Podcast appearances and mentions of michael ackerman

Friends and family of three climbers lost on Aoraki Mount Cook have been told to expect the worst with equipment found on the mountain suggesting the group may have suffered a catastrophic fall. One of the missing men, Kurt Blair, was a qualified international mountain guide. Silverton Avalanche School executive director Michael Ackerman, is a long time friend, colleague and climbing partner of his. He told Lisa Owen New Zealand authorities contacted him at the weekend to see if he'd been satellite tracking Blair and if he knew of his last location or communication.

Dr. Amit Goyal, along with episode chair Dr. Dinu Balanescu (Mayo Clinic, Rochester), and FIT leads Dr. Sonu Abraham (University of Kentucky) and Dr. Natasha Vedage (MGH), dive into the fascinating topic of channelopathies with Dr. Michael Ackerman, a genetic cardiologist and professor of medicine, pediatrics, and pharmacology at Mayo Clinic, Rochester, Minnesota. Using a case-based approach, they review the nuances of diagnosis and treatment of channelopathies, including Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and long QT syndrome. Dr. Sonu Abraham drafted show notes. Audio engineering for this episode was expertly handled by CardioNerds intern, Christiana Dangas. The CardioNerds Beyond the Boards Series was inspired by the Mayo Clinic Cardiovascular Board Review Course and designed in collaboration with the course directors Dr. Amy Pollak, Dr. Jeffrey Geske, and Dr. Michael Cullen. CardioNerds Beyond the Boards SeriesCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Channelopathies One cannot equate the presence of type 1 Brugada ECG pattern to the diagnosis of Brugada syndrome. Clinical history, family history, and/or genetic testing results are required to make a definitive diagnosis. The loss-of-function variants in the SCN5A gene, which encodes for the α-subunit of the NaV1.5 sodium channel, is the only Brugada susceptibility gene with sufficient evidence supporting pathogenicity. Exertional syncope is an “alarm” symptom that demands a comprehensive evaluation with 4 diagnostic tests: ECG, echocardiography, exercise treadmill test, and Holter monitor. Think of catecholaminergic polymorphic ventricular tachycardia (CPVT) in a patient with exertional syncope and normal EKG! ICD therapy is never prescribed as monotherapy in patients with CPVT. Medical therapy with a combination of nadolol plus flecainide is the current standard of care. Long QT syndrome is one of the few clinical scenarios where genetic testing clearly guides management, particularly with respect to variability in beta-blocker responsiveness. Notes - Channelopathies 1. What are the diagnostic criteria for Brugada syndrome (BrS)? Three repolarization patterns are associated with Brugada syndrome in the right precordial leads (V1-V2): Type 1: Prominent coved ST-segment elevation displaying J-point amplitude or ST-segment elevation ≥2 mm, followed by a negative T wave. Type 2/3: Saddleback ST-segment configuration with variable levels of ST-segment elevation. It is important to note that only a type 1 pattern is diagnostic for Brugada syndrome, whereas patients with type 2/3 patterns may benefit from further testing. The Shanghai score acknowledges that relying solely on induced type 1 ECG changes has limitations. Therefore, one cannot equate the presence of a type 1 Brugada ECG pattern alone to the diagnosis of Brugada syndrome. The score suggests incorporating additional information—such as clinical history, family history, and/or genetic testing results—to achieve a definitive diagnosis. 2. What is the significance of genetic testing in Brugada syndrome? There are 23 alleged Brugada syndrome susceptibility genes published with varying levels of evidence. However, only one gene mutation, the loss-of-function variants in the SCN5A gene encoding for the α-subunit of the NaV1.5 sodium channel, is considered to have sufficient evidence. The overall yield of BrS genetic testing is 20%. The presence of PR prolongation (>200 ms) along with type I EKG pattern increases the yield to 40%. On the contrary, in the presence of a normal PR interval, the likelihood of SCN5A positivity drops to

Michael Ackerman was born in Tel Aviv, Israel, in 1967. When he was seven years old his family emigrated to New York City, where he grew up and began photographing at the age of eighteen. Michael has exhibited internationally and published five books, including End Time City, by Robert Delpire, which won the Prix Nadar in 1999. His other books are Epilogue (Void, 2019) Half Life (Delpire, 2010) Fiction (Delpire, 2001) and Smoke (l'axolotl, 2023). His work is in the permanent collection of The Museum of Fine Arts, Houston, The Museum of Modern Art, New York, The Brooklyn Museum, and The Biliothèque National, France among others, as well as in many private collections.“In Michael Ackerman's work, documentary and autobiography conspire with fiction, and all of the above dissolve into hallucination. His photography explores time and timelessness, personal history and the history of places, immediate family and love, with all it's complexities and contradictions. “ Jem Cohen. Michael currently lives in Berlin and is represented by Galerie Camera Obscura, Paris, Spot Home Gallery, Naples and MC2 Gallery, Milan. In episode 229, Michael discusses, among other things:A little family historyWhy he put that info on his websiteCollating family photos on becoming a fatherWhy he loves New YorkHow he started photography thereBeing ‘very, very slow'Why he uses cheap plastic camerasWhat he likes about photographing animalsMoodAnders PetersenLonging being the human conditionPhotographing ‘life'Text and contextTranscending the facts while keeping a strong hold on a deeper truthHis life in Berlin with an impossible ‘to do' list Referenced:Teru KuwayamaSylvia PlachyLorenzo CastoreAnders PetersenRobert FrankMasao YamamotoBoris MikhailovJem Cohen Website | Instagram“For me photography is always a negotiation between confrontation and avoidance. And I think my pictures show that. I think my pictures are very intimate and they do get close to something and they are an attempt at getting close, but there's also a lot of fear in them I see, because I know it in myself, and a lot of solitude.” Become a full tier 1 member here to access exclusive additional subscriber-only content and the full archive of previous episodes for £5 per month.For the tier 2 archive-only membership, to access the full library of past episodes for £3 per month, go here.

Après avoir rencontré Marie-Ève Bouillon, responsable de la mission photographique des Archives nationales, Caroline Stein, en charge de la collection photographique de Neuflize OBC, et Fiammetta Horvat, responsable de la collection de son regretté père, Frank Horvat, décédé en octobre 2020, nous clôturons cette exploration de la collection avec, dans ce dernier numéro, une incursion au sein de la collection de deux collectionneurs privés qui ont accepté — et nous les en remercions chaleureusement — d'ouvrir leurs portes à Yannick Le Guillanton. Liste non exhaustive des œuvres citées - Jean-Michel Fauquet, Untitled ; 2009 - Joel-Peter Witkin, Waiting for de Chirico in the Artist's Section of Purgatory, New Mexico ; 1994 - Denis Dailleux, Deux frères chez le garagiste de Kom el-Dik, Egypte, Alexandrie ; juin 2002 - Denis Dailleux, Mères et Fils - Raed Bawayah, Série « les veines de la terre », Palestine ; 2012 - Michael Ackerman, Napoli ; 2000 - Reza Aramesh, Action 68 South Vietnamese soldiers show of a Viet Cong prisoner captured near Tan Son Nhut Airbase, May 6; 2009 - Matt Collishaw, Série « Last Meal on Death Row », David Allen Castillo ; 2010 - Jean-Michel Pancin, Pelote P29T ; 2011 - Brian Hubble, Electric Love Seat (or the Love Destroyer) - Bogdan Konopka, Sedletz-Ossarium - Eva Koťátková, Out of Sight ; 2013 - Hicham Benohoud, Half Couple ; 2004 - Pierre Molinier, Série « Mon cul » ; Ca 1965 - Lea Crespi, Lieux - Olivier Valsecchi, selfportrait with bubble ; 2009 - Markus Lupertz, Satyr + Nymphe 1, Mixed media on canvas ; 2014 - Alberto García-Alix, Mi un pelo en la cabeza ; 2007 - Luca Giordano, San Sebastiano curato da Sant'Irene, Huile sur toile ; 1670 - Dieter Appelt, Sans titre ; 1979 - Patrick Faigenbaum, Famille Pallavicini, Rome ; 1987

Axolotl, c'est le nom choisi par Caroline Bénichou pour sa maison d'édition. Un projet qui mûrit depuis longtemps, en parallèle de son poste de directrice de la galerie VU'. Cet amphibien assez peu connu du grand public malgré une caractéristique étonnante, celle de pouvoir régénérer n'importe quelle partie de son corps sera désormais l'emblème de ce projet éditorial et artistique photographique. Pour le lancement de son premier ouvrage « Smoke », de Michael Ackerman, en septembre prochain, toutes les planètes se sont parfaitement alignées. L'ouvrage est en appel à souscription à un prix préférentiel, dépêchez-vous, il n'y en aura pas pour tout le monde !

This week's episode of the podcast is supported by the SADS Foundation (SADS.ORG) and is on the topic of the overdiagnosis of LQTS. What sorts of conditions can lengthen the QT interval without true congenital LQTS syndrome? What are the most common errors of ECG interpretation that account for misdiagnosis of this condition and are there leads of the ECG that might help or hurt when attempting to accurately measure the QT interval. What is the role of the ICD in the LQTS patient? We speak with Professor of Pediatrics, Medicine and Pharmacology at the Mayo Clinic Alix School of Medicine, Dr. Michael Ackerman about a recent work he published on this important topic.doi: 10.1016/j.jacc.2022.11.036.

Michael Ackerman is currently the director of the Master in Healthcare Innovation Program and Professor of Clinical Nursing and the director of the Center for Healthcare Innovation and Leadership at the Ohio State University College of Nursing. He also maintains a clinical practice as an acute care nurse practitioner at St. Joseph's Neighborhood Hospital in Rochester, New York. Today, we talk about nursing, healthcare innovation, and opportunities for designers in the healthcare industry. Listen to learn about: The role of nurses in nursing/healthcare innovation The unique challenges of innovation in healthcare Improving the healthcare innovation cycle OSU's Center for Healthcare Innovation and Leadership Our Guest Michael Ackerman is currently the Director of the Master in Healthcare Innovation Program and Professor of Clinical Nursing, and the Director of the Center for Healthcare Innovation and Leadership at the Ohio State University College of Nursing. He also maintains a clinical practice as an acute care nurse practitioner at St Joseph's Neighborhood in Rochester, NY.  He is also the Owner of Ackerman Consultants. Dr. Ackerman has held just about every position a nurse could hold in academia and clinical practice from candy striper to senior director. His entire career has been dedicated to critical care with numerous publications as well as invitations to speak nationally and internationally. His research and writing has focused on a variety of clinical topics including sepsis, airway management, hemodynamics, innovation and leadership. His innovation work has led to many disruptions in clinical practice and health system change. He has been recognized for his various contributions with various fellowships including; Fellow in Critical Care Medicine, Fellow in the National Academy of Practice, and Fellow in American Academy of Nurse Practitioners. Dr. Ackerman completed his BSN from Niagara University, his MSN and DNS from The State University of New York at Buffalo, a post-masters certificate as an Acute Care Nurse Practitioner from the University of Rochester and is currently enrolled in a Design Thinking certificate program at Rochester Institute of Technology.   Show Highlights [01:18] Michael talks about his love of nursing, and starting his career in the ICU. [01:46] Finding his way into the healthcare innovation space. [03:27] What people, and especially designers, should understand about bedside nursing. [04:33] The three “P's” of nursing and design. [07:22] Co-creating with nurses via the Center for Healthcare. [09:52] Nurses are moving into the innovation space. [11:59] Michael's wishlist of things designers should do when working in the healthcare innovation space. [12:37] The healthcare industry is risk-averse. [14:46] A look at the different viewpoints of healthcare executives. [16:41] Michael talks about one project – a new feeding tube device. [19:07] The healthcare innovation cycle is often slow. [20:20} How the COVID-19 pandemic sped up the innovation cycle. [22:18] How designers and healthcare leadership can help improve the healthcare innovation cycle. [23:27] Democratizing innovation and inviting healthcare staff to the table. [26:00] Ohio State's innovation studios for healthcare and nursing. [27:42] Working with the architecture school on creating healthier work environments. [28:48] OSU's Masters in Healthcare Innovation program. [30:12] OSU's Center for Healthcare Innovation and Leadership. [32:42] The importance of creativity, and logic-brain versus creative-brain. [34:21] Designers need to help people find ways to turn off their logic-brain to allow their creative-brain to turn on. [35:43] Giving people permission to experiment and create. [38:37] The patient harm threshold for rapid healthcare innovation. [39:49] The need for innovation leadership roles in hospitals and healthcare. [43:01] All leaders would benefit from being familiar with design thinking and being able to lead teams using a design mindset and methods. [44:51] A culture of innovation and creativity starts at the top. [47:22] Hospitals and healthcare are complex adaptive systems. [49:59] Michael's and Dawan's advice for innovators.   Links Michael on LinkedIn Michael on Twitter Ackerman Consulting Michael on ResearchGate The Handoff: Nurse Burnout with Michael Ackerman Google Scholar list of articles where Michael is an author/co-author The #HCBIZ Show: The Novation Dynamic: 3 Pillars for Healthcare Innovation Success with Michael Ackerman SONSEIL   Other Design Thinking 101 Episodes You Might Like Healthcare Design Teams + Wellness + ScienceXDesign with Chris McCarthy — DT101 E24 Nursing + Service Design + Healthcare Innovation with Brittany Merkle — DT101 E38 Seeing, Reframing, and Pursuing Problems with Thomas Wedell-Wedellsborg — DT101 E86

Michael Ackerman is currently the director of the Master in Healthcare Innovation Program and Professor of Clinical Nursing and the director of the Center for Healthcare Innovation and Leadership at the Ohio State University College of Nursing. He also maintains a clinical practice as an acute care nurse practitioner at St. Joseph's Neighborhood Hospital in Rochester, New York. Today, we talk about nursing, healthcare innovation, and opportunities for designers in the healthcare industry. Listen to learn about: The role of nurses in nursing/healthcare innovation The unique challenges of innovation in healthcare Improving the healthcare innovation cycle OSU's Center for Healthcare Innovation and Leadership Our Guest Michael Ackerman is currently the Director of the Master in Healthcare Innovation Program and Professor of Clinical Nursing, and the Director of the Center for Healthcare Innovation and Leadership at the Ohio State University College of Nursing. He also maintains a clinical practice as an acute care nurse practitioner at St Joseph's Neighborhood in Rochester, NY.  He is also the Owner of Ackerman Consultants. Dr. Ackerman has held just about every position a nurse could hold in academia and clinical practice from candy striper to senior director. His entire career has been dedicated to critical care with numerous publications as well as invitations to speak nationally and internationally. His research and writing has focused on a variety of clinical topics including sepsis, airway management, hemodynamics, innovation and leadership. His innovation work has led to many disruptions in clinical practice and health system change. He has been recognized for his various contributions with various fellowships including; Fellow in Critical Care Medicine, Fellow in the National Academy of Practice, and Fellow in American Academy of Nurse Practitioners. Dr. Ackerman completed his BSN from Niagara University, his MSN and DNS from The State University of New York at Buffalo, a post-masters certificate as an Acute Care Nurse Practitioner from the University of Rochester and is currently enrolled in a Design Thinking certificate program at Rochester Institute of Technology.   Show Highlights [01:18] Michael talks about his love of nursing, and starting his career in the ICU. [01:46] Finding his way into the healthcare innovation space. [03:27] What people, and especially designers, should understand about bedside nursing. [04:33] The three “P's” of nursing and design. [07:22] Co-creating with nurses via the Center for Healthcare. [09:52] Nurses are moving into the innovation space. [11:59] Michael's wishlist of things designers should do when working in the healthcare innovation space. [12:37] The healthcare industry is risk-averse. [14:46] A look at the different viewpoints of healthcare executives. [16:41] Michael talks about one project – a new feeding tube device. [19:07] The healthcare innovation cycle is often slow. [20:20} How the COVID-19 pandemic sped up the innovation cycle. [22:18] How designers and healthcare leadership can help improve the healthcare innovation cycle. [23:27] Democratizing innovation and inviting healthcare staff to the table. [26:00] Ohio State's innovation studios for healthcare and nursing. [27:42] Working with the architecture school on creating healthier work environments. [28:48] OSU's Masters in Healthcare Innovation program. [30:12] OSU's Center for Healthcare Innovation and Leadership. [32:42] The importance of creativity, and logic-brain versus creative-brain. [34:21] Designers need to help people find ways to turn off their logic-brain to allow their creative-brain to turn on. [35:43] Giving people permission to experiment and create. [38:37] The patient harm threshold for rapid healthcare innovation. [39:49] The need for innovation leadership roles in hospitals and healthcare. [43:01] All leaders would benefit from being familiar with design thinking and being able to lead teams using a design mindset and methods. [44:51] A culture of innovation and creativity starts at the top. [47:22] Hospitals and healthcare are complex adaptive systems. [49:59] Michael's and Dawan's advice for innovators.   Links Michael on LinkedIn Michael on Twitter Ackerman Consulting Michael on ResearchGate The Handoff: Nurse Burnout with Michael Ackerman Google Scholar list of articles where Michael is an author/co-author The #HCBIZ Show: The Novation Dynamic: 3 Pillars for Healthcare Innovation Success with Michael Ackerman SONSEIL   Other Design Thinking 101 Episodes You Might Like Healthcare Design Teams + Wellness + ScienceXDesign with Chris McCarthy — DT101 E24 Nursing + Service Design + Healthcare Innovation with Brittany Merkle — DT101 E38 Seeing, Reframing, and Pursuing Problems with Thomas Wedell-Wedellsborg — DT101 E86

It was a true thrill to be able to talk with photographer Michael Ackerman. His deeply thoughtful approach to his work, and his dedication to his art is an inspiration to me. A true meeting of the minds.Links:Michael Ackerman websiteEnd Time City bookHunger: Epilogue book

A veces la única manera de conocerse es alejarse, desconectar de todo, encontrar un lugar en el que un ruido nuevo nos permita sintonizar con nuestra propia voz. A veces, para encontrarse, hay que perderse, hacer borrón y empezar de nuevo, escribiendo a base de imágenes para, fotografiando hacia afuera, mirar hacia dentro. Hoy, en Calle Oscura, Jorquera. En este episodio hablamos de - Hacer cosas con las manos. - La libertad de tomar fotos. - Reconocer un lugar a través de la cámara. - Y de reconocerse en las fotos propias. - Viajes reales y viajes ficticios. - Profundizar deliberadamente. - Trabajar con distancia. - Mostrarse vulnerable. - Documentar la vida. - Apostar fuerte por aquello en lo que crees. Y de mucho más, como siempre. Quién nos acompaña Jorquera nace circunstancialmente en Galicia en 1972. La fotografía hace que se olvide de la ingeniería agrónoma, aprendió al lado de Luis Asín y trabajó como positivador en el laboratorio de Juan Manuel Castro Prieto. Antes de establecerse de nuevo en Madrid, donde reside actualmente, vivió en Wuhan, la ciudad que ha quedado marcada por la pandemia de la COVID-19. Es miembro fundador del colectivo Nophoto, ha editado varios trabajos personales en forma de libros de autor y recibió la beca FotoPres por su proyecto Radiochina. En 2007 la fundación Azcona hace posible un viaje que iba a durar 1 año y que finalmente se convirtió en una estancia de 9 y en el libro Wuhan Before Wuhan, que es tanto un trabajo sobre aquella ciudad y la sociedad china como sobre sí mismo. Escucha nuestra charla Referencias y enlaces Autores y colectivos - Alberto García-Alix. - Antoine D´Agata. - Cristina García Rodero. - David Jiménez. (https://jotabarros.com/calle-oscura-david-jimenez/) - Daido Moriyama. (https://jotabarros.com/curso/14-introduccion-fotografia-japonesa/) - Eduardo Nave. - Henri Cartier-Bresson. (https://jotabarros.com/curso/22-monografico-henri-cartier-bresson/) - Jonás Bel. - José A. Carrera. - Juan Manuel Castro Prieto. - Juan Valbuena. - Liyu + Liubo. (https://archivo.getxophoto.com/archivo/festival-2009/autores-2009/liyu-liubo/) - Luis Asín. - Michael Ackerman. - Paco Gómez. - Rafael Trapiello. - Ricky Dávila. - Rafael Sanz Lobato. (https://jotabarros.com/grandes-fotografias-rafael-sanz-lobato-genova-1969/) - Sergio Larraín. (https://jotabarros.com/lectura-carta-sergio-larrain-sobrino-amor-fotografia/) - Tanit Plana. - Wong Kar-Wai. - Zhang Yimou. Trabajos - Cuaderno Uno y Tao, de Jorquera. - Wuhan Before Wuhan, de Jorquera. (https://lasalbooks.com/products/wuhan-before-wuhan-jorquera) Jorquera y lo demás Encontraréis a Jorquera en la página web de su colectivo (http://nophoto.org/jorquera) y en Instagram como @jorquera_wuhan (https://www.instagram.com/jorquera_wuhan/). Gracias por tu escucha Ojalá hayáis disfrutado de esta charla con Jorquera tanto como yo. Estoy deseando saber qué os ha parecido, podéis contármelo a través de los comentarios y así la conversación prosigue. Si os ha gustado, no olvidéis dejar 5 estrellas, compartir este capítulo en vuestras redes y recomendarlo a vuestra gente. Algo tan sencillo supone una gran diferencia. Antes de la despedida, como siempre, gracias a Ricoh y a su modelo GR3 (https://www.tiendapentaxeros.com/camaras/compactas/ricoh-gr/) por apoyar la emisión de Calle Oscura. Desde aquí, todo mi agradecimiento por acompañarme, por acompañarnos, desde ese otro lado que se siente muy cercano. Volvemos a escucharnos pronto. Hasta entonces… Nos vemos en la calle! Jota.

