Podcasts about hutchinson gilford

“Wisdom is not just about knowledge. Wisdom adds to knowledge with discernment, with understanding, with a moral sense of what's right and wrong.” We live in a time of overflowing and interweaving crises. A global pandemic exacerbates a mental health crisis caused social media technology. The upheaval of American electoral politics caused by an erosion (or breakdown?) of social and relational trust. The rise of nationalism, the proliferation of war, and longing for justice in the realms of gender and race. Underneath it all appears to be a crisis of knowledge and its convergence around skepticism of science, a culture of suspicion, and confusion about basic factual information, let alone right and wrong. We need wisdom. Badly. But in times of crisis and chaos, where are we to turn for wisdom? In this episode Mark Labberton is joined by longtime friend Francis Collins, physician, researcher, and former director of the National Institutes of Health (NIH). Known for his leadership in mapping the human genome, his public service at the NIH spanned three presidencies and culminated with overseeing the national response to Covid-19 pandemic. The author of many books, including his bestselling The Language of God, Collins's new book is *The Road to Wisdom: On Truth, Science, Faith, and Trust,* a reflection on the crisis of truth, science, faith, and trust, and how the exhausted middle might chart a path toward a better future. About Francis Collins Francis S. Collins, MD, PhD, is the former director of the National Institutes of Health (NIH). As the longest serving director of NIH—spanning twelve years and three presidencies—he oversaw the work of the largest supporter of biomedical research in the world, from basic to clinical research. Collins is a physician-geneticist noted for his landmark discoveries of disease genes and his leadership of the international Human Genome Project, which culminated in April 2003 with the completion of a finished sequence of the human DNA instruction book. He served as director of the National Human Genome Research Institute at the NIH from 1993 to 2008. Collins's research laboratory has discovered a number of important genes, including those responsible for cystic fibrosis, neurofibromatosis, Huntington's disease, a familial endocrine cancer syndrome, and most recently, genes for type 2 diabetes, and the gene that causes Hutchinson-Gilford progeria syndrome, a rare condition that causes premature aging. Collins received a BS in chemistry from the University of Virginia, a PhD in physical chemistry from Yale University, and an MD with honours from the University of North Carolina at Chapel Hill. Prior to coming to the NIH in 1993, he spent nine years on the faculty of the University of Michigan, where he was a Howard Hughes Medical Institute investigator. He is an elected member of the Institute of Medicine and the National Academy of Sciences. Collins was awarded the Presidential Medal of Freedom in November 2007 and the National Medal of Science in 2009. Show Notes Get your copy of The Road to Wisdom: On Truth, Science, Faith, and Trust “The crisis behind the crisis. It's the crisis of culture. It's the crisis of mind and heart. It's the crisis of society. It's the crisis of faith.” Collins occupying various roles through this book: professor, advocate, mentor, philosopher, coach, scientist, pathologist, and perhaps most saliently, cultural diagnostician. Being on the road to wisdom Helping those in the exhausted middle, to offer ways to do something to address cultural crises Collins summarizes the arc of the book TRUTH: “There is such a thing as objective truth. But it is not necessarily very popular in many circumstances.” “Facts—*established facts—*are now sometimes called into question because somebody doesn't like the fact.” Jonathan Rauch on the “Constitution of Knowledge” “You will know the truth and the truth will set you free. He doesn't say the counter that lies will imprison you, but you might have to think about that.” Science as a pathway to the truth Anecdotes vs. empirical science “We have to bring faith into this conversation if we're trying to shape a future that it gives you a chance to tap into all the wisdom that's there.” TRUST: “I found in my own experience, some of the information that turned out to be most life-changing came from a source that I never would have considered as part of my reliable circle of buddies, but I needed to hear it.” “Wisdom is not just about knowledge. Wisdom adds to knowledge with discernment, with understanding, with a moral sense of what's right and wrong.” “Our society is in trouble.” Where will the solution come from? No politicians, not media, but only us. Empowering people to be part of the solution “Love is your calling. Anger and fear are not your calling.” “Listen to understand.” Don't distribute information unless you're sure it's true. Build bridges with neighbours and within communities. Braver Angels Website “If you put information in front of people that's well established, they'll make rational decisions. And I assume that's what science is all about.” Collins's experience leading the charge to develop Covid-19 vaccines, and then managing the resistance to vaccines “People of faith in many instances were the most likely to fall into the category of not trusting what science had to say.” The cultural crisis beneath the medical crisis of Covid vaccine skepticism Collins reflects on public health responses to Covid-19 (school closures, mask mandates, etc.) Systemic breakdown caused by fear, anxiety, distrust, and suspicion Collins comments on Anthony Fauci's public service throughout Covid-19 Discrediting and redefining science, subverting faith Postmodernism and the erasure of objectivity and reason in science “Nothing is true except our perspective.” Francis Collins's perspectives on the Christian church Christians' ungrounded fear that this is a war Tim Alberta's book The Kingdom, the Power, and the Glory “Seeing through a glass darkly.” (1 Cor 13) A book of hope and whole human experience “There are profound reasons for each of us to engage. This is an argument about not standing aside. It's crucial to see that what we are fighting for is great and glorious, and worth every bit of the effort from each of us. Truth, science, faith, and trust are not just sources of relief from a painful period in our country's life. They represent the grandest achievements and insights of human civilization. They literally hold down the promise of a better life for every person on this planet in material terms, in spiritual terms, and in social and cultural terms. To take up this challenge is therefore not an act one of exhaustion or desperation. But one arising from the hopeful pursuit of the promise of greater flourishing of our entire humandom.” Production Credits Conversing is produced and distributed in partnership with Comment magazine and Fuller Seminary.

Send us a textDr. Francis S. Collins, M.D., Ph.D., ( https://www.francisscollins.com/ ) is the former Director of the U.S. National Institutes of Health (NIH), where as the longest serving director of NIH (spanning 12 years and three presidencies) he oversaw the work of the largest supporter of biomedical research in the world, from basic to clinical research.  Dr. Collins continues to serve as NIH Distinguished Investigator, Center for Precision Health Research, at the National Human Genome Research Institute ( NHGRI - https://irp.nih.gov/pi/francis-collins ).Dr. Collins is a physician-geneticist noted for his landmark discoveries of disease genes and his leadership of the international Human Genome Project, which culminated in April 2003 with the completion of a finished sequence of the human DNA instruction book. He served as director of the National Human Genome Research Institute at the NIH from 1993-2008.Dr. Collins' research laboratory has discovered a number of important genes, including those responsible for cystic fibrosis, neurofibromatosis, Huntington's disease, a familial endocrine cancer syndrome, and most recently, genes for type 2 diabetes, and the gene that causes Hutchinson-Gilford progeria syndrome, a rare condition that causes premature aging.Dr. Collins received a B.S. in chemistry from the University of Virginia, a Ph.D. in physical chemistry from Yale University, and an M.D. with honors from the University of North Carolina at Chapel Hill. Prior to coming to the NIH in 1993, he spent nine years on the faculty of the University of Michigan, where he was a Howard Hughes Medical Institute investigator. He is an elected member of the Institute of Medicine and the National Academy of Sciences. Dr. Collins was awarded the Presidential Medal of Freedom in November 2007 and the National Medal of Science in 2009.Dr. Collins also founded and served as President of The BioLogos Foundation ( https://biologos.org/ ), which promotes discourse on the relationship between science and religion.Dr. Collins is also an accomplished author with many available titles including The Language of Life: DNA and the Revolution in Personalized Medicine, The Language of God: A Scientist Presents Evidence for Belief, Music and Mind: Harnessing the Arts for Health and Wellness, and a new book coming out The Road to Wisdom: On Truth, Science, Faith, and Trust - Sep 17, 2024 ( https://www.amazon.com/Road-Wisdom-Truth-Science-Faith/dp/0316576301 ).#FrancisCollins #NationalInstitutesOfHealth #HumanGenomeProject #NIH #Progeria #Cancer #Diabetes #Repurposing #Wisdom #Faith #Truth #Trust #BioLogosFoundation #ProgressPotentialAndPossibilities #IraPastor #Podcast #Podcaster #ViralPodcast  #STEM #Innovation #Technology #Science #ResearchSupport the show

