Podcasts about Reconstitution

Pauline Revenaz, en compagnie de Laurent Valdiguié, revient sur de grandes affaires policières et judiciaires faisant l'actualité. Chaque week-end, l'émission pilotée par Pauline Revenaz avec à ses côtés Laurent Valdiguié, consultant police/justice BFMTV, traite d'un événement majeur de la semaine, ainsi que d'autres affaires qui sont revenues sur le devant de la scène. BFMTV, 1ère chaine d'information en continu de France, vous propose toute l'info en temps réel avec 18h d'antenne live par jour et des directs partout à travers le monde où l'actualité le nécessite. BFMTV, c'est aussi les débats et les grands reportages d'actualité. Retrouvez BFMTV sur le canal 15 de la TNT et sur BFMTV.com.

39 ans après la disparition de Marie-Thérèse Bonfanti dans l'Isère, une reconstitution a été organisée jeudi 15 mai à Pontcharra, en présence de l'homme qui a avoué avoir tué la mère de famille en mai 1986. Pendant quatre heures, le suspect, Yves Châtain, s'est plié aux demandes du magistrat instructeur et de l'avocat des parties civiles, rejouant le meurtre selon le scénario qu'il a rapporté aux enquêteurs. Les deux enfants de la victime, son mari et ses frères et sœurs étaient également présents en tant que parties civiles. Mais alors que 39 ans se sont écoulés depuis le crime, organiser une reconstitution présente des difficultés.Comment organise-t-on une reconstitution dans un cold case, lorsque les faits se sont déroulés il y a plusieurs dizaines d'années? Quelles sont les contraintes que les enquêteurs doivent prendre en compte?Elisa Trannin et Elisa Fernandez, journaliste police-justice à BFMTV.com, reçoivent dans Affaire suivante Jacques Dallest, ancien procureur et juge d'instruction, auteur de "Sur les chemins du crime" aux éditions Mareuil.  

Worship Service

Informations pratiquesSamedi 17 mai :Accès au village: 11h—18hAccès à la mine : 13h—18h/dernier départ pour la mine à 17h Dimanche 18 mai :Accès au village: 10h—17hAccès à la mine : 11h—17h/dernier départ pour la mine à 16hTARIFS : L'accès au village des mineurs, aux ateliers et aux animations qui s'y déroulent est gratuit.Visite de la mine Saint-Louis Eisenthür (1h de visite): Adulte—17€/Enfant (5-12 ans)—10€Les interviews sont également à retrouver sur les plateformes Spotify, Deezer, Apple Podcasts, Podcast Addict ou encore Amazon Music.Hébergé par Ausha. Visitez ausha.co/politique-de-confidentialite pour plus d'informations.

durée : 00:13:02 - La commémoration du 8 mai 1945 sous forme de reconstitution historique à St Geniès

Tous les samedis et dimanches, dans Europe 1 Matin week-end, Alexandre Devecchio, rédacteur en chef du service débats du Figaro, livre son édito.Distribué par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Tous les samedis et dimanches, dans Europe 1 Matin week-end, Alexandre Devecchio, rédacteur en chef du service débats du Figaro, livre son édito.Distribué par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Aujourd'hui, Barbara Lefebvre, Didier Giraud et Flora Ghebali débattent de l'actualité autour d'Alain Marschall et Olivier Truchot.

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Host Timothy Regan welcomes Elia Paz, creator and leader at the Wise Heart Community. She is the author of the new book, Life Serving Boundaries: 6 Skills for Creating Thriving Relationships.  She also hosts “The Wise Heart Podcast: Relationships as Spiritual Practice.” We explore the current efforts within our U.S. Federal Governement to implement extreme policies with extreme impact, and how to respond through the lens of healthy human relationship principles and truths. This episode is about your own power to respond with life-serving awareness and action to the big issues of our collective time in history. The post The Cremation and Reconstitution of Care in the U.S. appeared first on KPFA.

Send us a text- On-Demand Programme Link - https://mailchi.mp/bb2a7b851246/kairos-centreUndistort your Cognitive Distortions. How?What are Cognitive Distortions? Examples might be: 'All guys do it', 'At least I am no longer visiting porn sites', 'I'll only be on here for 5 minutes, no longer', 'What I do, is not as bad as...', 'What an horrendous day. I deserve....', 'I can't help it'It is reasonable for you to have a conversation with your brain, like this: "Brain, you are supposed to be on my side. There are times when I have found you out. You have not been telling me the whole truth. Whose side are you on in this Addiction Recovery journey? What is this that I am learning about you giving me Cognitive Distortions?"Unless you spot a Cognitive Distortion, you won't realise that you are just 10 Minutes away from 'Acting out' and you are at Preparation Stage on the Cycle of Sex Addiction:ACTING OUT ---> REGRET --> RECONSTITUTION -->DORMANT -->TRIGGER --PREPARATION -->ACTING OUT -->When you recognise and see the Cognitive Distortion, don't debate with it; don't question its truth; don't linger; don't procrastinate. Immediately R.U.N. (We will look at R.U.N in a future episode).For now, you need space away from the place where the 'Acting out' WILL take place, in order to undistorted your Cognition - your Thinking.Get some help from The Kairos Centre. See what you cannot see. Begin to change that which you begin to better understand.Give a little to my fund raising page. Help someone access the Recovery Programme: https://igg.me/at/ThekairosCentreHelp is here: bit.ly/pornaddictionhelpThe world's first Online Webinar Sex, Porn, Love Addiction video-on-demand Recovery Programme. Discover the real, authentic you. email info@kairos-centre.comNow launched: A Video-on-Demand Online Course (for Singles, Couples/Marrieds/Partners) Access here - https://www.kairos-centre.com/changement-on-demand/Gary McFarlane (BA, LLM, Dip, Certs), Accredited EMDR Practitioner.Episode Keywords: Sex Addiction | Porn Addiction | Love Addiction | Root Causes | Brain Impact | Self-Soothing Behaviors | Family Conflict | Emotional Neglect | Peer Pressure | Performance Pressure | Separation | Divorce | Fear | Anxiety | Stress | Pain | Dissociation| Recovery Program | EMDR Therapy | Emotional Event | Trauma Healing | Neuroplasticity | Online Therapy | Sex Addiction Recovery Program | Compulsive Behaviors | Intimacy Issues | Sexual Dysfunction | Obsessive Thoughts | Guilt | Infidelity | Traumatic Bonding | Objectification | Hypersexualization | Pornography Industry | Love Addiction Patterns | Attachment Styles | Sexual Compulsivity | Behavioral Therapy | Relapse Prevention | Emotional Regulation | Healing Journeys | Intimacy Building |  

In Episode 323 of Devolution Power Hour, Jon Herold, Patrick Gunnels, and Chris Paul, delve into the rapid transformations under President Trump's second term. They explore the reconstitution phase of government, Trump's decisive executive orders targeting cartels, DEI policies, and birthright citizenship, and the geopolitical implications of his World Economic Forum appearance. The hosts also analyze Trump's bold tax reform proposals, AI infrastructure initiatives, and efforts to restore constitutional governance. Packed with sharp insights, lively discussions, and thought-provoking theories, this episode highlights the unfolding changes reshaping America's political and global landscape.

CME credits: 1.00 Valid until: 24-01-2026 Claim your CME credit at https://reachmd.com/programs/cme/balancing-act-immune-reconstitution-vs-immune-suppression/32227/ This series of bite-sized episodes contains important information on the use of high-efficacy disease-modifying therapies (DMTs) in multiple sclerosis (MS). Drs. Ahmed Obeidat and Mark Freedman discuss the role of inflammation in MS pathology, treatment strategies for high-efficacy DMTs, impact on cognition, and use in special populations.

In this episode of Devolution Power Hour, Jon Herold and Burning Bright delve into the sweeping changes unfolding during President Trump's second term. They explore the revocation of EO 13961, marking the shift from devolution to reconstitution, and analyze its implications. Key discussions include Trump's bold executive orders dismantling DEI policies, strengthening border security, and imposing significant trade tariffs. The episode also addresses the controversy surrounding Larry Ellison's AI-driven mRNA cancer vaccine initiative, the growing role of AI in governance and innovation, and Trump's strategic moves in foreign and domestic policy. Packed with sharp insights and engaging commentary, this episode captures the rapid transformations shaping America's future.

Durant votre récré de midi à Jurbise on joue avec Salvatore di Bennardo et Juan d'Oultremont, comparses d'un jour d'Etienne et Jerry, on s'étonne des habitudes des Belges avec le micro-trottoir de Raoul Reyers, on apprend grâce aux questions de Walid, qui tournent autour de George Orwell, d'une cloche qui a joué à cache-cache dans la commune boraine, de légume oublié et de héraldique, et on se souvient en compagnie de notre invité du jour, Cédric Rocher, la vingtaine, passionné d'histoire militaire de la seconde guerre mondiale, qui outre la tenue d'un petit musée, organise chaque année la reconstitution du Camp de la Butte des Fusillés à Masnuy-Saint-Jean. Un riche programme d'activités pour tous est proposé pour l'occasion : convois militaires, exposition de matériel d'époque, reconstitution d'un hôpital de campagne U.S., repas, soirées, cérémonie pour la Mémoire, spectacle de claquettes... https://www.jurbise.be/ Merci pour votre écoute Salut les copions, c'est également en direct tous les jours de la semaine de 16h à 17h sur www.rtbf.be/lapremiere Retrouvez tous les épisodes de Salut les copions sur notre plateforme Auvio.be : https://auvio.rtbf.be/emission/19688 Et si vous avez apprécié ce podcast, n'hésitez pas à nous donner des étoiles ou des commentaires, cela nous aide à le faire connaître plus largement.

