. MRC can help limit unexpected, covered repairs as your vehicle ages, potentially saving you thousands of dollars. Learn more about MRC and how to get it today at Triangle Credit Union. Visit trianglecu.org to check it out!  If there are any other tips or topics you'd like us to cover, let us know at tcupodcast@trianglecu.org. Also, remember to like and follow our Making Money Personal Facebook and Instagram to share your thoughts. Finally, remember to look for our sponsor, Triangle Credit Union, on Facebook and LinkedIn.         Thanks for listening to today's Money Tip Tuesday. Check out our other tips and episodes on the Making Money Personal podcast.    

Jerry Giordano, author of Your 7 Words to a Happier You: Unlock the Story Sabotaging Your Relationships? With personal insights and a lot of humor, Jerry will talk about why we do what we do and how it's sabotaging our relationships and ourselves. Jerry has put his 7-word philosophy into practice by interviewing over 200 people from ages thirteen to ninety-four. He can share: How he tried every form of therapy, seminar, retreat, life coach, past-life regression, psychic and self-help book available, but still felt the same His realization that these were all left-brained approaches (logic) to a right-brained problem (emotion)Hitting rock bottom -- in the span of weeks, he lost his mother to cancer and his fiancée broke up with him How his newfound mindfulness practice and meditations helped him discover that his easygoing, people-pleasing persona was fake How he discovered the 7 words approach and how that's led to an in-depth understanding of the unconscious story that was affecting his life “As a psychotherapist, introducing a number of clients to their 7 Words has been an effective tool for uncovering their unconscious stories and circumventing their sabotaging lifelong patterns. The discovery of my own words was the breakthrough I was unknowingly in search of for decades! Jerry's writing exudes an uncommon vulnerability, clarity and authenticity, and this book takes self-help/self-discovery to a transcendent level.”— Melissa D. Borski, MRC, CFRC, LPCBecome a supporter of this podcast: https://www.spreaker.com/podcast/arroe-collins-like-it-s-live--4113802/support.

George O'Connor returns to help MRC finish off August of 1967 with Fantastic Four 65, Strange Tales 159 with SHIELD and Dr. Strange, Tales of Suspense 92 with Iron Man and Captain America, and Avengers 43! Auras of Negativism! Contessa Valentina Allegra de Fontaine! La Leche Es Verde! 4/5ths Face! The Ultimate No-Prize! Convenient Homing-Beam Gizmos! Check it out!