Sammy Basso"Antenorea"1 - Il Consigliere di PriamoRonzani Editorewww.ronzanieditore.itSammy Basso entra nella mente dei personaggi, svelandone passioni e desideri e creando un affresco su temi universali che affondano le loro radici nella parte più profonda dell'animo umano in cui tutti noi possiamo riconoscerci.Quando gli Achei giungono alle spiagge della Troade, Antenore ha già più anni alle spalle di quanti gliene rimangono da vivere. Fautore della pace, anziano saggio di Troia, dovrà mettere in gioco la sua intera esistenza per una missione più grande di quella che un solo uomo può portare a termine. Diviso tra la fedeltà a Re Priamo, suo amico fidato, che sembra non essere più in grado di tenere unita la città, e il senso di ciò che è giusto, dovrà mettere da parte ogni principio per compiere il suo dovere verso la Patria. E mentre i suoi figli scendono in battaglia a fianco di eroi come Ettore ed Enea, ed incrociano le spade contro i micidiali Achille e Diomede, Antenore intraprenderà un lungo viaggio, lontano dalle sicure pendici del Monte Ida, per richiamare a sé potenti alleati e antichi nemici in grado di rovesciare le sorti della città. Tra pericoli, intrighi di corte, vecchi rancori o amicizie dai contorni non ben definiti, Antenore si troverà a capeggiare una quinta colonna di audaci, con il sostegno della sua famiglia e l'appoggio assoluto del popolo degli Eneti. Dopo dieci anni di battaglia, è giunto il momento di decretare la vittoria o la completa distruzione di Troia, in un mondo antico, dove fedeltà e tradimento si intrecciano. Antenore si appresta a vivere gli ultimi atti di una guerra totale, una guerra che nemmeno gli dèi si sottraggono dal combattere. Attraverso la narrazione romanzata di un mito, espressione di una struttura senza tempo della psiche, Sammy Basso entra nella mente dei personaggi, svelandone passioni e desideri e creando un affresco su temi universali che affondano le loro radici nella parte più profonda dell'animo umano in cui tutti noi possiamo riconoscerci.Sammy Basso, classe 1995, nato a Schio, in provincia di Vicenza. Laureato in Scienze Naturali e Biologia Molecolare all'Università di Padova, è affetto dalla nascita da Progeria di Hutchinson-Gilford, motivo per cui, fin da bambino, è impegnato nella divulgazione scientifica e nel sostegno alla ricerca verso questa malattia. Per tale impegno, nel 2019 è stato nominato Cavaliere all'Ordine al Merito della Repubblica italiana. Ricercatore e consulente scientifico per professione, è sempre stato affascinato dalla mitologia, dalla storia e dalle tradizioni dei popoli, passione dalla quale è nato questo suo primo scritto che vuole raccontare in maniera romanzata, l'etnogenesi del popolo veneto, di cui, essendo italiano, si sente parte per nascita e per cultura. È inoltre coautore, con Valentino Baron, di Scolpire il corpo, scoprire l'anima (Biblos, 2014) e autore de Il Viaggio di Sammy (Rizzoli 2015).IL POSTO DELLE PAROLEascoltare fa pensarewww.ilpostodelleparole.itDiventa un supporter di questo podcast: https://www.spreaker.com/show/tracce-di-il-posto-delle-parole_1/support.

A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 12, entitled, “Hepatic hydrogen sulfide levels are reduced in mouse model of Hutchinson-Gilford progeria syndrome.” Hutchinson-Gilford progeria syndrome (HGPS) is a rare human disease characterized by accelerated biological aging. Current treatments are limited, and most patients die before 15 years of age. Hydrogen sulfide (H2S) is an important gaseous signaling molecule that is central to multiple cellular homeostasis mechanisms. Dysregulation of tissue H2S levels is thought to contribute to an aging phenotype in many tissues across animal models. Whether H2S is altered in HGPS is unknown. In a new study, researchers Stephen E. Wilkie, Diana E. Marcu, Roderick N. Carter, Nicholas M. Morton, Susana Gonzalo, and Colin Selman from the University of Glasgow, University of Edinburgh, Saint Louis University, and Karolinska Institute investigated hepatic H2S production capacity and transcript, protein and enzymatic activity of proteins that regulate hepatic H2S production and disposal in a mouse model of HGPS (G609G mice, mutated Lmna gene equivalent to a causative mutation in HGPS patients). “This study was designed and undertaken due to the lack of understanding in the mechanistic targets of known treatments against HGPS and considering the positive association between H2S and longevity in model organisms.” Here, the researchers employed the HGPS mouse model G609G to test the hypothesis that, in contrast to anti-aging increases in H2S production, the accelerated aging typical of progeroid mice is associated with reduced hepatic H2S production. G609G mice were maintained on either regular chow (RC) or high fat diet (HFD). HFD has been previously shown to significantly extend lifespan of G609G mice, and compared to wild type (WT) mice maintained on RC. RC-fed G609G mice had significantly reduced hepatic H2S production capacity relative to WT mice, with a compensatory elevation in mRNA transcripts associated with several H2S production enzymes, including cystathionine-γ-lyase (CSE). H2S levels and CSE protein were partially rescued in HFD fed G609G mice. The data acquired here confirmed some aspects of the relevance of H2S in HGPS but raises more questions about the specific mechanisms at play. “Regardless, the work presented here addresses an area of research that remains critically understudied and provides new evidence that the accelerated ageing phenotype observed in HGPS may be partially explained by a reduction in hepatic H2S levels.” DOI - https://doi.org/10.18632/aging.204835 Corresponding authors - Colin Selman - colin.selman@glasgow.ac.uk, and Stephen E. Wilkie - stephen.wilkie@ki.se Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204835 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, progeria, hydrogen sulfide, high-fat diet, ageing, lamin A About Aging-US: Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us on social media. MEDIA@IMPACTJOURNALS.COM

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.04.527139v1?rss=1 Authors: Hasper, J., Welle, K., Swovick, K., Hryhorenko, J., Ghaemmaghami, S., Buchwalter, A. Abstract: Mutations to the LMNA gene cause laminopathies including Hutchinson-Gilford progeria syndrome (HGPS). The origins of tissue specificity in these diseases are unclear, as the A-type Lamins are abundant and broadly expressed proteins. We show that A-type Lamin protein and transcript levels are uncorrelated across tissues. As protein-transcript discordance can be caused by variations in protein lifetime, we applied quantitative proteomics to profile protein turnover rates in healthy and progeroid tissues. We discover that tissue context and disease mutation each influence A-type Lamin protein lifetime. Lamin A/C has a weeks-long lifetime in the aorta, heart, and fat, but a days-long lifetime in tissues spared from disease. Progerin is even more long-lived than Lamin A/C in the cardiovascular system and accumulates there over time. These proteins are insoluble and densely bundled in cardiovascular tissues, which may present an energetic barrier to degradation. We reveal that human disease alleles are significantly over-represented in the long-lived proteome. These findings indicate that gene therapy interventions will have significant latency and limited potency in disrupting long-lived disease-linked proteins such as Progerin. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

A rare, fatal, genetic condition, characterized by premature aging beginning at childhood