Mes chers camarades, bien le bonjour ! Je suis sûr que près de chez vous, il y a déjà eu des événements où des personnes ont enfilé des costumes du passé et se sont comportés comme s'ils vivaient à l'époque. Eh bien ça, c'est de la reconstitution historique ! Mais plus concrètement, en quoi ça consiste ? Depuis quand ça existe, et comment les reconstituteurs savent-ils comment c'était avant ? Pour le découvrir, j'ai reçu en entretien Martin Bostal, qui est docteur en histoire et en archéologie spécialisé dans l'étude des représentations contemporaines et de la culture matérielle du passé, et donc spécialiste de la reconstitution. Vous allez le découvrir dans un instant, le sujet est vaste et passionnant, alors ne tardons pas plus ! Je vous souhaite une bonne écoute sur Nota Bene ! Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

Mes chers camarades, bien le bonjour ! Vous avez déjà vu des gens costumés en chevaliers dans la fête médiévale du coin ? Eh bien ça, c'est de la reconstitution historique, et d'ailleurs ça ne se limite pas aux chevaliers et au Moyen Âge ! Pour découvrir le domaine dans son ensemble, j'ai eu la chance de recevoir en entretien un spécialiste de la question, Martin Bostal, entretien qui sera disponible sur le podcast dans quelques jours. Mais ces personnes qui font de la reconstitution, comment font-elles pour savoir comment c'était avant ? Il doit bien y avoir une méthode ? Et d'ailleurs, si j'avais envie de me lancer en reconstitution, qu'est-ce qui serait à faire ou à éviter ? Martin va nous répondre dans un instant, alors bonne écoute ! Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

Écoutez l'émission du 20 décembre 2024.

durée : 00:04:52 - Le Zoom de France Inter - Jusqu'en 1989, la seule évocation du nom de la police secrète est-allemande faisait frémir la population. Avec la chute du Mur, la police secrète a bien évidemment disparu. Mais elle a laissé des traces : des milliers de documents que des archivistes tentent aujourd'hui de reconstituer.

durée : 00:03:43 - L'info d'ici de 06h30

durée : 00:59:41 - invitée : Airelle Besson - par : Nicolas Pommaret - Parution de "Surprise !" de Airelle Besson chez Papillon Jaune - Deutschlandfunk / L'Autre Distribution.

Destination finale de l'été parano : la Côte d'Azur. Dans cet épisode, Gaël et Geoffroy reviennent sur les zones d'ombre qui entourent la mort du célèbre humoriste et décortiquent les théories du complot qui soutiennent que le fondateur des Restos du Coeur a été assassiné par les services secrets français sur ordre de l'Elysée. Musique : Thibaud R. Habillage sonore / mixage : Alexandre Lechaux Facebook  Instagram  Twitter  www.toutsavoir.fr Contact : tousparano@gmail.com

The Krulak Center's new Russia SME, MR. James Harvey, discusses Russian military reconstruction with Dr. Dmitry Gorenburg. This is a new episode in our on going 'On Russia' series. All opinions expressed here are those of the individual and do not necessarily reflect those of the Krulak Center, Marine Corps University, the United States Marine Corps, or any other agency of the US Government. Enjoyed this episode? Think there's room for improvement? Share your thoughts in this quick survey - all feedback is welcome! The survey may be found here: https://docs.google.com/forms/d/e/1FAIpQLSenRutN5m31Pfe9h7FAIppPWoN1s_2ZJyBeA7HhYhvDbazdCw/viewform?usp=sf_link Intro/outro music is "Epic" from BenSound.com (https://www.bensound.com) Follow the Krulak Center: Facebook: https://www.facebook.com/thekrulakcenter Instagram: https://www.instagram.com/thekrulakcenter/ Twitter: @TheKrulakCenter BlueSky Social: @thekrulakcenter.bsky.social LinkedIn: https://www.linkedin.com/company/brute-krulak-center-for-innovation-and-future-warfare

La Tour du Temple à Paris a été, durant la Révolution, la prison de Louis XVI, de Marie-Antoinette et de leurs enfants, dont le jeune Louis XVII. Ce qui est moins connu est que, pendant près de 800 ans, la tour du Temple faisait partie d'une véritable ville dans la ville, qu'on appelait l'Enclos du Temple. Il était entouré de hautes murailles fortifiées de tourelles. Aujourd'hui, il n'en reste pratiquement plus rien, sinon le nom qu'il a donné au quartier du Temple.   Adhérez à cette chaîne pour obtenir des avantages : https://www.youtube.com/channel/UCN4TCCaX-gqBNkrUqXdgGRA/join Pour soutenir la chaîne, au choix: 1. Cliquez sur le bouton « Adhérer » sous la vidéo. 2. Patreon: https://www.patreon.com/hndl Script: Simon Dagenais, https://www.facebook.com/simon.dagenais.39 Montage: Théo Dussault Drainville   Abonnez-vous à ma chaine: https://www.youtube.com/c/LHistoirenousledira Instagram: https://www.instagram.com/laurentturcot Musique issue du site : https://epidemicsound.com Images provenant de https://www.storyblocks.com Les vidéos sont utilisées à des fins éducatives selon l'article 107 du Copyright Act de 1976 sur le Fair-Use. Sources et pour aller plus loin: -Henri de Curzon, La maison du temple de Paris: Histoire et description, Paris, 1888 -J. J. Barillet, Recherches historiques sur le Temple, Paris, 1809 -Frédéric Bussman, Un prince collectionneur: Louis-François de Bourbon Conti et ses collections au palais du Temple à Paris, Paris, 2012 Images : Maquette du Temple au musée Carnavalet: https://paris-promeneurs.com/l-enclos-du-temple-detruit/ Thé à l'Anglaise au Temple : (Mozart et la cour de Conti) https://fr.wikipedia.org/wiki/Fichier:Le_Th%C3%A9_%C3%A0_l%27anglaise.jpg Souper du prince de Conti au Temple : https://wikioo.org/paintings.php?refarticle=AQSUQP&titlepainting=SOUPER%20DU%20PRINCE%20DE%20CONTI%20AU%20TEMPLE%201766&artistname=Michel%20Barth%C3%A9l%C3%A9my%20Ollivier Tour du Temple : https://commons.wikimedia.org/wiki/File:Tour_du_Temple_circa_1795_Ecole_Francaise_18th_century.jpg Vidéo d'Assassins Creed Unity : Viewpoint court, soleil https://www.youtube.com/watch?v=egKpK2b1MCU Temple médiéval vs temple 18e siècle https://www.youtube.com/watch?v=Ygl4NgWFyKw (certains passages lents, bon pour extraits) Images AC Unity : Guillaume Béland et intérieur du Temple : https://www.artstation.com/artwork/qva22 Autres reconstitutions 3d : Reconstitution 3d du Temple: https://www.lepoint.fr/culture/journees-du-patrimoine-visitez-l-enclos-du-temple-sa-prison-son-eglise-ses-hotels-18-09-2014-1864194_3.php Autres références disponibles sur demande. #histoire #documentaire #templiers #Paris #quartierdutemple

In the final chapter of Military Culture Shift, I reference a theory of reconstitution written by Stoney Portis, after he commanded the 3-61 CAV troops that survived the now historic Battle of COP Keating and needed to somehow become mission-ready again. Reading his reflection on what it took to wholistically serve the battle-weary troops who had earned every right to hang up the one tattered uniform they had left, I knew it was a case study on what it would take to reconstitute an entire culture as well. So I invited now LT COL Stoney Portis to join Matt and me in a discussion about their shared sacred space in hopes it could validate the sacred spaces in your own life, but also inspire the healing of us all. Read Stoney's Paper on Reconstitution: https://www.corieweathers.com/wp-content/uploads/Stoneys-Paper.-full-1.pdf Read about the Battle of Cop Keating here Watch the movie "The Outpost": https://www.netflix.com/title/81276140?source=35 This podcast is based on the book Military Culture Shift by clinical consultant and SME on military family culture, Corie Weathers.  Order your copy of Military Culture Shift https://militaryfamilybooks.com/products/military-culture-shift-by-corie-weathers Listen to Corie's Lifegiver Podcast https://corieweathers.podbean.com/ Find out more about how you can work with and contact Corie https://www.corieweathers.com Final Credits song is "The Hard Way" by Moda Spira https://modaspira.bandcamp.com/track/the-hard-way  

durée : 00:44:06 - franceinfo: Les informés - par : Jean-François ACHILLI - Autour Victor Matet, les informés débattent de l'actualité du dimanche 5 mai 2024.