Dr. John Sweetenham and Dr. James Foran discuss the evolving treatment landscape in acute myeloid leukemia, including new targeted therapies, advances in immunotherapy, and the current role for allogeneic transplantation. TRANSCRIPT Dr. John Sweetenham: Hello, I'm Dr. John Sweetenham, the host of the ASCO Daily News Podcast. There has been steady progress in the therapies for acute myeloid leukemia (AML) in recent years, largely based on an increasing understanding of the molecular mechanisms which underlie the disease. On today's episode, we'll be discussing the evolving treatment landscape in AML. We'll explore risk group stratification, new targeted therapies, advances in immunotherapy for AML, and also a little about the current role for allogenic transplantation in this disease.  I'm delighted to welcome Dr. James Foran to this discussion. Dr. Foran is a professor of medicine and chair of the Myeloid Malignancies and Blood and Marrow Transplant Disease Group at the Mayo Clinic Comprehensive Cancer Center. He's based in Jacksonville, Florida.  Our full disclosures are available in the transcript of this episode.  James, it's great to have you join us on the podcast today, and thanks so much for being here. Dr. James Foran: I'm delighted and thank you for the invitation. Thank you very much. Dr. John Sweetenham: Sure, James, let's get right into it. So, our understanding of the molecular mechanisms underlying AML has resulted not only in new methods for risk stratification in this disease, which have added refinement to cytogenetics, but also has resulted in the development of many new targeted agents. Understanding that this is a complex area of investigation, and our time is somewhat limited, can you give us a high-level update on the current state of the art in terms of how risk factors are being used for treatment selection now? Dr. James Foran: Absolutely. I think in the past, you know, we had things broken down pretty simply into make a diagnosis based on morphology, do cytogenetics, break patients into the groups of those who were more likely to benefit from therapy – so-called favorable risk – those where the intensive therapies were less likely to work – so-called poor adverse risk, and then this large intermediate group that really had variable outcomes, some better, some worse. And for a long time, the progress was in just identifying new subtle cytogenetic risk groups. And then, late 1990s, we began to understand that FLT3 mutations or NRAS mutations may be more adverse than others that came along. In the first part of this millennium, in the, you know, 2000-2010 range, a lot of work was being done to understand better or worse risk factors with single genes. The ability to do multiplex PCR, and then more recently NGS platforms, have allowed us to really look at many genes and identify many mutations in patients. At the beginning that was used just to sort of refine – who did a little better, who did a little worse with intensive therapy – helped us decide who may benefit more from an allogeneic transplanter for whom that would not be necessary.  But the good news is that really, we're now starting to target those mutations. One of the first molecularly targeted treatments in leukemia was FLT3 mutations, where we knew they were adverse. Then along came targeted treatments. I was involved in some of those early studies looking at sunitinib, sorafenib, more recently midostaurin, now quizartinib, FDA approved, and gilteritinib in the relapse refractory setting.  So we're moving into a state where we're not just refining prognosis, we're identifying targets. You know, it's been slow progress, but definite incremental progress in terms of outcomes by looking for FLT3 mutations, then looking for IDH mutations, and more recently, mutations involving NPM1 or rearrangement of what we used to call the MLL gene, now the lysine methyltransferase 2A or KMT2A rearrangement, where we now have targets. And it's not just for refinement of prognosis, but now we're identifying therapeutic targets for patients and ways to even look for measurable residual disease which is impacting our care. Dr. John Sweetenham: That's great, James. And I'm going to expand on that theme just a little bit and perhaps ask you to elaborate a little bit more on how the introduction of these new therapies have specifically impacted frontline therapy. And a couple of ancillary questions maybe to go along with that: First of all, is ‘7+3' a standard therapy for anybody in 2025? And maybe secondly, you know, could you comment also maybe briefly on older patients with AML and how you think maybe the treatment landscape is changing for them compared with, say, 5 or 10 years ago? Dr. James Foran: I'll start with the therapy and then work my way back. So we've had ‘7+3' cytarabine daunorubicin or cytarabine anthracycline since 1976, and we're still using it as the backbone of our intensive therapy. There is still an important role for it, particularly in younger or fitter patients, and particularly for those with intermediate or favorable risk genetic groups or cytogenetic risk groups just because we achieve high rates of remission. Our 30-day induction mortality rates are lower now than they were 10 and 20 years ago. Our supportive care is better. And we still have a busy inpatient hospital service here at Mayo Florida and my colleagues in Rochester and Arizona as well giving intensive therapy. So that remains the backbone of curative therapy for younger adults. We are trying to be a little more discriminating about who we administer that to. We are trying to add targeted agents. We know from, now, two different randomized trials that the addition of a FLT3 inhibitor, either midostaurin or more recently quizartinib, has a survival advantage in patients with a FLT3 mutation, or for quizartinib, a FLT3/ITD mutation. And so yes, ‘7+3' remains important.  Off protocol for somebody who just comes in with acute leukemia in a 40-year-old or 30-year-old or even early 60s and fit, we would still be considering ‘7+3' therapy and then waiting for an expedited gene mutation panel and an expedited cytogenetics panel to come back to help us discriminate is that a patient for whom we should be giving a FLT3 inhibitor? I think there's a little more nuance about when we do a day 14 bone marrow, do they really matter as much anymore? I still do them. Some of my colleagues find them less important. But we're still giving intensive therapy. We're still giving high-dose ARA-C consolidation for younger patients who achieve complete remission.  In older adults, it's a different story. You know, it was only in the early part of the 2000s – 2004, 2007 range – where we really got buy-in from randomized studies that low-dose therapy was better than no therapy. There was a lot of nihilism before then about therapy for older adults, especially over age 75. We know that low-dose ARA-C is better than nothing. It looked like azacitidine was better than ARA-C or at least equivalent or slightly better. But with the advent of venetoclax it was a game changer. I ran a national randomized study of intensive therapy in AML. It was the last national randomized study of intensive therapy in older patients right before venetoclax got approved. And we were very excited about our results, and we thought we had some really interesting clinical results. And suddenly that's a little bit obsolete in patients over 70 and particularly over age 75 because of the high remission rates with azacytidine venetoclax or hypomethylating agents, so-called HMAs and venetoclax and the survival advantage. Now, it's not a home run for everybody. We quote 60% to 70% remission rates, but it's a little different based on your cytogenetics and your mutation profile. You have to continue on therapy so it's continuous treatment. It's not with curative intent, although there are some people with long-term remission in it. And the median survival went from 10 months to 15 months. So home run? No, but definitely improved remissions, meaningful for patients off transfusions and better survival. So right now it's hard to find an older adult who you wouldn't give azacitidine and venetoclax or something similar, decitabine, for instance, and venetoclax, unless somebody really was moribund or had very poor performance status or some reason not to. And so ‘7+3' is still relevant in younger adults. We're trying to get better results with ‘7+3' by adding targeted agents and azacitine and venetoclax in older adults.  I think the area of controversy, I guess there are two of them, is what to do in that overlap age between 60 and 75. Should people in that age still get intensive therapy, which we've used for years – the VIALE-A trial of aza-venetoclax was age 75 plus – or with cardiac comorbidities? And I think if you're 68 or 72, many of us are starting to bias towards aza-venetoclax as generally being better tolerated, generally being more outpatient, generally being slow and steady way to get a remission. And it doesn't stop you from going to transplant for somebody who might still be a candidate.  The other area of controversy is somebody under 60 who has adverse cytogenetics where we don't do very well with ‘7+3,' we still give it and we might do just as well with decitabine venetoclax. A lot of us feel that there's equipoise in the 60 to 75 group where we really can ask a question of a randomized study. Retrospective studies might suggest that intensive therapy is a little better, but there are now a couple of randomized studies happening saying, “Can we replace ‘7+3' in that intermediate age with aza-venetoclax?” And for younger adults similarly, we're looking to see how we apply that technology. Those are the areas where we're really trying to investigate what's optimal for patients and that's going to require randomized trials. Dr. John Sweetenham: Oh, that's great, thank you. And I'll just extend that question a little bit more, particularly with respect to the new targeted therapies. How much are they impacting the treatment of these patients in the relapse and refractory setting now? Dr. James Foran: Oh, they're definitely impacting it. When I trained and probably when you trained, AML was still a medical emergency. But that was the thing that you admitted to the hospital immediately, you started therapy immediately. The rule was always that's the one thing that brings the fellow and the consultant in at night to see that new patient on a Friday or Saturday. Now, we'll still admit a patient for monitoring, but we try not to start therapy for the first three or five or seven days if they're stable, until we get those genetics and those genomics back, because it helps us discriminate what therapy to pursue. And certainly, with FLT3 mutations, especially FLT3/ITD mutations, we're adding FLT3 inhibitors and we're seeing a survival advantage. Now, on the surface, that survival advantage is in the range of 7% or 10%. But if you then pursue an allogeneic transplant in first remission, you're taking disease where we used to see 30%, 40% long-term survival, maybe less, and you're pushing that to 60%, 70% in some studies. And so we're now taking a disease that– I don't want to get off topic and talk about Ph+ ALL. But that's a disease where we're actually a little excited. We have a target now, and it used to be something really adverse and now we can do a lot for it and a lot about it.  The other mutations, it's a little more subtle. Now, who knew until 2010 that a mutation in a sugar metabolism gene, in isocitrate dehydrogenase, or IDH was going to be so important, or even that it existed. We know that IDH1 and IDH2 mutations are still a minority of AML, certainly less than 10% to 15%, maybe overall. But we're able to target those with specific IDH1 and IDH2 inhibitors. We get single-agent responses. There are now two approved IDH1 inhibitors on the market. We don't yet have the randomized data that adding those to intensive therapy is better, but we're getting a very strong hint that it might be better in older adults who have an IDH mutation, maybe adding those is helpful and maybe adding those to low-intensity therapy is helpful. Those studies are ongoing, and we're also trying with low-intensity treatments to add these agents and get higher remission rates, deeper remissions, longer remissions. I think a lot of work has to be done to delineate the safety of that and the long-term efficacy. But we're getting hints it's better, so I think it is impacting.  The other area it's impacting is when you pick up adverse mutations and those have crept into our classification systems like an ASXL1 mutation or RUNX1 mutation for instance, or some of the secondary AML mutations like BCOR and others, where that's helping us discriminate intermediate-risk patients who we think aren't going to do as well and really helping us select a group who's more likely to get benefit from allogeneic transplant or for whom at least our cure rates without allo transplant are low. And so I think it's impacting a lot. Dr. John Sweetenham: Great. And I'm going to pick up now, if I may, on a couple of things that you've just mentioned and continue the theme of the relapsed and refractory setting. We've started to see some reports which have looked at the role of immune strategies for patients with AML, in particular CAR T or NK cells. Can you comment a little on this and let us know whether you think either these two strategies or other immune strategies are likely to have a significant role in AML in the future? Dr. James Foran: They are, but I think we're still a step behind finding the right target or the right way to do it. If you think of allogeneic transplantation as the definitive immune therapy, and we know for adverse AML we can improve survival rates and cure rates with an allotransplant, then we know inherently that immune therapy matters. And so how do we do what they've done in large cell lymphoma or in CD19 targeting for B cell malignancies? How do we bring that to acute myeloid leukemia? There have been a number of efforts. There have been at least 50 trials looking at different targets. CD33, CD123, CD7, others, CLL-1. So, there have been a number of different trials looking at how to bind a CAR T or a CAR T construct that can be active. And we have hints of efficacy. There was kind of a provocative paper in the New England Journal of Medicine a year ago in April of last year from a Chinese group that looked at a CD7-based CAR T and it was 10 patients, but they used CD7 positive acute leukemia, AML or ALL and had a CD7-targeted CAR T and they actually incorporated that with a haploidentical transplant and they had really high remission rates. People tolerated it quite well. It was provocative. It hasn't yet been reproduced on a larger scale, but the strong hints that the strategy is going to work.  Now, CD33 is a little tricky to have a CAR T when CD33 is expressed on normal hematopoietic cells. CD123 likewise. That's been something where there's, I think, still promise, but we've struggled to find the trials that make that work. Right now, there's a lot of interest in leveraging NK cells and looking, for a couple of reasons, but NK cells are attractive and NK cell markers might be attractive targets. NK cells might have similar degrees of immune efficacy. It's speculative, but they are likely to have less cytokine release syndrome and less neurotoxicity than you see with CAR T. And so it's kind of attractive to leverage that. We have had some ongoing trials looking at it with bispecifics and there certainly are trials looking at it with CAR NK-based strategies. One of the antigens that people looked at is the NK group 2D. NK group 2D or NKG2D is overexpressed in AML and its ligands overexpressed. And so that's a particular potential target. So, John, it's happening and we're looking for the hints of efficacy that could then drive a pivotal trial to get something approved.  