La conocí en Formentera, allá por 2020, a ella y a su cómplice de laboratorio. Entonces aún trataba de domesticar un laberinto que recientemente, y tras ocho años de trabajo, se ha transfigurado en un libro maravilloso que me ha tenido atrapado, felizmente atrapado, durante semanas. Hace dos años supe que solo era cuestión de tiempo que nuestros caminos volvieran a cruzarse, y es que esto ni siquiera había empezado. Hoy, en Calle Oscura, Camilla De Maffei. En este episodio hablamos de - Empezar tarde. - Amar la complejidad. - Belleza y dolor. - Identidad, territorio y memoria. - Imágenes-puerta. - Formular preguntas. - Trabajo colaborativo. - Curiosidad. - Derribar barreras personales. - Adentrarse en uno mismo al explorar un lugar. Y, qué poco me sorprende esto, de muchas otras cosas que salieron al paso. Quién nos acompaña Camilla nace en 1981 en Cles, una pequeña localidad italiana al borde del Lago di Santa Giustina, en la provincia de Trento. Su trabajo mezcla lo documental y una narrativa personal que en lugar de ilustrar y describir busca interpretar, atribuyendo nuevos significados a los elementos cercanos. Camilla ha mirado sobre todo hacia los Balcanes, explorando y conectando las nociones de identidad, memoria y paisaje. Lleva más de una década enseñando, está especializada en la tutoría de proyectos a largo plazo y es cofundadora, con Eugeni Gay Marín, de El Observatorio, un espacio que definen como un laboratorio didáctico orientado a la fotografía y la narrativa visual. Su trabajo Delta se alzó con el Premio Mallorca de Fotografía Contemporánea y se ha convertido en una exposición y en un libro con Ediciones Anómalas. Pero Camilla lleva desde 2010 acumulando reconocimientos y colgando sus imágenes en las paredes de los festivales más prestigiosos. Referencias y enlaces Autores y colectivos - Eugeni Gay Marín. - Mario Giacomelli. - Michael Ackerman. Trabajos - Delta, Camilla de Maffei. - El Observatorio Creación. (http://www.elobservatoriocreacion.com/) - Stalker, de Tarkovski. Alex y lo demás Podeis encontrar a Camilla en Instagram (https://www.instagram.com/camilla_demaffei/), pero os aconsejo, como siempre, que os paséis por su web (https://camillademaffei.com/), donde podéis ver sus trabajos con la pausa que merecen. Recordad que el libro Delta está disponible en la página de Ediciones Anómalas (https://www.edicionesanomalas.com/en/producto/delta-3/). Gracias por tu escucha Hasta aquí el trigésimo pimer episodio de Calle Oscura, ojalá hayáis disfrutado de esta charla con Camilla tanto como yo. Si ha sido así no olvidéis dejar 5 estrellas, compartir este capítulo en vuestras redes y recomendarlo a vuestra gente. Algo tan tan sencillo supone, en realidad, una gran diferencia. Antes de la despedida, gracias a Ricoh y a su modelo GR3 (https://www.tiendapentaxeros.com/camaras/compactas/ricoh-gr/) por apoyar la emisión de Calle Oscura. Desde aquí, todo mi agradecimiento por acompañarme, por acompañarnos, desde ese otro lado que se siente muy cercano. Volvemos a escucharnos pronto. Hasta entonces… Nos vemos en la calle! Jota.

As COVID-19 progressed and vaccines became available, reports of professional soccer players collapsing on the field became more prevalent. To better understand this phenomenon, I sat down with Dr. Michael Ackerman, a Mayo Clinic genetic cardiologist and the president of the Sudden Arrhythmic Death Syndrome (SADS) Foundation, to get his expert opinion on how COVID and the vaccine affect heart conditions in people under 35. Dr. Ackerman also explains what SADS is, how its diagnosed, and what can be done to mitigate the chances of becoming one of the 5,000 to 10,000 Americans that die from SADS every year. ⭕️ Sign up for our NEWSLETTER and stay in touch

This episode finds our crew waiting in the woods, hoping to catch the attention of Barnaby's friends. Mysterious friends that he hasn't been completely up front about. Friends who may not be so friendly anymore. Although it may not matter if something else finds them first...Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.com"Waiting and Hoping" was written, directed and audio designed by Becky McLaughlin and features the voice talents of:Jon Furr as BarnabyCaitlin Stafford as GrimalkinMaddox Butler as BazAstoria McLaughlin as NaomiKrynn McLaughlin as OliviaRiley Meehan as AriBecky McLaughlin as Coro"The Golden Hand" was directed and audio designed by Becky McLaughlin and features the voice talents of:Caitlin Stafford as Grimalkin the NarratorSean Carey as FrancisSarah Thompson as ColetteSandy Scott as Elizabeth"The Emerald Ring" was directed and audio designed by Becky McLaughlin and features the voice talents of:Michael Ackerman as EdmundSandy Scott as EleanorWe are also now accepting fan art to put on our YouTube channel, and YOUR original scary stories for us to dramatize! See below for links:Send your fan mail to grimalkinthegreat@gmail.comSend your fan art to thewitchinthewoodspod@gmail.comSend your original scary stories to the witchinthewoodspod@gmail.com and visit our website for guidelines!Follow us on social media @thewitchinthewoodspodSupport us on Patreon to get great perks like extra scary stories and original spooky art in our sticker of the month club! https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin. Theme music by Ken Ashford with sounds from Zapsplat.com.

Paul is so excited! Not only has he found a good job with a nice family, they also have a place for him to stay. A cabin of his very own! One with a ready supply of firewood, one with a fireplace that is somehow still warm from the last resident, one that might have a surprise in store for Paul...This episode was directed and audio designed by Becky McLaughlin and features the voice talents of Michael Ackerman as Paul, Sandy Scott as Annie, Sean Carey as Winston and Jon Furr as Barnaby who is the narrator for this story.We are also now accepting fan art to put on our YouTube channel, and YOUR original scary stories for us to dramatize! See below for links:Send your fan mail to grimalkinthegreat@gmail.comSend your fan art to thewitchinthewoodspod@gmail.comSend your original scary stories to the witchinthewoodspod@gmail.com and visit our website for guidelines!Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon to get great perks like extra scary stories and original spooky art in our sticker of the month club! https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin. Theme music by Ken Ashford with sounds from Zapsplat.com

Chaque vision est singulière, porteuse de sens et de changement. Le but de ce format est de rassembler de nombreux artistes et que chacun nous délivre sa vision et son expérience de la photographie. Pour ce podcast, j'ai rendez-vous en plein Marais, dans le 3ème arrondissement de Paris. Grégoire Eloy, gagnant du Prix Niepce 2021,  m'accueille d'une voix douce et posée, un œil porté sur l'ouvrier qui termine les travaux dans la cour extérieure. Nous prenons le temps de discuter. Grégoire semble être un vrai passionné, au vu de la grande bibliothèque remplie de livres photos qui longe l'escalier. « Ça, c'est la rangée des livres scandinaves, là il y a les livres japonais. Les français sont là. Tiens, il manque un livre. » Quel bonheur de se retrouver avec un photographe qui transmet un tel enthousiasme ! Nous commençons l'enregistrement. Sa fille, qui rentre de l'école, se place dans l'escalier « pour capter le wifi » et aussi sûrement, pour écouter son père. Le chat familial, très craintif, fait des allers-retours à pas feutrés. Une heure de discussion captivante. ☄️ Ce podcast a été propulsé par Adobe France. Vivez l'expérience l'expérience Creative Cloud :  http://urlr.me/xtDGT 

Grimalkin has taken it upon herself to update a classic that we dramatized in Season One: "The Call is Coming from Inside the House".  In this version, Ben is once again babysitting the Garcia children but instead of the landline phone ringing with a raspy voice on the other end, his cell lights up with cryptic messages and pictures over Snapchat. Will this version turn out differently than the first? You'll have to listen to find out!This episode was directed and audio designed by Becky McLaughlin and features the voice talents of Michael Ackerman as Ben, Ben Hill as Mr. Garcia, and Caitlin Stafford as Grimalkin who narrated this story. We are also now accepting fan art to put on our YouTube channel, and YOUR original scary stories for us to dramatize! See below for links:Send your fan mail to grimalkinthegreat@gmail.comSend your fan art to thewitchinthewoodspod@gmail.comSend your original scary stories to the witchinthewoodspod@gmail.com and visit our website for guidelines!Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon to get great perks like extra scary stories and original spooky art in our sticker of the month club! https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin. Theme music by Ken Ashford with sounds from Zapsplat.com

Happy Halloween! To celebrate, we've created a special holiday episode! This episode is a stand alone story and doesn't contain any spoilers for Season One, so feel free to listen no matter where you are in the season.In this episode, the children visit the witch's crew on Halloween. They've brought treats and their own scary stories to share, and Rosa also tells the story of how Jack O' Lanterns came to be. It's a spooky good time!In this episode we also invite people of all ages to send in their original scary stories for the chance to have us turn them into audio dramas as we all anxiously await Season Two! Any story will be considered, and strong writing skills are not required. The major thing to keep in mind is that we are a family friendly podcast, so please keep your stories PG. We are happy to guide you if you have questions! Please email your stories to thewitchinthewoodspod@gmail.com. We can't wait to make them come to life!Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon at https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa.The Halloween Special was directed, audio designed and edited by Becky McLaughlin. "The Tale of Jack of the Lantern" features the voice talents of Michael Ackerman as Jack, Josh McLaughlin as Jacob, and Lara Ianni as The Devil."The Winds of Winston-Salem" was written by Astoria McLaughlin at age 11. 

The final episode of Season One puts the kids in mortal danger and reveals Rosa's true identity. Need we say more?Thank you so much for listening to Season One. The Witch in the Woods will return for Season Two, but we'll also continue to release scary stories and other fun content weekly in between seasons. Keep an eye on our social media for updates!Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon at https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa.Episode Twelve also featured Janel Fuller as The Changeling Mother.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley Meehan

There's something wrong with Naomi and the witch's crew knows exactly what it is. That means that everything will be alright! Won't it?Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon at https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley Meehan

We see a rare side of Barnaby this episode when Grimalkin crosses a line and reveals a precious secret to the children. He is trying to protect Rosa and her secrets, but Naomi drops a hint that reveals his fears might have come true after all because... they know.Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comSupport us on Patreon at https://www.patreon.com/thewitchinthewoodspodFollow us on social media @thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."Aren't You Glad You Didn't Turn On The Light?" was directed by Janel Fuller and Becky McLaughlin and stars Lara Ianni as Julie and Sarah Jenkins as Lizzie. It was edited by Becky McLaughlin with sounds from Zapsplat.com."The Reflection in the Window" was directed by Ken Ashford and stars Lara Ianni as Nadja, Janice Lovett as Ms. Lorne, Caleb Cabiness as Henry and Becky McLaughlin as the newscaster. It was edited by Becky McLaughlin with sounds from Zapsplat.com.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley MeehanEpisode Artwork by Astoria McLaughlin

Naomi is very worried about her older brother and she has good reason to be. He's sick with a mystery illness and Ari is still convinced they've seen something... supernatural happen with Dave's eyes. It's time to ask the witch's crew for help. Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comSupport us on Patreon at https://www.patreon.com/thewitchinthewoodspodFollow us on social media @thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."The Beast of Bladenboro" was directed and audio designed by Sara Butner and stars Josh McLaughlin as the Farmer and Sally Meehan as C.E. Kinlaw. It was edited by Becky McLaughlin with sounds from Zapsplat.com."Pinned in the Graveyard" was directed by Caleb Cabiness and stars Lara Ianni as Annie, Michael Ackerman as Randy, Janel Fuller as Emilia, Matt Crawford as Chuck, and Becky McLaughlin as Carly. It was edited by Becky McLaughlin with sounds from Zapsplat.com.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley MeehanEpisode Artwork by Astoria McLaughlin

Danger is around every corner in this episode and the plot thickens when the witch's crew has a close call with whoever it is they're hiding from. The witch's crew might be in trouble, but the kids shouldn't have anything to fear... right?Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."White Riders" was directed by Caleb Cabiness and stars Matt Crawford as Wyatt, Ben Hill as Everett,  and Caleb Cabiness as both the White Rider and Cowboy. Edited by Becky McLaughlin with sounds by Zapsplat.com"The French Broad Siren" was directed by Lara Ianni and features original music written and performed by Claire Walton and Zac Messick of Bug Street. You can check them out at https://bugstreet.bandcamp.com/Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley MeehanEpisode Artwork by Astoria McLaughlin

“Festival du Regard“ 6ème éditionIntime & Autofictionsà Cergy-Pontoisedu 1er octobre au 21 novembre 2021Interview de Sylvie Hugues et de Mathilde Terraube, directrices artistiques du Festival du Regard,par Anne-Frédérique Fer, à Cergy-Pontoise, le 23 septembre 2021, durée 26'12.© FranceFineArt.Communiqué de presseDirection artistique : Sylvie Hugues et Mathilde TerraubeÉdito – Intime & AutofictionsL'approche autobiographique a toujours existé dans la photographie, mais elle est longtemps restée à l'arrière-plan… Si on peut considérer que la première photo de l'intime est, en 1840, l'incroyable autoportrait d'Hippolyte Bayard en noyé (protestant ainsi contre l'oubli par l'Etat de sa propre invention de la photographie), pendant longtemps la mission du photographe était de montrer le monde extérieur, d'être un témoin, un observateur, un reporter. Bien sûr on peut retrouver des traces d'intimité chez Edward Weston, dès 1935, quand il réalise des nus de Charis Wilson qui deviendra sa compagne. Mais celui qui va définitivement ancrer l'intime dans une photographie de témoignage, c'est Robert Frank dans « Les Américains », qui se clôt par une photo prise au petit matin sur une route où l'on devine sa famille endormie dans un véhicule mal garé le long de la route. Quelques figures titulaires ont définitivement fait basculer la photographie dans l'autobiographie et l'intime. On peut citer Nan Goldin et sa « ballade de la dépendance sexuelle » (1986), toute l'école japonaise issue de Nobuyoshi Araki et de Daido Moriyama, ainsi que la filiation nordique qui s'ouvre avec Christer Strömholm, s'épanouit avec Anders Petersen et se multiplie au XXIème siècle avec JH Engstrom, Jacob Aue Sobol et beaucoup d'autres… En France, l'arrivée quasi simultanée dans le sillage de Christian Caujolle de l'agence Vu d'Antoine d'Agata et de Michael Ackerman, à la fin des années 1990, ancrent définitivement le corps du photographe comme étant un élément constitutif du travail artistique. Désormais, le photographe est autant derrière l'appareil que devant, dans une sorte de dédoublement de personnalité. En accueillant dans cette édition quelques photographies emblématiques de Michael Ackerman et un film sur Antoine d'Agata, nous mettons justement en valeur ce basculement où l'intimité du photographe dialogue en prise directe avec le monde extérieur. Cette façon d'affirmer le « je » (que l'on pourrait prendre pour une forme d'égotisme quand il est mal géré) va aussi permettre de renouveler et de revivifier la photographie créative. En se rapprochant d'une forme de narration, les « mises en scènes » de l'intime vont devenir le pendant photographique de ce que l'on nomme en littérature « l'autofiction ». Ce genre mal défini nous a paru intéressant à mettre en parallèle avec la notion de l'intime photographique. Comment se dévoiler sans aller trop loin ? Comment faire de sa propre personne un personnage « extérieur » ? Comment éviter le piège de l'autocongratulation ou de l'autoflagellation ? Comment trouver la bonne distance quand on est à la fois l'auteur et l'acteur, le sujet et l'objet ? Mais surtout comment mêler fiction et réalité dans ce qui est à la fois une création artistique et un témoignage documentaire ?Sylvie Hugues et Mathilde Terraube, Directrices artistiques du Festival du RegardLes lieux et les expositions -> À l'ancienne poste• Alberto Garcia Alix : De donde no se vuelve• Jen Davis : Eleven Years, et sa suite Stephen and I• Marc Riboud et Catherine Chaine : Clémence• Patrick Taberna : Autres journées• Eva Rubinstein : Elégies• Lolita Bourdet : Plamondon• Marilia Destot : La Promesse• Sylvia Ney : De l'autre côté de l'eau• Patrick Cockpit : Franco et moi• Franck Landron : Ex Time• Kourtney Roy : Enter as Fiction• Robert Doisneau : Meilleurs voeux• Deanna Dikeman : Leaving and waving• L'intime et l'autofiction vus par : Hippolyte Bayard, Araki, Lucienne Bloch, Miroslav Tichý, Ralph Eugene Meatyard, Michael Ackerman et une sélection de tirages du XIXème.• Projections des court-métrages de Kourtney Roy et des films documentaires de Franck Landron (Limite(s) d'Antoine d'Agata et Un flirt photographique sur l'oeuvre de Claude Nori)-> Sur la place des arts• Exposition Bambino (le Festival du Regard à destination du jeune public) Voir Acast.com/privacy pour les informations sur la vie privée et l'opt-out.