Download The Peptide Cheat Sheet: https://peptidecheatsheet.carrd.co/

Aujourd'hui dans "Punchline", Laurence Ferrari et ses invités débattent de la reconstitution de la disparition du petit Émile, réalisée dans le Haut-Vernet.

Qui était le mystérieux Joséphine que Lisadol prétend avoir rencontré par hasard ? Notre reporter Julien Cernobori mène une enquête sur les circonstances de la rencontre avant de se rendre sur les lieux... CERNO est un podcast créé par Julien Cernobori Reportage, montage, réalisation et mixage : Julien Cernobori Musique originale : Théo Boulenger Ecoutez les épisodes suivants sur patreon.com/cerno !

Jeff, Jim, David, Brian, and Paul compare and contrast the Human Subject of chapter 7 and the reconstituted Subject of Romans chapter 8. Become a Patron! If you enjoyed this podcast, please consider donating to support our work.

Dominique Rizet, en compagnie de Ronald Guintrange, revient sur de grandes affaires policières et judiciaires faisant l'actualité. Chaque dimanche, l'émission pilotée par Ronald Guintrange avec à ses côtés Dominique Rizet, consultant police/justice BFMTV, traite d'un événement majeur de la semaine, ainsi que d'autres affaires qui sont revenues sur le devant de la scène. BFMTV, 1ère chaine d'information en continu de France, vous propose toute l'info en temps réel avec 18h d'antenne live par jour et des directs partout à travers le monde où l'actualité le nécessite. BFMTV, c'est aussi les débats et les grands reportages d'actualité. Retrouvez BFMTV sur le canal 15 de la TNT et sur BFMTV.com.

Download The Peptide Cheat Sheet: https://peptidecheatsheet.carrd.co/Join The Fully Optimized Health Private Membership Group: https://www.fullyoptimizedhealth.com/start-here1 On 1 Coaching Application: https://hunterwilliamscoaching.carrd.co/Book A Call With Me: Book A Call With Me: https://hunterwilliamscall.carrd.co/Supplement Sources: https://hunterwilliamssupplements.carrd.co/Today, I'm publishing a video about how to reconstitute peptides.This video is the END ALL-BE ALL video on reconstituting. After watching it you should be able to mix your own peptides for life!Here's what you'll learn in the video:Bacteriostatic Water and Peptide Reconstitution:How to prep all your peptides. This guide includes details about necessary materials like bacteriostatic water, sample peptides, and syringes.Detailed Guide on Peptide Reconstitution: The video provides a step-by-step process for adding the right amount of bacteriostatic water to your peptides, based on the specific peptide you're using.Dosing and Measurement Tips:I explain how to measure and dose peptides, giving helpful tips and showing how to use a peptide calculator. This helps ensure accurate and effective reconstitution.Guidelines for Water Addition in Vials: Here's a crucial part of the process – determining how much water to add to your peptide vials:For peptides with 1-5 milligrams: Add 1 mL of bacteriostatic water.For peptides with 6-10 milligrams: Add 2 mL of bacteriostatic water.For peptides over 10 milligrams: Add 3 mL of bacteriostatic water.Post-Reconstitution Steps and Storage: Post-reconstitution, I discuss how to store your peptides properly. Keeping them refrigerated ensures they remain potent for 12 to 16 weeks.Here's the video:I'd love to hear your feedback and as always, use the link in the footer of the email if you have questions or suggestions for video topics.Best,Hunter

durée : 00:07:00 - Tendez l'oreille du samedi 06 janvier 2024 - par : Christophe Dilys - Christophe Dilys a mis la main sur les "Sam Fox Moving Pictures Music" (1913) et nous explique comment ça marche : une page de musique par émotion, comme une sorte d'annuaire à destination des pianistes pour films muets. Est-ce que cela fonctionne sur des films d'aujourd'hui ?

Vermont, au nord des Etats-Unis. Notre histoire du jour commence sous un temps radieux, qui ravit les ouvriers en train de se démener avec force et entrain pour boucler un chantier ferroviaire qui s'éternise. Phineas Gage est l'un d'entre eux. Il est tendu, et donc, assez peu patient. Il faut dire que son gars est en train de transporter de la poudre noire, et qu'il en a plein les mains. Un geste de travers, et c'est le grand BOUM. Un peu plus prudemment, l'homme qui vient d'éviter l'accident se dirige vers le rocher qui bloque l'avancée du chantier. Rien de plus simple qu'un bon coup d'explosif pour se rendre la vie plus facile, n'est-ce pas ? Gage, qui s'est mis à l'ombre du pied de la montagne, un peu plus loin, ne peut retenir un soupir d'exaspération. Cet ouvrier est nouveau, et chacun de ses gestes prend des plombes. Exaspéré, Gage écarte l'ouvrier et bourre la poudre lui-même, sans ménagement dans une faille de la roche. Attention, Phineas, si la chance sourit aux audacieux, la malchance, elle, est le lot des imprudents. Nous sommes le 13 septembre 1848, un léger vent se lève et se prend dans les cheveux de ces hommes qui travaillent de leurs mains. Il est un peu moins de 16 heures 30, et c'est l'heure H de mon histoire. Merci pour votre écoute Retrouvez l'ensemble des épisodes de l'Heure H sur notre plateforme Auvio.be : https://auvio.rtbf.be/emission/22750 Et si vous avez apprécié ce podcast, n'hésitez pas à nous donner des étoiles ou des commentaires, cela nous aide à le faire connaître plus largement.

On this episode of Defence Deconstructed, Charlotte Duval-Lantoine speaks to Lieutenant-General Jocelyn Paul about the Canadian Army's efforts to reconstitute and change its culture. Dave Perry is joined by Kate Todd to discuss the week in defence news. This episode is part of a series exploring the challenges facing CAF Reconstitution and culture change, made possible thanks to the Department of National Defence's MINDS Program. Defence Deconstructed is brought to you by Irving Shipbuilding Participants' bio Lieutenant-General Paul is the Commander of the Canadian Army – https://www.canada.ca/en/army/corporate/senior-leaders/commander.html Host bio
- Charlotte Duval-Lantoine is CGAI's Ottawa Operations Manager and one of its fellows. www.cgai.ca/staff#Lantoine Recording Date: 29 June 2023 Follow the Canadian Global Affairs Institute on Facebook, Twitter (@CAGlobalAffairs), or on LinkedIn. Head over to our website at www.cgai.ca for more commentary. Produced by Charlotte Duval-Lantoine. Music credits to Drew Phillips

Vous êtes peut être déjà allé vous promener dans une des nombreuses fêtes médiévales de France, et vous avez peut être déjà rencontré ces drôles de personnes qui font de la reconstitution médiévale, habillés comme à l'époque et qui donnent l'illusion d'avoir fait un voyage dans le temps. Et bien dans cet épisode je vous propose de passer 24h, enfin presque, avec une de ces troupes de reconstitution, la Confrérie du Cerbère. Je les ai rencontré lors des fêtes médiévales de Provins, une des plus grandes fêtes médiévales de France, début juin 2023. Une fête médiévale est comme un grand festival où le public est invité à se replonger dans le Moyen Âge avec des spectacles, des animations, des boutiques, et dans la ville en elle même et ses rues médiévales, inscrite au Patrimoine Mondial de l'UNESCO depuis 2001. Mais dans cet épisode, nous n'allons pas directement parlons des fêtes médiévales, mais surtout de la reconstitution historique, sous plein d'aspects. Nous y parlons du combat, de la vie quotidienne, la cuisine, les vêtements, et d'autres choses encore, mais aussi toute la réflexion derrière cette volonté de reconstituer la vie au Moyen Âge. Je remercie bien sûr énormément toute la Confrérie du Cerbère pour leur accueil très chaleureux, vraiment je n'aurais pas pu rêver mieux pour cet épisode. Si vous les croisez lors d'une fête médiévale n'hésitez pas à les saluer de ma part. Et merci aux auditeurs et auditrices qui m'ont accompagné une partie du samedi après midi et qui ont pris des photos quand j'avais les mains prises par le micro. ▪ Infos sur le podcast Créé et produit par Fanny Cohen Moreau depuis 2017. ➡ Soutenir le podcast > https://passionmedievistes.fr/soutenir/ ➡ Instagram > https://instagram.com/passionmedievistes/ ➡ Facebook > https://facebook.com/PassionMedievistes ➡ Twitter > twitter.com/PMedievistes ➡ Plus d'info sur cet épisode > https://passionmedievistes.fr/hlm-8-reconstitution Préparation, enregistrement, montage et mixage : Fanny Cohen Moreau Montage et mixage du générique : Moustaclem Et si vous avez des idées d'endroits qui pourraient être les sujets des prochains épisodes de ce format envoyez moi un mail à passionmedievistes@gmail.com

On this episode of Defence Deconstructed, Charlotte Duval-Lantoine speaks to Vice-Admiral Angus Topshee about culture change and reconstitution in the Royal Canadian Navy. This episode is part of a series exploring the challenges facing CAF Reconstitution and culture change, made possible thanks to the Department of National Defence's MINDS Program. Defence Deconstructed is brought to you by Irving Shipbuilding Participants' bio Vice-Admiral Angus Topshee is the Commander of the Royal Canadian Navy – www.canada.ca/en/navy/corporate/…adership/crcn.html Host bio
- Charlotte Duval-Lantoine is CGAI's Ottawa Operations Manager and one of its fellows. https://www.cgai.ca/staff#Lantoine Recording Date: 26 May 2023 Follow the Canadian Global Affairs Institute on Facebook, Twitter (@CAGlobalAffairs), or on LinkedIn. Head over to our website at www.cgai.ca for more commentary. Produced by Charlotte Duval-Lantoine. Music credits to Drew Phillips

This week I finally bond with the bartender that was making me not want to go into my favorite bar anymore all thanks to my new Octopussy watch. Hmmm. Those two words are even funny in print. Classic. Also, spending all day at the track and dinner with the Mayor of Red Bank, NJ; A big date at the place they notoriously won't give me parmesan cheese; and as usual - a restaurant that we get kicked out of after an 8:30 reservation. Juskow in the CITY is getting angry at the CITY! But -- that's always hilarious.