Please join first author Cecilia Bahit and Associate Editor Graeme Hankey as they discuss the article "Predictors of Development of Atrial Fibrillation in Patients With Embolic Stroke Of Undetermined Source: An Analysis of the RE-SPECT ESUS Trial." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center, and Duke; National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, Associate Editor and Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well, Carolyn, this week's feature, we're going to analyze the RE-SPECT ESUS trial. What does that pertain to? Well, you're going to have to wait and find out, but it relates to atrial fibrillation and embolic stroke. But before we get to that, how about we grab a cup of coffee and go through some of the other articles in the issue? Would you like to go first? Dr. Carolyn Lam: I sure would. Greg, we know that Chronic kidney disease is associated with adverse outcomes among patients with established cardiovascular disease or diabetes. The question is: What are the effects of Icosapent Ethyl across the range of kidney function in patients with established cardiovascular disease or diabetes from the REDUCE-IT trial? Dr. Greg Hundley: Ah, Carolyn, can you remind us what was the REDUCE-IT trial? What did it encompass there? Dr. Carolyn Lam: The REDUCE-IT trial was a multicenter double-blind, placebo-controlled trial that randomized statin treated patients with elevated triglycerides, who had cardiovascular disease or diabetes, and one additional risk factor, two treatment with icosapent ethyl at 4g daily versus placebo. After a median follow up period of 4.9 years, the study drug demonstrated a 25% relative risk reduction in the primary composite endpoint of cardiovascular death, myocardial infarction, stroke, coronary revascularization, or unstable angina. Dr. Greg Hundley: Ah, great summary of the original paper, but now this is sort of a follow-up paper. What did this paper research? Dr. Carolyn Lam: Well first, remember they focused on renal function and the median baseline GFR was 75 ml/min with a range of 17 to 123 mL/min/1.73 m2. Treatment with Icosapent Ethyl led to consistent reduction in both primary and secondary composite endpoints across the baseline GFR categories. Patients with the GFR >60 treated with Icosapent Ethyl had the largest absolute, but similar relative risk reduction for the primary composite endpoint. And while patients with GFR >60 treated with Icosapent Ethyl had the highest numerical rates of atrial fibrillation of flutter and serious bleeding. The hazard ratios for atrial fibrillation flutter and serious bleeding were similar across GFR categories. In summary Icosapent Ethyl reduced cardiovascular events among patients with elevated triglycerides in a well-controlled LDL on statin therapy across a wide range of baseline renal function. Dr. Greg Hundley: Oh, Carolyn. Beautiful presentation. That presentation was so good that I know you are ready for a quiz. We haven't had Carolyn's quiz in a week, so we've got to get right back to that. Dr. Carolyn Lam: No, we don't (laughs). Dr. Greg Hundley: Can you describe the primary sequelae of Hutchinson-Gilford progeria syndrome? Dr. Carolyn Lam: Oh wow. Okay. So this is the syndrome where there's premature aging, there's a lot of vascular stiffening, calcification. I'm going to guess some sort of atherosclerotic consequence (laughs). Dr. Greg Hundley: Very nicely done Carolyn. Oh my goodness. I need to get you to take my ABIM recertification- Dr. Carolyn Lam: (laughing) Dr. Greg Hundley: Beautifully done. So Carolyn, this paper comes to us from Dr. Vicente Andrés from Centro Nacional De Investigaciones Cardiovasculares Carlos III, and Hutchinson-Gilford progeria syndrome is a rare disorder characterized, just like you said, Carolyn by premature aging and death, mainly due to myocardial infarction, stroke or heart failure. The disease is provoked by progerin, a variant of lamin A expressed in most differentiated cells. Carolyn, these patients look healthy at birth and symptoms typically emerge in the first or second year of life. In assessing the reversibility of progerin induced damage, and the relative contribution of specific cell types is critical to determining the potential benefits of late treatment and to developing new therapies. Dr. Carolyn Lam: Wow, you've really, really piqued my interest. So what did these investigators do and what did they find? Dr. Greg Hundley: Oh Carolyn, very clever design. So the authors use CRISPR-Cas9 technology to generate mice engineers to ubiquitously express progerin while lacking lain A and allowing progestin suppression in lain A restoration in a time and cell type specific manner upon CRE recombinase activation. They characterize the phenotype of these engineered mice and cross them with CRE transgenic lines to assess the effects of suppressing progestin and restoring lain A ubiquitously at different disease stages, as well as specifically in vascular smooth muscle cells and cardiomyocytes. So Carolyn, what did they find? Well, number one, like Hutchinson-Milford progenia syndrome patients, their engineered mice appeared healthy at birth, and progressively developed Hutchinson-Milford progenia syndrome symptoms, including failure to thrive, Lipodystrophy, vascular smooth muscle cell loss, vascular fibrosis, electric cardiographic anomalies and early death. Their median lifespan was 15 months versus 26 months in the wild types. Dr. Greg Hundley: Second, ubiquitous progestin suppression in lain A restoration significantly extended lifespan, when induced in six month old, mildly symptomatic mice, and even in severely ill animals aged 13 months, although the benefit was much more pronounced upon the early intervention. And then finally, Carolyn remarkably major vascular alterations were prevented and lifespan normalized in engineered Hutchinson-Milford progenia syndrome mice when progestin suppression and lain A restoration were restricted to: just Vascular smooth muscle cells and Cardiomyocytes. Dr. Carolyn Lam: Wow, just fascinating, but, okay. What is the clinical take home message? Dr. Greg Hundley: Right, Carolyn. So these authors findings suggest that it is never too late to treat Hutchinson-Milford progenia syndrome, although the benefit is much more pronounced when progestin is targeted early in mice with mild symptoms. Also, restricting its suppression to Vascular smooth muscle cells in Cardiomyocytes is sufficient to prevent Vascular disease and normalize lifespan in mice, and therefore these data suggest that strategies to treat Hutchinson-Milford progenia syndrome through gene therapy or RNA therapy should consider targeting Vascular smooth muscle cells and Cardiomyocytes. Dr. Carolyn Lam: Oh wow. Very, very cool. Well, my next paper is a basic science paper that's significant for both its methods and its results. Dr. Greg Hundley: Oh wow, Carolyn, I can't wait. So tell us about this novel methodology. Dr. Carolyn Lam: Well, this paper is from Dr. Chang from Westlake University in Hangzhou, China, and colleagues who use a gene editing approach to efficiently institute Exon Skipping without introducing DNA double-strand breaks. So harnessing a fusion of a nuclease defective Case protein, and a cytidine deaminase, which is, we're going to abbreviate it as Targeted AID-induced mutagenesis (TAM) or base editor three (BE3), their approach precisely edited conserved guanines at splice sites, thus abrogating Exon recognition resulting in a programmable skipping of the targeted Exons. Isn't that neat? Dr. Greg Hundley: Yeah, it really is sophisticated Carolyn, wow. So what did they do using these methods? Dr. Carolyn Lam: A novel mirroring model of Duchenne muscular dystrophy was generated, which recapitulated many cardiac defects observed in the human form of the disease, including dilated cardiomyopathy, reduced left ventricular function and extensive cardiac fibrosis. Using this model, they examined the feasibility of using a cytidine base editor to install Exon Skipping and rescue the dystrophic cardiomyopathy in vivo. A single dose administration of an Adenovirus 9EtAm, instituted over 50% targeted Exon Skipping in the Chengdu muscular dystrophy transcripts and restored up to 90% dystrophin in the heart. And as a result, early ventricular remodeling was prevented and cardiac and skeletal muscle function were improved, leading to an increased lifespan of the mice. Despite gradual decline of the Adenovirus vector and base editor expression, the dystrophin restoration and pathophysiological rescue of muscular dystrophy lasted for at least a year. And so this technique really has the potential to be applied to monogenic human diseases, to modulate Exon Skipping or inclusion. Isn't that cool? Dr. Greg Hundley: Absolutely, Carolyn. Beautifully explained. Dr. Carolyn Lam: Well, let me end by sharing what else is in today's issue. There's a Perspective piece by Dr. Alexander on “Chest Pain Redux: Updated and Patient Centered.” There is an In Depth paper by Dr. Kroemer on NAD plus metabolism in cardiac health, aging and disease. And there's a Research Letter by Dr. Shepherd on sudden death in female athletes, with insights from a large regional registry in the United Kingdom. Dr. Greg Hundley: Very good, Carolyn. What a great issue. Now, how about we get to that feature discussion? Dr. Carolyn Lam: Let's go, Greg. Dr. Greg Hundley: Welcome listeners to our feature discussion today on this November 30th. And we have with us Dr. Cecilia Bahit from Rosario, Argentina and our own associate editor, Dr. Graeme Hankey from Perth, Australia to talk to us about a paper pertaining to Atrial Fibrillation. Welcome to you both, and Cecilia, we'll start with you. Could you describe for us a little bit of the background information that went into formulating your study, and then what hypothesis did you want to address? Dr. Cecilia Bahit: Thank you for the invitation. So we all know that embolic stroke of undetermined source, which is called ESUS isn't just a subset of cryptogenic stroke, and is associated with stroke recurrence about 3-6% per year. And on the other hand, we know that continuous cardiac monitoring in this patient population shows that atrial fibrillation can be detected between 10% at six months or 30% at three years. So the underlying atrial fibrillation may be a mechanism for the recurrent thromboembolic stroke in this patient population. So we know that prior studies have identified some predictors of atrial fibrillation in these patients. And if we are able to identify which patients could benefit from cardiac monitoring and have a higher yield to detect atrial fibrillation, we could do a better job at treating them. So, that was our idea behind the paper. So using the RE-SPECT ESUS trial, which was a trial that included patient with ESUS stroke and were randomized to the bigger trend versus Aspirin, we look at predictors of atrial fibrillation unassociated regarding stroke. Dr. Greg Hundley: Very nice. And so, now was this a sub-study here and maybe define for us a little bit, your study design and specific study population. Dr. Cecilia Bahit: So this was a secondary analysis of a randomized clinical trial that as mentioned it was not a sub-study, it was a secondary analysis. We thought all along to do it because of the interest of the clinical question. We look at the total patient population was 5,390 patients. And we looked at those patients who developed atrial fibrillation during the 19 months of follow-up. And it was 7.5%, 403 patients developed atrial fibrillation. Dr. Greg Hundley: Very good. And what were your results? Dr. Cecilia Bahit: So, as I mentioned, we saw that 7.5% of our patient population developed atrial fibrillation during the follow-up. And we know those patients were older, were like, have higher morbidities, and we assessed, we did an one variable analysis and then a multi-variable analysis, trying to identify predictors for atrial fibrillation. And for our model, we identified different predictors, older age, hypertension, lack of diabetes, and higher body mass index, were independent predictors of atrial fibrillation. So the patients who have atrial fibrillation have a higher recurrence of stroke, it was 7.2 versus four, compared to those that did not have atrial fibrillation. Dr. Cecilia Bahit: So I think there's an important part, that 20% of the patient population of the overall trial, this is a little more than a thousand patients, had NT-prob measure at baseline. And when we included this biomarker into the model, only older age and NT-prob were independent predictors of atrial fibrillation. In addition, even though this was not the objective of this analysis, we look at the treatment effect of the bigger trend. And even though we saw that there was a statistical benefit of the bigger trend versus Aspirin in the higher group of these in our score, the overall treatment effect was not there. So we couldn't assess the fact that the bigger trend was better compared to Aspirin in patient with atrial fibrillation, but of course the numbers were very small. Dr. Greg Hundley: Very good. Thank you so much for that wonderful description. And Graeae, now we'll turn to you as associate editor for us at Circulation, and also the editorialist on this particular paper. What caught your attention about this particular study and the results from the many papers that really come across your desk. Dr. Graeme Hankey: Thank you, Greg. And congratulations to Cecilia and her RE-SPECT ESUS colleagues. I mean, this is a landmark study, the RE-SPECT ESUS study, and just to go back, embolic stroke of undetermined source is really common. About one in four ischemic strokes, we don't know the cause of, and it's one of the major subtypes of cryptogenic stroke is an embolic ischemic stroke in which the source could have come from the heart or the aortic arch or the carotids. And we're not really sure. And we think that some of these patients have occult atrial fibrillation, but we can't pick it up at the time. So one way is to try and monitor them with prolonged ECG monitoring. And another way is to actually treat them with anticoagulation because we know that, that's more effective in people with cardio embolic stroke. And so RE-SPECT ESUS and NAVIGATE ESUS used the latter strategy and said, let's see if treating people with ESUS with anticoagulation is more effective than antiplatelet therapy. Dr. Graeme Hankey: And both studies were not significant in terms of showing that Dabigatran or Parovarian for NAVIGATE ESUS was more effective than antiplatelet therapy. So we're left now with this default that all patients with ESUS just get Aspirin, but we have a hunch that some of them actually have cardiogenic embolism and are being undertreated with Aspirin and need anticoagulation. So it's a heterogeneous entity, but we're treating it homogeneously with a sort of weak antiplatelet. So we want to try and find out who's going to get AF or who's already got it that is occult. And this study is a really great and prospective study with 5,000 patients as Cecilia said, who of whom 7% did develop AF just through annual ECG reporting and just with symptom reporting. And that's probably an under report. You know, if they'd had monitoring, they probably would've found about 20 or 30% would've developed AF during that time of 19 months follow up. Dr. Graeme Hankey: And it's the first study to really then show that not just the AF people had a higher stroke rate, but in that group who they predicted to be at high risk of AF with older age and the NT-prob, that the high risk group had a significant reduction with Dabigatran versus Aspirin in that high risk group. It's just, when you look for hetero homogeneity or heterogeneity across the risk groups, it wasn't quite significant. And that might be because it's not significant or it might be that study was underpowered to look at those three, across those three risk subgroups. And also it might be a bit confounded because of it, the patients weren't randomized according to their risk status for AF, they were just randomized, whether they had ESUS, so it's further excited us that there might be a subgroup who needs anticoagulation. And that's why the ARCADIA trial is ongoing now, looking at where the people with ESUS who have high risk of AF benefit from a apixaban versus aspirin. Dr. Greg Hundley: Very nice. And so, with these results that we have here, maybe come back to Cecilia, what do you think would be the next series of studies that needs to be performed in this area of research? Dr. Cecilia Bahit: Well, there's one side that's ongoing as Dr. Hankie mentioned, but I think we should be able to identify which patients have a higher risk of atrial fibrillation and those patients who use cardiac monitoring for long term to identify atrial fibrillation and to treat properly. So I think that would be key in this area. Dr. Greg Hundley: Very nice. And Graeae, what are your thoughts? Dr. Graeme Hankey: Yes. Well, one way is to have our ESUS patients have prolonged ECG monitoring by implantable loop recorders, for example, and then those who develop AF randomizing them to anticoagulation versus antiplatelet therapy. Although if they declare themselves with AF they're usually just go straight onto anticoagulation therapy. So the burning question is, in these people with ESUS who haven't declared themselves as AF, but have predictors of AF like those shown in RESPECT ESUS, like older age, high blood pressure, high BMI ,prob, and perhaps echo features, like left atrial size or ECG features like lots of premature atrial contractions or P wave of abnormalities. Dr. Graeme Hankey: Are these, the subgroups or even LV dysfunction, are these subgroups who need to be more specifically targeted in a randomized trial rather than the whole group of ESUS. And also with longer follow up. NAVIGATE ESUS stopped after 11 months. The bigger RESPECT ESUS stopped after a median follow up of 16 months and the curves were diverging. Maybe with five years follow up, a lot of these people would've developed AF and would've benefited from longer term anticoagulation, but the trials were stopped early, because there wasn't a signal of benefit and there was an early risk of bleeding with anticoagulation. Dr. Greg Hundley: Very good. Well listeners, this has been a really interesting study and we want to thank Cecilia and Graeme for sharing results of the RESPECT ESUS study, highlighting that, in patients with embolic stroke of undetermined source, atrial fibrillation occurs and is a possible source of this stroke, and then also older age, and elevation of NT-prob can be associated with development of atrial fibrillation, subsequent to that stroke event. Dr. Greg Hundley: Well listeners, we want to wish you a great week. And on behalf of Carolyn and myself, look forward to catching you next week on The Run. This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more visit ahajournals.org.