Ari has something important to talk to Olivia about that's very concerning... and also a little hard to believe. One thing's for sure... Naomi's not going to like it.Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon! https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."Brown Mountain Lights" was directed by Janel Fuller and Becky McLaughlin and stars Sally Meehan as Faith and Chris Cohen as Jesse. It was audio designed and edited by Becky McLaughlin with sounds from Zapsplat.com."The Choking Dog" was directed by Ken Ashford and stars Janice Lovett as Myrtle, Lara Ianni as Woman, Charlie Lovett as the Vet and Chris Cohen as both the Man and the Officer. It was edited by Becky McLaughlin with sounds from Zapsplat.com.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley MeehanEpisode Artwork by Astoria McLaughlin

This episode reveals more clues about Rosa's mysterious past, but it's unclear how helpful these cryptic hints really are. We're now halfway through Season One... will we ever discover the truth?Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon at https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."Bloody Mary" was audio designed, edited and directed by Becky McLaughlin. Featuring the voice talents of Alonna Rauton as Lily, Piper Machado as Chloe, and Stella McLaughlin as Grace. Sounds from Zapsplat.com."Bloody Mary Origin Story" was audio designed and directed by Lara Ianni and features the voice talents of Lara Ianni as Ginger and Sarah Jenkins as Mary. It was edited by Becky McLaughlin with sounds from Zapsplat.com with original music composed by Kevin MacCloud.Echoes of Time v2 by Kevin MacLeod http://incompetech.comCreative Commons — Attribution 4.0 International — CC BY 4.0Free Download / Stream: https://bit.ly/echoes-of-time-v2Music promoted by Audio Library https://youtu.be/BNE9uj3CQ6s Evening of Chaos by Kevin MacLeod is licensed under a Creative Commons Attribution license (https://creativecommons.org/licenses/...)Source: http://incompetech.com/music/royalty-...Artist: 

The kids and witch's crew seem to have found  a groove this episode. The kids bring food, the crew tells stories, and Grimalkin's catnip has worn off so she's remarkably calm. Everything is normal. Right?Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon! https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."The Call is Coming from Inside the House" was sound designed and directed by Sara Butner and stars Michael Ackerman as Ben, Ben Hill as Mr. Garcia and The Caller, and Janel Fuller as the 911 Operator. It was edited by Becky McLaughlin with sounds from Zapsplat.com."The Clown Statue" was sound designed and directed by Sara Butner and stars Sarah Jenkins as Hannah and Janice Lovett as Ms. Lorne. Featuring the voice of Gavi McLaughlin as Nick. It was edited by Becky McLaughlin with sounds from Zapsplat.com.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman, utilizing sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Original Art for Season One by Riley MeehanEpisode Artwork by Astoria McLaughlin

The story of Johann Krohmann and Michael Ackerman, who in 1872, had a Reef Mining lease on Hawkins Hill in the golden quarter mile.Their story is told by Lorraine Miller a descendent who lives in Hill End

Grimalkin is especially annoying this episode, although it's not clear if that's because the kids couldn't predict her reaction to catnip or if it's because she's a little homesick. Which leaves us to wonder, where exactly IS home?Rated PG: light peril and ghostly subjects. More guidance for parents is available on our website. https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodSupport us on Patreon! https://www.patreon.com/thewitchinthewoodspodEpisodes will also be available SOON on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa."High Beams" was directed by Becky McLaughlin and Mike Burke, and features the voice talents of Janel Fuller as Jenny, Sarah Jenkins as Robin, Caleb Cabiness as the Man and Sara Butner as the Officer. Sound design and editing by Becky McLaughlin, with sounds from Zapsplat.com"The Briefcase" was directed and audio designed by Caleb Cabiness and features the voice talents of Sarah Jenkins as Laura, Michael Ackerman as the Man and Chris Cohen as Husband. Edited by Becky McLaughlin with sounds from Zapsplat.com.Season One is edited by Becky McLaughlin, with audio design by Becky McLaughlin and Michael Ackerman with sounds from Zapsplat.com. The theme music for Season One was created by Ken Ashford, based on the composition Dance Macabre by Camille Sans Sons.Original Art for Season One by Riley MeehanEpisode Artwork by Astoria McLaughlin

The children find out more about the witch's trusty familiars when their ages are revealed. Could they really be as old as they say? Rated PG with light peril and ghostly subjects. You can find out more about our content to judge if it's right for your family on our website:   https://www.thewitchinthewoodspodcast.squarespace.comYouTube videos of our episodes are coming soon! https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gFollow us on social media @thewitchinthewoodspodSupport us on Patreon to get extra scary stories and other perks you won't want to miss!https://www.patreon.com/thewitchinthewoodspod?fan_landing=trueThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa. The Black Ribbon Necklace was directed by Becky McLaughlin and Janel Fuller, and featured the voice talents of Michael Ackerman and Danny and Sara Butner as Camille. Sound Design and editing by Becky McLaughlin, with sounds from Zapsplat.com. The Keyhole was directed and audio designed by Lara Ianni and edited by Becky McLaughlin. It featured the voice talents of Janice Lovett as The Receptionist and Ben Hill as Charles with original music titled “Cryptic Sorrow” by Kevin MacLeod.Link: https://incompetech.filmmusic.io/song/3568-cryptic-sorrowLicense: https://filmmusic.io/standard-licenseThe theme music for Season One was created by Ken Ashford, based on the composition "Dance Macabre" by Camille Sans Sons.Season One artwork by Riley Meehan.Episode Three thumbnail by Astoria McLaughlin.

New insights into our witch reveal that she might have ulterior motives and a haunting past. Rated PG with light peril. Visit our website for more information on content at https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodFor full episodes with closed captioning and fan art visit our YouTube channel at https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production and was written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa. The Hook Hand was directed by Becky McLaughlin and Mike Burke, and featured the voice talents of Chris Cohen as Brad and Lara Ianni as Janet; additional voices by Charlie Lovett and Josh McLaughlin. Sound design and editing by Becky McLaughlin, featuring sound effects from Zapsplat.com.The Licked Hand was directed, designed and edited by Ken Ashford and featured the voice talents of Sally Meehan as Selene and Ken Ashford as the Newscaster.The audio for Episode Two was designed and edited By Becky McLaughlin. The theme music for Season One was created by Ken Ashford, based on the composition Dance Macabre by Camille Sans Sons.Season One artwork by Riley Meehan.Episode Two artwork by Astoria McLaughlin.

Four friends follow through on a dare to seek out the witch in the woods. Will they find her? And what will happen if they do?Rated PG: light peril and ghostly subjects. More information regarding content is available on our website: https://www.thewitchinthewoodspodcast.squarespace.comFollow us on social media @thewitchinthewoodspodEpisodes are also available on our YouTube channel with captions and original fan art!https://www.youtube.com/channel/UCNFDMW4T279qmYLw3u8936gThe Witch in the Woods Podcast is a Zombie Burrito Production.  It was created, written and executive produced by Becky McLaughlin.Season One was directed by Michael Ackerman and stars Maddox Butler as Baz, Riley Meehan as Ari, Krynn McLaughlin as Olivia, Astoria McLaughlin as Naomi, Becky McLaughlin as Coro, Jon Furr as Barnaby, Caitlin Stafford as Grimalkin, and Emily Emerson as Rosa. The Vanishing Hitchhiker was directed by Becky McLaughlin and Mike Burke, and featured the voice talents of Michael Ackerman as Bob, Christopher Cohen as Jim, Sarah Jenkins as Lydia, and Janice Lovett as Lydia's Mom.Audio for Episode One and The Vanishing Hitchhiker was designed and edited by Becky McLaughlin, featuring sounds from Zapsplat.com and original music by Kevin McCloud. The theme music for Season One was created by Ken Ashford, based on the composition Dance Macabre by Camille Sans Sons.Original artwork for Season One by Riley Meehan.Original artwork for Episode One by Astoria McLaughlin.

Coming August 19, 2021! The Witch in the Woods is a family friendly horror podcast.  Check us out at www.thewitchinthewoodspodcast.squarespace.com or follow us on social media @thewitchinthewoodspod to learn more! SEASON ONE CAST:Starring:Jonathan Furr, Caitlin Stafford, Emily Emerson, Maddox Butler, Krynn McLaughlin, Astoria McLaughlin and Riley Meehan.Featuring: Ken Ashford, Janice Lovett, Chris Cohen, Sarah Jenkins, Lara Ianni, Michael Ackerman, Becky McLaughlin, Caleb Cabiness, Matt Crawford, Ben Hill, Charlie Lovett, Sara Butner, Janel Fuller, Sally Meehan, Piper Machado, Alonna Rauton and Stella McLaughlin.Production Crew:Written and Created by Becky McLaughlin. Executive Produced by Becky McLaughlin.Directing and Sound Design by Michael Ackerman, Ken Ashford, Sara Butner, Lara Ianni, Caleb Cabiness and Becky McLaughlin.Edited by Becky McLaughlin.Original Artwork by Riley Meehan.The Witch in the Woods Podcast is a product of Zombie Burrito Productions. Trailer Sound Credits:Sounds from Zapsplat.comMusic: Dopplerette by Kevin McCloud (https://incompetech.filmmusic.io/song/3668-dopplerette) edited slightly by eliminating abrupt ending. Link to license here: https://incompetech.filmmusic.io/standard-licenseCinematic Movie Trailer Epic Ending Sound Effect from Sound Effects Factory:https://www.youtube.com/watch?v=eURQPmqz36s

'Sode 5.29 features Michael Ackerman who is the Deputy Director of the Silverton Avalanche School. We recorded this episode before the snow started to fly in the fall. Ack and I chat about his career path, how SAS planned to tackle the challenges posed by a global pandemic, some of the ways SAS has evolved and continues to evolve, and his hopes for a bright future for all backcountry users. Enjoy! Music by Ketsa

For this week's Feature Discussion, please join authors Igor Klem, Pasquale Santangeli, Mark N.A. Estes III, and Associate Editor Victoria Delgado as they discuss, in a panel forum, the articles: " The Relationship of LVEF and Myocardial Scar to Long-Term Mortality Risk and Mode of Death in Patients with Non-Ischemic Cardiomyopathy," "Prognostic Value of Non-Ischemic Ring-Like Left Ventricular Scar in Patients with Apparently Idiopathic Non-Sustained Ventricular Arrhythmias," and "Cardiac Magnetic Resonance Imaging in Nonischemic Cardiomyopathy: Prediction Without Prevention of Sudden Death." 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, Director of the Pauley Heart Center in Richmond, Virginia. Well Carolyn, this week we've got another sort of double feature with a forum and our focus is going to be on myocardial scar that's observed with late gadolinium enhancement during cardiovascular magnetic resonance and the two author groups we'll be discussing the impact of that scar on the development of ventricular arrhythmias. But before we get to that, how about we grab a cup of coffee and jump into the other articles in the issue? Would you like to go first? Dr. Carolyn Lam: I certainly would. Although I have to say, can't wait for the double feature. I love those, and this is right up your alley too. All right. But first, the first paper I want to talk about provides new randomized trial information regarding the benefits of catheter ablation in atrial fibrillation in patients who also have heart failure. Now, this is a sub-study of the CABANA trial. Dr. Greg Hundley: So Carolyn, remind us a little bit about the CABANA trial first. Dr. Carolyn Lam: I thought you might ask. Well, CABANA randomized 2,204 patients with atrial fibrillation who were 65 years or older or less than 65 with one or more risk factors for stroke at, it was huge at 126 sites, and they were randomized to ablation with pulmonary vein isolation or drug therapy. Now of these, 35% of 778 patients had New York Heart Association Class II or higher at baseline, and really formed the subject of the current paper. Although this sub-study was not specifically designed to evaluate patients with heart failure with preserved ejection fraction, about 91% of the patients with a clinical diagnosis of heart failure participating in CABANA for whom such data on injection fraction were available, really had an ejection fraction of above 40% and fully 79% had an ejection fraction above 50%. So excitingly, this is really majority talking about, have HFpEF. Now, what did they find well in patients with New York heart Association Class II or III heart failure at trial entry, most of whom did not have a reduced ejection fraction. Dr. Carolyn Lam: There was substantial clinical outcome benefits with the ablation over drug therapy with a 36% relative reduction in the primary composite endpoint of death, disabling stroke, serious bleeding or cardiac arrest. Benefits were evident for both all-cause mortality and atrial fibrillation reduction. However, the effects on heart failure hospitalization were small and not significant. Authors also caution that these results should not be viewed as practice changing until they are reproduced in a confirmatory trial of ablation in the same population. And this is beautifully discussed in an editorial by Lynda Rosenfeld and Alan Enriquez from Yale University School of Medicine. Dr. Greg Hundley: Oh, wow. Thanks Carolyn. Well, my first paper comes from the world of basic science and it's from Professor Thomas Braun, from the Max Planck Institute for Heart and Lung Research. So Carolyn, vascular smooth muscle cells show a remarkable phenotypic plasticity allowing acquisition of contractile or synthetic states, but critical information is missing about the physiological signals that promote formation and maintenance of contractile vascular smooth muscle cells in vivo. So BMP-9 and BMP-10 are known to regulate endothelial quiescence after secretion from the liver and right atrium. And these investigators are studied the role of BMP-9 and 10 for controlling formation of contract, all vascular smooth muscle cells. Dr. Carolyn Lam: Greg, talking about vascular smooth muscle cells always reminds me of their role in pulmonary hypertension, am I right? Dr. Greg Hundley: Yes, Carolyn. So these investigators found that in mouse models, BMP-9 and BMP-10 act directly on vascular smooth muscle cells for induction and maintenance of their contractile state, and surprisingly the effects of BMP-9 and 10 in vascular smooth muscle cells are mediated by different combinations of BMP type 1 receptors in a vessel bed specific manner. And therefore, just as you suggest, Carolyn, these results may offer new opportunities to manipulate blood pressure in the pulmonary circulation. Dr. Carolyn Lam: Thank you, Greg. Well, my next paper provides the first proof of principle of gene therapy for complete correction of Type 1 Long QT syndrome. Dr. Greg Hundley: Ah, so tell us a little bit about Type 1 Long QT syndrome, Carolyn. Dr. Carolyn Lam: Okay. Well Type 1 long QT syndrome is caused by loss of function variants in the KCNQ1 and coded potassium channel alpha sub-unit. And that is essential for cardiac repolarization providing the slow delayed rectifier current. Now no current therapies target the molecular cause of this Type 1 long QT syndrome. Well, this study from Dr. Michael Ackerman colleagues from Mayo Clinic Rochester really established a novel dual component suppression and replacement KCNQ1 gene therapy approach for Type 1 long QT syndrome. And it's the type that contains the KCNQ1 short hairpin RNA to suppress endogenous expression and a codeine altered short hairpin RNA immune copy of this KCNQ1 for gene replacement. Dr. Carolyn Lam: So this very novel approach rescued the prolonged action potential duration in inducible pluripotent STEM cell cardiomyocytes derived from four patients with unique Type 1 Long QT syndrome, causative, KCNQ1 variants. So it's super cool. Just go have a look. Dr. Greg Hundley: Well, thanks Carolyn. Dr. Carolyn Lam: I want to also tell you about other things in the mail bag. We have ECG Challenge by Dr. Dai on “Severe Arrhythmia Caused by a Chinese Herbal Liqueur. What's the Diagnosis?” I'm not going to tell you. You have to go see. We have Dr. Karen Sliwa writing a beautiful Joint Opinion paper from the World Heart Federation and American College of Cardiology, American Heart Association, and European Society of Cardiology on "Taking a Stand Against Air Pollution, the Impact on Cardiovascular Disease." Dr. Greg Hundley: Well, thanks Carolyn. So I've got a couple other articles. First Professor Yacoub has a global rounds describing and working towards meeting the challenges of improving cardiovascular health in Egypt. Those are really interesting features to learn about cardiovascular care worldwide. Next there's an In Depth article by Professor Thum entitled, "Therapeutic and Diagnostic Translation of Extracellular Vesicles in Cardiovascular Diseases, Roadmap to the Clinic." And then finally, a Research Letter from Dr. Bottá entitled, "Risk of Coronary Artery Disease Conferred by Low Density Lipoprotein Cholesterol Depends on Apologetic Background." Well, Carolyn, what a great issue and how about now we proceed on to that double feature? Dr. Carolyn Lam: Oh, I can't wait. Thanks Greg. Dr. Greg Hundley: Well, listeners, we are here for a really exciting feature discussion today that's going to focus on imaging, in particular magnetic, resonance imaging, and some new findings in that era and how those findings may pertain to ventricular dysrhythmias. With us today, we have Dr. Igor Klem from Duke University who will be discussing a paper, Dr. Pasquale Santangeli from University of Pennsylvania, our own associate editor, Dr. Victoria Delgado from Leiden and an editorialist, Dr. Mark Estes from UPMC in Pittsburgh. Welcome to all of you. Well, Igor, we're going to start with you. Could you tell us what was the hypothesis for your study and what was your study population in study design? Dr. Igor Klem: Yes. Good morning, Greg and thanks for the invitation. We wanted to know if you have a patient who you diagnosed with non ischemic cardiomyopathy based on clinical grounds and you refer him for a cardiac MRI study with contrast, what is the additional information that you get from the MRI study? And so we wanted to compare, and that's primarily related to the findings on scar imaging with late gadolinium enhancement. And we wanted to compare that to one of the most robust clinical parameters in cardiology, which is left ventricular ejection fraction, and in particular using a cutoff of 35%, which somehow in our clinical management has sort of as established as a break point for many clinical decisions. Dr. Igor Klem: And so we created a registry among three centers of patients who undergo a cardiac MRI study, where we found an LVEF of less than 50% and we followed them for a number of outcomes. One is all caused death. And then we wanted to separate a little bit the events into those who have cardiac mortality to look at a little epidemiology because in those patients, we have two major adverse events: one as heart failure related mortality. One is arrhythmia related mortality. Dr. Greg Hundley: And how many subjects did you include? Dr. Igor Klem: We included about a thousand patients from three centers and coming to the major findings of our study, we found that both left ventricular ejection fraction, as we know, is a robust marker of all cause mortality and cardiac death. And so it was the presence of myocardial scar on cardiac MRI. But the major difference was in relation to the arrhythmic events. We founded left ventricular ejection fraction in particular, when we use the 35% cutoff actually had very little predictive power to inform us who is at risk of arrhythmic events. In contrast, there was a very strong and robust relationship or multiple statistical methods to stratify patients who are at risk for sudden cardiac death, appropriate ICD shock, as well as arrhythmic cardiac death. Dr. Greg Hundley: Very good. Well, Pasquale understand you also performed a research study utilizing cardiovascular magnetic resonance. Could you describe for us your hypothesis as well as what was your population and your study design? Dr. Pasquale Santangeli: Thank you, Greg. And of course, thanks to the editor for the interest in our paper. I need to thank also the first call authors Daniele Muser and Gaetano Nucifora for putting together a registry of 70 institutions throughout the U.S., Europe, and Japan and the our hypothesis came from a clinical need. We do know that patients with idiopathic ventricular re we ask, which includes not sustain a weakness like PVCs or non-sustained VT. Very few of them, but there is a group of them that have a higher risk of ending malignant and up comes in terms of your ethnic events over follow-up. And prior studies have shown that by doing an MRI and showings and the detecting scar related announcement, there is an increase with how we make events of a follow-up. However, if you do look at those studies late, an answer's been reported in up to 70% of these patients, which you never view is a highly practical way of re-stratifying these patients, because you have a risk factor that is present 70% of those, then it's hard to use it for clinical decision-making. Dr. Pasquale Santangeli: So in this registry, which you put it again at 686 patients with panel data idiopathic, not sustained ventricular arrhythmias, which were defined by a normal WBC gene status, a normal echocardiogram and a normal stress test. We looked at whether there is a specific pattern of late announcement. So how basically I believe lands, and it looks on the MRI, they may predict better or outcomes over follow-up. And again, we use a composite and Pauline the full cost mortality, but associated cardiac arrest due to ventricular fibrillation or a hemodynamically unstable BP, or in a subgroup of patients that underwent ICD therapy. We also looked at, I approve SED shocks. Dr. Pasquale Santangeli: The groups were divided in three different categories. The first one, which is a larger group of 85% of patients and no late announcement. The second group, the one with late announcement, which represents the remaining 50% of 15% of patients, we divided it into a ring light pattern, which was defined as that word says, as a ring like distribution of the lead announcement in the mid-market segments, which involves a three consecutive continuous segments in a short axis view. It looks like really at least half the ring or three-quarters of the ring. Dr. Pasquale Santangeli: And the other group is the one that had the leader announcement without a ring light pattern. And it's interesting that the third and the latest announcement was not that similar between the ring light and the one without ring light late announcement. What we did find though for our follow-up the patient with a ring light pattern, a significantly higher rate of the primary composite endpoint, which happened in the median follow-up about 61 months so it was quite long. And the composite outcome occurred in 50% of patients in the ring light group versus 19% in the no ring light a positive announcement group and a 0.3%. So really, really rare in patients. So then concluded that of course, late announcement does provide some information in general, particularly the type of announcement that increases the risk significantly. Probably although this has to be confirmed prospective fashion patient with a ring light pattern may benefit from other forms of interventions, including potentially defibrillator therapy in a prophylactic fashion. Dr. Greg Hundley: Very nice. So now listeners, we're going to turn to our associate editor. One of the imaging experts here at Circulation, Dr. Victoria Delgado. Victoria, you see a lot of papers come across your desk and as an imaging expert, what attracted you to these two papers? And what do you think are their significance? Dr. Victoria Delgado: Thank you, Greg. I think that these two papers are important because right now, if we follow the clinical guidelines, we decide implantation. For example, of an ICD based on the ejection fraction, and we see that in many patients based on ejection fraction, they may not benefit ever from an ICD because they don't have arrhythmias. What other patients who do not meet the criteria often injection fraction below 35%. They may have still arrhythmias. So the article by Igor highlights the relevance of the amount of burden of late government Huntsman with CMR, in patients with non ischemic cardiomyopathy, which are sometimes very challenging patients on how to decide when we implant an ICD or not. We need sometimes to base the decision on genetics. Dr. Victoria Delgado: If we have an on the other hand, the paper of Pasquale, these were patients with normal echocardiogram. So what patient, having arrhythmias where we don't see on echocardiogram, that is the first imaging technique that we usually use to evaluate these patients. We don't see anything, but CMR can give us more information in terms of structural abnormalities and particularly not only the burden of scar, but also the pattern of the scar. And we have seen in other studies that for example, not only for ICD implantation, but for ventricular tachycardia ablation. The characteristics of that scar and some areas where these are short of panel that can be targeted for that ventricular tachycardia ablation can lead to much more precise treatment if you want of these patients. Dr. Greg Hundley: Thank you, Victoria. So it sounds like listeners we're hearing late gadolinium enhancement, regardless of EF could be forecasting, future arrhythmic events. And then also the pattern of late gadolinium enhancement, where contiguous segments in a ring-like fashion may also offer additional prognostic information. Well, now we're going to turn to our editorialists and as you know, listeners at Circulation, we'll bring in an editorialist to really help put things together and uniquely here today, we have Dr. Mark Estes, who is really not an imager per se, but like many of us uses the information from imaging to make clinical decisions. Mark, how do you see this late gadolinium enhancement as perhaps a new consideration for placement of devices? Dr. N.A. Mark Estes: Greg, that's one of the key questions. There's no doubt, not only based on these two studies, which extend our prior information about LGE and patients with valid and non ischemic cardiomyopathies that scar burden is important in predicting not only total mortality, but arrhythmic events. All of the criteria that were used in the original ICD studies, which include the definite, the Skuid half Danish and made it our it trials use only ejection fraction and functional status, no imaging. These are legacy trials. Now, many of them, a decade or more older. And the treatment of advanced heart failure has progressed to the point that the total mortality is dramatically lower than it was at the time of these studies. In some instances down to 4 or 5% per year. The studies are important in that they identify a subgroup of patients with low ejection fractions, less than 35%, who might qualify for ICDs, who are unlikely to benefit. Dr. N.A. Mark Estes: They also identify a group of patients with preserved ejection fraction greater than 35%, less than 50 in whom the risk of sudden death may be substantial. And it extends prior observations about patchy, mid Meyer, cardio wall fibrosis, subendocardial, subepicardial and important ways. But the key issue here, and it was alluded to with Pasquale's comments about prospective validation, is that when one has a risk stratifier and identifies a high risk population that has to be linked to an unequivocal therapy, it improves survival. And we don't have that link quite yet. Dr. N.A. Mark Estes: Prospective randomized trials are unlikely to be done in the low ejection fraction because they would probably be considered unethical. Given the trials that have shown the benefit you can't randomize to defibrillator versus an implantable loop recorders. I think the future really lies in risk stratification for people with preserved ejection fractions greater than 35%, less than 50 using LG in that patient population. Currently, I think the best information we can give to clinicians is to stick with the AHA guidelines, which is PF less than 35% with dilated, nonischemic class II symptoms who have had optimal medical therapy for at least three months using perhaps in that patient population LGE for shared decision-making in patients about the magnitude of the risk. And I think that's as far as we can go pending future studies, and there is one which we can discuss later on the CMR study at just that preserved ejection fraction LGE randomizing to defibrillator versus ILR. Dr. Greg Hundley: Thank you, Mark. So listeners just really quickly, let's go back to each of our experts and ask them, you know, in 20 seconds, Igor, Pasquale, Victoria, and Mark, what's the next study that needs to be performed in this space? Igor, we'll start with you. Dr. Igor Klem: Well, number one, following on Mark's comment on the less than 35% population, I think that it's unlikely that they're randomized clinical trial is ethical in this population, but we may consider a wealth of registry data by now that shows that there is a subgroup of patients who have a lower risk or lower benefit from an ICD. I think in the preserved ejection fraction above 35%, maybe up to 45%, 50%. That's an interesting study that's coming up. Maybe there's more trials that can provide us that robust information that we need today in order to change the guidelines to risk stratify, not based on the LVF, but on the presence of scar or maybe subgroups of scar. Dr. Greg Hundley: Pasquale? Dr. Pasquale Santangeli: Yes. So I think of course, one of the major studies is the one already alluded by this, which is a prospective study that links as specific therapy like ICD or even additional risk factors like we've been using program's stimulation some of these patients to further risk for the five to see what they can benefit. Dr. Pasquale Santangeli: Based another one that I think is important for the study that we did is a mechanistic more study to understand why the ring light pattern was there, as opposed to other patterns. We do believe we think that some of these patients may have an initial form of lb dominant arrhythmogenic paramount. There wasn't really a detective before and ran. Now, if we actually extending our study and have a registry to try to screen also the family members or patients with ring light pattern to understand whether there is a familiar component to it, because really we do not see this type of pattern that commonly and it'd been associated with lb dominant. Magnetic kind of alpha in some others, small studies. Dr. Pasquale Santangeli: So that's the other part to dig in a little bit more into the field type for these patients to understand why one pattern versus another happens and whether that gets main to, to explain why there's a higher risk in one population versus another. Dr. Greg Hundley: Victoria. Dr. Victoria Delgado: Yeah. Following what has been said. I think that from the imaging point of view, we are always criticizing in a way that we increase the burden or the cost of healthcare. But I think that these studies or any randomized study where MRI or echo is used in order to design a therapy and show the value of using that imaging technique to optimize the health care costs is important. So I will not add much on which sort of populations, but probably patients within non ischemic cardiomyopathy with preserved ejection fraction that do not fulfill the recent scores, for example, in hypertrophic cardiomyopathy to be implanted with an ICD. But probably if we see a lot of scar on a AGE where specific patterns that can help to decide which are the patients that have benefited from an ICD implantation, for example. Dr. Greg Hundley: Thank you. And finally Mark. Dr. N.A. Mark Estes: But I think all the major points have been hit here. And unfortunately we have a bit of a dilemma. And that dilemma is that these legacy trials for ICDs, which selected based on low ejection fraction and functional class II were done at a time when contemporary heart failure treatment was not as good as it currently is pharmacologically. And it's been reflected with a lower total mortality. When the mortality in this patient population gets down to the 4 and 5% per year, it's unlikely that any intervention for prevention of sudden death is going to impact on that total mortality. Dr. N.A. Mark Estes: So I do think that the registries hold a lot of promise, giving us insights into the subgroup of patients that previously would have been selected for defibrillators who may not have as much benefit or who may benefit the most. And I think that they will play an important part in perhaps refining the risk stratification with greater sensitivity and specificity in the patient population, less than 35%. I think the CMR guide trial is going to be a critical trial and looking at ICDs in the patient population between 35 and 50%, but we need to be mindful of one thing. And that in the Danish trial, they get a sub study looking at about 240 patients using LGE. And they found that ICD in patients with LGE that was positive, did not make a difference in survival or total mortality. So again, we need to get the data. I think the best clinical practice has come out of the best clinical evidence. You'll clearly be limitations to what we can do, but I think in the future, we'll have much better data to make these judgment calls. Dr. Greg Hundley: Very good. Well listeners, we want to thank our panelists, Dr. Igor Clem, Pasquale, Santangeli, Victoria Delgado, and Dr. Mark Estes for this wonderful discussion related to magnetic resonance imaging, late gadolinium enhancement, and how it may be useful in identifying those at risk for future arrhythmic events. On behalf of both Carolyn and myself, want to wish you a great week and we will catch you next week on the run. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021.  