We discuss World War II and how it impacted the world since its end, especially the world consciousness and humanity's capacity to bring about the Afro-Asiatic reconfiguration of the world. We continue our deep reading of Hegel's Science of Logic here: https://drive.google.com/.../1eXesdzt13OZSmq0SUEUy4t.../view

durée : 00:28:50 - Les Nuits de France Culture - par : Albane Penaranda - Par Stéphane Pizella - Avec les policiers du quai des Orfèvres

Layman meets with the founding framer of The Reconstitution project, Ari Allen, to talk about the genesis and goals of The Reconstitution: a collective experiment in revising the United States' Constitution and drafting a series of amendments responsive to some of the deepest challenges confronting the country, its people, and its governing bodies: polarization and corruption, the influence of money in elections, limitations to meaningful participation in government and self-governance, imbalances in representation, the status of corporations and the need to address corporate influence on democratic process, the role of advertising in a free society, and much more. Ari reflects on the historical justification for such an experiment, what he has learned through convening this imaginal Constitutional Convention, and how the resulting document might be used going forward, to foster dialogue, stimulate creative thinking, and hopefully catalyze meaningful change. Ari Allen earned his JD from Georgetown Law and has worked at Sidley Austin, representing clients on Capitol Hill during the 2008 financial crisis and the subsequent Dodd-Frank Wall Street Reform. He holds a Masters in Psychology degree from the California Institute of Integral Studies, and currently works in the education technology industry. He is also a writer, philosopher, and a DJ. The Reconstitution Project https://www.thereconstitution.com/ Follow The Integral Stage on Fathom! https://hello.fathom.fm/ 2Subscribe, and support The Integral Stage on Patreon to make more of these conversations possible! https://www.patreon.com/theintegralstage Special thanks and big love to Shai Newman, Brandon LaChance, Mike McElroy, Brandon Norgaard, Brendan Graham Dempsey, Francesca, and all of our other Patreon supporters!