Old is a supernatural mystery thriller starring Jumanji co-star Alex Wolff about a family on a tropical holiday who discover a secluded beach where relaxing causes aging rapidly in a single day taking of your entire life.We examine this movie to see if it properly considered the progeria condition which is also known as Hutchinson-Gilford syndrome, an extremely rare, progressive genetic disorder, that causes children starting in the first two years to age rapidly.What are your thoughts?Subscribe to the "Beyond the Natural Podcast" on any podcast app or by going to YouTube!

Progeria is an ultra rare genetic condition. Sufferers age extremely rapidly and usually die within 20 years. Before the turn of the millenium, almost nothing was known about the disease, which is also called Hutchinson-Gilford syndrome. The Progeria Research Foundation is spearheading the search for a cure. Find out how you can help fund research that drastically improves the quality of life of Progeria children. Want to support the Progeria Research Foundation? https://www.progeriaresearch.org/  Find the episode on Great.com: https://great.com/great-talks-with/progeria-research-foundation/

https://astralcodexten.substack.com/p/what-do-treatments-for-accelerated   Progeria is a rare disease that makes people age unnaturally quickly. Babies born with progeria can lose their hair in toddlerhood, get wrinkles by grade school age, and die - apparently of old age - in their early teens. You can see a picture of a progeroid child here, though I don't recommend it. There's been a lot of research on one important form - Hutchinson-Gilford Syndrome - and just last year, the FDA approved the first treatment, a drug called lornafarnib. In the study, a few hundred children averaging around 7 years old took the drug for two years; 3% died during that time. In an ad hoc group of untreated comparison children, about 30% died during the same period. I'm a little confused by the methodology - it seems like the "comparison children" were chosen partly because they died too early to get into the trial, which sounds like a pretty major confounder - but everyone seems to treat this as reasonable so I will assume they adjusted for this in some way. If that's true, then lornafarnib cuts mortality by 90%. That's great for the 300 or so children worldwide with Hutchinson-Gilford progeria (it's a really rare disease). But none of the discussion about this answered the question I wanted to know: can lornafarnib also prevent normal aging? After looking into this more, I find some evidence the the answer is no, but also some reasons why maybe it's less clear cut than that? Hutchinson-Gilford progeria (I'll just say "progeria" from here on, even though that's kind of inaccurate) is what's called a laminopathy. It's a disease of the nuclear lamina, a weblike structure that helps support and give shape to the cell nucleus. The lamina is partly made of a protein called lamin A. Children with progeria have a mutation in the relevant gene; instead of producing lamin A, they produce a defective mutant protein called progerin. The cell tries to build the nuclear lamina out of defective progerin instead of normal lamin A, and as a result the cell nucleus is screwed up and can't maintain a normal shape.

El Dr. Frank G. Hammond, Médico Genetista, conversa con Peter T. sobre la progeria (síndrome de envejecimiento prematuro Hutchinson-Gilford) y las esperanzas que ofrecen recientes investigaciones para quienes sufren esta condición, en la sección de ciencia y salud de TecnologiaHechaPalabra. El eminente investigador y académico de Genética Médica en la Universidad Lisandro Alvarado de Barquisimeto, detalla las características de la progeria, que la produce y su incidencia, además, asoma importantes desarrollos de la investigación médica que podrían ralentizar el deterioro característico del envejecimiento prematuro. - - - Duración = 00:25:35. - - - - - - Artículos relacionados: - Progeria (http://www.tecnologiahechapalabra.com/salud/especialidades/articulo.asp?i=7244). - Medicina regenerativa: avances en celulas madres contra la progeria (http://www.tecnologiahechapalabra.com/salud/salud_instante/articulo.asp?i=7200). - Esperanza contra la progeria y para ralentizar el envejecimiento (http://www.tecnologiahechapalabra.com/ciencia/actacientifica/articulo.asp?i=7243). - Nuevos avances contra el envejecimiento (http://www.tecnologiahechapalabra.com/ciencia/biociencias/articulo.asp?i=10803). - The Curious Case of Benjamin Button (http://www.tecnologiahechapalabra.com/entretenimiento/record_report/cinevideo/articulo.asp?i=3464).