For this week's Feature Discussion, please join authors Michael Ackerman, Christopher Haggerty, editorialist Michael Rosenberg, and Associate Editor Nicholas Mills as they discuss the original research articles “Artificial Intelligence-Enabled Assessment of the Heart Rate Corrected QT Interval Using a Mobile Electrocardiogram Device,” “ Deep Neural Networks Can Predict New-Onset Atrial Fibrillation From the 12-Lead Electrocardiogram and Help Identify Those at Risk of AF-Related Stroke,” and “Trusting Magic: Interpretability of Predictions from Machine Learning Algorithms.”   TRANSCRIPT BELOW: 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 cohosts. I'm doctor Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: And I'm Greg Hundley, associate editor, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well Carolyn, this week's feature, it's kind of a new thing for us. It's more than our double feature; it's actually a forum, where we're going to have two papers discussed, we'll have both authors represented from each of those two papers, we'll have an editorialist, and we'll have one of our associate editors. And the topic, Carolyn, just to keep you in suspense, is really on machine learning and actually how that can be applied to 12 lead electrocardiograms. But before we get to that, how about we grab a cup of coffee and start off on some of the other articles in this issue? Would you like to go first? Dr. Carolyn Lam: Yes, I would, but you're really keeping me in suspense. But first, let's focus on health related quality of life. We know that poor quality of life is common in heart failure, but there are few data on heart health related quality of life and its association with mortality outside of the Western countries. Well, until today's paper. And it's from the Global Congestive Heart Failure, or GCHF study, the largest study that has systematically examined health-related quality of life as measured by the Kansas City cardiomyopathy questionnaire 12, or KCCQ, and its association with outcomes in more than 23,000 patients with heart failure across 40 countries, in eight major geographic regions, spanning five continents. Dr. Greg Hundley: Wow, Carolyn. That KCCQ 12, that has been such an interesting tool for us to use in patients with heart failure. So what did they find in this study? Dr. Carolyn Lam: Really important. So the health-related quality of life differs considerably between geographic regions with markedly lower quality of life related to heart failure in Africa than elsewhere. Quality of life was a strong predictor of death and heart failure hospitalization in all regions, irrespective of symptoms class, and in both preserved and reduced ejection fraction. So there are some important clinical implications, namely that health-related quality of life is an inexpensive and simple prognostic marker that may be useful in characterizing symptom severity and prognosis in patients with heart failure. And there is certainly a need to address disparities that impact quality of life in patients with heart failure in different regions of the world. Dr. Greg Hundley: Very nice, Carolyn. Well, I'm going to turn to the world of basic science and bring us a paper from David Merryman from Vanderbilt University. So Carolyn, myocardial infarction induces an intense injury response, which ultimately generates a collagen dominated scar. Cardiac myofibroblasts are the cells tasked with depositing and remodeling collagen and are a prime target to limit the fibrotic process post myocardial infarction. Now Carolyn, serotonin 2B receptor signaling has been shown to be harmful in a variety of cardiopulmonary pathologies, and could play an important role in mediating scar formation after MI. So Carolyn, these investigators employed two pharmacologic antagonists to explore the effect of serotonin 2B receptor inhibition on outcomes post myocardial infarction and characterized the histological and micro structural changes involved in tissue remodeling. Dr. Carolyn Lam: Oh, that's very interesting, Greg. What did they find? Dr. Greg Hundley: So Carolyn, serotonin 2B receptor antagonism preserved cardiac structure and function by facilitating a less fibrotic scar, indicated in their results by decreased scar thickness and decreased border zone area. Serotonin 2B receptor antagonism resulted in collagen fiber redistribution to a thinner collagen fiber. And they were more anisotropic. They enhanced left ventricular contractility and the fibrotic tissue stiffness was decreased, thereby limiting the hypertrophic response of the uninjured cardiomyocytes. Dr. Carolyn Lam: Wow. That is really fascinating, Greg. Summarize it for us. Dr. Greg Hundley: Yeah, sure. So this study, Carolyn, suggests that early inhibition of serotonin 2B receptor signaling after myocardial infarction is sufficient to optimize scar formation, resulting in a functional scar, which is less likely to expand beyond the initial infarct and cause long-term remodeling. The prolonged presence of the antagonist was not required to maintain the benefits observed in the early stages after injury, indicating that acute treatment can alter chronic remodeling. So Carolyn, it's really going to be interesting to see how this research question is pursued in studies of larger animals, including us, or human subjects. Dr. Carolyn Lam: Wow, that is really interesting. And so is this next paper. Well, we know that genetic variation in coding regions of genes are known to cause inherited cardiomyopathies and heart failure. For example, mutations in MYH7 are a common cause of hypertrophic cardiomyopathy, while mutations in LMNA are a common cause of dilated cardiomyopathy with arrhythmias. Now, to define the contribution of non-coding variations, though, today's authors, led by Dr. Elizabeth McNelly from Northwestern University Feinberg School of Medicine in Chicago and colleagues evaluated the regulatory regions for these two commonly mutated cardiomyopathy genes, namely MYH7 and LMNA. Dr. Greg Hundley: Wow, Carolyn. So this is really interesting. So how did they do this and what did they find? Dr. Carolyn Lam: You asked the top questions, because the method is just as interesting as the findings here. They used an integrative analysis that relied on more than 20 heart enhancer function and enhancer target datasets to identify MYH7 and LMNA left ventricular enhancer regions. They confirmed the activity of these regions using reporter assay and CRISPR mediated deletion of human cardiomyocytes derived from induced pluripotent STEM cells. These regulatory regions contained sequence variants within transcription factor binding sites that altered enhancer function. Extending the strategy genome-wide, they identified an enhancer modifying variant upstream of MYH7. One specific genetic variant correlated with cardiomyopathy features derived from biobank and electronic health record information, including a more dilated left ventricle over time. So these findings really link non-coding enhancer variation to cardiomyopathy phenotypes, and provide direct evidence of the importance of genetic background. Beautiful paper. Dr. Greg Hundley: Very nice, Carolyn. Dr. Carolyn Lam: But let me quickly tell you what else is in this issue. We have an ECG Challenge by Dr. Lutz on flash pulmonary edema in a 70-year-old; there's an On My Mind paper by Dr. Halushka, entitled (An) Urgent Need for Studies of the Late Effects of SARS-CoV-2 on the Cardiovascular System. Dr. Greg Hundley: Ah, Carolyn. Well, in the mailbox, there are two Research Letters, one from Dr. Soman entitled (The) Prevalence of Atrial Fibrillation and Thromboembolic Risk in Wild-Type Transthyretin Amyloid Cardiomyopathy, and a second letter from Dr. Berger entitled Multiple Biomarker Approaches to Risk Stratification in COVID-19. Well Carolyn, now let's get on to that forum discussion and hear a little bit more about using machine learning in the interpretation of a 12 lead ECG. Dr. Carolyn Lam: Wow, can't wait. Thanks, Greg. Dr. Greg Hundley: Well listeners, we are here today for a double feature, but this double feature is somewhat unique, in that we are going to discuss together two papers that focus on machine learning applications as they relate to the interpretation of the electrocardiogram. With us today, we have Mike Ackerman from Mayo Clinic, Chris Haggerty from Geisinger, Mike Rosenberg as an editorialist from University of Colorado, and then our own Nick Mills, an associate editor with Circulation. Welcome, gentlemen. Well, Mike Ackerman, we will start with you first. Could you describe for us the hypothesis that you wanted to test, and what was your study population and your study design? Dr. Michael Ackerman: Thanks, Greg. The hypothesis was pretty simple, and that is could an artificial intelligence based approach, machine learning, deep neural network, could that solve the QT problem? Which is one of the big secrets among cardiologists, which, as you know, one of your associate editors, Sammy Biskin, published a sobering paper over a decade ago, showing and revealing the secret that cardiologists are not so hot at measuring the QT interval, and heart rhythm specialists sometimes don't get it right either. And we all know that the 12 lead ECG itself is vexed by its computer algorithms at getting the QTC just right, compared to those of us who would view ourselves as QT aficionados. And so we were hoping that a machine learning approach would solve this and help us glean, one, a very accurate QTC, as accurate as I can make it when I measure it, or core labs that do QT measuring for living. Dr. Michael Ackerman: And two, could we get that QTC from just a couple of leads to be as accurate as what the whole 12 lead ECG would be seeing so that we can move it to a mobile smartphone enabled solution? And so that was our hypothesis going forward, and we studied a lot of patients. And that's something that machine learning and the power of computation does, that in my world, I'm used to studying a hundred or a thousand patients with congenital long QT syndrome and thinking that I've assembled a large cohort, but for this study, we started with over two and a half million ECGs from over 650,000 people. And then ultimately, through training, testing, and validation of about 1.6 million ECGs from over a half a million individuals to sort of teach the computer or have the AI algorithm get the QT interval not too hot, not too cold, but just right. And as we'll discuss, I think we hit the mark. Dr. Greg Hundley: Thanks so much, Mike, what did you find? Dr. Michael Ackerman: Ultimately, we were able to show that with this drill, we could get the deep neural network derived QTC to be give or take two plus minus 20 milliseconds from what would the standard of care, and that being a technician over-read QTC. But then we took, I would say, pretty unique to AI studies, as many AI studies, just do training, testing, and validation for study number one. And then a future paper of a prospective study. But we did that prospective study within this single paper with a subsequent about two year enrollment of nearly 700 patients that I evaluated in our genetic heart rhythm clinic at Mayo Clinic. And half of those patients have congenital long QT syndrome, half did not. And what we showed was that the deep neural network derived QTC from a mobile ECG approximated the subsequent or the just prior 12 lead ECG within one millisecond, +/- 20 millisecond territory. Dr. Michael Ackerman: And it's ability to say is the QTC above or below 500, which we all know is sort of a warning sign, that's a very actionable ECG finding, do something about it, that that 500 millisecond cutoff by the deep neural network gave us an area under the curve of 0.97, which from a screening perspective, that AUC is far higher than a lot of AUCs for a lot of screening tests done in the cancer world and so forth. And so we think we are very close to what I've called a pivot point, where we will soon pivot from the way we've been doing the QTC since Eindhoven over a century ago to a fundamentally new way of deriving a QTC that's precise and accurate and mobile enabled. Dr. Greg Hundley: Very nice, Mike. So using machine learning to accurately assess the QTC from just two leads of an electrocardiogram. Well Chris, you also have a paper in this issue of circulation that pertains to another application of machine learning and looking at the electrocardiogram. Can you describe for us your study population, study design, and then also the question you were trying to address? Dr. Christopher Haggerty: Sure. Yeah, thanks Greg. Great to be here with you all today. Very similar to Mike's study, the motivation for us was we believe very strongly that there's opportunities with using deep learning applied to ECG data to uncover not only new knowledge latent in the ECG itself related to the current patient context, but also to try to predict future outcomes, future events. And that was really our motivation, was to take that paradigm of looking forward, in this case to predict new onset of atrial fibrillation within a year. We used our Geisinger patient cohort, which is a largely rural population in central Pennsylvania. We have very longitudinal data for a lot of our patients, which allows us to have this kind of design going back in our electronic health records, in this case, our ECG database to 30 plus years. Dr. Christopher Haggerty: Similar big numbers that Mike described, and in our case, 1.6 million ECGs over 430,000 patients used to train the model. And we had several different study designs that we employed. One just being a simple proof of concept, asking can we accurately predict new onset atrial fibrillation one year? And then a second study design that was intended to simulate a real world deployment scenario. Obviously the main rationale for trying to predict atrial fibrillation is to then be able to treat and try to prevent stroke. And so we tried to, as best we can in a retrospective fashion, simulate a scenario in which we might use this model to identify patients who went on to have a presumably AFib associated stroke. Dr. Greg Hundley: And what did you find, Chris? Dr. Christopher Haggerty: So I think there are three main findings that we highlighted here. So first, obviously we were building on the great work that Mike and some of his colleagues at the Mayo Clinic have done, showing that looking at AFib using deep neural networks needs to be feasible. We extended it in this case by looking out further than just an acute sense, looking at that one-year outcome. And we had an area under the curve for our proof of concept of 0.85. So area under the curve of 0.85 to identify patients with new onset of atrial fibrillation within one year in our millions of ECGs. Looking at it another way, the second main finding was that that one year prediction was shown to have prognostic significance beyond that one year, which is really interesting and warrants a lot of further study. Looking over 30 years of follow-up, patients predicted to be at high risk at baseline had a hazard ratio of 7.2 for developing atrial fibrillation, compared to those deemed to be low risk. Dr. Christopher Haggerty: And then really the third, and I think perhaps the most exciting finding that we had here, was this simulated stroke experiment that we had, where we identified patients from an internal stroke registry and identified patients who had new diagnosis of AFib at the time or up to a year after the stroke. So we can assume that they were an AFib associated stroke. And subsequently, or I should say previously, had an ECG that we could use to run through the algorithm to predict their atrial fibrillation risk. And we showed that the model performed well in this setting, that of the 375 strokes that we identified, for example, over a five-year period in our registry, we were able to identify 62% of them within three years based on that ECG. So a number needed to screen for an atrial fibrillation associated with stroke about 162, which compares favorably well to other screening techniques that are out there, obviously. So we took that as a great proof of concept that this type of AI technique might have benefits for screening for atrial fibrillation and preventing strokes. Dr. Greg Hundley: Well congratulations, Chris. Well, we're now going to turn to our associate editor, Dr. Nick Mills. And Nick, you have a lot of manuscripts come across your desk. What attracted you to these two papers, and what are the significance of the results as they apply to ECG applications as we move forward? Nick Mills: Thanks, Greg. Yeah, this is a rapidly growing field, where the availability of data scale with digital archiving and lots of really interesting new methodologies are available to our researchers. So we are receiving a lot of content in this area. What I loved about these two papers is not just the quality of the work, but also the really tangible benefits, potentially, for patients. So AI does not need to be complex, but it does need to solve a tangible problem. I guess what we look for in the journal, beyond the kind of innovation and methodology, is quality, and these studies used prospective validation, really reliable end points, ascertainments, transparency, reporting, all the things that we know are important for high quality clinical research. I think the idea that we can bring QT monitoring to the drug store on a portable device for our patients is potentially transformative. I also think that to take a technology, the electrocardiogram that we've been using for over a century, and provide new insights that go way beyond my ability to interpret the ECG, that might help us recommend a different course of action for our patients is also just really exciting. Dr. Greg Hundley: Very nice. Thank you, Nick. Well Mike ... we're going to turn to Mike Rosenberg now, listeners. And Mike wrote a wonderful editorial, and I would invite you to work through this. As you have an opportunity to read the journal and interact with it. Mike, there are two different types of machine learning, I think, that you described were used by the two respective investigative groups. Could you describe those for our cardiology listeners? What were the differences in those two approaches? Dr. Michael Rosenberg: Yeah, sure. And thank you for the opportunity to write the editorial. Two very fascinating papers. I should say that they both use the same approach of what's called supervised learning, where you basically have a set of data inputs, and you're trying to predict a labeled outcome. And what I talk about in the paper is that what we've learned is if you have enough data and enough computing power, you can predict almost anything highly accurately. What's interesting about the two papers, and what I sort of tried to contrast in the editorial, is that the one from the Mayo Group and Dr. Ackerman, was basically predicting what's already a known biomarker for sudden death, which is the QT interval. And essentially, almost trying to automate that process of predicting it accurately and in a way that, in essence, could allow a home monitoring of patients for QT prolongation, which obviously would be a huge benefit for clinicians, all those alerts and things, to be able to have patients taking drugs that are known to prolong the QT interval and feeling comfortable that if they have any prolongation, it could be detected accurately. Dr. Michael Rosenberg: The second one, which is sort of interesting, and in contrast is from the Geisinger Group and Dr. Haggerty, was the approach of ... where actually the prediction itself is actually the biomarker. And we don't actually know exactly what it's using, which I talk about a little bit of what that means and the implications clinically, but in essence, what they showed was that it actually is a very good biomarker and on par with what a lot of us would consider to be very strong predictors of agents. So I think it was two very interesting approaches to, again, applying the same type of machine learning, but really approaching it one from a more discovery side and another from sort of validated or almost automating something that we do on a daily basis. Dr. Greg Hundley: Thank you, Mike. So Mike, just coming back to you again, as we read the literature, and most of us are clinicians or researchers practicing, what should we look for when these new machine learning manuscripts and research studies come out as to gauge, "Ah, this is a really good study," or maybe not so much? Dr. Michael Rosenberg: Yeah. And it's a good question. I think one of the biggest challenges, as I talked about, is interpretability. I think in the clinical world, we're used to understanding the code for the variables that go into our risk prediction model. And so I think first and foremost is can I even understand what this is predicting or am I sort of expected to take the predictions as sort of a black box, it is what it is type of approach? I think that there's other things that I just look at when I'm reviewing these manuscripts. I mean, as I sort of mentioned, what these models are really doing, it's not anything magical. What they're doing is identifying patterns in the data and then using those to make predictions, again, toward whatever label that you've assigned them to. Dr. Michael Rosenberg: It's important that your data sets are split and that you're training at one data set and then testing it in one that's separate. And again, you can't ignore epidemiology. Is the data set that you're training it reflective of the population that you're going to be using those models in? And we know from outside of healthcare, there's issues with models that have been trained in one population where it's potentially biased or it's potentially offering predictions that are using information we may not necessarily want to use. Recidivism is a big example of that. So I think that that's, first and foremost, it's sort of taking a step back as a clinician and saying, "If this was a biomarker that someone was proposing to use to predict some new disease, what would I expect to use to evaluate that?" And that's probably what I would start with. Dr. Greg Hundley: Excellent. Well, I'm going to turn back and go back to our panelists here, listeners. And we're going to ask each of our panelists in about 20 seconds to describe for us what they think is the next most important aspect of research in their respective areas. So first I'll start with Mike Ackerman. Mike, can you tell us what's coming next in this area of assessment of QT prolongation or other aspects of the electrocardiogram? Dr. Michael Ackerman: I think next is implementing this in the real world. We are having our suite of the AI ECG as a  hypertrophic cardiomyopathy detector. We've shown that as an ejection fraction detector, and now as a QT detector in AFib, from our work and Chris's work. And for the QT itself, I think where we are is we're really, really close to now having a mobile enabled digital QT meter. And a digital QT meter, once FDA cleared, then allows the QTC to truly emerge as the next vital sign. And it really deserves to be a vital sign. We use it as a vital sign. We know I want to know my patient's QTC every bit as I want to know his or her weight, blood pressure, saturation. It's an actionable finding, and we're now getting really close. We're just on the cusp of having a true digital QT meter. Dr. Greg Hundley: Excellent. Chris? Dr. Christopher Haggerty: I think for us to, in part address some of the comments that Mike brought up about the reproducibility of these types of models, we're very keen to demonstrate the prospective capabilities of our models to enroll patients in a prospective fashion, run their ECG through our predictor, and then screen them for AFib to determine how well we actually do moving forward, instead of just relying solely on our retrospective data. So we're very excited to do that. We're ramping up for that trial now and hope to be able to demonstrate similarly positive findings from our technique. Dr. Greg Hundley: Great. How about you, Nick? Nick Mills: I'd like to see the same quality and rigor applied to the implementation of these technologies as we have to other important areas in cardiovascular medicine. I think that's a really important step, not just to develop the tools, but to demonstrate their value. But I also think what we've done so far is relatively simplistic. We've taken an ECG and we've ignored almost all the other information that we have in front of us. And as these algorithms are trained and evolved, these and other vital clinical biomarkers and information, and integrating them into these neural networks will really enhance their performance for predicting things that are less tangible, like sudden death in the future or stroke. Dr. Greg Hundley: And then finally, Mike Rosenberg. Dr. Michael Rosenberg: Yeah, I actually see two challenging areas in this field. One is the access to data. And I think one of the things that a lot of companies are realizing is that even if they make hardware, that the data may be more valuable than the technology that they're getting the data from. So I think one is figuring out ways to get access to data so that people can reproduce findings from these studies. And the second is deliverable. A bottle like this is not like the CHADS-VASc score that I can calculate in my head in the clinic. I mean I need a way to actually run these models within an EHR, within a computer system like that. And I think it's going to be a big challenge to take a model like this and to deploy it at scale the way we would with the drug or any other innovation. Dr. Greg Hundley: Fantastic. Well listeners, we want to thank Mike Ackerman from Mayo Clinic, Chris Haggerty from Geisinger, Mike Rosenberg from University of Colorado, and Nick Mills from University of Edinburgh for really providing us with a wonderful discussion regarding the use of machine learning applications in one study to predict the QTC interval from two leads that may be applicable to wearable devices. And in the second study, predicting the future occurrence of atrial fibrillation and even stroke as an adverse event in people at risk. Dr. Greg Hundley: On behalf of both Carolyn and myself, I want to wish you a great week and we will catch you next week on the run. This program is copyright of the American Heart Association, 2021.  