This month on Episode 45 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the February 3rd and February 17th issues of Circulation Research. This episode also features an interview with Dr Hind Lal and Dr Tousif Sultan from the University of Alabama at Birmingham about their study Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation.   Article highlights:   Pi, et al. Metabolomic Signatures in PAH   Carnevale, et al. Thrombosis TLR4-Mediated in SARS-CoV-2 Infection   Cai, et al. Macrophage ADAR1 in AAA   Koide, et al. sEVs Accelerate Vascular Calcification in CKD   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cynthia St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'm going to be highlighting the articles from our February 3rd and 17th issues of Circulation Research. I'm also going to have a chat with Dr Hind Lal and Dr Tousif Sultan from the University of Alabama at Birmingham about their study, Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation. But before I get to the interviews, here are a few article highlights.   Cindy St. Hilaire:        The first article I want to highlight comes from the laboratory of Dr Peter Leary at the University of Washington, and the title is Metabolomic Signatures Associated With Pulmonary Arterial Hypertension Outcomes. Pulmonary Arterial Hypertension or PAH is a rare but life-threatening disease in which progressive thickening of the walls of the lung's blood vessels causes increased blood pressure and that increased blood pressure ultimately damages the heart's right ventricle.   Interestingly, progression to heart failure varies considerably among patients, but the reasons why there is variability are not well understood. To find out, this group turned their attention to patient metabolomes, which differ significantly from those of healthy people and thus may also change with severity. Blood samples from 117 PAH patients were analyzed for more than a thousand metabolites by mass spectrometry and the patient's progress was followed for the next three years. 22 patients died within a three-year period and 27 developed significant right ventricle dilation. Other measures of severity included pulmonary vascular resistance, exercise capacity and levels of BNP, which is a metric of heart health. Two metabolic pathways, those relating to polyamine and histidine metabolism, were found to be linked with all measures of severity suggesting a key role for them in disease pathology. While determining how these pathways influence disease as a subject for further study, the current findings may nevertheless lead to new prognostic indicators to inform patient care.   Cindy St. Hilaire:        The next article I want to discuss is coming from our February 3rd issue of Circulation Research and this is coming from the laboratory of Dr Francisco Violi at the University of Rome and the title is Toll-Like Receptor 4-Dependent Platelet-Related Thrombosis in SARS-CoV-2 Infection. Thrombosis can be a complication of COVID-19 and it is associated with poor outcomes, including death. However, the exact mechanism by which the virus activates platelets, which are the cells that drive thrombosis, is not clear. For one thing, platelets do not appear to express the receptor for SARS-CoV-2. They do however, express the TLR4 receptor and that's a receptor that mediates entry of other viruses as part of the immune response. And TLR4 is ramped up in COVID-19 patient platelets. This group now confirms that, indeed, SARS-CoV-2 interacts with TLR4, which in turn triggers thrombosis.   The team analyzed platelets from 25 patients and 10 healthy controls and they found that the platelet activation and thrombic activity were both boosted in the patient samples and could not be blocked using a TLR4 inhibitor. Additionally, immunoprecipitation and immunofluorescent experiments further revealed colocalization between the virus protein and the TLR4 receptor on patient platelets. The team went on to show that the signaling pathway involved reactive oxygen species producing factors p47phox and Nox2, and that inhibition of phox 47, like that of the TLR4 receptor itsel,f could prevent platelet activation. As such, this study suggests that inhibiting either of these proteins may form the basis of an antithrombotic treatment for COVID-19.   Cindy St. Hilaire:        The third article I want to highlight is coming from the lab of Shi-You Chen at University of Missouri and the title of this article is ADAR1 Non-Editing Function in Macrophage Activation and Abdominal Aortic Aneurysm. Macrophage activation plays a critical role in abdominal aortic aneurysm development, or AAA development. Inflammation is a component of this pathology; however, the mechanisms controlling macrophage activation and vascular inflammation in AAA are largely unknown. The ADAR1 enzyme catalyzes the conversion of adenosine to inosine in RNA molecules and thus this conversion can serve as a rheostat to regulate RNA structure or the gene coding sequence of proteins. Several studies have explored the role of ADAR1 in inflammation, but its precise contribution is not fully understood, so the objective of this group was to study the role of ADAR1 in macrophage activation and AAA formation.   Aortic transplantation was conducted to determine the importance of nonvascular ADAR1 in AAA development and dissection and angiotensin II infusion of ApoE knockout mice combined with a macrophage specific knockout of ADAR1 was used to study the role of ADAR1 macrophage specific contributions to AAA formation and dissection. Allograft transplantation of wild type abdominal aortas to ADAR1 haploinsufficient recipient mice significantly attenuated AAA formation. ADAR1 deficiency in hematopoietic stem cells also decreased the prevalence and the severity of AAA and it also inhibited macrophage infiltration into the aortic wall. ADAR1 deletion blocked the classic macrophage activation pathway. It diminished NF-κB signaling and it enhanced the expression of a number of anti-inflammatory microRNAs. Reconstitution of ADAR1 deficient but not wild type human monocytes to immunodeficient mice blocked the aneurysm formation in transplanted human arteries. Together these results suggest that macrophage ADAR1 promotes aneurysm formation in both mouse and human arteries through a novel mechanism of editing the microRNAs that target NF-κB signaling, which ultimately promotes vascular inflammation in AAA.     Cindy St. Hilaire:        The last article I want to highlight is also from our February 17th issue of Circulation Research and it is coming from the lab of Shintaro Mandai at Tokyo Medical and Dental University and the title of the article is Circulating Extracellular Vesicle Propagated MicroRNA signatures as a Vascular Calcification Factor in Chronic Kidney Disease. Chronic Kidney Disease or CKD accelerates vascular calcification in part by promoting the phenotypic switching of vascular smooth muscle cells to osteoblast like cells. This study investigated the role of circulating small extracellular vesicles or SUVs from the kidneys in promoting this osteogenic switch. CKD was induced in rats and in mice by an adenine induced tubular interstitial fibrosis and serum from these animals induced calcification in in vitro cultures of A-10 embryonic rat smooth muscle cells. Intraperitoneal administration of a compound that prevents SEV biosynthesis and release inhibited thoracic aortic calcification in CKD mice under a high phosphorus diet. In Chronic Kidney Disease, the microRNA transcriptome of SUVs revealed a depletion of four microRNAs and the expression of the microRNAs inversely correlated with kidney function in CKD patients.   In vitro studies found that transected microRNA mimics prevented smooth muscle cell calcification in vitro. In silico analyses revealed that VEGF-A was a convergent target of all four microRNAs and leveraging this, the group used in vitro and in vivo models of calcification to show the inhibition of the VEGF-A, VEGFR-2 signaling pathway mitigated calcification. So in addition to identifying a new potential therapeutic target, these SUV propagated microRNAs are a potential biomarker that can be used for screening patients to determine the severity of CKD and possibly even vascular calcification.   Cindy St. Hilaire:        Today I have with me Dr Hind Lal who's an associate professor of medicine at the University of Alabama Birmingham and his post-doctoral fellow and the lead author of the study Dr Tousif Sultan. And their manuscript is titled Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation. And this article is in our February 3rd issue of Circulation Research. So thank you both so much for joining me today.   Tousif Sultan:              Thank you.   Hind Lal:                     Thank you for taking time.   Cindy St. Hilaire:        So ponatinib, it's a tyrosine kinase inhibitor and from my understanding it's the only treatment option for a specific group of patients who have chronic myelogenous leukemia and they have to harbor a specific mutation. And while this drug helps to keep these patients alive essentially, it's extremely cardiotoxic. So cardiotoxicity is somewhat of a new field. So Dr Lal, I was wondering how did you get into this line of research?    Hind Lal:                    So I was fortunate enough to be in the lab of Dr Tom Force and he was kind of father of this new area, now is very developed, it's called cardio-oncology. On those days there were basically everything started in cardio-oncology. So I just recall the first tyrosine kinase approved by FDA was in 2000 and that was... Imagine and our paper came in Nature Medicine 2005 and discovering there is... so to elaborate it a little bit, the cancer therapy broadly divided in two parts. One is called non-targeted therapy like chemotherapy, radiations, et cetera, and then there are cytotoxic drugs. So those cytotoxic drugs because they do not have any targeted name on it so they are, cardiotoxic are toxic to any organ was very obvious and understanding. When these targeted therapy came, which is mainly kinase inhibitor are monoclonal antibodies. So these are targeted to a specific pathway that is activated only in the cancer cells but not in any other cells in the body so they were proposed as like magic bullets that can take off the cancer without any cardiotoxity or minimal side effects. But even in the early phase like 2005 to 2010, these came out, these so-called targeted, they are not very targeted and they are not also the magic bullets and they have serious cardiotoxicity.   Cindy St. Hilaire:        And so what's the mechanism of action of ponatinib in the leukemia and how does that intersect with the cardiovascular system?   Hind Lal:                     Yeah, so this is very good question I must say. So what we believe at this point because, so leukemia if you know is driven by the famous Philadelphia chromosome, which is a translicational gene, one part of human chromosome nine and one part of human chromosome 22 and they translocate make a new gene which is BCR-ABL gene. And because it was discovered in Philadelphia UPENN, is named that Philadelphia chromosome, which is very established mechanism, that's how CML is driven. But what we have discovered that the cardiotoxicity driven by totally, totally different from the ponatinib is one of the inflammatory So it's kind of goodening. So this question is so good. One kind of toxicity is called on-target, when toxicity is mediated by the same mechanism, what is the mechanism of the drug to cure the cancer? So in that case your absolute is minimal because if you manipulate that, the drug's ability to cure the cancer will be affected but if the toxicity and the efficacy is driven by two different mechanism, then as in case of ponatinib seems like it's NLRP3 and inflammasome related mechanism. So this can be managed by manipulating this pathway without hampering the drug efficacy on the cancer.   Cindy St. Hilaire:        So what exactly is cardiotoxicity and how does it present itself in these patients?   Hind Lal:                     So these drugs like ponatinib, they call broader CVD effects. So it's not just cardiac, so they also in hypertensives and atherosclerosis and thrombosis, those kind of thing. But our lab is primarily focused on the heart. So that's why in this paper we have given impresses on the heart. So what we believe at this point that ponatinib lead to this proinflammatory pathway described in this paper, which is just 108A9-NLRP3-IL-1β and this inflammatory pathway lead to a cytokine storm very much like in the COVID-19 and these cytokine storms lead to excessive myocarditis and then finally cardiac dysfunction.   Cindy St. Hilaire:        Is the cytokine storm just local in the cardiac tissue or is it also systemic in the patients? Is cardiotoxicity localized only or is it a more systemic problem?   Tousif Sultan:              I would like to add in this paper we have included that we look this cytokine things and explain blood circulation, bone marrow. So the effect is everywhere, it's not local. So we didn't check other organs, maybe other organs also being affected with the ponatinib treatment.   Cindy St. Hilaire:        And what's the initial phenotype of a patient has when they start to get cardiotoxicity, what's kind of like a telltale symptom?   Hind Lal:                     So good thing that in recent years cardio-oncology developed. So initially the patient that were going for cancer treatment, they were not monitored very closely. So they only end up in cardiology clinic when they are having some cardiac events already. So thanks to the lot of development and growth in the cardio-oncology field, now most patients who going for a long-term cancer treatment, they are closely monitored by cardiology clinics.   Cindy St. Hilaire:        Got it. So they can often catch it before a symptom or an event. That's wonderful.   Hind Lal:                     Yeah, so there's a lot of development in monitoring.   Cindy St. Hilaire:        Wonderful. So you were really interested in figuring out why ponatinib induces cardiotoxicity and you mentioned that really up until now it's been very difficult to study and that's because of the limitation of available murine models. If you just inject a wild type mouse with ponatinib, nothing happens really. So what was your approach to finding relatively good murine models? How did you go about that?   Hind Lal:                     So this is the top scientific question you can ask. So like science, the field is try and try again. So initially this is the first paper with the ponatinib toxicity using the real in vivo models. Any paper before this including ours studies published, they were done on the cellular model in hiPSC, that isolated cardiomyocytes. So you directly putting the ponatinib directly the isolated cells. So this is first case when we were trying to do in vivo, maybe other attempt in vivo but at least not published. So first we also treated the animals with ponatinib and that failed, we don't see any cardiotoxic effect. And then when we going back to the literature, the clinical data is very, very clear from pharmacovigilance that ponatinib is cardiotoxic in humans. So when we're not able to see any phenotype in mouse, we realize that we are not mimicking what's happening in the humans.   So we certainly missing something. Now once again I quote this COVID-19, so many people get infected with COVID-19 but people are having preexisting conditions are on high risk to developing CVD. So there was some literature on that line. So we use this very, very same concept that if there is preexisting conditions, so likely who'd have developing future cardiac event will be more. So we use two model in this paper one atherosclerosis model which is APoE null mice mice, another is tag branding which is pressure overload model for the heart and as soon as we start using what we call comorbidity model like patient is having some preexisting conditions and we very clearly see the robust defect of ponatinib on cardiac dysfunction.   Cindy St. Hilaire:        Yeah, it's really, really well done and I really like that you use kind of two different models of this. Do you think it's also going to be operative in maybe like the diabetic mirroring models? Do you think if we expand to other comorbidities, you might also recapitulate the cardiotoxicity?   Hind Lal:                     So you got all the best questions.   Cindy St. Hilaire:        Thank you. I try.   Hind Lal:                     So because this is CML drug and lot of the risk factor for cardiovascular and cancer are common and even metabolic disease. So most of the time these patients are elderly patients and they're having metabolic conditions and most of the time they have blood pressure or something CVD risk factors. So I agree with you, it'll be very relevant to expand this to the diabetes or metabolic models, but these were the first study, we put all our focus to get this one out so news is there then we can expand the field adding additional models et cetera. But I agree with you that will be very logical next step to do.   Cindy St. Hilaire:        Yeah. And so I guess going back to what you know from the human study or the clinical trials or the human observations, are different populations of patients with CML more predisposed to cardio toxicity than others or is that not known yet?   Hind Lal:                     So one other area called pharmacovigilance. So what pharmacovigilance does patient all over the world taking these drugs. So WHO have their own vigilance system and FDA have their own, so it's called BG-Base for the WHO and it's called the FAERS for the FDA. So one can go back in those data sets and see if X patient taking this Y drug and what kind of symptoms or adverse effect they are seeing and if these symptoms are associated with something else. So there is data that if patients having CVD risk factor, they are more prone to develop ponatinib induced cardiac events. But it needs more polish like you asked the just previous question, diabetes versus maybe blood pressure means hypertension, atherosclerosis, or thrombosis. So it has not been delineated further but in a one big bucket if patients are having CVD risk factor before they are more prone and more likely to develop the cardiac events.   Cindy St. Hilaire:        So after you established that these two murine models could pretty robustly recapitulate the human phenotype, what did you do next? How did you come upon the S100A8/A9-NLRP3-IL-1β signaling circuit? How did you get to that?   Hind Lal:                     So in basic science work, whenever we do mouse is called until we get there is cardiac dysfunction, it's called phenotype, right? So mouse had a cardiac phenotype. So next step is, "Why? What is leading to that phenotype?" That's what we call mechanism. So there the best idea to fit the mechanism is using one of the unbiased approaches like you do unbiased proteomics, unbiased RNC analysis, something like this that will analyze the entire transcript like RNC and say, "Okay, these pathway are," then you can do further analysis that will indicate these pathway are different, are altered. So in this case we used RNC analysis and it came out that this yes A8 and yes A9, 100A8 and nine, they were the most upregulated in this whole set. And thereafter we were very lucky. So we started this study at Vanderbilt, where my lab was and thereafter we very lucky to move here and found Sultan who had a lot of experience with this inflammation and immune system and then Sultan may add something on this so he'll be the better person to say something on this.   Tousif Sultan:              So after our RNC analysis, so we got this S100A8 and nine as top hit with the ponatinib treatment. So then we validated this finding with our flow cytometric, qRT PCR aand then we started which pathway is going to release cytokine and all that. So we found that is NLRP3 inflammasome.   Cindy St. Hilaire:        Yeah and well and I guess maybe step back, what is S100A8/A9? What are those? Tousif Sultan:              Yeah, S10A8/A9 is a calcium binding protein. So that's also called alarmin and they basically binds with the pathogen associated pattern and other TLR2 like receptors and then start inflammatory pathway to release cytokine and all that and it's stable in heterodimer form. So S100A8 heterodimer with A9 and then bind with TLR and a start in this inflammatory pathway.   Cindy St. Hilaire:        And what type of cell is that happening in? Is that happening in the immune cells only or is it also in the cardiomyocyte, or...?   Tousif Sultan:              Yeah, we have included all this data. So from where this alarmin is coming with ponatinib treatment, so literature also suggested that neutrophils and monocytes, those cells are the potential to release the alarmin. So here we also found these two type of cells, neutrophils and monocytes. They release huge alarmin with the treatment of ponatinib.   Cindy St. Hilaire:        And so really taking this really neat mechanism to the next level, you then tried attenuating it by using broad anti-inflammatory steroid dexamethasone but also by targeting these specific components, the NLRP and the S100A specific inhibitors and they worked well. It worked really nicely. Does your data show that any of these therapies work better than the other and then are these viable options to use in humans?   Hind Lal:                     Yeah, we have some data in the paper. Are very broad which help a lot in COVID patients, far very acute infections. So in this case, situation is very different cause most of CML patients will going to take ponatinib for lifelong, there is no remission, right? So in those case, its certainly not a very attractive option. We have shown data in the paper that dexamethasone help with the heart but lead to some metabolic changes. So we have compared those with the NLRP3 inhibitors, those metabolic alterations, dexa versus the NLRP3 inhibitors, CY-09. And we demonstrated that targeting is specifically with paquinimod, our NLRP3 inhibitor CY-09, feel better. It can still rescue the cardiac phenotype without having those adverse effect on metabolic parameters.   Cindy St. Hilaire:        That's wonderful. Do you think though that because you have to take ponatinib for life, that long-term NLRP inhibition would also cause problems or...?   Hind Lal:                     So because not every patient who taking ponatinib would develop the cardiac phenotype, right? Which is like a 10%, 12%, patient developing cardiac dysfunction. So I think someone like I strongly believe paquinimod, which is inhibitor of S100A9, will be really good option or at least we have enough data that make us nail for at least a small clinical trial. And we quickly moving on that. At UAB we have our clinical cardio-oncology program and we are already in touch with the director for the clinical cardio-oncology program. So what we trying to do in that small trial is if one of the standard therapy for heart like beta blocker or ARBs inhibitor, is there any preference like one work better than the other in the standard care? So first we doing that project, then we obviously looking forward if one small clinical trial can be done with paquinimod. I strongly believe it should be helpful.   Cindy St. Hilaire:        That is wonderful. And so do you think... There's other chemotherapeutic agents or probably even other non-cancer drugs that cause cardiotoxicity, do you think this mechanism, this pathway, this S100A-NLRP-IL-1β axis is operative in all cardiotoxicities or do you think it's going to be very specific to the ponatinib?   Hind Lal:                     So it's certainly not all, but it'll be certainly more than ponatinib. So in our lab we are using another kinase inhibitor, which is osimertinib and it's not published yet, but now we know that it's also cardiotoxic because it's taking metabolic root or energetics disruption but not this pro-inflammatory part, but we're doing another project which is strep pneumonia induced cardiac dysfunction, which is called pneumonia. So strep pneumoniae, which leads to the pneumonia ,and lot patient die because of the failing heart we see here in the hospitals and we see these pathways operational over there and we gearing up to do clinical trial on that aspect as well, but it's not generalized like all kind of heart will have the same mechanism.   Cindy St. Hilaire:        It's wonderful to see you're already taking those next steps towards really kind of bringing this to a translational/clinical study. So what was the most challenging aspect of this study?   Tousif Sultan:              The challenging aspect, ponatinib is a kinase inhibitor and that was surprising for us how it's activating immune cells. Generally kinase inhibitors, inhibits all the cells like that. So that was challenging. So we repeated it many times did in vitro experiment to confirm that. So we just added, just treated in vitro immune cells with the ponatinib and confirmed it. So that was little challenging.   Cindy St. Hilaire:        So what's next? You mentioned you're going to try some clinical trials, early stage clinical trials. What's next mechanistically, what do you want to go after?   Hind Lal:                     So what we are doing next and we are very, very eagerly trying to do that. So what it was done, we used the cardiac comorbidity models, but as you know, anybody who will take ponatinib will have cancer, right? So we strongly believe that we miss one factor. There was no cancer on these. So that is very logical next step. What that will allow us to do, what rescue experiment we'll have done in this paper. So we saw, "Okay, this rescue the cardiac phenotype, which is taken care of now," but very same time, we not able to demonstrate that this is happening without hurting the cancer efficacy. So if we have the dual comorbid mouse, which have CML a real thing and we have cardiac thing, then that will allow us to demonstrate, "Okay, we got something that can take care of the cardiac problem without hurting the efficacy on the cancer." And it will be best if you also help little bit to more potentiate the cancer efficacy.   Cindy St. Hilaire:        Yes. Excellent. Well, congratulations on a beautiful study, really exciting findings. Dr Lal and Dr Sultan, thank you so much for taking the time to talk with me today.   Tousif Sultan:              Thank you so much.   Hind Lal:                     Well thank you, Cynthia. We really appreciate your time. Thank you for having us.   Cindy St. Hilaire:        Yeah, it was great.   Cindy St. Hilaire:        That's it for our highlights from the February 3rd and February 17th issues of Circulation Research. Thank you so much for listening. Please check out the Circulation Research Facebook page and follow us on Twitter and Instagram with the handle @CircRes and #DiscoverCircRes. Thank you to our guests, Dr Hind Lal and Dr Tousif Sultan. This podcast is produced by Ishara Ratnayake, edited by Melissa Stoner and supported by the editorial team at Circulation Research. Some of the copy text for the highlighted articles was provided by Ruth Williams. I'm your host, Dr Cynthia St. Hilaire, and this is Discover CircRes, you're on-the-go source for most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2023. And the opinions expressed by the speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, please visit ahajournals.org.  

Reconstitution. This operation is often misunderstood in that most at the Tactical Level of War have yet to experience what actually happens. Is it a sustainment operation? Are there different kinds of reconstitution operations? In this episode of Breaking Doctrine, our host, Captain Wyatt Harper sat down to discuss reconstitution with the Commanding General of the Combined Arms Support Command, the Sustainment Center of Excellence, and Fort Lee, Major General Mark Simerly and Colonel Andy Morgado, the Director of the School of Advanced Military Studies (SAMS) here at Fort Leavenworth.

Pre-IPO Stock Market Update - Jan 06, 2023Topics include;- Canva launches new products; Canva Docs + Magic Write- 409A (internal) valuation updates from Stripe, Checkout.com, Instacart, Databricks- Capital raises from Asimov, Synthekine, ChartHop, Immune-Onc Therapeutics, Ensoma- 40+ new indexes published ... AG Dillon Pre-IPO Equity Vintage Indexes- Exits from Magic Leap, Evernote, FTX (bankrupt)- Quarterly update of AG Dillon Pre-IPO Equity Index; average of last 40 quarterly vintage indexes- Reconstitution of AG Dillon Pre-IPO Equity Secondary Investable Market Index- Canva company spotlight- Autonomous driving emerging technology spotlightView full video here = https://youtu.be/mZdVx2z8TZgRegister for the live weekly webinar here www.agdillon.com/webinar.www.agdillon.com/agdillon_vcfund for more on AG Dillon & Co venture capital funds.

“Radio 5G” Nancy Hopkins and Mark Joseph discussing interviews with Todd Callender & Jeffrey Prather on "Surveillance Under the Skin? WE ARE ALREADY THERE." - The Connection Between 5G, Crystal Oscillators, CBDCs, Luciferase-Based Biosensors & the mRNA-Modifying Shots. SHOW PHOTOS Thrivetime Show Clay Clark Todd Callender www.VaxxChoice.com and www.DrAdvocates.com Jeffrey Prather www.JeffreyPrather.com Jan Shaw's 12/31/22 SCOTUS LEGAL CASE DOCUMENT SCOTUS LEGAL CASE VIDEO INSTRUCTIONS ON HOW TO WRITE SCOTUS New shows of Radio 5G can be heard Wednesdays at 12-2 pm EST https://www.cosmicreality.com/radio.html Archived Podcasts: https://www.cosmicreality.com/5g-know-radio-archives.html Nancy's books - free PDF copies https://www.cosmicreality.com/books--blogs.html Nancy's Shungite Recommendations: https://www.cosmicreality.com/shungite-recommendations.html Shungite Store https://mysticalwares.com/ 

Episode 120: Immune Reconstitution Inflammatory Syndrome (IRIS) Abeda Faharti and Dr. Schlaerth present the definition, diagnosis, and treatment of IRIS. Moderated by Dr. Arreaza. Written by Abeda Farhati, MS4, Ross University School of Medicine. Editing and comments by Katherine Schlaerth, MD, and Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Definition.Have you heard of IRIS? No, not the color portion of our eyes. IRIS is short for Immune Reconstitution Inflammatory Syndrome. This condition occurs in immunocompromised patients with HIV/AIDS due to an overactive inflammatory response. In most cases, it occurs after initiating antiretroviral therapy (ART). To understand IRIS in HIV patients, we must first understand HIV.HIV.The Human Immunodeficiency Virus (HIV) infection was first reported in 1981. The virus attacks the immune system, destroying white blood cells called CD4+ T lymphocytes, which are part of our body's defense mechanism. These cells are also known as "helper T cells" and are responsible for destroying viruses, bacteria, and other germs that make us sick.When your CD4+ count is low, you are more likely to get serious infections from viruses, bacteria, and fungi, which usually do not cause problems in otherwise healthy individuals. These infections are called Opportunistic infections, and they can be deadly. To restore CD4+ T lymphocytes, HIV patients are started on ART to normalize their immune response to pathogens. As a result of these treatments, HIV patients' lives have been significantly improved and prolonged. [Comment by Dr. Arreaza: It is paradoxical, but some HIV patients are among the healthiest patients I have seen.]Despite this, no treatment is guaranteed to be without side effects. Increases in CD4+ T lymphocytes trigger the immune system to respond to any persisting antigen, regardless of whether it is fragments or intact organisms. As a result, a hyperinflammatory response may occur.Diagnosis.There are no established criteria for diagnosing IRIS. It is generally accepted that IRIS requires the worsening of an existing infection or an unrecognized, preexisting infection in the context of improved immune function. For a diagnosis to be made, most, if not all of the following features must be present:The presence of a low CD4 count (less than 100 cells) before initiating treatment with ART (Except IRIS secondary to preexisting TB infection can occur with CD4 counts >200 cells).The presence of an inflammatory condition, especially after ART is initiated.The absence of drug-resistant infection, bacterial superinfection, drug allergy, or other adverse drug reactions.The absence of patient noncompliance or reduced drug levels due to drug-drug interactions or malabsorption.Clinical Manifestations.IRIS can be presented in patients in 2 ways:Patient's with a preexisting infectious disease that has NOT been treated, getting paradoxically worse after initiating treatment with ART ---this is known as “unmasking IRIS” ORPatient's with a preexisting infectious disease that has been previously diagnosed and treated but regained capacity after treatment with ART, causing it to mount an inflammatory response – this is known as “paradoxical IRIS.”In summary: Unmasking IRIS and paradoxical IRIS.Patients with IRIS have clinical features that vary widely. The presentations are strongly dependent on the type of preexisting opportunistic infection. For example, about 75% of patients with a mycobacterial or cryptococcal-related infection will develop a fever. In contrast, fever is rarely seen in cytomegalovirus (CMV) infections.Risk & Prevention.Researchers have found that lower CD4 cell counts or high HIV RNA levels at the time of anti-retroviral treatment initiation increase the risk of developing IRIS. One way to prevent IRIS development is to treat opportunistic infections prior to starting ART. Although this reduces the risk of IRIS development, it does not guarantee it.Treatment.In “unmasking IRIS,” patients can be treated with antibiotics, antivirals, or antifungals against the underlying infectious organism. In severe cases, steroids can also be used to suppress inflammation until the infection has been eradicated. Unfortunately, there is no treatment for paradoxical IRIS. Most patients who experience “paradoxical IRIS” reactions will get better spontaneously without additional therapy.Incidence of IRIS.The overall incidence of IRIS is unknown; however, studies have shown that anywhere from 25 to 30% of HIV patients who start antiretroviral treatment develop IRIS in the first six months. You may ask, which preexisting infections can lead to patients developing IRIS?Pathogens associated with IRIS.Different pathogens have been associated with the development of IRIS. The leading pathogens include:Mycobacterium tuberculosisMycobacterium avium complexCytomegalovirusCryptococcus neoformansPneumocystis jiroveciiHerpes simplex virusHepatitis B virusHuman herpes virus 8 (associated with Kaposi sarcoma)Non-HIV etiologies.IRIS can also be seen in other immunocompromised conditions, such as:Solid organ transplant recipients Postpartum period – 3 to 6 weeks after giving birthNeutropenic patients – with an absolute neutrophil count of less than 500Patients on Tumor Necrosis Factor Antagonists (TNF antagonists)- are used to treat chronic conditions such as ulcerative colitis, Crohn's disease, or sarcoidosis.In summary, Immune Reconstitution Inflammatory Syndrome (IRIS) is a hyper-inflammatory state seen after initiating ART in HIV patients whose improved immune system responds to previously acquired opportunistic infection, whether treated or not.The treatment is directed to the unmasked specific opportunistic infection or support therapy if no active infection is found.____________________________Conclusion: Now we conclude episode number 121, “Immune Reconstitution Inflammatory Syndrome (IRIS).” This syndrome presents in about 30% of HIV patients when they start ART. A stronger immune system means a stronger immune reaction. So, keep in mind this diagnosis when your HIV patients get sicker when they are supposed to get better after starting ART. This week we thank Hector Arreaza, Abeda Farhati, and Katherine Schlaerth. Audio edition by Adrianne Silva.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________Links:“CD4 Lymphocyte Count: MedlinePlus Medical Test.” Medlineplus.gov, accessed on November 4, 2022.https://medlineplus.gov/lab-tests/cd4-lymphocyte-count/#:~:text=A%20CD4%20count%20is%20mostly,have%20trouble%20fighting%20off%20infections.Sun HY, Singh N. Immune reconstitution inflammatory syndrome in non-HIV immunocompromised patients. Curr Opin Infect Dis. 2009 Aug;22(4):394-402. doi: 10.1097/QCO.0b013e32832d7aff. PMID: 19483618. https://pubmed.ncbi.nlm.nih.gov/19483618/Thapa, Sushma, and Utsav Shrestha. “Immune Reconstitution Inflammatory Syndrome.” PubMed, StatPearls Publishing, 2022, www.ncbi.nlm.nih.gov/books/NBK567803/.Wolfe, Cameron. Immune reconstitution inflammatory syndrome, UpToDate. ww.uptodate.com, https://www.uptodate.com/contents/immune-reconstitution-inflammatory-syndrome. Accessed November 14, 2022.Royalty-free music used for this episode: “Keeping Watch,” New Age Landscapes. Downloaded on October 13, 2022, from https://www.videvo.net/royalty-free-music-albums/new-age-landscapes/. 

Episode 105:This week we're continuing Russia in Revolution An Empire in Crisis 1890 - 1928 by S. A. Smith[Part 1]Introduction[Part 2-5]1. Roots of Revolution, 1880s–1905[Part 6-8]2. From Reform to War, 1906-1917[Part 9-12]3. From February to October 1917[Part 13 - 16]4. Civil War and Bolshevik PowerThe Expansion of SovietsNational Self-Determination and the Reconstitution of EmpireViolence and TerrorThe Suppression of the Socialist Opposition[Part 17 - This Week]4. Civil War and Bolshevik PowerOne Party Dictatorship in Action - 0:20Discussion - 23:42[Part 18 - 20?]5. War Communism[Part 21 - 23?]6. The New Economic Policy: Politics and the Economy[Part 24 - 27?]7. The New Economic Policy: Society and Culture[Part 28?]ConclusionFootnotes:77) 2:44Gimpel'son, Formirovanie, 78.78) 6:01Sovetskaia derevnia glazami VChK-OGPU, vol. 1:, 1918–22: Dokumenty i materialy (Moscow: ROSSPEN, 1998), 32.79) 6:42A. I. Chernykh, Stanovlenie Rossii Sovetskoi: 20-e gody v zerkale sotsiologii (Moscow: Pamiatniki Istoricheskoi Mysli, 1998), 262; Richard Sakwa, Soviet Communists in Power: A Study of Moscow during the Civil War, 1918–21 (New York: St Martin's, 1988).80) 7:22State Archive of Perm' Oblast', ГАПО ф. 201, оп.1, д.11, л.7.81) 8:08Robert V. Daniels, The Conscience of the Revolution: Communist Opposition in Soviet Russia (Cambridge, MA: Harvard University Press, 1960).82) 9:30James Harris, ‘Stalin as General Secretary: The Appointments Process and the Nature of Stalin's Power', in Sarah Davies and James Harris (eds), Stalin: A New History (Cambridge: Cambridge University Press, 2005), 66.83) 12:58G. Gimpel'son, Sovetskie upravlentsy, 1917–1920gg. (Moscow: RAN, 1998), 167.84) 13:33I. S. Rat'kovskii and M. V. Khodiakov, Istoriia sovetskoi Rossii (St Petersburg: Lan', 1999), 54.85) 14:01S. A. Pavliuchenkov, Voennyi kommunizm v Rossii: vlast' i massy (Moscow: RKT-Istoriia, 1997), 189.86) 14:31I. V. Pavlova, Stalinizm: Stanovlenie mekhanizma vlasti (Novosibirsk: Sibirskii khronograf, 1993), 50.87) 15:09Gimpel'son, Sovetskie upravlentsy, 203.88) 19:15Bertram D. Wolfe, Strange Communists I Have Known (London: George Allen and Unwin, 1966), 88.89) 20:23Balabanoff, Impressions of Lenin, 102–3.90) 21:03.91) 22:10.92) 23:01Service, Lenin: A Biography, 299; V. I. Lenin, ‘Second All-Russian Congress of Miners', 23 Jan. 1921, .

Episode 104:This week we're continuing Russia in Revolution An Empire in Crisis 1890 - 1928 by S. A. Smith[Part 1]Introduction[Part 2-5]1. Roots of Revolution, 1880s–1905[Part 6-8]2. From Reform to War, 1906-1917[Part 9-12]3. From February to October 1917[Part 13 - 15]4. Civil War and Bolshevik PowerThe Expansion of SovietsNational Self-Determination and the Reconstitution of Empire[Part 16 - This Week]4. Civil War and Bolshevik PowerViolence and Terror - 0:19The Suppression of the Socialist Opposition - 19:56[Part 17]4. Civil War and Bolshevik Power[Part 18 - 20?]5. War Communism[Part 21 - 23?]6. The New Economic Policy: Politics and the Economy[Part 24 - 27?]7. The New Economic Policy: Society and Culture[Part 28?]ConclusionFootnotes:57) 0:36James Ryan, Lenin's Terror: The Ideological Origins of Early Soviet State Violence (London: Routledge, 2012).58) 3:26Latsis, ‘Pravda of krasnom terrore', Izvestiia, 26, 6 Feb. 1920, 1.59) 3:57Michael Melancon, ‘Revolutionary Culture in the Early Soviet Republic: Communist Executive Committees versus the Cheka', Jahrbücher für Geschichte Osteuropas, 57:1 (2009), 1–22 (9).60) 6:14George Leggett, The Cheka: Lenin's Political Police: The All-Russian Extraordinary Commission for Combatting Counter-Revolution and Sabotage, 1917–1922 (Oxford: Clarendon Press, 1981), 467.61) 7:06The use of torture by the Cheka was hinted at in the press. See the complaint by a party member who had fallen into the clutches of the Cheka in Moscow. Izvestiia, 18, 26 Jan. 1919, 2.62) 8:45I. N. Kamardin, ‘Rabochii protest v Povolzh'e v 1919–1920gg'. .63) 9:41; .64) 11:55A. G. Tepliakov, ‘Chekisty Kryma v nachale 1920-kh gg', Voprosy istorii, 11, Nov. 2015, 139–45.65) 14:06.66) 15:36Dietrich Beyrau, ‘Brutalization Revisited: The Case of Russia', Journal of Contemporary History, 50:1 (2015), 15–37.67) 16:32Martin Conway and Robert Gerwarth, ‘Revolution and Counter-Revolution', in Donald Bloxham and Robert Gerwarth (eds), Political Violence in Twentieth-Century Europe (Cambridge: Cambridge University Press, 2011), 140–76 (141). Stathis Kalyvas, The Logic of Violence in Civil War (Cambridge University Press, 2006), 365–87.68) 16:59Hoffmann and Kotsonis (eds), Russian Modernity; Peter Holquist, ‘Violent Russia, Deadly Marxism? Russia in the Epoch of Violence, 1905–21', Kritika, 4:3 (2003), 627–52.69) 17:18Holquist, Making War, ch. 6.70) 17:59Cited in Mawdsley, Russian Civil War, 67.71) 19:26Smele, Historical Dictionary, 138–41, 1142–3, 92. I am grateful to Erik Landis for drawing my attention to Marat Khairulin, ‘Boi za Kazan' (avgust–sentiabr' 1918g.). Khronika deistvii aviatsii', .72) 20:07Vladimir N. Brovkin, Behind the Front Lines of the Civil War: Political Parties and Social Movements in Russia, 1918–1922 (Princeton, NJ: Princeton University Press, 1994).73) 20:49Scott B. Smith, Captives of Revolution: The Socialist Revolutionaries and the Bolshevik Dictatorship, 1918–1923 (Pittsburgh: University of Pittsburgh Press, 2011).74) 22:55Z. Galili and A. Nenarokov (eds), Men'sheviki v 1918 godu (Moscow: ROSSPEN, 1999).75) 24:12D. B. Pavlov, Bol'shevistskaia diktatura protiv sotsialistov i anarkhistov 1917—seredina 1950-kh godov (Moscow: ROSSPEN, 1999), 63.76) 30:08Brovkin, Behind the Front Lines, 268.

Episode 103:This week we're continuing Russia in Revolution An Empire in Crisis 1890 - 1928 by S. A. Smith[Part 1]Introduction[Part 2-5]1. Roots of Revolution, 1880s–1905[Part 6-8]2. From Reform to War, 1906-1917[Part 9-12]3. From February to October 1917[Part 13 - 14]4. Civil War and Bolshevik PowerThe Expansion of Soviets[Part 15 - This Week]4. Civil War and Bolshevik PowerNational Self-Determination and the Reconstitution of Empire - 0:20[Part 15 - 16?]4. Civil War and Bolshevik Power[Part 17 - 19?]5. War Communism[Part 20 - 22?]6. The New Economic Policy: Politics and the Economy[Part 23 - 26?]7. The New Economic Policy: Society and Culture[Part 27?]ConclusionFootnotes:46) 0:50Richard Pipes, The Formation of the Soviet Union: Communism and Nationalism, 1917–1923 (Cambridge, MA: Harvard University Press, 1954); Jeremy Smith, The Bolsheviks and the National Question, 1917–1923 (New York: St Martin's, 1999).47) 4:21Izvestiia, 11, 16 Jan. 1918, 3; Izvestiia, 12, 17 Jan. 1918, 2.48) 8:56Alfred E. Senn, The Emergence of Modern Lithuania (New York: Columbia University Press, 1959).49) 16:03O. V. Budnitskii, Rossiiskie evrei mezhdu krasnymi i belymi (1917–1920) (Moscow: ROSSPEN, 2006), 275–6; Oleg Budnitskii, ‘Shots in the Back: On the Origin of the Anti-Jewish Pogroms of 1918–1921', in E. M Avrutin and H. Murav (eds), Jews in the East European Borderlands (Boston: Academic Studies Press, 2012), 187–210.50) 18:00.51) 18:51Peter Holquist, Making War, Forging Revolution: Russia's Continuum of Crisis, 1914–1921 (Cambridge, MA: Harvard University Press, 2002).52) 25:35Adeeb Khalid, ‘Nationalizing the Revolution in Central Asia: The Transformation of Jadidism, 1917–1920', in Ronald G. Suny and Terry Martin (eds), A State of Nations: Empire and Nation-Making in the Age of Lenin and Stalin (Oxford: Oxford University Press, 2001), 145–64.53) 28:45Marco Buttino, La Rivoluzione capovolta: L'Asia centrale tra il crollo dell'impero Zarista e la formazione dell'URSS (Naples: L'ancora del Mediterraneo, 2003).54) 30:13Daniel E. Schafer, ‘Local Politics and the Birth of the Republic of Bashkortostan, 1919–1920', in Suny and Martin (eds), A State of Nations, 165–90.55) 33:25M. A. Persits, ‘Vostochnye internatsionalisty v Rossii i nekotorye voprosy natsional'no-osvoboditel'nogo dvizheniia (1918–iul' 1920)', Komintern i Vostok: bor'ba za leninskuiu strategiiu i taktiku v natsional'no-osvoboditel'nom dvizhenii (Moscow: Nauka, 1969), 53–109 (96).56) 33:56‘Biuro Sekretariata TsK RKP (iiun'1923g.)', in Tainy natsional'noi politiki TsK RKP: stenograficheskii otchet sekretnogo IV soveshchaniia TsK RKP 1923g. (Moscow: INSAN, 1992), 74; .