For this week's Feature Discussion, please join authors Erik Näslund, Mehran Anvari, Editorialist Philip Schauer, and Associate Editor Ian Neeland as they discuss, in a panel forum, the articles: "Association of Metabolic Surgery With Major Adverse Cardiovascular Outcomes in Patients With Previous Myocardial Infarction and Severe Obesity: A Nationwide Cohort Study," "Bariatric Surgery and Cardiovascular Outcomes in Patients With Obesity and Cardiovascular Disease: A Population-Based Retrospective Cohort Study," and accompanying editorial "After 70 Years, Metabolic Surgery has Earned a Cardiovascular Outcome Trial." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary, and backstage pass to the journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, Director of the Pauley Heart Center in Richmond, Virginia with VCU Health. Well, Carolyn, another double feature this week and investigating the world of metabolic, or as we also know, bariatric surgery and the impact of bariatric surgery on cardiovascular outcomes. Dr. Greg Hundley: But before we get to that double feature discussion today, how about we grab a cup of coffee and we jump into some of the other articles in the issue. I'll go first this week, Carolyn. The first article comes from Professor Andreas Schuster from University Medical Center in Göttingen. Carolyn, as you know, right heart catheterization using exercise stress represents a key method for the diagnosis of heart failure with preserved ejection fraction but carries the risk of that invasive procedure. These authors hypothesized that real time cardiovascular magnetic resonance exercise imaging with pathophysiologic data at excellent temporal and spatial resolution may represent a contemporary non-invasive alternative for diagnosing HFpEF. Dr. Carolyn Lam: Wow, Greg, you know how I love talking about HFpEF? I actually managed this paper. Could you just describe what they found? It's so exciting. Dr. Greg Hundley: Yeah, Carolyn. Even the methods are interesting here, where these authors created a situation where you're riding a bicycle and obtaining an MRI scan at the same time. Let's get to the results. The HFpEF stress trial, prospectively recruited 75 patients with echocardiographic signs of diastolic dysfunction and dyspnea on exertion with E to E primes greater than eight, New York Heart Association class greater than or equal to two. To then, undergo echocardiography, right heart catheterization and then this real time pedaling a bicycle CMR exam at rest and during exercise stress. And so what they found Carolyn, the real time CMR allowed a highly accurate identification of HFpEF during physiological exercise and qualifies, perhaps, as a suitable non-invasive diagnostic alternative to the invasive procedures. So Carolyn, I think these results will need to be confirmed in a multicenter prospective approach, but really interesting innovation here, in this particular study. Dr. Carolyn Lam: So Greg, the paper I want to talk about, actually, is the first indicative critical role of cardiac macrophages in pressure overload-induced cardiac fibrosis and dysfunction and reveal macrophage micro RNA-21 as a key molecule for the pro-fibrotic role of cardiac macrophages. Now, this comes from Dr. Engelhardt from Munich, Germany, and colleagues who show that within the myocardium, micro RNA-21 has the strongest expression in cardiac macrophages. Where it is also the single strongest express micro RNA among all micro RNAs. Targeted genetic deletion of micro RNA-21 in macrophages of mice prevented their pro-inflammatory polarization and subsequent pressure overload-induced cardiac fibrosis and dysfunction. Analysis of intercellular communication using cell sequencing identified the cardiac fibroblasts as the primary recipient cell of intercellular signals that emanate from activated cardiac macrophages and that are controlled by micro RNA-21. Dr. Greg Hundley: Oh, Carolyn, really interesting findings. What are the clinical implications? Dr. Carolyn Lam: Ah, glad you asked? What this implies is that interference with the activation of cardiac macrophages represents a promising therapeutic strategy in myocardial remodeling and dysfunction. In fact, synthetic oligonucleotide inhibitors against micro RNA-21 are currently undergoing clinical testing against fibrotic disease. This is really, really fascinating. Dr. Greg Hundley: Well, Carolyn, my next paper also comes from the world of basic science and it's from Dr. Anke Tijsen from Amsterdam University Medical Center, University of Amsterdam. Carolyn, as you know, titin, the largest protein in human, forms the molecular spring that spans half of the sarcomere to provide passive elasticity to cardiomyocytes. Mutations that disrupt the titin transcript are the most frequent cause of hereditary heart failure. These investigators evaluated the role of titin and specifically a class of circular RNAs for regulating splicing of key muscle genes in the heart. Dr. Carolyn Lam: Fascinating. Tell us what do they find. Dr. Greg Hundley: Yeah, Carolyn. In this study, the authors found that the back splice junction formed by circular RNAs creates a unique motif, which binds SRSF10, to enable it to regulate splicing. And furthermore, they show that one of these circular RNAs, cTTN1, distorts both localization of, and splicing of, RBM20. Carolyn, the authors demonstrate with this work that circular RNAs formed from the titin transcript are essential for normal splicing of key muscle genes by enabling splice regulators, RBM20 and SRSF10. This shows that the titin transcript also has regulatory roles besides its well-known signaling and structural function. So, really interesting new work involving titin. Dr. Greg Hundley: Well, Carolyn, as we transitioned to the other articles in the issue, I want to tell you about Dr. Maskoun. He has a cardiovascular case series entitled, A Plumbing and Electrical Problem: An Unusual Cause of Syncope. Dr. Carolyn Lam: I like that title. Well, there's also a perspective fees by Dr. Lindman on unloading the stenotic path to identifying medical therapy for calcific aortic valve disease, talking about its barriers and opportunities. Dr. Carolyn Lam: Tracy Hampton reviews the literature and fascinatingly highlights papers like how DNA base editing treats Hutchinson-Gilford progeria syndrome in mice, how some researchers have identified the protein involved in cardiac repair, which is the ZEB2 protein and more information on mapping early heart formation in the embryonic mouse heart. Dr. Carolyn Lam: We've got a research letter by Dr. Levine. This one is so fascinating. It's about the cardiac effects of repeated weightlessness during extreme duration swimming and how that compares with spaceflight. Is that cool? Dr. Greg Hundley: Yeah. Dr. Carolyn Lam: Anyways, this was just such a power-packed issue. Now, let's just go to our feature discussion. Shall we? I can't wait, Greg. Dr. Greg Hundley: You bet. Dr. Greg Hundley: Well listeners, we have got another exciting feature discussion today on this April 13th issue. We have with us Erik Naslünd from Karolinska Institute in Stockholm, Ari Doumouras from McMaster Institution in Ontario, Canada, Ian Neeland our own associate editor from Cleveland, Ohio, and Phil Schauer from Pennington Biomedical Research Center-LSU. Welcome gentlemen. Let's start with you today, Erik. Could you describe for us, what was the hypothesis that your study wanted to address and what were your study population and design? Dr. Erik Naslünd: Well, what we want to study was if metabolic surgery affects the outcome in patients with previous myocardial infarction. And in Sweden, we are lucky that every Swede has their personal identification number, which is connected to essentially anything that we do, including all healthcare and we then have several registries. One is in a metabolic surgery registry, and then we also have one for cardiovascular disease called SWEDEHEART. What we did was, we went into these registries and we found patients who had undergone metabolic surgery. And then, we went to the SWEDEHEART registry and we looked at those patients who'd had a previous myocardial infarction. And then, we were able to get a match cohort, the same BMI and so on, in the SWEDEHEART registry. We were able to compare these two. We got a cohort then of roughly 500 patients who'd had metabolic surgery without a prior myocardial infarction and 500 who'd had a myocardial infarction. We then, assessed to see what the outcome was. Dr. Greg Hundley: Very nice. And can you describe for us your results? Dr. Erik Naslünd: Yeah, what we found was... Our main outcome measure was in the major adverse cardiovascular event and we found that, that was lower in the group that underwent metabolic surgery. We also then looked at death, which was also lower. We also looked at the risk for new onset of heart failure, which was also reduced. We also then assessed the risk for a major complication of the surgery in the group that had undergone metabolic surgery. We compare that to our surgical registry and we found that that was essentially the same. There was not really difference in terms of outcomes in terms of severe complications after the surgery. Dr. Greg Hundley: Excellent. Now, Ari, you also have a study that is involving bariatric surgery or metabolic surgery. Could you describe for us your hypothesis and your study population and design? Dr. Aristithes Doumouras: Yes. Thanks, Greg. Our hypothesis, first and foremost, was very similar to Erik's that patients who underwent metabolic surgery, who already had a history of heart disease when compared to a group that didn't receive bariatrics or metabolic surgery would decrease the future cardiovascular risk through a MACE outcome. Our secondary hypothesis we had, that was that those with heart failure would actually have a greater effect of metabolic surgery because of the decrease in obesity compared to those without heart failure or patients with ischemic, just ischemic heart disease with no heart failure. Dr. Aristithes Doumouras: The setting of the study was Ontario, Canada, where we have a centralized bariatric surgery network called the Ontario Bariatric Network. Like Erik, in Ontario, we're able to have multiple databases that are connected. They have one unique identifier for each patient. And so we looked at all patients who underwent bariatric surgery in Ontario during a timeframe. To note, we have a very large private system. Most bariatric surgeries, more than 95%, happen in the public system so we're able to track a lot of our bariatric surgery patients and don't lose a lot. We tracked all of our bariatric patients and matched them, on a one-to-one ratio, with very similar patients who also had heart disease and access to cardiology care, access to family physician care and followed them over 10 years. And so the design was a retrospective matched cohort in this way, comparing these two groups. Dr. Greg Hundley: Thank you, Ari. And Ari, what did you find? Dr. Aristithes Doumouras: Once again, like Erik, we found that there was a lower rate of MACE outcomes in the patients who underwent metabolic surgery and the absolute values were actually quite high. The absolute risk difference between the two groups was 8% and actually that went up to almost 19% in patients with heart failure. There was no action causing interaction between ischemic heart disease and heart failure, so they were the same. And the risk was about 40% lower for future MACE events in the surgery group. Dr. Greg Hundley: Wow, a large difference. Ian, as an editorialist for Circulation, the American Heart Association, you see a lot of papers come across your desk, what attracted you to these two manuscripts?   Dr. Ian Neeland: When I first read these excellent papers, I thought that first of all, it was globally diverse. One study was in Europe, the other one in North America. And nevertheless, they showed strikingly similar relative risk reductions in MACE. One of them showed between 40 to 50% and so did the other. That was one really striking thing, was the consistency of a risk reduction despite being globally diverse with different systems in each country. Second of all, the absolute risk reduction was astounding. Assuming you could translate the absolute risk reduction to a clinical trial, to real-world experience, you're looking at a number needed treat between five to 12 for MACE, which is astounding and much greater than many of the evidence-based therapies we have today. The magnitude of the findings were striking and the ability to generalize globally were really interesting. Dr. Greg Hundley: Thank you, Ian. Well listeners, we also have an editorialist that can help us put all of this in context of what we known previously about bariatric surgery or what we are calling metabolic surgery. So we're going to turn to Phil. Phil help us put the results of these two studies in the context of cardiovascular medicine specialists or even family practitioners, internists that are managing patients with cardiovascular disease that happened to be morbidly obese. Dr. Phillip Schauer: Yeah, Greg. Well, these are both outstanding observational studies. And congrats to Erik and Ari and their teams for putting these studies together. Now, what's unique about these studies, is that I think these are the first to actually look at metabolic surgery for secondary prevention. Now, there are nearly 30 studies looking at metabolic surgery as primary prevention. These are all observational. They're not prospective randomized trials, but they all show, nearly all of them, show mortality reduction and MACE event reductions. These two studies are the first to show that metabolic surgery is good for secondary prevention. This is really important because I think, up till now, cardiologists have been very reluctant to refer patients to metabolic surgery. Patients who've already had a heart attack because of the least perceived operative risk and surgeons have been reluctant to operate on these patients. And both Erik and Ari have showed that the perioperative risks were remarkably low for this population, operative mortality way below 1%. Dr. Phillip Schauer: And so within a very short period, within a year or two, the mortality reduction, by far, supersedes any perioperative risk. I think this is really very good news. We now have quite a large amount of observational data in the primary prevention side. These two studies, nearly identical, showing mortality, MACE event reductions, as Ian pointed out, 40 to 50%. That's a lot. That rivals almost anything else out there in terms of mortality reduction, whether it's an SGLT2 inhibitor, a GLP-1, or a statin, I mean, people dance in the street when you see a five and 10% reduction. With surgery, it looks like we're seeing 40 to 50%. So, this is remarkable news but we do have a little more work to do. Perhaps we can talk about that, your next question. Dr. Greg Hundley: What a great lead-in Phil. So listeners, striking results with this surgical intervention for patients with cardiovascular disease that have morbid obesity. Erik, let's start with you, but we'll go through all of our expert panelists here. Erik, what do you think is the next study that needs to be performed in this sort of area of research? Dr. Erik Naslünd: Well, I mean, the obvious answer to that is that we need to do a randomized control trial to verify these results. That's the number one. Number two, I think, we also need to tease out, if we can, which are the most suitable patients. And is there a difference between the most commonly performed metabolic surgery procedures. That's where I would suggest that you need to do next. Dr. Greg Hundley: Ari, how about you? Dr. Aristithes Doumouras: I agree with Erik. I think everyone's going to say the same thing. That I think a randomized trial is the next step when looking at bariatric surgery and the role of secondary prevention-based patients, as these are all observational studies. And they just need to be confirmed. We're starting on a pilot study for this exact randomized trial at our institution and obviously looking for more partners later on, but yeah, that's definitely the next step in the process for sure. Dr. Greg Hundley: Ian, what would you like to add? Dr. Ian Neeland: No, I definitely agree an RCT is needed. I think one that combines both primary and secondary prevention patients is important to try to understand that the difference. One could imagine that secondary patients may actually derive much greater benefit than prime prevention patients given their baseline risk. And if one can show that the operative morbidity, mortality is low in both populations, as both papers showed observationally, then I think there's a lot of benefit there. I also think it's important to try to randomize people to different procedures, to really try to understand is it the gastric sleeve? Is it the bypass? And which one has greater benefit in the setting of a RCT as well as how do the risks and safety outcomes differ between those two in the real-world RCT setting. Dr. Greg Hundley: Very nice. Well, Phil we've heard randomized trials, maybe also, do we need longer follow-up? Dr. Phillip Schauer: Yeah, Greg. In the title of my editorial, and I hope that the listeners actually do read it, is after 70 years, metabolic surgery has earned a prospective randomized trial, and it's true. This field is 70 years old, there's not a single prospective large randomized controlled trial. There are quite a few small studies that were powered for biomarkers, but not hard clinical end points. We need this and it is doable. For example, for coronary artery bypass surgery, there's over a hundred prospective randomized controlled trials. So we definitely need this type of study. It needs to be long follow-up, probably five years or more. As Erik and Ari pointed out, it should have a mixture of primary and secondary prevention. Dr. Phillip Schauer: I'll share with you right now, I'm working with a group in the US. Along with Steve Nissen, a very noted cardiologist, Bob Eckel, who's currently the president of the American Diabetes Association and a number of other experts. David Aterburn, Sonia Thomas, who are working together to try to develop a study. The question is who will fund this? And frankly, we've been talking to various funding organizations. And frankly, we need the help of the cardiology community to help us support this. This information is very important. Dr. Phillip Schauer: If I may say one more thing, it's interesting the entire field of obesity treatment, everybody who has obesity gets treatment to cause weight loss. Yet in 2021, we do not have data that shows that weight loss actually reduces morbidity and mortality. The closest thing we have is a look ahead trial, and it looked at weight loss via a lifestyle intervention. After 10 years, they got 6% weight loss, 6% weight loss is not enough. With metabolic surgery, we can get 25 to 30% weight loss. So we need to do this study, not just to show that metabolic surgery is effective, but to show that weight loss itself could actually reduce morbidity and mortality. And frankly, it's not just cardiovascular. The second most common cause of death in these studies is cancer. And that's the other interesting thing that should be looked at. Hopefully, we can get organizations like NCI to come in and support this initiative. Dr. Greg Hundley: Thank you. Well, listeners, what a wonderful discussion today, really a feature symposium. And we want to thank Erik Naslünd, Dr. Aristithes Doumouras, Ian Neeland and Phil Schauer for their time and expertise and sharing that with us today. Especially on this topic of bariatric, but now maybe more commonly called metabolic surgery, where these two studies have been demonstrating efficacy of these procedures now in patients with cardiovascular disease and even those post myocardial infarction. Dr. Greg Hundley: On behalf of Carolyn and myself, I want to wish you another great week ahead and we will catch you in that next week, on the run. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021.  