En un mundo de pantallas y pixels, donde consumimos miles de imágenes a diario casi sin ser conscientes, los libros de Fotografía y fotolibros – que no son lo mismo, aunque pueda parecerlo – siguen manteniendo intacta su capacidad para atraparnos y llevarnos de la mano a un mundo propio. Así que aquí está este nuevo episodio de Calle Oscura, en el que me siento a charlar de Fotografía y páginas de libros con alguien a quien le gustan tanto como a mí y de quien no dejo de aprender constantemente. En este episodio hablamos de - La experiencia de adentrarse en un fotolibro. - Cómo la inspiración puede colarse desde el lugar más inesperado. - La importancia de cultivar nuestra cultura visual. - Las conexiones entre palabra e imagen y cómo se influyen mutuamente. - La relación entre fotografía y otras formas artísticas. - La conveniencia de interesarte por lo aquello que está en las antípodas de lo que haces (y de lo que te gusta). - Que empezar copiando puede ser una gran manera de cultivar una mirada propia. - Por qué los trabajos clásicos son imprescindibles. - Que hay distintos fotolibros para diferentes momentos vitales. - Cómo acercarse a ese mundo desde cero. Y, claro, de muchas otras cosas que fueron saliendo durante la charla. Quién me acompaña Leire Etxazarra es una apasionada de la Fotografía y de los fotolibros, algo que se nota – y mucho – en todos sus proyectos. El primero fue un blog muy bien escrito y lleno de información valiosa (y entretenida, una combinación irresistible), a aquello le siguió un canal de Youtube dedicado a sus libros favoritos, que comparte y analiza desde una óptica muy personal. Disfruto muchísimo con todo lo que hace Leire y he aprendido tanto de su mano que no veía el momento de sentarme a charlar con ella de fotos, libros y – algo que sospechaba que sucedería – un buen puñado de cosas más. No olvides localizar y seguir a Leire en las redes a través de: - Su blog Cartier-Bressson no es un reloj (http://www.cartierbressonnoesunreloj.com). - El canal de Youtube con el mismo nombre (http://bit.ly/3asmOE9). - Su perfil de Instagram (http://www.instagram.com/leiremiska/). Referencias y enlaces Autores y autoras - Alan Schaller. - Alex Webb. - Bego Antón. - Duane Michaels (este catálogo es una gran manera de conocer su trabajo https://amzn.to/3u0cDOK). - Francesca Woodman (y sus libros On Being an Angel https://amzn.to/3qobH4B y Portrait of a Reputation https://amzn.to/3dyvzyz). Gabriele Croppi. - Jonas Bendiksen y esa fotografía que parece magia: http://jotabarros.com/grandes-fotografias-jonas-bendiksen-satellites/. - José Manuel Navia (http://jotabarros.com/aprende-de-jose-manuel-navia/). - Michael Ackerman. - Rafael Roa. Libros y trabajos - Hojas de Contacto, el libro de Magmun: http://jotabarros.com/libro-fotografia-magnum-contact-sheets/. - Garry Winogrand (el catálogo de la exposición: https://amzn.to/2ZrLW7w). - La Visión Fotográfica de Eduardo Momeñe (http://jotabarros.com/la-vision-fotografica-de-eduardo-momene/). - Mirar de Joel Meyerowitz (http://jotabarros.com/libro-fotografia-mirar-joel-meyerowitz/). Cómo Hago Fotografías, también de Meyerowitz (http://jotabarros.com/libro-como-hago-fotografias-20-consejos-joel-meyerowitz/). - The Americans de Robert Frank (http://jotabarros.com/the-americans-los-americanos-de-robert-frank/). - The Suffering of Light de Alex Webb (http://jotabarros.com/libro-fotografia-calle-the-suffering-of-light-alex-webb/). - Ravens de Fukase (http://jotabarros.com/libro-fotografia-callejera-ravens-masahisa-fukase/). - Street Photography Now (https://amzn.to/3jXnK6H). Muchas gracias por tu escucha Si te ha gustado este capítulo de Calle Oscura, deja tu valoración positiva en Ivoox, Apple Podcast y Spotify, donde también puedes encontrar este podcast. No olvides suscribirte a través de cualquiera de esas plataformas para no perderte ningún episodio. Por favor, comparte este contenido entre tus redes para que llegue a más gente, puede suponer una gran diferencia. Y ahí abajo tienes los comentarios, para seguir conversando sobre los temas abordados con Leire. Muchas gracias por estar ahí, al otro lado. Hasta pronto. Jota.

On Episode 80 of Totally Deep Podcast, Doug Stenclik and Randy Young of www.cripplecreekbc.com bring you the lowdown on the world of uphill and backcountry skiing and boarding. Gear, technique, fashion, jargon, guests, and assorted spray from folks who know how to earn it in the backcountry. The world's best backcountry skiing podcast. More info about TDP at Totally Deep Podcast Blog on Cripplecreekbc.com or wildsnow.com. On Episode 80 of Totally Deep Podcast: 1. Josh Jespersen and Michael "Ack" Ackerman of Silverton Avalanche School. 2. History of Avalanche "Science". 3. School for you. 4. Why Avy 1 makes you a menace. 5. Quick hit starter: Avalanche Rescue course. 6. Crowded backcountry doesn't mean you get to be a dick. Comments: info@cripplecreekbc.com Or leave a voicemail: 970-510-0450 Backcountry Skiing, Uphill Skiing, Rando (skimo?) Racing, Splitboarding, its all here.  

Dr. Michael Ackerman (@MJAckermanMdPhd) of the Mayo Clinic joins @SicEm365Radio to talk about how much his national profile has changed after his thoughts on myocarditis went viral, how the world takes in medical data in 2020, and how fast the medical community has had to try to turn around info on Covid-19.

3:15pm-Don Hyde, La Vega Football Coach on Replacing Opening Game3:30pm-Dave Aranda Comments from Saturday Media Session3:45pm-Kevin Hoffman, Mart Football Coach3:50pm-Greg Jacobs, Crawford Football Coach4:00pm-Dr. Michael Ackerman, The Mayo Clinic 4:30pm-Bob Bowlsby, Big 12 Commissioner5:00pm-Chuck Cooperstein, Mavericks Play-By-Play Broadcaster5:30pm-Jerry Forrest, PigskinPrep.com

Dan is joined by Mayo Clinic Cardiologist Dr. Michael Ackerman to discuss what myocarditis is and what impact it may have on Covid-19 patients.

Dan Barreiro & JG broadcast live from Vikings practice at TCO Performance Center! Mike Zimmer joins the show after practice to discuss defense, and how this season is different among a wide range of other topics. Ben Goessling calls in to break down ...

What is COVID myocarditis and how strong is the data to create a link between COVID and potential arrhythmias? Was COVID myocarditis the leading factor in the recent decisions of some American athletic conferences to shut-down the fall sports season? What are the criteria to start participation again?On this episode of the AMSSM Sports Medcast, host Devin McFadden, MD is joined by sports medicine physicians and internationally renowned experts on Sports Cardiology Jonathan Drezner, MD, FAMSSM and Michael Ackerman, MD, who have both been influential in the debate on whether a Collegiate Athletic season can safely occur in the midst of the ongoing COVID-19 Pandemic.Dr. Jonathan Drezner is a Professor from the Department of Family Medicine and Director of the University of Washington Center for Sports Cardiology, past president of the AMSSM, team physician for the Seattle Seahawks, UW Huskies, and OL Reign and deputy editor of the BJSM. Dr. Michael Ackerman is a Professor of Medicine, Pediatrics, and Pharmacology at the Mayo Clinic College of Medicine and Science. He is the Director of the Windland Smith Rice Genetic Heart Rhythm Clinic and Windland Smith Rice Sudden Death Genomics Laboratory, as well as the president of the Sudden Arrhythmia Death Syndromes (SADS) Foundation.In this 40 minute conversation Drs. Drezner and Ackerman addressed the following topics:What is COVID myocarditis and why is it so concerning?How strong is the link between COVID-19 and was this a driving factor in the cancelling of the FALL sports season by some collegiate conferences?What metrics need to be satisfied in order to safely return to play, and will that occur this year?Health and Well Being Considerations for PAC-12 Institutions: Guidance for Local Planning for Return to Sporting Activity https://xs.pac-12.com/2020-08/Pac-12%20Covid-19%20Return%20to%20Play%20Considerations%2008.10.2020.pdf Puntmann VO, Carerj ML, Weiters I. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19) https://jamanetwork.com/journals/jamacardiology/fullarticle/2768916 Baggish A, Drezner JA, Kim J, et al. Resurgence of sport in the wake of COVID-19: cardiac considerations in competitive athletes https://bjsm.bmj.com/content/early/2020/06/18/bjsports-2020-102516 Maron BJ, Zipes DP, Kovacs RJ, et al. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: a scientific statement from the American Heart Association and the American College of Cardiology. Copublished in Circulation and the Journal of the American College of Cardiology 2015. https://www.acc.org/~/media/fb92803045d249ae91b715650dd0ebe4.pdf Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology (EAPC). European Heart Journal 2019;40:19.https://academic.oup.com/eurheartj/article/40/1/19/5248228

What is COVID myocarditis and how strong is the data to create a link between COVID and potential arrhythmias? Was COVID myocarditis the leading factor in the recent decisions of some American athletic conferences to shut-down the fall sports season? What are the criteria to start participation again? On this episode of the AMSSM Sports Medcast (T: @TheAMSSM) host Dr. Devin McFadden, MD is joined by sports medicine physicians and internationally renowned experts on Sports Cardiology Dr. Jonathan Drezner and Dr. Michael Ackerman, who have both been influential in the debate on whether a Collegiate Athletic season can safely occur in the midst of the ongoing COVID-19 Pandemic. Dr. Jonathan Drezner is a Professor from the Department of Family Medicine and Director of the University of Washington Center for Sports Cardiology, past president of the AMSSM, team physician for the Seattle Seahawks, UW Huskies, and OL Reign and deputy editor of the BJSM. Dr. Michael Ackerman is a Professor of Medicine, Pediatrics, and Pharmacology at the Mayo Clinic College of Medicine and Science. He is the Director of the Windland Smith Rice Genetic Heart Rhythm Clinic and Windland Smith Rice Sudden Death Genomics Laboratory, as well as the president of the Sudden Arrhythmia Death Syndromes (SADS) Foundation. In this 40 minute conversation Drs. Drezner and Ackerman addressed the following topics: What is COVID myocarditis and why is it so concerning? How strong is the link between COVID-19 and was this a driving factor in the cancelling of the FALL sports season by some collegiate conferences? What metrics need to be satisfied in order to safely return to play, and will that occur this year. Health and Well Being Considerations for PAC-12 Institutions: Guidance for Local Planning for Return to Sporting Activity https://xs.pac-12.com/2020-08/Pac-12%20Covid-19%20Return%20to%20Play%20Considerations%2008.10.2020.pdf Puntmann VO, Carerj ML, Weiters I. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19) https://jamanetwork.com/journals/jamacardiology/fullarticle/2768916 Baggish A, Drezner JA, Kim J, et al. Resurgence of sport in the wake of COVID-19: cardiac considerations in competitive athletes https://bjsm.bmj.com/content/early/2020/06/18/bjsports-2020-102516 Maron BJ, Zipes DP, Kovacs RJ, et al. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: a scientific statement from the American Heart Association and the American College of Cardiology. Copublished in Circulation and the Journal of the American College of Cardiology 2015. https://www.acc.org/~/media/fb92803045d249ae91b715650dd0ebe4.pdf Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology (EAPC). European Heart Journal 2019;40:19. https://academic.oup.com/eurheartj/article/40/1/19/5248228

On today's show, we welcome Dr. Michael Ackerman, M.D., Ph.D. of the Mayo Clinic, Baylor AD Mack Rhoades, Tim Brando of Fox Sports, David Helman of DallasCowboys.com, & John McClain of the Houston Chronicle.

Michael Ackerman, director of the Master in Healthcare Innovation Program at The Ohio State University, believes that every innovation program must do three things in tandem:   Innovation – filling gaps where no solution currently exists, in a way that adds value Renovation – quality improvement and process improvement Exnovation – removing functions that no longer add value; also known as de-implementation   When practiced together, and ideally led by different teams within the organization, the 3 pillars of The Novation Dynamic help us overcome the notorious friction that has slowed healthcare innovation for too long.   You'll Learn: The 3 pillars of The Novation Dynamic and how to apply them in your organization The 3 things that make innovation so hard in healthcare and how to address them How to do evidenced-based innovation even though innovation is, by definition, void of evidence Why we're seeing so much innovation right now during the pandemic, and what we can learn from the experience to make sure we never slow back down. How to create a culture of innovation (plus, a killer idea to make your end of year reviews meaningful at the same time). Why no innovation should be deployed without a scheduled reevaluation date. How to tap the tremendous potential of nurses to drive innovation   Today's Guest: Michael H. Ackerman, DNS, RN, FCCM, FNAP, FAANP, FAAP is director of the Master in Healthcare Innovation Program and professor of clinical nursing at the College of Nursing, The Ohio State University, in Columbus, Ohio.   LinkedIn: https://www.linkedin.com/in/michael-ackerman-dns/ Facebook Group: Stop the Silence in Healthcare   Resources: The Novation Dynamic Getting Rid of Stupid Stuff (NEJM) The #HCBiz Show! #133: Keeping Your Innovation Engine Humming During the COVID-19 Crisis w/ Karen Murphy, PhD, RN The #HCBiz Show! #7: Redefining Sepsis | Michael Ackerman   Sponsor: This episode is sponsored by Formstack. Formstack is a workplace productivity platform that simplifies healthcare data processes. Healthcare teams can transform piles of paperwork into automated workflows that are easy to administer and 100% HIPAA compliant. From appointment scheduling to insurance verification, Formstack makes it easy to breeze through administrative tasks, reduce security risks, and improve patient care and satisfaction. 