One of the other areas is not restricting yourself just to a single antigen. For instance, there is a compound that's looking at a multi-tumor-associated antigen-specific T-cell therapy, looking at multiple antigens in AML that could be overexpressed. And there were some hints of activity and efficacy and actually a new trial looking at a so-called multi-tumor associated antigen-specific T cell therapy. So without getting into specific conflicts of interest or trials, I do think that's an exciting area and an evolving area, but still an investigational area. I'll stop there and say that we're excited about it. A lot of work's going there, but I'm not quite sure which direction the field's going to pivot to there. I think that's going to take us some time to sort out. Dr. John Sweetenham: Yeah, absolutely. But as you say, exciting area and I guess continue to watch this space for now.  So you've mentioned allogeneic stem cell transplants two or three times during this discussion. Recognizing that we don't have an imatinib for AML, which has kind of pushed transplant a long way further back in the treatment algorithm, can you comment a little on, you know, whether you think the role of stem cell transplantation is changing in AML or whether it remains pretty much as it was maybe 10 years ago? Dr. James Foran: By the way, I love that you use imatinib as an introduction because that was 6 TKIs ago, and it tells you the evolution in CML and you know, now we're looking at myristoyl pocket as a target, and so on. That's a great way to sort of show you the evolution of the field.  Allogeneic transplant, it remains a core treatment for AML, and I think we're getting much smarter and much better about learning how to use it. And I'm just going to introduce the topic of measurable residual disease to tell you about that. So I am a little bit of a believer. Part of my job is I support our allogeneic transplant program, although my focus is acute myeloid leukemia, and I've trained in transplant and done it for years and did a transplant fellowship and all that. I'm much more interested in finding people who don't need a transplant than people who do. So I'm sort of looking for where can we move away from it. But it still has a core role. I'll sidestep and tell you there was an MDS trial that looked at intermediate or high-risk MDS and the role of allogeneic transplant that shows that you about double your survival. It was a BMT CTN trial published several years ago that showed you about double your three-year survival if you can find a donor within three months and get to a transplant within six months. And so it just tells you the value of allotransplant and myeloid malignancy in general. In AML we continue to use it for adverse risk disease – TP53 is its own category, I can talk about that separately – but adverse risk AML otherwise, or for patients who don't achieve a really good remission. And I still teach our fellows that an allotransplant decreases your risk of relapse by about 50%. That's still true, but you have to have a group of patients who are at high enough risk of relapse to merit the non-relapse mortality and the chronic graft versus host disease that comes with it. Now, our outcomes with transplant are better because we're better at preventing graft versus host disease with the newer strategies such as post-transplant cyclophosphamide. There are now new FDA-approved drugs for acute and chronic graft versus host disease, ruxolitinib, belumosudil, axatilimab now. So we have better ways of treating it, but we still want to be discriminating about who should get it.  And it's not just a single-minded one-size-fits-all. We learned from the MORPHO study that was published in the JCO last year that if you have FLIT3-positive AML, FLIT3/IDT-positive AML, where we would have said from retrospective studies that your post-transplant survival is 60% give or take, as opposed to 15% or 20% without it, that we can discriminate who should or shouldn't get a transplant. Now that trial was a little bit nuanced because it did not meet its primary endpoint, but it had an embedded randomization based upon MRD status and they used a very sensitive test of measurable residual disease. They used a commercial assay by Invivoscribe that could look at the presence of a FLT3/ITD in the level of 10 to the minus 5th or 10 to the minus 6th. And if you were MRD-negative and you went through a transplant, you didn't seem to get an advantage versus not. That was of maintenance with gilteritinib, I'll just sort of put that on there. But it's telling us more about who should get a transplant and who shouldn't and who should get maintenance after transplant and who shouldn't.  A really compelling study a year ago from I don't know what to call the British group now, we used to call them the MRC and then the NCRI. I'm not quite sure what to call their studies at the moment. But Dr. Jad Othman did a retrospective study a year ago that looked at patients who had NPM1 mutation, the most common mutation AML, and looked to see if you were MRD positive or MRD negative, what the impact of a transplant was. And if you're MRD negative there was not an advantage of a transplant, whereas if you're MRD positive there was. And when they stratified that by having a FLT3 mutation that cracked. If you had a FLT3 mutation at diagnosis but your NPM1 was negative in remission, it was hard to show an advantage of a transplant. So I think we're getting much more discriminating about who should or should not get a transplant by MRD testing for NPM1 and that includes the patients who have a concomitant FLT3 mutation. And we're really trying to learn more and more. Do we really need to be doing transplants in those who are MRD-negative? If you have adverse risk genetics and you're MRD-negative, I'll really need good data to tell me not to do a transplant, but I suspect bit by bit, we'll get that data. And we're looking to see if that's really the case there, too. So measurable residual disease testing is helping us discriminate, but there is still a core role of allogeneic transplant. And to reassure you, compared to, I think your allotransplant days were some time ago if I'm right. Dr. John Sweetenham: Yes. Dr. James Foran: Yeah. Well, compared to when you were doing transplants, they're better now and better for patients now. And we get people through graft versus host disease better, and we prevent it better. Dr. John Sweetenham: That's a great answer, James. Thanks for that. It really does help to put it in context, and I think it also leads us on very nicely into what's going to be my final question for you today and perhaps the trickiest, in a way. I think that everything you've told us today really emphasizes the fact that the complexity of AML treatment has increased, primarily because of an improved understanding of the molecular landscape of the disease. And it's a complicated area now. So do you have any thoughts on what type of clinical environment patients with AML should be evaluated and treated in in 2025? Dr. James Foran: Yeah, I want to give you a kind of a cautious answer to that because, you know, I'm a leukemia doctor. I work at a leukemia center and it's what we focus on. And we really pride ourselves on our outcomes and our diagnostics and our clinical trials and so on. I am very aware that the very best oncologists in America work in private practice and work in community practice or in networks, not necessarily at an academic site. And I also know they have a much harder job than I have. They have to know lung cancer, which is molecularly as complicated now as leukemia, and they have to know about breast cancer and things that I don't even know how to spell anymore. So it's not a question of competence or knowledge. It's a question of infrastructure. I'll also put a little caveat saying that I have been taught by Rich Stone at Dana-Farber, where I did a fellowship a long time ago, and believe Rich is right, that I see different patients than the community oncologists see with AML, they're seeing different people. But with that caveat, I think the first thing is you really want to make sure you've got access to excellence, specialized hematopathology, that you can get expedited cytogenetics and NGS testing results back. There was a new drug, approved just a few months ago, actually, for relapsed AML with a KMT2A rearrangement, revumenib. We didn't talk about the menin inhibitors. I'll mention them in just a second. That's a huge area of expansion and growth for us. But they're not found on NGS platforms. And normal cytogenetics might miss a KMT2A-rearrangement. And we're actually going back to FISH panels, believe it or not, on AML, to try to identify who has a KMT2A-rearrangement. And so you really want to make sure you can access the diagnostic platforms for that.  I think the National Referral Labs do an excellent job. Not always a really fast job, but an excellent job. At my institution, I get NGS results back within three days or four days. We just have an expedited platform. Not everybody has that. So that's the key, is you have to be able to make the diagnosis, trust the pathologist, get expedited results. And then it's the question of trying to access the targeted medications because a lot of them are not carried in hospital on formulary or take time to go through an insurance approval process. So that's its own little headache, getting venetoclax, getting gilteritinib, getting an IDH1 inhibitor in first line, if that's what you're going for. And so I think that requires some infrastructure. We have case managers and nurses who really expedite that and help us with it, but that's a lot of work. The other piece of the puzzle is that we're still with AML in the first month and maybe even the second month. We make everybody worse before we make them better. And you have to have really good blood bank support. I can give an outpatient platelet transfusion or red cell transfusion seven days a week. We're just built for that. That's harder to do if you're in a community hospital and you have to be collaborating with a local blood bank. And that's not always dead easy for somebody in practice. So with those caveats, I do find that my colleagues in community practice do a really good job making the diagnosis, starting people on therapy, asking for help. I think the real thing is to be able to have a regional leukemia center that you can collaborate with, connect with, text, call to make sure that you're finding the right patients who need the next level of diagnostics, clinical trial, transplant consults, to really get the best results.  There was some data at ASH a couple of years ago that looked at – the American Society of Hematology and ASCOs had similar reports – that looked at how do we do in academic centers versus community practice for keeping people on therapy. And on average, people were more likely to get six cycles of therapy instead of three cycles of therapy with azacitidine venetoclax at an academic center. Now, maybe it's different patients and maybe they had different cytogenetics and so on, but I think you have to be patient, I think you have to collaborate. But you can treat those patients in the community as long as you've got the infrastructure in place. And we've learned with virtual medicine, with Zoom and other platforms that we can deliver virtual care more effectively with the pandemic and beyond. So I think we're trying to offer virtual consults or virtual support for patients so they can stay in their home, stay in their community, stay with their oncologists, but still get access to excellent diagnostics and supportive care and transplant consults, and so on. I hope that's a reasonable answer to that question. It's a bit of a nuanced answer, which is, I think there's an important role of a leukemia center, and I think there's a really fundamental role of keeping somebody in the community they live in, and how we collaborate is the key to that. And we've spent a lot of time and effort working with the oncologists in our community to try to accomplish that.  John, I want to say two other things. I didn't mention in the molecular platforms that NPM1 mutations, we can now target those on clinical trials with menin inhibitors. We know that NPM1 signals through the Hoxa9/Meis1 pathway. We know that similar pathways are important in KMT2A rearrangements. We know that there are some other rare leukemias like those with NUP98 rearrangement. We can target those with menin inhibitors. The first menin inhibitor, revuminib, was approved by the FDA for KMT2A. We have others going to the FDA later this year for NPM1. There are now pivotal trials and advanced expanded phase 1/2 studies that are showing 30% response rates. And we're looking to see can we add those into the first-line therapy. So, we're finding more targets.  I'll say one last thing about molecular medicine. I know I'm a little off topic here, but I always told patients that getting AML was kind of like being struck by lightning. It's not something you did. Now, obviously, there are risk factors for AML, smoking or obesity or certain farm environments, or radioactive exposures and so on. But bit by bit, we're starting to learn about who's predisposed to AML genetically. We've identified really just in the last five or eight years that DDX41 mutations can be germline half the time. And you always think germline mutations are going to cause AML in a younger patient, but the median age is 60 to 70 just like other AMLs. They actually might do pretty well once they get AML. We've reported that in several papers. And so we're trying to understand who that has a RUNX1 mutation needs germline testing, who with a DDX41 needs germline testing. And we're trying to actually come up with a cleaner pathway for germline testing in patients to really understand predisposition, to help with donor selection, to help with family counseling. So I think those are other areas where a leukemia center can contribute for somebody in who's community practice to understand genomic or genetic complexity in these patients. And we're starting to develop the databases that support that. Dr. John Sweetenham: Yeah, great. Thanks, James. I loved your answer about the clinical environment too. And I know from a patient-centric perspective that I know that patients would certainly appreciate the fact that we're in a situation now where the folks taking care of them will make every effort to keep them close to home if they possibly can.  I want to thank you, James, for an incredible review of a very complex subject and I think you did a great job. I think we all will have learned a lot. And thanks again for being willing to share your insights with us today on the ASCO Daily News Podcast. Dr. James Foran: John, it's my pleasure. And as you know, I'll do anything for a latte, so no problem at all. Dr. John Sweetenham: Okay. I owe you one, so thank you for that.  And thank you to our listeners for your time today. You'll find links to the studies we've discussed today in the transcript of this episode. And finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity or therapy should not be construed as an ASCO endorsement. Find out more about today's speakers:  Dr. John Sweetenham  Dr. James Foran Follow ASCO on social media: @ASCO on Twitter ASCO on Bluesky ASCO on Facebook  ASCO on LinkedIn  Disclosures:    Dr. John Sweetenham:    No relationships to disclose Dr. James Foran: Stock and Other Ownership Interests: Aurinia Pharmaceuticals Consulting or Advisory Role: Peerview, CTI BioPharma Corp, Remix Therapeutics, Cardinal Health, Medscape, Syndax, Autolus Therapeutics Research Funding (Inst.): Chordia Therapeutics, Abbvie, Actinium Pharmaceuticals, Kura Oncology, Sellas Life Sciences, Novartis, Roivant, Celgene/Bristol-Myers Squibb, Astellas Pharma, SERVIER Travel, Accommodations, Expenses: Peerview