In this episode Daniel and Nate talk about recent technology breakthroughs, how those things will impact our culture, and how the church will respond to those changes.Like what will be the implications gene editing becoming more and more affordable.   Here's a link to an article about a major leap forward with Hutchinson-Gilford progeria syndrome and gene editing. How far can we take gene editing and how could it be used to heal and change our bodies?  Will the church take a zero tolerance stance on gene editing because it is playing God or will we have a more nuanced response about the time and place to use this technology? After Tesla, Elon Musk, and others roll out full self-driving cars, will we need church parking lots anymore? Will we want to own cars anymore and deal with the maintenance and headaches? What will churches do with their unused parking lots? Will they turn them into gardens that are managed by Humanoid Autonomous Robots that garden, manage animals, harvest produce, eggs, milk, etc and can cook, process, store, and distribute these resources to the community?Nate and Daniel also discuss the implications of the Boston Dynamics dancing robots. It's not CGI. The video is totally real. Personal robots are coming to every home and business in this decade. Robots that can learn and work and help us and also put us out of the work we're doing today.  Is a machine that can do the job of 100 humans a good thing? Is our goal to replace humans in all systems possible and what would humans go on to do if those things are automated?Why are we here?Where are we going?Why is so much wrong with the world?What's the remedy?Here's a link to the book "When Helping Hurts" as you think about how you can really help those who are in need in ways that accomplish the intended goals. Support the show (https://www.patreon.com/jubileefreedomshalom)

Here are the links for everything discussed in Episode 46, I'm also including times here so feel free to skip ahead to the topics that interest you. I hope everyone has a safe, happy, and socially distanced holiday! (1:08) Approval of Zokinvy for Hutchinson-Gilford progeria syndrome (4:37) New EUA authorized for banlamivimab for treatment of COVID19 CDC updates on COVID-19 & influenza reportingConnect with The Rx Daily Dose:Twitter      Instagram      YouTube      Linkedin       WebsiteEmail: therxdailydose@gmail.comConnect with Ian Parnigoni PharmD. on social media:Twitter       Instagram       Linkedin  ★ Support this podcast on Patreon ★

Des chercheurs taïwanais ont découvert qu'une carence en cil primaire sur les cellules pourrait être la clé pour comprendre la progéria, une maladie génétique progressive rare connue sous l’appellation de la maladie des enfants-vieillards. Les résultats de l’avancée scientifico-médicale taiwanaise ont été publiés en tant qu'étude-phare dans une édition récente des EMBO Reports, une revue scientifique consacrée à la biologie moléculaire. Les patients atteints de progéria, ou syndrome de Hutchinson-Gilford, développent des symptômes néonatals aigüs et ont une espérance de vie moyenne de 13-14 ans à peine. Les traits cliniquement observables comprennent un retard de croissance sévère, une perte de graisse sous-cutanée, une peau ridée, une perte des cheveux, une ostéoporose, une raideur corporelle et le développement de maladies cardiovasculaires. Chen Hong-chen (陳鴻震), professeur de biologie moléculaire à l'Université nationale Yang-Ming qui a dirigé l'équipe de recherche, a présenté les travaux de recherche de son équipe et détaillé qu’ils ont trouvé un lien entre l’anomalie du noyau et le cil primaire à la surface de la cellule. Étant donné que le cil primaire fonctionne comme une antenne cellulaire qui détecte les changements dans les environnements extracellulaires et transmet les signaux à l'intérieur de la cellule pour répondre à ces changements, il est possible que le dysfonctionnement des cils primaires puisse provoquer une progéria. Le ministère des sciences et technologies salue cette dévouverte qui « fournit non seulement de nouvelles perspectives sur la pathogenèse du syndrome de progéria, mais qui met également en lumière de nouvelles stratégies thérapeutiques pour les maladies apparentées. »

Um bebê nasce com a aparência e os interesses de um idoso. Assim inicia a vida de Benjamin Button, esperança de felicidade e prosperidade para a sua família, que acaba tendo que lidar com um corpo que nasce velho e rejuvenesce à medida que o tempo passa. A nossa conversa neste episódio apresenta spoilers, pois trata-se de um conto extremamente curto e já adaptado para o cinema. No entanto, buscamos ir além de comentar a leitura, trazendo personagens da vida real que passam pelo que o personagem de Fitzgerald passou. Enfim, o episódio está curto mas com uma boa dose de reflexão. Aperte o play e venha refletir sobre o tempo e a vida com a gente! A Rádio Caractere é Associada Amazon.com.br! O curioso caso de Benjamin Button: https://amzn.to/2NTSQg8 Reportagens mencionadas no episódio: Síndrome de Hutchinson-Gilford: http://www.fiocruz.br/biosseguranca/Bis/infantil/sindrome-hutchinson-gilford.htm Sobre o italiano Sammy Basso: https://www.gazetadopovo.com.br/viver-bem/saude-e-bem-estar/saude/com-progeria-jovem-se-torna-cientista-e-busca-cura-para-a-doenca/ Sobre Bayezid Hossain: https://br.blastingnews.com/mundo/2017/05/o-curioso-caso-de-benjamim-button-da-vida-real-veja-o-que-acontece-com-o-menino-001665447.html Sobre os irmãos indianos que sofrem com a síndrome: https://www.megacurioso.com.br/medicina-e-psicologia/90666-irmaos-indianos-sofrem-de-condicao-rara-que-os-faz-parecer-velhinhos.htm Nossos links: https://linktr.ee/Caractere Receba os podcasts da Rádio Caractere no seu app favorito, Spotify ou no YouTube! Envie uma mensagem de voz para a Rádio Caractere! https://anchor.fm/radio-caractere/message Direção e Conteúdo: Suzane Madruga Produção e Edição: Glenio Madruga --- Send in a voice message: https://anchor.fm/radio-caractere/message Support this podcast: https://anchor.fm/radio-caractere/support

El Dr. Frank G. Hammond, Médico Genetista, conversa con Peter T. sobre la progeria (síndrome de envejecimiento prematuro o Hutchinson-Gilford) y las esperanzas que ofrecen recientes investigaciones para quienes sufren esta condición, en la sección de ciencia y salud de TecnologiaHechaPalabra.- -El eminente investigador y academico de Genética Médica en la Universidad Lisandro Alvarado de Barquisimeto, detalla las características de la progeria, que la produce y su incidencia, además, asoma importantes desarrollos de la investigación médica que podrían ralentizar el deterioro característico del envejecimiento prematuro.- - -Duración = 00:25:35.- - - - - -Artículos relacionados:- Progeria (http://www.tecnologiahechapalabra.com/salud/especialidades/articulo.asp?i=7244).- Medicina regenerativa: avances en celulas madres contra la progeria (http://www.tecnologiahechapalabra.com/salud/salud_instante/articulo.asp?i=7200).- Esperanza contra la progeria y para ralentizar el envejecimiento (http://www.tecnologiahechapalabra.com/ciencia/actacientifica/articulo.asp?i=7243).- Nuevos avances contra el envejecimiento (http://www.tecnologiahechapalabra.com/ciencia/biociencias/articulo.asp?i=10803).- The Curious Case of Benjamin Button (http://www.tecnologiahechapalabra.com/entretenimiento/record_report/cinevideo/articulo.asp?i=3464).

Sejam bem-vindos ao quadringentésimo nonagésimo sexto Spin de Notícias, o seu giro diário de informações científicas... em escala sub-atômica.E nesse Spin de Notícias falaremos sobre... Biomedicina!*Este episódio, assim como tantos outros projetos vindouros, só foi possível por conta do Patronato do SciCast. Se você quiser mais episódios assim, contribua conosco!*

Sejam bem-vindos ao quadringentésimo nonagésimo sexto Spin de Notícias, o seu giro diário de informações científicas... em escala sub-atômica.E nesse Spin de Notícias falaremos sobre... Biomedicina!*Este episódio, assim como tantos outros projetos vindouros, só foi possível por conta do Patronato do SciCast. Se você quiser mais episódios assim, contribua conosco!*

En este episodio comentamos una nueva estrategia terapéutica basada en la técnica de CRISPR-Cas9 y dirigida a paliar los efectos del síndrome de Hutchinson-Gilford (progeria) que causa envejecimiento prematuro. También discutimos una reciente investigación sobre la co-evolución de moléculas de adhesión en bacterias y los receptores encargados de reconocerlas en las células del sistema inmune. Además, comentamos una prometedora opción terapéutica contra el cáncer de mama triple negativo, basada en el reposicionamiento de fármacos ya aprobados para otras patologías. Todo ello, además de las (bio)noticias de la semana y una entrevista a Lluís Montoliú y Laura Morrón, autor y editora, respectivamente, del libro sobre CRISPR "Editando Genes: recorta, pega y colorea".

La tertulia semanal en la que repasamos las últimas noticias de la actualidad científica. En el episodio de hoy: Operación Rescate: Nos vamos a Marte a liberar a Opportunity; Ecofísica para el modelado de la evolución lingüística; Creando textos con una IA; CRISPR para el tratamiento del síndrome Hutchinson–Gilford, o progeria; Primera imagen 3D de viroides; Guiando el crecimiento neuronal. En la foto, de arriba a abajo y de izquierda a derecha: Ignacio Crespo, Sara Robisco, Bea Ruiz, Héctor Socas, Carlos Westendorp. Todos los comentarios vertidos durante la tertulia representan únicamente la opinión de quien los hace… y a veces ni eso. CB:SyR es una colaboración entre el Área de Investigación y la Unidad de Comunicación y Cultura Científica (UC3) del Instituto de Astrofísica de Canarias.

La tertulia semanal en la que repasamos las últimas noticias de la actualidad científica. En el episodio de hoy: Operación Rescate: Nos vamos a Marte a liberar a Opportunity; Ecofísica para el modelado de la evolución lingüística; Creando textos con una IA; CRISPR para el tratamiento del síndrome Hutchinson–Gilford, o progeria; Primera imagen 3D de viroides; Guiando el crecimiento neuronal. En la foto, de arriba a abajo y de izquierda a derecha: Ignacio Crespo, Sara Robisco, Bea Ruiz, Héctor Socas, Carlos Westendorp. Todos los comentarios vertidos durante la tertulia representan únicamente la opinión de quien los hace… y a veces ni eso. CB:SyR es una colaboración entre el Área de Investigación y la Unidad de Comunicación y Cultura Científica (UC3) del Instituto de Astrofísica de Canarias.