New York and New Jersey have the highest number of coronavirus cases and related deaths in the U.S. As leaders in other states plan to reopen businesses amid the pandemic, New Jersey Governor Phil Murphy weighs the country’s preparedness for crisis and the state-by-state financial troubles brought on by widespread shutdowns. The New York Times Foreign Affairs columnist Tom Friedman highlights America’s need for strong and transparent leadership, especially in a pandemic. Plus genetic cardiologist at the Mayo Clinic Dr. Michael Ackerman, issues a warning about the cardiac risks that may accompany the widely-praised Covid-19 treatment, hydroxychloroquine.  Learn more about your ad choices. Visit megaphone.fm/adchoices

A study published recently in Mayo Clinic Proceedings details information about potential cardiac side effects when using off-label drugs to treat COVID-19. Off-label means the drug has been approved by the Food and Drug Administration to treat a different condition. Some of the off-label drugs being used to treat COVID-19 have a risk of sudden cardiac arrest and death. On the Mayo Clinic Q&A podcast, Dr. Michael Ackerman, a Mayo Clinic genetic cardiologist and director of the  Windland Smith Rice Sudden Death Genomics Laboratory, explains how heart monitoring is important to identify at-risk patients.

This episode was recorded on April 3, 2020Claim credit here: https://ce.mayo.edu/covid19podcastGuest:  Michael J. Ackerman, M.D., Ph.D. (@MJAckermanMDPhD)Host: Amit K. Ghosh, M.D., M.B.A. (@AmitGhosh006)The administration of hydroxychloroquine and azithromycin, along with other very common medications could result in drug-induced sudden cardiac death caused by drug-induced QT prolongation, in some patients. In order to avoid the wrong medication, for the wrong patient, at the wrong time, Dr. Michael Ackerman shares how to assess your patient’s risk, how to find and measure their QTc value, and neutralize the threat.Deeper Dive:Link to Journal Pre-Proof:https://mayoclinicproceedings.org/pb/assets/raw/Health%20Advance/journals/jmcp/jmcp_covid19.pdfLink to COVID-19 QTc Calculator and other resources:https://www.covidqtc.com/#WRchTxt7-12veGiudicessi JR, Noseworthy PA, Friedman PA, Ackerman MJ. Urgent guidance for navigating and circumventing the QTc prolonging and torsadogenic potential of possible pharmacotherapies for COVID-19 [published online ahead of print March 25, 2020]. Mayo Clin Proc. https://doi.org/10.1016/j.mayocp.2020.03.024.FDA Emergency Use Authorization (EUA) of hydroxychloroquine sulfate: https://www.fda.gov/media/136538/downloadMayo Clinic Connected Care - Genetic Heart Rhythm Diseases https://connect.mayoclinic.org/page/genetic-heart-rhythm-disorders/tab/covid-19/#Connect with the Mayo Clinic’s School of Continuous Professional Development online at https://ce.mayo.edu/ or on Twitter @MayoMedEd.

Nos ocupamos de la obra de Erwin Blumenfeld (1987 - 1969) un fotógrafo, en sus inicios, revolucionariamente iconoclasta y dadaísta que, además de en uno de los fotógrafos más influyentes y mejor pagados de la Historia, se convirtió en uno de los grandes innovadores y estilistas de la fotografía de moda a la que aplicó algunos lenguajes propios del surrealismo. De Diane Arbus (1923 - 1971), fallecida por suicidio igual que Blumenfeld, leemos una de sus imágenes más icónicas. Y, finalmente, analizamos "Half Life", un fotolibro de culto de Michael Ackerman (Tel Aviv, 1967), un fotógrafo perturbador que bucea en la oscuridad, la alienación y el extrañamiento del ser humano en poderosas pero atormentadas imágenes en blanco y negro. Dirige y presenta: Juan María Rodríguez Con: Alfredo Oliva, Leire Etxazarra y Miguel Solís Emisión: 21 / 01 / 20

Nos ocupamos de la obra de Erwin Blumenfeld (1987 - 1969) un fotógrafo, en sus inicios, revolucionariamente iconoclasta y dadaísta que, además de en uno de los fotógrafos más influyentes y mejor pagados de la Historia, se convirtió en uno de los grandes innovadores y estilistas de la fotografía de moda a la que aplicó algunos lenguajes propios del surrealismo. De Diane Arbus (1923 - 1971), fallecida por suicidio igual que Blumenfeld, leemos una de sus imágenes más icónicas. Y, finalmente, analizamos "Half Life", un fotolibro de culto de Michael Ackerman (Tel Aviv, 1967), un fotógrafo perturbador que bucea en la oscuridad, la alienación y el extrañamiento del ser humano en poderosas pero atormentadas imágenes en blanco y negro. Dirige y presenta: Juan María Rodríguez Con: Alfredo Oliva, Leire Etxazarra y Miguel Solís Emisión: 21 / 01 / 20

Jane Ferguson:                  Hi there. Welcome to the November 2019 issue of Getting Personal: Omics of the Heart. I'm Jane Ferguson. This is your podcast from Circulation: Genomic and Precision Medicine. Let's get started.                                                 First up from Eric Curruth, Christopher Haggerty and colleagues from Geisinger, we have a paper entitled, “Prevalence and Electronic Health Record-based Phenotype of Loss-of-function Genetic Variance in Arrhythmogenic Right Ventricular Cardiomyopathy-associated Genes”. In this study, the team set out to understand the phenotypic consequences of variants and desmosome genes which has been associated with a arrhythmogenic right ventricular cardiomyopathy or ARVC. In clinical genetic testing, secondary findings of pathogenic or likely pathogenic variants in desmosome genes are recommended for clinical reporting. However, relatively little is known about the phenotypic consequences of these variants in a general clinical population.                                                 The team obtained whole exome sequencing data for over 61,000 individuals from the DiscovEHR cohort, part of the Geisinger MyCode Community Health Initiative. They then screened individuals for a putative loss of function variants in PKP2, DSC2, DSG2, and DSP. They evaluated ARVC diagnostic criteria using previously conducted ECG and echocardiograms and performed a phenom-wide association study or PHeWAS using EHR derived phenotypes. They found 140 people with an ARVC variant in one of the four genes, none of whom had an existing diagnosis of ARVC in the EHR.                                                 Further, there were no measurable differences in their ECG or echocardiogram findings compared with matched controls. There were also no associations with any heart disease phenotypes as assessed by PHeWAS. Overall, they report a prevalence of ARVC loss of function variants of around one in 435 in a general clinical population of predominantly European descent, but they did not find evidence that these variants associated with specific phenotypes. Thus, the clinical relevance of putative loss of function variants in desmosome genes still remains to be determined.                                                 The next paper is titled, “MRAS Variants Cause Cardiomyocyte Hypertrophy in Patients-specific iPSC-derived Cardiomyocytes”. Additional evidence for MRS as a definitive Noonan syndrome susceptibility gene. This comes from Erin Higgins, Michael Ackerman, and colleagues from the Mayo Clinic. They were interested in understanding whether a recently identified Noonan syndrome variant in the MRS gene was necessary and sufficient to cause Noonan syndrome with cardiac hypertrophy. They generated induced pluripotent STEM cell or IPS C lines from patient derived cells carrying the glycine 23 veiling variant and MRS. In addition to isogenic control cells where the pathogenic variant was corrected back to wild-type using CRISPR CAS nine gene editing, they also created a disease model cell line by introducing the MRS variant into unrelated control cells.                                                 They then comprehensively characterized the phenotypes of the three cell lines using a variety of approaches including microscopy, immunofluorescence, single cell RNA seek, Western blot, qPCR, and live cell calcium imaging. Both the patient derived and the disease model IPS cardiomyocytes were larger than control cells and demonstrated changes in gene expression and intracellular pathway signaling characteristic of cardiac hypertrophy. The patient and disease model cells also displayed impaired calcium handling. Through in-vitro phenotyping, the team was able to demonstrate that the glycine 23 veiling MRS variant elicits a cardiac hypertrophy phenotype and IPSC cardiomyocytes, that strongly suggests that this variant is responsible for the observed Noonan syndrome associated cardiac hypertrophy in the effected patients.                                                 Next up is a review from Christopher Lee, Iftikhar Kullo, and colleagues also from the Mayo Clinic on “New Case Detection by Cascade Testing in Familial Hypercholesterolemia: A Systematic Review of the Literature”. In this review they set out to systematically assess cascade testing programs for familial hypercholesterolemia, a disease which has a prevalence of about one and 250 but is estimated to be diagnosed in under 10% of patients. They identified published studies across the world which had conducted cascade testing and had reported the number of index cases and number of relatives tested and had also specified their methods of contacting relatives and testing.                                                 Using these criteria, they identified 10 studies for inclusion spanning several European countries, South Africa, New Zealand, Australia, and Brazil. The team calculated the proportion of relatives testing positive and the number of new cases per index case to facilitate comparison between studies. The mean number of programs was 242 with an average of 826 relatives per study. The average yield was 45%, ranging from 30 to 60%. the mean new cases per index case was 1.65 with a range of 0.22 to 8.0. Studies that use direct contact versus indirect contact for relatives and those that tested beyond first degree relatives had a greater yield. Further, active sample collection versus collection at clinic and using genetic testing versus biochemical testing was similarly associated with a higher yield. Despite differences between the United States and other countries, applying these strategies when establishing new cascade testing programs in the US may help promote success of these programs.                                                 Our next paper concerns “Randomization of Left-right Asymmetry and Congenital Heart Defects: The Role of DNAH5 in Humans and Mice”. And this was conducted by Tabea Nöthe-Menchen, Heymut Omran, and colleagues from University Children's Hospital Muenster and the PCD study group. They were interested in understanding the relationship between congenital heart defects and laterality defects where internal organs are atypically positioned, such as in a mirror image as occurs in situs inversus. Ciliary dyskinesia is thought to play a role in situs inversus and the most frequently mutated gene in primary ciliary dyskinesia is DNAH5. The team does hypothesize that DNAH5 mutations may play a role in congenital heart disease. They characterized phenotypes in 132 patients with primary ciliary dyskinesia carrying disease causing DNAH5 mutations and also studied left right access establishment using a DNAH5 mutant mouse model.                                                 66% of patients in their study had laterality defects, 88% of whom presented with situs inversus totalis and 6% presented with congenital heart disease. In the mass model, they observed immotile cilia, impaired flow with the left right organizer and randomization of nodal signaling with normal reversed or bilateral expression of key molecules. Their study thus demonstrates that mutation of DNAH5 is associated with congenital heart defects and they further highlight the ciliary mechanisms underlying defects and development of left right positioning during embryogenesis. Consideration of celiopathy related symptoms may be warranted when examining patients with congenital heart defects.                                                 Next up, we have a research letter from William Goodyear, Marco Perez and colleagues from Stanford University on “Broad Genetic Testing in a Clinical Setting Uncovers a High Prevalence of Titan Loss-of-Function Variants in Very Early-Onset Atrial Fibrillation”. They were interested in understanding genetic determinants of atrial fibrillation and hypothesized that causal genetic variants would be enriched in individuals with very early onset AF, who are diagnosed with AF under the age of 45 with no other significant comorbidities. They identified 25 families comprising 23 unrelated patients with very early onset AF who had been evaluated and received genetic counseling at Stanford between 2014 and 2018.                                                 The mean age of AF diagnosis was 27.2 years and 76% of patients were male. 40% of patients had a first or second degree relative with very early onset AF, while 36% at first or second degree relatives with either early onset idiopathic cardiomyopathy, unexplained sudden death or strokes. 85% of patients were identified as having at least one rare variant in a cardiomyopathy associated gene. Six patients carried actionable pathogenic or likely pathogenic variants, four of which were in the titan gene.                                                 A subset of individuals were further evaluated by MRI or computed tomography on average 817 days after their first presentation and this revealed high rates of cardiac abnormalities including reduced ventricular function, chamber enlargement, borderline LV non compaction, or late gadolinium enhancement. These were not noted on echocardiogram at presentation, suggesting there may have been subsequent disease development or progression. Overall, this study highlights a high rate of familial disease and implicates an association between very early onset AF and rare variants in titan before the clinical onset of cardiomyopathy.                                                 The final letter this month comes from Yu Xia, Shaoxian Chen, Ping Li, Jian Zhuang and colleagues from Guangdong Academy of Medical Sciences and is entitled, “A Novel Mutation in MYH6 in Two Unrelated Chinese Han Families with Familial Atrial Septal Defect”. They report on two unrelated families who presented with secundum atrial septal defect or ASD2. Whole exome sequencing revealed a novel variant and the MYH6 gene in both families, with the same variant present in all effected individuals but not in unaffected family members or unrelated controls. Because other variants in MYH6 have been reported to effect myofibril formation. The team studied the effect of the novel variant on the myofibrillar organization through transient transfection of CTC 12 cells. The MYH6 E526K variant was associated with a reduced striated I pattern and increased non-striated patterning. There was no effect on ATPase activity.                                                 Protein modeling suggested a variant of the effective position would reduce hydrogen bonding between alpha helices in the actin interface two region, increasing the volume of the cavity between the alpha helices and promoting the exposure of the alkaline side chain in the actin binding region. This could impair the interaction between the myosin motor head and actin. What these data suggests are that this novel MYH6 heterozygous variant may underlie ASD2 in two unrelated Chinese Han families by impairing myofibrillar organization.                                                 That's all for November 2019. Thank you for listening and I look forward to being back in December for the final episode of 2019.                                                 This podcast was brought to you by Circulation: Genomic and Precision Medicine and the American Heart Association council on genomic and precision medicine. This program is copyright American Heart Association 2019.

Sepsis is not an infection. Rather, it's your body's overwhelming reaction to an infection and can lead to some serious health issues. In fact, sepsis is the #1 cause of death for patients in hospitals. Sepsis definitions and protocols have been around for some time, but have been undergoing major changes. Additionally, sepsis is under scrutiny from CMS at the federal level and is subject to public reporting in many states. All of this, plus the importance of quickly diagnosing and treating the condition puts clinicians in a difficult spot. Many times they'll find themselves treating to the protocol, even when their clinical instincts suggest something else. In that regard, sepsis proves to be a very instructive topic in our never-ending quest to unravel the business of healthcare. On this episode, we'll talk with Michael Ackerman who's Director of the Master in Healthcare Innovation Program and Professor of Clinical Nursing at The Ohio State University. Michael is an expert on the topic who speaks on it across the country. He'll help us understand what we're up against and why it's so complicated from both a clinical and administrative standpoint. We discuss: What is sepsis? How is sepsis diagnosed? Why it's so important to diagnose and treat quickly. Why protocols and definitions continue to change. How new definitions of sepsis seem to be at odds with public reporting. How this impacts the clinicians and their ability to treat. How public reporting and media impact the approach. How proper identification and treatment impact healthcare costs. Why we need to focus on quality, but can't ignore the patient experience, the costs of care or the value that you bring to that care. What it all means to the patient and how we can protect ourselves. Why hospital administrators need to take the long-view. How a Sepsis-team can drive tremendous value to the hospital. The importance of incorporating new technology.   This episode originally aired on The #HCBiz Show! on May 3rd, 2017.   For more details visit DeepDive.tips

Jane Ferguson:                Hello, and welcome to Getting Personal, Omics of the Heart, your monthly podcast from Circulation: Genomic and Precision Medicine. I'm Jane Ferguson. It is August, 2019, and this is episode 31. Let's get started.                                            Our first paper comes from Freyja van Lint and Cynthia James, from University Medical Center Utrecht, and is entitled Arrhythmogenic Right Ventricular Cardiomyopathy-Associated Desmosomal Variants Are Rarely De Novo, Segregation and Haplotype Analysis of a Multinational Cohort. In this study, the team was interested in exploring variants that are associated with arrhythmogenic right ventricular cardiomyopathy or ARVC. ARVC is often attributable to pathogenic variants in genes encoding cardiac desmosomal proteins, but the origin of these variants had not been comprehensively studied.                                            The investigators identified ARVC probands meeting 2010 task force criteria from three ARVC registries in the United States and Europe and who had undergone sequencing of desmosomal genes. All 501 probands, 322 of them, or over 64%, carried a pathogenic or likely pathogenic variant in the desmosomal genes PKP2, DSP DSG2, DSC2, and JUP. The majority of these, over 75%, we're not unique with these variants occurring in more than one proband.                                            The team performed cascade screening and were able to identify the parental origin of almost all of the variants. However, they identified three de novo variants, including two whole gene deletions. They conducted haplotype analysis for 24 PKP2 variants across 183 seemingly unrelated families and concluded that all of these variants originated from common founders.                                            This analysis sheds light on the origin of variants in desmosomal genes and suggests that the vast majority of these ARVC variants originate from ancient founders with only a very small proportion of de novo variants. These data can inform clinical care particularly concerning genetic counseling and cascade screening of relatives.                                            The next paper continues a theme of cardiomyopathy and comes from Derk Frank, Ashraf Yusuf Rangrez, Corinna Friedrich, Sven Dittmann, Norbert Frey, Eric Schulze-Bahr and colleagues from University Medical Center Schleswig-Holstein. In this paper, Cardiac α-Actin Gene Mutation Causes Atrial-Septal Defects Associated with Late-Onset Dilated Cardiomyopathy, the team was interested in understanding the genetics of familial atrial-septal defect. They studied large multi-generational family with 78 family members and mapped a causal variant on chromosome 15q14, which caused nonsynonymous change in exon 5 of the ACTC1 gene.                                            In silico tools predicted this variant to be deleterious. Analysis of myocardial tissue from an affected individual revealed sarcomeric disarray, myofibrillar degeneration, and increased apoptosis. Proteomic analysis highlighted extracellular matrix proteins as being affected. The team over-expressed the mutation in rats and found structural defects and increased apoptosis in neonatal rat ventricular cardiomyocytes and confirmed defects in actin polymerization and turnover which affected contractility. These data implicate the variant in ACTC1 as causing atrial-septal defects and late-onset cardiomyopathy in this family and revealed the underlying molecular mechanisms affecting development and contractility.                                            The next paper is entitled Characterization of the CACNA1C-R518C Missense Mutation in the Pathobiology of Long-QT Syndrome Using Human Induced Pluripotent Stem Cell Cardiomyocytes Shows Action Potential Prolongation and L-Type Calcium Channel Perturbation, and it comes from Steven Estes, Michael Ackerman and colleagues at the Mayo Clinic. They set out to use patient-derived human induced pluripotent stem cells to understand the pathogenicity of a variant in the CACNA1C gene in Long-QT Syndrome.                                            They obtained cells from dermal punch biopsy from an individual with long-QT and a family history of sudden cardiac death who carried an R518C missense mutation in CACNA1C. Starting with fibroblasts, they reprogrammed the cells into iPSCs and then differentiated these into cardiomyocytes. They corrected the mutation back to wild type using CRISPR/Cas9 and then compared the cardiomyocytes carrying the original patient mutation with isogenic corrected cardiomyocyte controls. They found significant differences in action, potential duration, and in calcium handling.                                            Patch clamp analysis revealed increased L-type calcium channel window current in the original mutation-carrying cells in addition to slow decay time and increased late calcium current compared with the isogenic corrected control human iPSC cardiomyocytes. These data strongly suggest that CACNA1C is a long-QT susceptibility gene and demonstrate the potential in using patient-derived iPSCs and CRISPR/Cas9 to understand underlying mechanisms linking variants to disease.                                            The final paper this month is Blood Pressure-Associated Genetic Variants in the Natriuretic Peptide Receptor-1 Gene Modulate Guanylate Cyclase Activity and comes from Sara Vandenwijngaert, Chris Newton-Cheh and colleagues on behalf of the CHARGE+ Exome Chip Blood Pressure Consortium, the CHD Exome+ Consortium, the Exome BP Consortium, the GoT2D Consortium, the T2D-GENES Consortium, and the UK Biobank CardioMetabolic Consortium Blood Pressure Working Group.                                            This team wanted to understand how variants in the NPR-1 gene affect the function of the atrial natriuretic peptide receptor-1. They performed a meta-analysis across over 491,000 unrelated individuals, including both low frequency and rare variants in NPR-1 to identify their association with blood pressure. They identified three nonsynonymous variants associated with altered blood pressure at genome-wide significance and examined the function of these variants in vitro.                                            Using cells expressing either wild type NPR-1 or one of the three identified variants, they explored the impact of the variants on the ability of cells to catalyzes the conversion of guanosine triphosphate to cyclic 3′,5′-guanosine monophosphate in response to binding of atrial or brain natriuretic peptide. Increased levels of cyclic GMP are known to decrease blood pressure by inducing by natriuresis, diuresis, and vasodilation.                                            Two variants which associated with high blood pressure in the population meta-analysis were associated with decreased cyclic GMP in response to ANP or BNP in vitro, while one variant which associated with lower blood pressure in humans was associated with higher cyclic GMP production in vitro. These data show that variants affecting loss or gain of function in guanylate cyclase activity could have downstream effects on blood pressure at the population level.                                            That's it for this month. Thank you for listening. We will be back with more next month. This podcast was brought to you by Circulation: Genomic and Precision Medicine and the American Heart Association Council on Genomic and Precision Medicine. This program is copyright American Heart Association 2019.  