Au Cameroun, le parti d'opposition SDF, Social Democratic Front, qui s'est réuni en congrès extraordinaire, vient de désigner Joshua Osih comme son candidat à la présidentielle du mois d'octobre prochain. Le SDF a été longtemps la principale force d'opposition dans le pays. Depuis la dernière élection de 2018, il est moins en vue, mais cette année, il croit de nouveau en ses chances. En ligne de Yaoundé, le député Joshua Osih dévoile sa stratégie, qui pourrait bien s'inspirer de celle de Félix Tshisekedi en RDC. RFI : Dans votre programme, vous dîtes vouloir mettre fin aux violences dans les provinces du Nord-ouest et du Sud-ouest en seulement 100 jours. Comment vous allez vous y prendre ?Joshua Osih : Je pense qu'aucun autre parti politique ne connaît mieux le Nord-ouest et le Sud-ouest que nous. Nous savons ce qui se passe. Nous avons largement consulté sur la question. Nous avons parlé à toutes les parties en conflit et nous sommes sereins qu'en trois mois ou un peu plus, nous pouvons faire cesser la violence. Cela ne veut pas dire que la crise politique va s'arrêter. C'est pour cela que nous proposons en même temps de lancer un grand chantier qui devra aboutir au bout de trois ans sur un référendum constitutionnel. Cela va nous permettre de rétablir les équilibres politiques dans ce pays pour éviter des crises futures.Le président Biya, qui vient de fêter ses 92 ans, laisse entendre qu'il sera candidat à sa réélection en octobre prochain. Est-ce que vous pensez que son âge pourrait être un paramètre à prendre en compte dans la campagne ?Nous pensons que certainement l'âge du président de la République serait un handicap pour le pays si jamais il est élu. Vous savez, un président de la République à 100 ans, cela veut tout simplement dire que, si monsieur Biya devenait président de la République pour un autre mandat, le pays allait s'arrêter pour attendre la fin de son mandat. Sept années encore dans le noir, c'est quelque chose que la jeunesse camerounaise ne va pas accepter. C'est quelque chose que tous les Camerounais ne vont pas accepter. Nous sommes confiants que, qu'il soit candidat ou pas, son parti est dans l'impossibilité de gagner les élections de 2025.Dans vos discours, Joshua Osih, vous êtes moins véhément que Maurice Kamto. Est-ce à dire que face au RDPC au pouvoir, le SDF est dans une stratégie moins frontale que le MRC ?Ce n'est pas une question d'être moins véhément ou moins dans une stratégie frontale. C'est tout simplement parce que moi, j'ai appris à faire la politique auprès d'un très grand homme, John Fru Ndi et j'ai compris que, dans la politique, aucun adversaire n'est permanent. C'est déjà le premier point. Deuxièmement, il faut pouvoir se parler, même quand on est en désaccord. Donc, quand on fait la politique par les injures, et là je ne vise aucun parti politique, il y a malheureusement trop de personnes qui pensent qu'il faut passer la journée à insulter les uns et les autres. Nous sommes des adversaires politiques. La première des choses, c'est que nous devons nous respecter. Donc, je respecte le MRC, je respecte le RDPC, je respecte le PCRN, je respecte tous les partis politiques sur la place en attendant aussi d'eux un respect réciproque.En 2018, face à Joseph Kabila, Martin Fayulu et Félix Tshisekedi avaient deux stratégies différentes et à la fin, c'est Félix Tshisekedi qui est devenu président. Est-ce que vous avez ce scénario congolais dans la tête pour octobre prochain ?Bien sûr et je pense que nous sommes très proches de l'UDPS. Nous avons accompagné l'UDPS lors de ces élections-là. Et donc nous sommes plutôt dans cette logique-là que dans celle de Martin Fayulu. En 1992, nous avons gagné l'élection présidentielle. Tous nous donnent raison que nous avons gagné cette élection. Mais nous avions oublié qu'il faut gagner l'élection et aussi pouvoir prendre le pouvoir. Ce sont deux choses complètement différentes et nous n'avons pas réussi à prendre le pouvoir en 1992. Plus jamais nous n'allons faire cette erreur. Quand on est en politique, il faut avoir la capacité de construire des ponts et de parler avec ceux qui ont perdu le pouvoir pour qu'ensemble, on arrive à construire ce pays. Il ne s'agit pas pour le SDF d'arriver au pouvoir et de mettre tout le monde du RDPC en prison, de les jeter en pâture etc. Non, il s'agit de démontrer que, quand je vais gagner, il n'y aura pas de chasse aux sorcières parce qu'on aura besoin des 30 millions de Camerounais pour rattraper les 43 années que nous avons perdues.Face au candidat du pouvoir, vous serez beaucoup d'opposants. Maurice Kamto, Cabral Libii , Akere Muna, Madame Hermine Patricia Tomaïno Ndam Njoya et vous-même. Est-ce que par vos divisions, vous n'ouvrez pas un boulevard au candidat du RDPC au pouvoir ?Mutualiser nos forces dans les bureaux de vote, c'est une voie que nous pensons très importante. Que ceux qui sont dans les bureaux de vote où nous sommes absents nous représentent mutuellement. Et si tous ces autres partis que vous avez cités peuvent être présents dans les 30 000 bureaux de vote avec nous, cela fera que dans les bureaux de vote, il y aura une majorité de représentants de l'opposition par rapport au parti au pouvoir. Et dans ce cas-là, il n'y aurait aucune chance pour que le parti au pouvoir essaie de truquer les résultats. Nous sommes confiants que nous aurons les résultats que nous attendons. À lire aussiPrésidentielle au Cameroun: les prises de position contre une candidature de Paul Biya divisent des fidèles catholiquesÀ lire aussiPrésidentielle au Cameroun: les chefs traditionnels apportent leur «soutien» au président Paul Biya

MRC welcomes special guest George O'Connor to cover the books of August, 1967! A discussion of George's Asgardians graphic novels leads right into Thor 143, then Amazing Spider-Man 51, Daredevil 31, Tales to Astonish 94 with Namor and the Hulk, and X-Men 35! Lots of heroes pretending they don't know how money works! Pre-Puzo Puzo! Convenient fire-fighter nets! Lost weekends! Check it out!

Jijo Reed, recognized by LA WEEKLY and NEW YORK POST as "Top Trendsetter in 2023" is an Emmy Winning Producer, 16 time Telly Award Winner, and Executive Producer of over 80 feature films and/or series.Latest feature films include Crescent City starring Alec Baldwin and Terrence Howard, THE BLACKENING directed by Tim Story for MRC, Village Roadshow's CINNAMON, and MENDING THE LINE starring Brian Cox (Succession)... also, MACHINE GUN KELLY'S LIFE IN PINK 2022 documentary for Hulu/Disney and BACK ON THE STRIP with Kevin Hart and Tiffany Haddish.A high point in his career is when he deep dived to the wreck site of TITANIC in the Russian submersible, MIR 1, while directing and producing a documentary about the famed, ill-fated ship...during which he became one of the very few men in the entire world to dive the actual wreckage of TITANIC at 2.5 miles below sea level. More people have been to outer space than this depth of the ocean. His "ground breaking, cinematic" footage of Titanic is recognized globally. Reed states: "This was the most life changing project of my career."Also, Reed was Visual Effects Supervisor for THE AVENGERS S.T.A.T.I.O.N 3D interactive exhibit, the innovative and revolutionary experience which is currently a main attraction in Times Square, NY and Las Vegas.Jijo was Executive Producer of the 2013 OBAMA PRESIDENTIAL INAUGURATION Concert in Washington DC featuring WIL I AM and JOHN LEGEND. Additionally, he has produced screen media for live music concert tours, including EMINEM's MTV Awards performance and GUNS & ROSES.In 2004, Jijo created the hit VH1 show "CELEBRITY REHAB" which has won numerous awards and has helped people all over the world overcome addictionThroughout the 1990's, he worked as Post Supervisor on the audio/visual ad campaigns of studio films such as Martin Scorsese's CASINO, Jim Cameron's TRUE LIES, STAR TREK, DIE HARD, LETHAL WEAPON 4, THE UNFORGIVEN, and many others.Jijo Reed is a third generation Los Angeles native and the grandson of Alan Reed who was the voice of FRED FLINSTONE and acted in such movies as Breakfast At Tiffany's and Postman Always Rings Twice. Jijo is also the nephew of FRED ASTAIR'S choreographer, Hermes Pan.

WMAL GUEST: 7:05 AM - INTERVIEW - TIM GRAHAM - Executive Editor, Media Research Center's NewsBusters – Discussed MSNBC shakeup and MRC’s Defund PBS & NPR mobile billboard truck circling DC SOCIAL MEDIA: https://x.com/timjgraham Media Research Center has a digital billboard truck driving all around the Capital Tuesday through Thursday and will be saying to defund PBS and NPR. MSNBC axes THREE more stars' shows after Joy Reid in network bloodbath MSNBC host Rachel Maddow rips own network for axing Joy Reid’s show and other ‘non-white’ hosts’ programs Lester Holt is stepping down as anchor of 'NBC Nightly News' after a decade Where to find more about WMAL's morning show: Follow the Show Podcasts on Apple podcasts, Audible and Spotify. Follow WMAL's "O'Connor and Company" on X: @WMALDC, @LarryOConnor, @Jgunlock, @patricepinkfile, and @heatherhunterdc. Facebook: WMALDC and Larry O'Connor Instagram: WMALDC Show Website: https://www.wmal.com/oconnor-company/ How to listen live weekdays from 5 to 9 AM: https://www.wmal.com/listenlive/ Episode: Tuesday, February 25, 2025 / 7 AM Hour See omnystudio.com/listener for privacy information.

In the 7 AM Hour: Larry O’Connor and Julie Gunlock discussed: WMAL GUEST: 7:05 AM - INTERVIEW - TIM GRAHAM - Executive Editor, Media Research Center's NewsBusters – Discussed MSNBC shakeup and MRC’s Defund PBS & NPR mobile billboard truck circling DC SOCIAL MEDIA: https://x.com/timjgraham Media Research Center has a digital billboard truck driving all around the Capital Tuesday through Thursday and will be saying to defund PBS and NPR. MSNBC axes THREE more stars' shows after Joy Reid in network bloodbath MSNBC host Rachel Maddow rips own network for axing Joy Reid’s show and other ‘non-white’ hosts’ programs Lester Holt is stepping down as anchor of 'NBC Nightly News' after a decade DeSantis announces Florida ‘DOGE task force’ WMAL GUEST: 7:35 AM -INTERVIEW - JIM HANSON - President of Security Studies Group and served in US Army Special Forces – discussed Ukraine talks Christopher F. Rufo ⚔️ on X: "EXCLUSIVE: @GrossmanHannah and I have obtained logs from the NSA’s secret transgender sex chatroom, in which NSA, CIA, and DIA employees discuss genital castration, artificial vaginas, piss fetishes, sex polycules, and gangbangs—all on government time. This is insane. Where to find more about WMAL's morning show: Follow the Show Podcasts on Apple podcasts, Audible and Spotify. Follow WMAL's "O'Connor and Company" on X: @WMALDC, @LarryOConnor, @Jgunlock, @patricepinkfile, and @heatherhunterdc. Facebook: WMALDC and Larry O'Connor Instagram: WMALDC Show Website: https://www.wmal.com/oconnor-company/ How to listen live weekdays from 5 to 9 AM: https://www.wmal.com/listenlive/ Episode: Tuesday, February 25, 2025 / 7 AM Hour See omnystudio.com/listener for privacy information.

Willie is back talking about the latest media hypocrisy. Daniel Greenfiled from Front Page Mag joins the show. Isreal Ellis talks on Israel, the hostages and America's support for Israel. Steve Milloy debunks the climate change hysteria. Curtis Houck from MRC breaks apart the left-wing media, defunding PBS, NPR and more. Dr Suzanne Barchers on the state of education in America.

In this episode of the Pencil Pushers Podcast, host Mike Rosado interviews local designer and illustrator Lauren Griffin. Lauren shares her journey, from growing up in multiple cities to settling in Durham, North Carolina. With an impressive portfolio that includes work for Helms Workshop and Pabst Blue Ribbon, Lauren discusses her passion for creating playful yet sophisticated illustrations and brand identity design. She also talks about her newfound love for neon design, featuring pieces in the Museum of Neon Art in Los Angeles, as well as her preparations for her first solo show in Steamboat Springs, Colorado.Lauren reflects on her early influences, including her creative mother and a supportive teacher who nudged her toward an art and design career. She also shares her experiences working for agencies, freelancing, and even collaborating with Mike himself at his studio MRC in Raleigh, NC. The conversation explores the importance of knowing one's self-worth, the challenges of freelancing, and the evolving role of technology—including AI—in the world of design and art.

MRC finishes up July of 1967, with Fantastic Four 64, Daredevil 30, Thor 142, Tales of Suspense 91 with Iron Man and Captain America, and Avengers 42! Wonder of Wonders! Matt as Mike as DD as Thor! Anti-Force! Centrifugal Rays! Check it out!

"Jack Riccardi talked about Mexico and Canada blinking on tariff threats, joined by Gordon Chang, who also talked about China, tariffs and the Panama Canal, plus Chuck Schumer's party props, the grift of politicians writing books, and SA closing the MRC."

Fraudology is presented by Persona.Join Karisse Hendrick and special guest Tracy Brown as they dive deep into the world of e-commerce fraud prevention in this captivating episode of the Fraudology Podcast. Tracy, a veteran in the field and current VP at the Merchant Risk Council (MRC), shares her unique origin story in fraud prevention and how it led to the formation of the MRC. The duo discusses the latest fraud trends keeping merchants up at night, including the surprising rise of refund abuse and the challenges posed by alternative payment methods. Tracy provides an exclusive preview of the upcoming MRC Vegas conference, showcasing the event's diverse offerings from educational sessions to networking opportunities. Learn about the conference's innovative features, such as a behind-the-scenes look at issuing bank operations and a preparation course for the industry-recognized CPFPP certification.The episode also touches on the importance of building relationships within the fraud prevention community and leveraging events like the MRC conference to stay ahead of emerging threats. With insider tips on making the most of the conference experience and insights into the future of fraud prevention, this episode is a goldmine for anyone involved in e-commerce security. Don't wait - listen now and arm yourself with the latest intel from the frontlines of fraud prevention!To connect with Tracy Brown:https://www.linkedin.com/in/tracykobedabrown/To learn more about the MRC Vegas Conference:https://events.merchantriskcouncil.org/event/vegas2025/aboutFraudology is hosted by Karisse Hendrick, a fraud fighter with decades of experience advising hundreds of the biggest ecommerce companies in the world on fraud, chargebacks, and other forms of abuse impacting a company's bottom line. Connect with her on LinkedIn She brings her experience, expertise, and extensive network of experts to this podcast semi weekly, on Tuesdays and Thursdays.

While falling snow may look pretty, it can also be pretty dangerous for drivers. Winterizing your vehicle is a good precaution as it can save you money on car repairs and help you stay safe while on the road. If you own a car, here are some tips to get it winter-proof if you haven't already. Links: Visit our Auto page to explore current rates and learn more about GAP and MRC coverage for your vehicle Check out TCU University for financial education tips and resources!  Follow us on Facebook, Instagram and Twitter!  Learn more about Triangle Credit Union Transcript: Welcome to Money Tip Tuesday from the Making Money Personal podcast.   Roads often become slippery during the winter months. To counteract this, consider putting winter tires on your vehicle. You can use all-season tires during the winter, but when it gets cold, the rubber in these tires hardens, decreasing the grip on the road. Winter tires use a special compound that can resist the cold and won't harden. Winter tires also have better traction in snowy and icy road conditions, which means that they have better acceleration and are better at stopping than all-season tires. However, winter tires can be costly. Winter tires can cost over $600, plus you'll have to pay for the tire-swapping fees unless you do it yourself. A cheap alternative is putting chains on your tires to help with traction.  Regardless of what tires your car has, you'll want to check the tire pressure. Tire pressures drop 1 pound per square inch, or PSI for short, every 10 degrees Fahrenheit. You can check the correct tire pressure for your car in the manual or on the car door jamb. Another way to get your car winter-ready is to have the battery tested. Your car battery is essential for starting your car. Colder temperatures can affect the chemicals in the battery, which may result in a car having trouble starting or not starting at all. Consider buying a portable jump starter for your vehicle in case your car doesn't start due to low temperatures. Next, you'll want to make sure you have good visibility while driving. Check your windshield wipers to see if they are working properly, and don't leave smudge marks on your windshield. Fill up your windshield wiper fluid too. You can also get a hydrophobic repellant to add to your windshield, making scraping ice and snow off your car windows easier. Headlights are another thing to consider when winterizing your car. Snow can cause limited visibility when driving, but having a good set of headlights can help you see better, especially during the dark hours of winter. If you've noticed that your headlights aren't as bright as they used to be, you should get a headlight restoration kit or replace them altogether.  You should have a winter emergency kit in your car. If you get stranded with your vehicle, this kit will help you get back on your drive or at least keep you comfortable while waiting for help to arrive. In this kit, you should include a snow shovel, a snow broom, an ice scraper, a portable jump starter, warm clothing, including hats and gloves, blankets, a first-aid kit, a basic tool kit, traction mats, and flashlights.  If you're considering buying a car that's more suitable for winter, look for one that has 4-wheel drive or all-wheel drive instead of front-wheel drive. Vehicles with 4-wheel drive and all-wheel drive provide better traction on icy roads than front-wheel drive vehicles.  If you decide to buy a more winter-proof car, Triangle Credit Union offers auto loans tailored to fit your ride. If you get into an accident, Guaranteed Asset Coverage, or GAP coverage, is designed to reduce or eliminate the difference between the insurance settlement and the loan balance. This protects you from owing more than the vehicle is worth. Mechanical Repair Coverage, or MRC, can help limit unexpected, covered repairs as your vehicle ages, potentially saving you thousands of dollars.  If you're interested in either one of these coverages, contact the credit union or visit your local branch to learn more. If there are any other tips or topics you'd like us to cover, let us know at tcupodcast@trianglecu.org. Also, remember to like and follow our Making Money Personal Facebook and Instagram to share your thoughts. Finally, remember to look for our sponsor, Triangle Credit Union, on Facebook and LinkedIn.        Thanks for listening to today's Money Tip Tuesday. Check out our other tips and episodes on the Making Money Personal podcast.   

Happy Wednesday. Bob kicks off the show talking about the confirmation hearings of RFK and more. Bob then talks with Senator Bernie Moreno about the Columian president situation, ICE and illegals and the Trump agenda. Bob the talks with newly appointed senator Jon Husted. They talk about his plans and his support of President Trump. Bob then talks with Bill D'Agostino from MRC about the coverage of the pardons between Trump and Biden.. Bob takes calls to wrap up the show.See omnystudio.com/listener for privacy information.

MRC welcome super-special guest Dan McCoy, Emmy-winning writer and co-host of The Flophouse! We discuss four books from July 1967: Amazing Spider-Man 50, Strange Tales 158 with SHIELD and Dr Strange, Tales to Astonish 93 with Namor and Hulk, and X-Men 34! Spidey No More! Monocle upon eye patch upon monocle! An actual Pink Floyd Album cover! Shameless swipes! Check it out!

LA is on fire and the politicians are at fault. No thinning of the forest.....little to no water pressure in the fire hydrants and reservoirs are empty. Bill chats with Wayne Allyn Root on this and more. Dan Schnider from the MRC is on and we wrap up the show with Grover Norquist talking taxes and more.

In the 6 AM Hour: Larry O’Connor and Emily Domenech discussed: Trump’s reaction to the CA fires Biden mocked for tone-deaf ‘good news’ while Californians flee wildfires WMAL GUEST: 6:35 AM - INTERVIEW - NICHOLAS FONDACARO - Associate Editor for MRC and Newsbusters SOCIAL MEDIA: https://x.com/NickFondacaro CNN heads to court for high-stakes defamation trial about Afghanistan segment Jury set for CNN defamation trial after multiple candidates expressed disdain for network: 'Not a fan of CNN' Where to find more about WMAL's morning show: Follow the Show Podcasts on Apple podcasts, Audible and Spotify. Follow WMAL's "O'Connor and Company" on X: @WMALDC, @LarryOConnor, @Jgunlock, @patricepinkfile, and @heatherhunterdc. Facebook: WMALDC and Larry O'Connor Instagram: WMALDC Show Website: https://www.wmal.com/oconnor-company/ How to listen live weekdays from 5 to 9 AM: https://www.wmal.com/listenlive/ Episode: Thursday, January 09, 2025 / 6 AM Hour See omnystudio.com/listener for privacy information.