Dr. Jed Fahey is a multi-decade veteran of isothiocyanate research and is the director of the Cullman Chemoprotection Center at Johns Hopkins University.   In this episode, you'll discover: 00:00:00 - the early history of sulforaphane research, including key initial discoveries. 00:00:37 - the serendipitous unfolding of events that lead to the converging of the research on the NRF2 stress response pathway with the sulforaphane-related research going on at the same institute Johns Hopkins. 00:05:06 - why cruciferous vegetables bother to create isothiocyanates in the first place. 00:07:26 - the involvement of the heat shock proteins, in addition to the increased activity of Nrf2, as an additional cellular response mechanism that's been observed in association with sulforaphane. 00:08:11 - how sulforaphane affects a diverse array of biochemical processes from glutathione synthesis to elimination of reactive oxygen species and detoxification of harmful compounds, including carcinogens. 00:15:01 - whether or not to cook your cruciferous vegetables. 00:15:34 - the epidemiological (associative) evidence that cruciferous vegetable consumption may help reduce the risk of cancer. 00:18:30 - the extremely unpredictable nature of endogenous conversion of glucorapahanin (the precursor) into sulforaphane between person to person. 00:22:14 - practical information surrounding supplementation of sulforaphane. 00:27:05 - the effect one particular french sulforaphane supplement had on the doubling rate of PSA, which is a marker for prostate cancer recurrence in prostate cancer patients. 00:28:17 - the role that the Cullman Chemoprotection Center at Johns Hopkins has played, in addition to fundamental research, in providing early, vital infrastructure enabling some of the efforts of the international research community in elucidating the effects of sulforaphane and related compounds and the underlying biological pathways. 00:28:26 - the incredible, almost geometric growth in new studies that has occurred since the advent of a few of the key discoveries about sulforaphane and its method of action. 00:32:48 - the practicality of probiotics as a way to improve endogenous myrosinase activity needed to convert the precursor to sulforaphane into the bioactive sulforaphane. 00:33:26 - the involvement of our gut bacteria in our ability to convert the precursor of sulforaphane into its active form. 00:37:13 - whether or not endogenous myrosinase activity improves as a function of repeated challenge with glucoraphanin (the precursor to sulforaphane). 00:39:30 - why probiotics may vary in their degree of efficacy. 00:43:00 - why consuming isothiocyanates to reduce the number of bacterial colonies of h. pylori, a risk factor for peptic ulcers and stomach cancer, may turn out to be a better intervention than complete eradication of the species with antibiotics. 00:47:21 - the bizarre relationship h. pylori has with childhood asthma, where it has been shown that having some h. pylori seems to reduce asthma incidence in childhood. 00:52:28 - the effect sulforaphane has on inflammation and why inflammation is often a great therapeutic target for many different diseases, including diseases of aging. 00:54:05 - the life extension properties broccoli has been shown to have in an insect model of aging. 00:59:27 - the underlying causes of Hutchinson-Gilford progeria and the promise sulforaphane may hold for this disease of rapid aging. 01:09:00 - the effects of sulforaphane or Nrf2 activation on diseases of the brain, such as autism (human evidence) and Alzheimer's (animal evidence), possibly through anti-oxidative or anti-inflammatory effects. 01:11:09 - the so-called autistic fever response whereby autistic patients report a sudden reversal of symptoms during brief periods of fever. 01:10:05 - the role heat shock proteins might play more broadly in the prevention of certain neurological diseases. 01:19:00 - the challenges inherent in clinical trials where scientists may be extremely optimistic about the effects that might be observed, but still have to exercise caution and choose trial conditions that may be conservative, for the good of the people whose lives and hopes hang in the balance. 01:27:01 - the role of inflammation and depression and what some studies on animals have demonstrated in terms of sulforaphane's potential as an antidepressant. 01:42:30 - a special isothiocyanate-containing plant known as Moringa or sometimes referred to as the drumstick tree or the horseradish tree. 01:46:32 - Dr. Fahey's inadvertent foray into the consumption of exotic meats during a visit to Africa. 01:51:15 - a compound commonly associated with broccoli: indole-3-carbinol and its downstream product diindolylmethane (DIIM). 01:57:00 - the practicality of using mustard seed powder as an extra source of myrosinase, possibly for your cooked cruciferous vegetables. 02:00:13 - whether or not it makes sense to freeze broccoli sprouts in order to extend their shelf life, and possibly even increase sulforaphane within certain contexts. 02:05:25 - Dr. Fahey's thoughts on where endogenous conversion of glucoraphanin occurs in the body, as well as how long it takes before sulforaphane metabolites hit the bloodstream after ingestion. 02:07:25 - Some general thoughts on frequency in terms of how often one might need to take sulforaphane to elicit its biological effects. 02:12:16 - why sulforaphane may one day be a component of sunscreen. 02:12:31 - what some of the upcoming trials involving sulforaphane are at the Cullman Chemoprotection Center. 02:17:07 - the incredible way in which a sulforaphane-rich broccoli sprout beverage was shown to dramatically enhance the detoxification of benzene through excretion: one study showed up to 61% starting immediately after supplementation.   If you're interested in learning more, you can read the full show notes here: https://www.foundmyfitness.com/episodes/jed-w-fahey Join over 300,000 people and get the latest distilled information straight to your inbox weekly: https://www.foundmyfitness.com/newsletter Become a FoundMyFitness premium member to get access to exclusive episodes, emails, live Q+A's with Rhonda and more: https://www.foundmyfitness.com/crowdsponsor

Dr. Jed Fahey is a multi-decade veteran of isothiocyanate research and is the director of the Cullman Chemoprotection Center at Johns Hopkins University. Much of this conversation, as you might expect given Dr. Fahey's pedigree as a research scientist, is focused on isothiocyanates and, indeed, sulforaphane! While we covered quite a lot on this very topic (isothiocyanates) via my solo podcast a few weeks ago, this covers everything that may have been overlooked.... and, indeed, so much more! Skip to the timeline below for a sampling. Dr. Fahey and his colleagues have been, in a big way, at the absolute center of what is a staggering amount of research on these very powerful compounds. There is hardly a topic which we can discuss in which he doesn't have an anecdote about a study he was involved in, or, in some cases, tribal knowledge that may not even be published but is nonetheless interesting and an important part of the story that is unique to his particular vantage point. In this 2-hour and 30-minute interview, we discuss... 00:00:00 - the early history of sulforaphane research, including key initial discoveries. 00:00:37 - the serendipitous unfolding of events that lead to the converging of the research on the NRF2 stress response pathway with the sulforaphane-related research going on at the same institute Johns Hopkins. 00:05:06 - why cruciferous vegetables bother to create isothiocyanates in the first place. 00:07:26 - the involvement of the heat shock proteins, in addition to the increased activity of Nrf2, as an additional cellular response mechanism that's been observed in association with sulforaphane. 00:08:11 - how sulforaphane affects a diverse array of biochemical processes from glutathione synthesis to elimination of reactive oxygen species and detoxification of harmful compounds, including carcinogens. 00:15:01 - whether or not to cook your cruciferous vegetables. 00:15:34 - the epidemiological (associative) evidence that cruciferous vegetable consumption may help reduce the risk of cancer. 00:18:30 - the extremely unpredictable nature of endogenous conversion of glucorapahanin (the precursor) into sulforaphane between person to person. 00:22:14 - practical information surrounding supplementation of sulforaphane. 00:27:05 - the effect one particular french sulforaphane supplement had on the doubling rate of PSA, which is a marker for prostate cancer recurrence in prostate cancer patients. 00:28:17 - the role that the Cullman Chemoprotection Center at Johns Hopkins has played, in addition to fundamental research, in providing early, vital infrastructure enabling some of the efforts of the international research community in elucidating the effects of sulforaphane and related compounds and the underlying biological pathways. 00:28:26 - the incredible, almost geometric growth in new studies that has occurred since the advent of a few of the key discoveries about sulforaphane and its method of action. 00:32:48 - the practicality of probiotics as a way to improve endogenous myrosinase activity needed to convert the precursor to sulforaphane into the bioactive sulforaphane. 00:33:26 - the involvement of our gut bacteria in our ability to convert the precursor of sulforaphane into its active form. 00:37:13 - whether or not endogenous myrosinase activity improves as a function of repeated challenge with glucoraphanin (the precursor to sulforaphane). 00:39:30 - why probiotics may vary in their degree of efficacy. 00:43:00 - why consuming isothiocyanates to reduce the number of bacterial colonies of h. pylori, a risk factor for peptic ulcers and stomach cancer, may turn out to be a better intervention than complete eradication of the species with antibiotics. 00:47:21 - the bizarre relationship h. pylori has with childhood asthma, where it has been shown that having some h. pylori seems to reduce asthma incidence in childhood. 00:52:28 - the effect sulforaphane has on inflammation and why inflammation is often a great therapeutic target for many different diseases, including diseases of aging. 00:54:05 - the life extension properties broccoli has been shown to have in an insect model of aging. 00:59:27 - the underlying causes of Hutchinson-Gilford progeria and the promise sulforaphane may hold for this disease of rapid aging. 01:09:00 - the effects of sulforaphane or Nrf2 activation on diseases of the brain, such as autism (human evidence) and Alzheimer's (animal evidence), possibly through anti-oxidative or anti-inflammatory effects. 01:11:09 - the so-called autistic fever response whereby autistic patients report a sudden reversal of symptoms during brief periods of fever. 01:10:05 - the role heat shock proteins might play more broadly in the prevention of certain neurological diseases. 01:19:00 - the challenges inherent in clinical trials where scientists may be extremely optimistic about the effects that might be observed, but still have to exercise caution and choose trial conditions that may be conservative, for the good of the people whose lives and hopes hang in the balance. 01:27:01 - the role of inflammation and depression and what some studies on animals have demonstrated in terms of sulforaphane's potential as an antidepressant. 01:42:30 - a special isothiocyanate-containing plant known as Moringa or sometimes referred to as the drumstick tree or the horseradish tree. 01:46:32 - Dr. Fahey's inadvertent foray into the consumption of exotic meats during a visit to Africa. 01:51:15 - a compound commonly associated with broccoli: indole-3-carbinol and its downstream product diindolylmethane (DIIM). 01:57:00 - the practicality of using mustard seed powder as an extra source of myrosinase, possibly for your cooked cruciferous vegetables. 02:00:13 - whether or not it makes sense to freeze broccoli sprouts in order to extend their shelf life, and possibly even increase sulforaphane within certain contexts. 02:05:25 - Dr. Fahey's thoughts on where endogenous conversion of glucoraphanin occurs in the body, as well as how long it takes before sulforaphane metabolites hit the bloodstream after ingestion. 02:07:25 - Some general thoughts on frequency in terms of how often one might need to take sulforaphane to elicit its biological effects. 02:12:16 - why sulforaphane may one day be a component of sunscreen. 02:12:31 - what some of the upcoming trials involving sulforaphane are at the Cullman Chemoprotection Center. 02:17:07 - the incredible way in which a sulforaphane-rich broccoli sprout beverage was shown to dramatically enhance the detoxification of benzene through excretion: one study showed up to 61% starting immediately after supplementation. You can find out more about Dr. Fahey and the Cullman Chemoprotection Center by visiting: The Cullman Chemoprotection Center Website (donation link) facebook.com/chemoprotectioncenter twitter.com/jedosan (Jed's twitter) jedfahey.com