Jane Ferguson:  Hi, everyone. Welcome to Getting Personal: Omics of the Heart, the podcast from Circulation: Genomic and Precision Medicine. It's May 2019, and this is episode 28. So let's see what papers we have in the journal this month.                              First up, a paper from Mengyao Yu, Nabila Bouatia-Naji and colleagues from the Inserm Cardiovascular Research Center in Paris, entitled GWAS-Driven Gene-set Analyses, Genetic and Functional Follow-Up Suggest Glis1 as a Susceptibility Gene for Mitral Valve Prolapse.                              In this paper, they set out to characterize the genetic contributions to mitral valve prolapse, or MVP, to better understand the biological mechanisms underlying disease. They applied the gene-set enrichment analysis for QWAS tool and the pathway enrichment tool DEPICT to existing GWAS for MVP in a French sample to identify gene sets associated with MVP. They find significant enrichment of genes involved in pathways of relevance to valve biology and enrichment for gene expression in tissues of relevance to cardiovascular disease.                              They zeroed in a Glis family zinc finger gene Glis1 with consistently strong pattern of evidence across the GWAS enrichment and transcription analyses. They replicated the association between Glis1 and MVP in a UK biobank sample. They found that Glis1 is expressed in valvular cells during embryonic development in mice, but is mostly absent at later times. They targeted two Glis1 orthologs in zebrafish and found that knockdown of Glis1 B was associated with a significant increase in the incidence of severe atrioventricular regurgitation. These data highlight Glis1 as a potential regulator of cardiac valve development with relevance for risk of mitral valve prolapse.                              Next up is a paper from Gina Peloso, Akihiro Namuro, Sek Kathiresan and colleagues from Boston University, Kanazawa University, and Mass General Hospital. In their paper, Rare Protein Truncating Variance in APOB, Lower LDL-C, and Protection Against Coronary Heart Disease, the team was interested in understanding whether protein truncating variance in APOB underlying familial hypobetalipoproteinemia confer any protection against coronary heart disease.                              They sequenced the APOB gene in 29 Japanese families with hypobetalipoproteinemia as well as in over 57,000 individuals, some with early onset CHD and some without CHD. They found that presence of an APOB truncating variant was associated with lower LDL cholesterol and lower triglycerides, and also with significantly lower risk for coronary heart disease. This study confirms that variance in APOB, leading to reduced LDL and triglycerides are also protective against coronary heart disease. :                            The next paper entitled Mortality Risk Associated with Truncating Founder Mutations in Titin comes to us from Mark Jansen, Dennis Dooijes, and colleagues from University Medical Center Utrecht. They analyzed the effect of titin truncating variance on mortality in Dutch families. Titin truncating variants are associated with dilated cardiomyopathy, but have a very variable penetrance.                              In this study, the authors looked at three titin truncating variants, established to be founder mutations, and traced the pedigrees back to 18th century ancestors. They looked at 61 individuals on the transmission line and 360 of their first-degree relatives. They find no evidence for excess mortality in variant carriers overall. However, when they restrict it to individuals over 60 years of age, they did find a significant difference in mortality, which was also observed in individuals born after 1965. What these data tell us is that these titin truncating variants have a relatively mild phenotype with effects on mortality only manifesting later in life in many carriers. Given increases in life expectancy over the past several decades, the prevalence of morbidity and mortality attributable to titin truncating variants may increase. Genetic screening may identify genotype-positive, phenotype-negative individuals who would benefit from preventative interventions.                              Continuing on the theme of genetic variance, we have a paper from John Giudicessi, Michael Ackerman, and colleagues from the Mayo Clinic, Assessment and Validation of a Phenotype-Enhanced Variant Classification Framework to Promote or Demote RYR2 Missense Variants of Uncertain Significance. In this paper, they aim to find a better way to classify variants of unknown significance, of VUS, in the RYR2 gene. Variants in this gene are commonly associated with catecholaminergic polymorphic ventricular tachycardia, or CPVT.                              They examined 72 distinct variants in 84 Mayo Clinic cases and find that 48% were classified as VUS under ACMG guidelines. The rate was similar in a second sample from the Netherlands, with 42% of variants originally classified as VUS. They developed a diagnostic scorecard to incorporate a pretest clinical probability of CPVT, which included various clinical criteria, including symptoms and stress test results. Application of the phenotype enhanced ACMG criteria brought the VUS rate down to 7% in Mayo Clinic and 9% in the Dutch samples. The majority of VUS were reclassified as likely pathogenic.                              This study highlights how incorporation of disease-specific phenotype information can help to improve variant classification and reduce the ambiguity of reporting variants of unknown significance.                              We also have a number of research letters in the journal this month. From Karine Ngoyen, Gilbert Habib, and coauthors from Marseilles, we have a paper entitled Whole Exome Sequencing Reveals a Large Genetic Heterogeneity and Revisits the Causes of Hypertrophic Cardiomyopathy, Experience of a Multicentric study of 200 French Patients. In this study, they examined the genetic contributions to hypertrophic cardiomyopathy, or HCM, in 200 individuals as part of the HYPERGEN study and compared the benefits of whole exome sequencing compared with targeted sequencing of candidates' sarcomeric genes. All subjects had HCM documented by echocardiography.                              In the whole exome sequencing data, they first looked for mutations within 167 genes known to be involved in cardiomyopathies or other hereditary diseases. Of these 167 virtual panel genes, they find variants in 101 genes. Following whole exome sequencing, over 87% of the patients had an identified pathogenic, or likely pathogenic, mutation compared with only 35% of patients who only had targeted sequencing of sarcomeric genes.                              This highlights the generic heterogeneity of HCM and suggests that whole exome sequencing has utility in identifying variants not covered by sarcomeric gene panels.                              The next letter is from Wouter Te Rijdt, Martin [Vandenberg] and colleagues from University Medical Center Groningen and states that [dissynchronopathy] can be a manifestation of heritable cardiomyopathy. They hypothesized that left bundle branch block, also designated as dissynchronopathy, may be a manifestation of familial cardiomyopathy.                              They analyzed patients from a database of cardiac resynchronization therapy and identified super-responders whose left ventricular dysfunction was normalized by therapy. They carried out targeted sequencing in 60 known cardiomyopathy genes in 16 of these super-responder individuals and identified several variants, including a pathogenic variant in troponin T in one individual and variants of unknown significance in nine individuals. Pedigree analysis identified multiple family members with dilated cardiomyopathy.                              This study highlights that dissynchronopathy can be a manifestation of DCM, but that affected individuals may still benefit from cardiac resynchronization therapy.                              The next letter entitled Targeted Long-Read RNA Sequencing Demonstrates Transcriptional Diversity Driven by Splice-Site Variation in MYBPC3 comes from Alexandra Dainis, Euan Ashley, and colleagues from Stanford University. They set out to understand whether transcriptome sequencing could improve the diagnostic yield over genome sequencing in patients with hypertrophic cardiomyopathy. In particular, they hypothesized that long-read sequencing would allow for identification of alternative splicing linked to disease variance. They used long-read RNA and DNA sequencing to target the MYBPC3 gene in an individual with severe HCM who carried a putative splice-site altering variant in the gene. They were able to obtain heart tissue for sequencing and included several HCM and control subjects in addition to the patient with the MYBPC3 variant.                              They identified several novel isoforms that were only present in the patient sample, as well as some additional isoforms, including retained introns, extended exons, and an additional cryptic exon, which would not have been predicted based on the DNA variant. While the effects on protein function is not known, the transcripts are predicted to be translated.                              This analysis highlights the effect of a rare variant on transcription of MYBPC3 and provides additional evidence to link the variant to disease. This is a really nice approach, which could be used to probe causality and mechanisms, not only for cardiovascular disease, but for other rare variants in many disease settings.                              We finish with a perspective piece from Nosheen Reza, Anjali Owens, and coauthors from the University of Pennsylvania entitled Good Intentions Gone Bad, The Dangers of Sponsored Personalized Genomics. They present a case of a 23-year-old woman who presented for genetic counseling and evaluation after discovering she carried a likely pathogenic MYH7 variant associated with cardiomyopathy. She had no significant medical history, but had participated in employer-sponsored genetic testing motivated to identify potential variants related to cancer given a family history of cancer.                              After receiving her results, she experienced considerable anxiety and stopped exercising out of fear of cardiac complications. She visited an ER after experiencing chest pain, something she had not experienced previously. There was no appropriate counseling available at her institution for her genetic test results, leading her to seek out the additional counseling. Thus, while she was initially motivated to complete genetic testing because her employer offered it free of change, she ended up incurring costs related to the followup evaluation and counseling. Ultimately, she had no significant clinical findings. Although the variant had been listed as likely pathogenic, other sources consider it to be of unknown significance.                              This story highlights the psychological and financial impact that genetic testing can have on individuals, particularly when carried out without any pretest counseling or accessible post-test support when variants are identified.                              Despite the considerable promise of personalized medicine, there are many complexities to be considered, particularly with direct-to-consumer testing and employer-sponsored testing. This perspective highlights the ethical considerations and urges caution to maintain the best interests of patients.                              That's all for this month. Thanks for listening. I look forward to bringing you more next month.                              This podcast was brought to you by Circulation Genomic and Precision Medicine and the American Heart Association Council on Genomic and Precision Medicine. This program is copyright American Heart Association 2019.  

Jane Ferguson:                Hi everybody. Welcome to Episode 25. I'm Jane Ferguson. This is Getting Personal: Omics of the Heart, the podcast from Circulation: Genomic and Precision Medicine, and it is February 2019. Let's get started.                                            The first paper this issue is a concurrent publication and comes to us from 29 different editors-in-chief of 27 major cardiovascular journals, led by Joseph Hill, editor-in-chief of Circulation. This editorial, entitled Medical Misinformation: Vet the Message! gives a pointed reminder of the real life risks of misinformation that spreads rapidly through social media and influences people who are making crucial decisions about healthcare for themselves and their families. Quoting directly from the paper they say, "We, the editors-in-chief of the major cardiovascular scientific journals around the globe, sound the alarm that human lives are at stake. People who decline to use a statin when recommended by their doctor, or parents who withhold vaccines from their children, put lives in harm’s way."                                            In this editorial they call on those in the media to do a better job of taking responsibility for the information they disseminate. In particular, in evaluating content before disseminating it, and avoiding false equivalencies where overwhelming scientific evidence favors one side of the so called "debate." I'll add to that that those of us who are medical or scientific professionals need to do our best to take the time to explain our science to those around us. The science underlying most of medicine is complex and hard to explain and sometimes incomplete, but we do a disservice to people if we don't at least try. Let's all join the editors in calling everyone to vet information and hold those with power in the media accountable for the spread of misinformation they enable.                                            Next up this issue, a paper from Jody Ingles, Birgit Funke, and co-authors from the University of Sydney, Harvard Medical School and others, entitled Evaluating the Clinical Validity of Hypertrophic Cardiomyopathy Genes. As panels for clinical genetic testing expands to include more genes, there are more and more variants that are detected and reported to patients, but do not necessarily have underlying evidence to support or disprove pathogenicity. This group aimed to systematically assess the validity of potential gene disease associations with hypertrophic cardiomyopathy and left ventricular hypertrophy by curating variants based on multiple lines of genetic and experimental evidence.                                            They categorized genes based on the strength of evidence of disease causation and reviewed HCM variant classification in the ClinVar variant and phenotype repository. They selected 57 genes to study based on those which were frequently included on test panels or had previous reports of association with HCM. Of HCM genes, only 24% were characterized as having definitive evidence for disease causation, 10% of the genes had moderate evidence, while 66% had limited or no evidence for disease causation. Of syndromic genes, 50% were definitively associated with left ventricular hypertrophy. Of over 4,000 HCM variants in ClinVar, 31% were in genes that, on review, had limited or no evidence for association with disease.                                            What this study shows is that many genes that are included on panels for diagnostic testing for HCM actually have little evidence for any relationship to disease. Systematic curation is required to improve the accuracy of information being acquired and reported to patients and families with HCM.                                            Moving on to the next paper. This manuscript describes the international Triadin Knockout Syndrome Registry: The Clinical Phenotype and Treatment Outcomes of Patients with Triadin Knockout Syndrome. It comes from Daniel Clemens, Michael Ackerman and colleagues from the Mayo Clinic. So, Triadin Knockout Syndrome is a rare inherited arrhythmia syndrome and it is caused by recessive null mutations in the cardiac triadin gene. To improve the ability to study this rare syndrome, this group established the International Triadin Knockout Syndrome Registry, with the goal of including patients across the world with homozygous or compound heterozygous triadin null mutations. The registry currently includes 21 patients from 16 families who have been carefully phenotyped and many of whom exhibit T wave inversions and have transient QTC prolongation.                                            The average age for first presentation with cardiac arrest or syncope was three years of age. Despite a variety of treatments, the majority still have recurrent breakthrough cardiac events. These data highlight the importance of conducting testing for triadin mutations in patients, particularly young children presenting with cardiac arrest, and as this registry grows it will enable a better understanding of the disease and hopefully pave the way for future triadin gene therapy trials.                                            The next paper comes from Daiane Hemerich, Folkert Asselbergs and colleagues from Utrecht University, and is entitled Integrative Functional Annotation of 52 Genetic Loci Influencing Myocardial Mass Identifies Candidate Regulatory Variants and Target Genes. They were interested in whether variants that have been associated with myocardial mass may exert their influence through regulatory elements. They analyze the hearts of hypertrophic cardiomyopathy patients and non-disease controls and ran ChIP-seq in 14 patients and 4 controls and RNA-seq in 11 patients and 11 controls.                                            They selected 52 loci that have been associated with electric cardiogram defined abnormalities in amplitude and duration of the QRS complex and looked specifically at these gene regions. They found differential expression of over 2,700 different genes between HCM and control. They further found differential acetylation over 7,000 regions. They identified over 1000 super enhancers that were unique to the HCM samples. They found significant enrichment for differential regulation between disease and control hearts within the loci previously associated with HCM, compared with loci not associated with HCM. They analyzed regions where putative causal SNPs overlapped regulatory regions, and identified 74 co-localized variants within 20 loci, with particular enrichment for SNPs in differentially expressed promoters. They confirmed associations with 18 previously implicated genes, as well as identifying 14 new genes. Overall, what this study demonstrates is that by looking at regulatory features that differ in affected tissues between disease and healthy individuals, we can learn more about the underlying mechanisms of disease.                                            Moving on, we have a paper entitled Interleukin-6 Receptor Signalling and Abdominal Aortic Aneurysm Growth Rates from Ellie Paige, Marc Clément, Daniel Freitag, Dirk Paul, Ziad Mallatt and colleagues from the University of Cambridge. They aimed to investigate a specific SNP in the Interleukin-6 receptor rs2228145, which has been associated with abdominal aortic aneurysms. Inflammation is thought to be a contributor to aneurism progression. The authors hypothesized that the IL-6 receptor's SNP may affect aneurysm growth. They use data from over 2,800 subjects from nine different prospective cohorts and examine the effect of genotype on annual change in aneurysm diameter. Although there was a significant association between genotype and baseline aneurysm size, there was no statistically significant association with growth over time. It appeared that growth was less in minor allele carriers, but the effect if true, was small and the analyses were not powered for small effect sizes.                                            Sample sizes are limited for cohorts with abdominal aortic aneurysms and the authors already used all available worldwide data. In complimentary experiments in mice, they examined the effect of blocking the IL-6 receptor pathway. They found that selective blockage of the IL-6 trans-signaling pathway mediated by soluble IL-6 receptor was associated with improved survival in two different mouse models. However, blocking the classical membrane-bound IL-6 signaling pathway in addition to the trans-signaling pathway did not lead to improved survival. Although the severe lack of enough subjects for well powered genetic analyses is a major limitation for the study of abdominal aortic aneurism and humans, this paper demonstrates the potential relevance of the IL-6 trans-signaling pathway and aneurysm growth, and suggests that further interrogation of this pathway may be informative in figuring out new ways to prevent aneurysm progression and rupture.                                            Next, we have the first of two research letters this issue. The letter on Common Genetic Variation in Relation to Brachial Vascular Dimensions and Flow-Mediated Vasodilation comes to us from Marcus Dorr, Renate Schnabel and co-authors from several institutions including University Heart Center in Hamburg. They were interested in gaining a better understanding of the genetics underlying vascular function. They ran a meta-analysis of brachial artery diameter, maximum brachial artery diameter adjusted for baseline diameter, and flow-mediated dilation in over 17,000 individuals of European ancestry from six different GWA studies. They sought to replicate findings in over 9,500 newly genotyped individuals. They identified two novel SNPs for baseline brachial artery diameter, but no SNPs reached significance or replication from maximum brachial artery diameter or flow-mediated dilation. One of the significant SNPs was located in the insulin-like growth factor binding protein 3, or IGFBP-3 gene. They analyzed plasma IGFBP-3 protein levels in 1,400 individuals and found a significant association with brachial artery diameter.                                            The second SNP they identified is located within the AS3MT gene for arsenite methyltransferase, and this SNP appears to be an eQTL for AS3MT expression in monocytes and arterial tissue. Along with identifying these two genes with potential involvement in baseline brachial artery diameter, this study also supports a low genetic component to flow-mediated dilation, indicating that environmental factors may be or more influential in FMD.                                            The final research letter comes from Alexis Williams, Craig Lee and colleagues from the University of North Carolina and is entitled CYP2C19 Genotype-Guided Antiplatelet Therapy and 30-Day Outcomes After Percutaneous Coronary Intervention. It is known that loss of function variants in CYP2C19 effect bioactivation of clopidogrel, and CYP2C19 genotyping is increasingly used to guide antiplatelet therapies. The authors were interested in whether genotype-guided therapy is effective in reducing major adverse cardiovascular events in the short term, specifically in the 30 days following percutaneous coronary intervention, when most MACE occurs. They followed over a thousand individuals undergoing PCI and CYP2C19 testing and looked at atherothrombotic and bleeding outcomes. Consistent with implementation of genotype-guided therapy, individuals carrying loss of function alleles were less likely to be prescribed clopidogrel.                                            However, out of loss of function carriers, those who did take clopidogrel had significantly higher risk of MACE with no difference in bleeding risk. There was no difference by therapy in individuals without a loss of function allele. What this study shows us is that even in the 30 days following PCI, genotype-guided therapy can be effective in protecting individuals carrying loss of function CYP2C19 variants.                                            And that's it from us for February. Go online to ahajournals.org/journal/circgen to read the full papers, access videos and more, and of course to delve into the podcast archives. Thank you for listening and I look forward to bringing you more next month. This podcast was brought to you by Circulation: Genomic and Precision Medicine and the American Heart Association Council on Genomic and Precision Medicine. This program is copyright American Heart Association 2019.  

Michael Ackerman, Joe Bagwell, Madison Rice and Alex Winkler examine the corruption surrounding the FIFA World Cup.

Dr Carolyn Lam:                Welcome to Circulation on The Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. This week's issue is so special. It is an autopsy issue. I think it's actually the first of its kind in the history of Circulation. I am so pleased to have with me today Dr Jeffrey Saffitz from Beth Israel Deaconess Medical Center, who's the content editor for Pathology for Circulation and the guest editor for this entire autopsy issue. Welcome, Jeff. Dr Jeffrey Saffitz:             Thank you. Dr Carolyn Lam:                We also have Dr Lee Goldman from Columbia University Medical Center who wrote a beautiful perspective piece on autopsy. Thank you and welcome, Lee. Dr Lee Goldman:              Morning. Dr Carolyn Lam:                Jeff, could you start us off? I mean, an autopsy issue. How in the world did this come about? Dr Jeffrey Saffitz:             I think it really began by coincidence. The journal received submissions from several authors, each involving studies of autopsies, and the editors approached me and asked if we might consider grouping them together in a special issue focused on the role of the autopsy and cardiovascular medicine. I thought that would be a very interesting idea and this evolved into actually something much greater. Two additional papers came in focusing on the autopsy and I think looking at these papers in the aggregate, they represent what we can now consider to be the contemporary utility of the autopsy in understanding the way cardiovascular disease works. So I was particularly pleased that the editors agreed to group these papers into a single issue focused on the autopsy. We were really delighted that Lee Goldman agreed to write a perspective. He has had a longstanding history of studying the role of the autopsy and I hope the readers will find this to be a really interesting and useful issue which will, I hope, chart the course for future discovery. Dr Carolyn Lam:                Just listening to you, I love the way you say it's a contemporary look at autopsy. I mean, we covered things like molecular genetic, proteomic, autopsies, even like electronic autopsies using device. That's really cool. Lee, thank you again for sharing your time and incredible perspectives with us. The long history of autopsy. Do you think it's still necessary now? Dr Lee Goldman:              Maybe give some perspective. I first got involved in this a number of decades ago, when as a junior faculty member, I was assigned to be on the medical audit committee of the hospital where I saw patients as a cardiologist. And two of the senior people in the committee got into a debate about whether autopsies were still important given the advent of CT scans and other modern diagnostic technology. And to listen to them debate for 15 or 20 minutes, I finally had the temerity to pipe in and say we can actually study this, and so we did. We looked at autopsies in three different decades: 1960, 1970, 1980, and much to everyone's surprise, I think found, A. that the rate of which autopsies found diagnoses that doctors had missed and for which treatment would almost certainly have prolonged life was about 10 percent, and it was 10 percent, 1960, 10 percent, 1970, 10 percent, 1980.                                                 But the difference was that doctors were missing different diagnoses. The things that got missed in 1960, and where autopsies showed there were being missed led to better diagnostic approaches and those things were rarely missed in 1980. But since people stayed alive longer, they got new things that we didn't really know much about in 1960. A big difference, fewer people missed heart attacks, pulmonary emboli, and things of that sort, but far more people had missed infections, especially fungal infections that were complication of multiple antibiotics or immunosuppressive therapies.                                                 And so, as I followed this in 1980, if you will, to now, 2018, we find this gets recapitulated over and over again. Medicine moves forward, things we used to miss, we no longer miss, but people still die, and they still die from things that we don't always diagnose. We've done statistical analyses to show that probably the rate of misdiagnosis is going down a little bit, but it's still substantial and we still estimate that thousands of people each year die in the U.S. from things that are not what the doctors thought they had, and if that diagnosis had been made, the patient would have lived longer. Dr Carolyn Lam:                Lee, I just love that perspective. I have to say, it's really humbling. I mean, 1960s and so on would predate me as well, so I'm really humbled, and I love that reminder. Jeff, in fact, quite a number of our papers illustrate exactly what Lee said. We have four papers just dealing with sudden cardiac death, and that is still what diagnosis was struggled with. Could you tell us a little bit more about those? Dr Jeffrey Saffitz:             Yes, of course. I think we all recognize that sudden death remains a huge public health issue. We also realize that most people who die suddenly and unexpectedly don't do so in the hospital when they're being followed and monitored; rather, they die out in the community, and in many cases, these are individuals in whom major risk for coronary disease or other potentially lethal cardiovascular conditions was really not known. So I think it remains a major public health issue, and we still have a great deal to learn. So perhaps it's not surprising that four of the five papers involved autopsy studies of sudden death victims of individuals who died out in the community. A couple of them focused on sudden death in young people.                                                 We know that these individuals often will have familial diseases, and the autopsy has been one mechanism for studying these individuals, so one of the papers from Michael Ackerman at Mayo Clinic, advanced the concept that they started many years ago, the so-called molecular autopsy in which they apply a whole exome sequencing in cases of sudden unexpected death in young people defined here as age under 40, and they identified some rare variants which were likely to be of potential pathogenic significance in sudden death. A related paper from Junttila et al in Finland looks at the finding of myocardial fibrosis in young victims of sudden death. They identified several cases in which that was the only structural change in the myocardium, and when they applied next gen sequencing, the identified variance that we typically associate with the familial non-ischemic cardiomyopathies, arrhythmogenic, dilated, and hypertrophic cardiomyopathy. But the key insight here is that we traditionally think of these diseases as having rather characteristic structural changes which we can recognize at autopsy. What they showed is that those structural changes might be limited to nothing more than some fibrosis. And so the key here is that this expands our potential opportunity to recognize these familial cardiomyopathies, and the overarching idea is we use the autopsy to serve the living. This is a way to gain information at autopsy that we can then use to help family members and other individuals by virtue of the insights gained at autopsy. Dr Lee Goldman:              When we did the estimates in my editorial, and I estimated that roughly 28,000 people die each year in America with diagnoses that doctors missed and for which treatment would have been different if they hadn't missed it, that's really based on, I'll call traditional autopsy methods, which are anatomical, include microscopic evaluation, include culture, but it's not historically included genetic testing. I believe, as these articles show, that the advent of genetic testing, which you could argue could have been done while the patient was alive, but we're not quite there yet in terms of testing everyone's genome, now help you autopsies find even more things that might've been missed. And as you just heard, also can have important information for the family. So, one of the issues you often get into in autopsies is what's in it for the family, and one of the problems here is that the pathologists don't get paid. For the family members, it's mostly an aggravation. The doctors are worried they're going to get sued if something that gets found. And so, to make this work you need to bring in some incentives. Doctors not getting sued if they find things because they should get credit for trying to learn more, some way to reimburse reasonably pathologists and hospitals who do the autopsies, and the understanding of family members that they not only will perhaps be more reassured about what happens to the loved one, but also may learn things that will affect their future, because certainly, these cardiomyopathies, instead of them being diagnosed, are familial and oftentimes will lead to testing and hopefully interventions in family members that'll be to their benefit. Dr Carolyn Lam:                Lee, what great comments about bringing this into the clinical perspective and I just love what you said, Jeff, about autopsy for the living. That is just a quotable quote. That's so cool. I noticed that you did ask Dr Judge to write an editorial specifically about bringing autopsies into the molecular genetic era. So I just want to encourage all our listeners to make sure you read that as well. But Jeff, back to you about the other two papers. Dr Jeffrey Saffitz:             Well, I think one that I found particularly significant is this idea that nowadays, patients come to autopsy with implantable cardiac electronic devices, and the point of this paper is that interrogation of these devices postmortem can provide really important information about the cause and timing of those deaths. I think the reality is that most pathologists who do these autopsies are entirely unprepared or ill equipped to do such interrogations, and so I think the point of this paper is simply to encourage pathologists who do these autopsies to develop partnerships and relationships with cardiologists who are able to get this type of information from these devices. And again, it not only provides information about what happened to that one individual and what the death was all about, but it provides important information to the family and potentially information that allows the family to recognize particular risks that might impact the living members. So I thought this was just another really interesting example of how information that is potentially available at autopsy may not be fully utilized, and I hope that this paper will have an impact in that regard. Dr Carolyn Lam:                That's great. Lee, did you have any perspectives on devices and its role in autopsy now? Dr Lee Goldman:              I guess that the point that I would just reinforce would be that diagnostic technologies, including the ability to monitor someone's heart rate, have helped us diagnose things that were missed in previous eras, but medicine is always pushing the frontier forward, and as long as we develop new therapies, develop new devices, there'll be new things to learn. I want to make one other point about what I'll call overconfidence in diagnoses. The published statistics for the accuracy of most diagnostic tests are based on what doctors think the diagnosis ends up being, not the autopsy, which is the ultimate gold standard. So, if you actually go through some not-so-complicated arithmetic, you'll find that many of the tests that we think are almost perfect at finding things really aren't because the people who die with those things found that autopsies that the test missed. There's something called a virtuous circle, there's also a vicious cycle. There's a bit of a vicious cycle here that if you don't do autopsies to be sure you aren't missing things, you become overconfident in the tests that you think are finding them, and therefore think you already know everything and don't need to do an autopsy. To me, in some ways, that's the most perverse result of the plummeting autopsy rate, which, by the way, can be linked directly to changes in how hospitals get accredited, that in prior years there was a minimal autopsy rate required for accreditation. When that was removed, not surprisingly, autopsy rates plummeted, and now, most autopsies done in the US are not done in hospitals because doctors aren't sure what's going on. They've done by medical examiners as part of the laws for autopsies least being considered and people who die without having had a medical attention to some degree. Dr Jeffrey Saffitz:             You are exactly right on all of these points. I'll just say this is the point of one of the other papers from Tseng et al. This was a prospective autopsy study of sudden death in the city and county of San Francisco, and what they showed here is that only about half of the deaths that were considered to be sudden cardiac deaths as defined by the conventional criteria actually turned out to be deaths due to a rhythmic disorder. So Lee's point is exactly right. Doctors think they know a lot of things, but they're not always right about that, and the autopsy is probably one of the best ways to bring some quality control to this, and to really provide, I think, objective data that often is the case flies in the face of what the previous thinking was, and I think this paper in this issue of Circulation really brings that point home very clearly. Dr Carolyn Lam:                Yikes. OK, so here I am, I practice in Asia, and I think the autopsy rates are even lower, so this is a great wake up call for me just listening. Let's switch gears a little bit. How about the paper by Dr Herrington? Now this goes to a proteomic bisection almost of maybe preclinical disease and atherosclerosis. Would you like to comment on that on, Jeff? Dr Jeffrey Saffitz:             In the perspective that I wrote with Gaetano Thiene, in addition to looking at the history of the autopsy, we looked to the future and just considered briefly what role will the autopsy play going forward, and I think the paper by Herrington is a great example of how we can use the autopsy to learn so much more about the way human disease works. The basic idea here is that something like coronary artery disease or atherosclerosis, we think of as being a disease that only involves the blood vessels, and we tend not to recognize it until it is rather advanced and clinically manifest, but we recognize that these diseases begin decades before they become clinically manifest. We really don't know how to identify the earliest antecedents, and without knowing that we really, I think, very much limit our ability to identify the disease way early before it becomes clinically manifest, and then be able to practice preventive measures and intervene to prevent the disease from occurring.                                                 So, what this paper showed is that it's an application of high-throughput proteomics looking at coronary artery and aortic samples obtained at autopsy, and these authors identified particular changes in proteins that they then were able to show in a prospective independent clinical cohort were able to predict the development of coronary artery disease. So I think going forward, we are going to redefine our understanding of human disease by learning about its earliest expressions and its full systemic distribution, and in doing so, we'll be much better prepared to diagnose earlier and intervene and prevent disease. So I think this was a great example of how the autopsy can help in that effort. Dr Carolyn Lam:                I feel like we are going full circle in history and going back to learn about how to go forward. I don't know if I expressed that well, but I am just in awe of what I've learned from both of you. Thank you so much, Jeff, for putting together this amazing issue, and thank you so much, Lee, for sharing your perspectives. Thank you, audience, for joining us this week. You've been listening to Circulation On The Run. Don't forget to tune in again next week.  

Sepsis is not an infection. Rather, it's your bodies overwhelming reaction to an infection and can lead to some serious health issues. In fact, sepsis is the #1 cause of death for patients in hospitals. Sepsis definitions and protocols have been around for some time, but have been undergoing major changes. Additionally, sepsis is under scrutiny from CMS at the federal level and is subject to public reporting in many states. All of this, plus the importance of quickly diagnosing and treating the condition puts clinicians in a difficult spot. Many times they'll find themselves treating to the protocol, even when their clinical instincts suggest something else. In that regard, sepsis proves to be a very instructive topic in our never-ending quest to unravel the business of healthcare. On this episode, we'll talk with Michael Ackerman who's an Acute Care Nurse Practitioner and an Associate Director and Professor at Niagara University School of Nursing. Michael is an expert on the topic who speaks on it across the country. He'll help us understand what we're up against and why it's so complicated from both a clinical and administrative standpoint. We discuss: What is sepsis? How is sepsis diagnosed? Why it's so important to diagnose and treat quickly. Why protocols and definitions continue to change. How new definitions of sepsis seem to be at odds with public reporting. How this impacts the clinicians and their ability to treat. How public reporting and media impact the approach. How proper identification and treatment impact healthcare costs. Why we need to focus on quality, but can't ignore the patient experience, the costs of care or the value that you bring to that care. What it all means to the patient and how we can protect ourselves. Why hospital administrators need to take the long-view. How a Sepsis-team can drive tremendous value to the hospital. The importance of incorporating new technology.   Weekly Updates If you like what we're doing here, then please consider signing up for our weekly newsletter. You'll get one email from me each week detailing: New podcast episodes and blog posts. Content or ideas that I've found valuable in the past week. Insider info about the show like stats, upcoming episodes and future plans that I won't put anywhere else. Plain text and straight from the heart :) No SPAM or fancy graphics and you can unsubscribe with a single click anytime. Michael Ackerman's Background: Michael (Mike) Ackerman has held just about every role nurse could; from Candy Striper to Senior Director. His entire career has been in the critical care arena from staff nurse, nurse manager, clinical nurse specialist, nurse practitioner and most recently senior director of nursing.  He has over 50 publications as well as several funded studies. In addition, he has held leadership roles in academia. Mike has a passion for critical care nursing. This is evident in his much sought after presentations on a variety of critical care topics. He also has a passion for the “Crucial Conversations” program which he has implemented in two of his recent institutions. This implementation has been a catalyst in much of Mike's work in the area of culture change. Mike is a skilled clinician, avid researcher, motivational speaker and caring leader. Leading from the bedside has been a consistent theme in Mike's career. Check out Mike's facebook group: Stop the Silence in Healthcare and learn more about him here: www.ackermanhealthcareconsulting.com Michael will be speaking at The National Teaching Institute & Critical Care Exposition in Houston from May 22-25. Mentioned on the Show Mike mentioned a book on the episode called Take this Book to the Hospital With You. It's a consumer guide to surviving your hospital stay. I've never read that one, but I'm currently reading The Patient Survival Guide: 8 simple solutions to prevent hospital and healthcare-associated infections by a friend of the show Dr. Maryanne McGuckin and Toni L. Goldfarb. Doctor Turns Up Possible Treatment For Deadly Sepsis - Dr. Paul Marik uses Vitamin C to treat Sepsis cases with great success. Sepsis Alliance - On a mission to save lives and reduce suffering by raising awareness of Sepsis as a medical emergency. About the Infection Prevention and Control Series This episode is part of The #HCBiz Show's Infection Prevention and Control (IPAC) series. We'd like to thank our partners InfectionControl.tips and the Center of Excellence for Infection Prevention and Control (COE IPAC) for their support and guidance with the series. About InfectionControl.tips InfectionControl.tips is a Pan-Access journal that extends globally and touches locally. www.IC.tips is: Free to Publish. Free to Access and provides Accessible Scientific Services. About Center of Excellence for Infection Prevention and Control (COE IPAC) Center of Excellence for Infection Prevention and Control (COE IPAC) is a collaborative effort to accelerate and support new solutions that hold the promise of significantly advancing infection prevention and control. On a quarterly basis, the Center of Excellence will evaluate at least 3 international innovations – giving them access to independent testing, publication as well as a US commercialization site The #HCBiz Show! is produced by Glide Health IT, LLC in partnership with Netspective Media.   Soundtrack credit: Acid Lounge by FoolBoyMedia

Det. Dan Ferrin from the Miami-Dade Metro Police Department joins us to discuss their incredible program Project HERO. We wish every department across the U.S. would implement this program. Also joining us will be Deputy Michael Ackerman from the Charleston County Sheriff's Department, S.C. He'll talk about his recovery from a violent critical incident, in which his partner was killed and he suffered a severe Gun Shot Wound from an AK-47. Michael also discusses his recovery from PTSD and the amazing things that he and the Charleston County Sheriff's Department are doing to help Law Enforcement Officers across the United States. Background song Hurricane used by permission from the band Dark Horse Flyer, www.DarkHorseFlyer.com See omnystudio.com/listener for privacy information.

Sudden cardiac death in the young, that's an apparently healthy person dying unexpectedly from heart-related issues under the age of 35, is rare but devastating. It is also something of a mystery to many scientists. So how can we try to prevent young people from dying unexpectedly like this? Could genetic screening be the answer? Georgia Mills caught up with Michael Ackerman, from the Mayo Clinic in Minnesota, at the British Cardiovascular Society Conference 2016. Like this podcast? Please help us by supporting the Naked Scientists

Sudden cardiac death in the young, that's an apparently healthy person dying unexpectedly from heart-related issues under the age of 35, is rare but devastating. It is also something of a mystery to many scientists. So how can we try to prevent young people from dying unexpectedly like this? Could genetic screening be the answer? Georgia Mills caught up with Michael Ackerman, from the Mayo Clinic in Minnesota, at the British Cardiovascular Society Conference 2016. Like this podcast? Please help us by supporting the Naked Scientists

Neil is back after two months off! He welcomes new co-host, Michael Ackerman, to the show. They start off with an intro of Michael and then dive right into bikepacking talk. Listen in for updates from Neil's time at Interbike and Outerbike, which includes discussion about bikes, packs, tires, and other new goods.   They also chat about Neil's recent White Rim in a Day trip and give a hint about the upcoming routes tool on Bikepackers Magazine. Neil and Michael wrap up this episode by reviewing some recent bikepacking races, including the Smoke and Fire 400, Alleghany Mountain Loop, Coconino Stage Bikepack, Trans North California, and the Cross Florida Individual Time Trail.     If you have an idea for a guest or would like to be on yourself, please contact Ben at Ben@Mountainbikeradio.com.    We also have advertising opportunities available if you would like to promote your race. Please contact us about advertising at info@mountainbikeradio.com.   ------------------------------------------------------   Related Show Links:   10 Notable Brands at Interbike Blackburn Design Apidura Bags Wanderlust Bags Chumba Cycles Smoke and Fire 400 Website Smoke and Fire 400 on Bikepackers Magazine Coconino Stage Bikepack on Bikepackers Magazine Bikepackers Magazine Bikepackers Magazine - Neil Beltchenko CTR report Contact Bikepackers Magazine Support Mountain Bike Radio    Bikepackers Magazine Social: Facebook Twitter Google+ Instagram Youtube

Michael Ackerman chats with Karlos Rodriguez Bernart, John Pickron, and Kevin Porter at the Junction Creek Trailhead at the end of the Colorado Trail Race. They talk about how they got into the sport and share some great experiences. They give a good shout out to Joe Polk at MTBCast.com for his role in growing bikepacking. Listen in for some great insight from three CTR riders.   Related Show Links: Bikepackers Magazine Bikepackers Magazine - Neil Beltchenko CTR report Colorado Trail Race Website Bikepackers Magazine Reviews Contact Bikepackers Magazine   Bikepackers Magazine Social: Facebook Twitter Google+ Instagram Youtube

Garrett Alexander chats with Michael Ackerman about his first attempt of racing the Colorado Trail. While he admits that he learned a ton and that he could go under six days, Garrett finished in 6 days and 13 hours, which is a really great time for the 500+ miles. Listen in as he shares the details of his ride, including what it's like to ride to home to Durango, his equipment, food, and more.      Related Show Links: Bikepackers Magazine Bikepackers Magazine - Neil Beltchenko CTR report Colorado Trail Race Website Bikepackers Magazine Reviews Contact Bikepackers Magazine   Bikepackers Magazine Social: Facebook Twitter Google+ Instagram Youtube

Mayo Clinic in collaboration with theheart.org brings you context to the latest news, trials, and trends in cardiovascular medicine.

Last year we visited Animas High School in Durango Colorado, and learned how this public school, which focuses on excellence, was founded. Now, Animas has grades 9-11 and will have its first graduating class in a bit over a year. My guest is Michael Ackerman, Head of School at Animas. He’ll tell us how Animas school is organized, following the … Read more about this episode...

I Tidsskriftets podkast for nr. 6/2009 kan du høre intervju med Trond Markestad, Erik Fosse og Michael Ackerman, om det er etisk riktig å bruke forskningsmateriale fra en henrettet fange. Reporter: Eline Feiring. Les artikkelen her: https://tidsskriftet.no/2009/03/aktuelt/bruk-av-datasettet-visible-human-project-i-forskning

A study published recently in Mayo Clinic Proceedings details information about potential cardiac side effects when using off-label drugs to treat COVID-19. Off-label means the drug has been approved by the Food and Drug Administration to treat a different condition. Some of the off-label drugs being used to treat COVID-19 have a risk of sudden cardiac arrest and death. On the Mayo Clinic Q&A podcast, Dr. Michael Ackerman, a Mayo Clinic genetic cardiologist and director of the  Windland Smith Rice Sudden Death Genomics Laboratory, explains how heart monitoring is important to identify at-risk patients. Advertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy