Podcasts about T2

This week's episode is all about Cine Gear, which took place at the beginning of the month in Los Angeles. We discuss what brands and new products Johnnie covered at the show — from the ZEISS Horizon Anamorphic lens to the Sony RIALTO 65 sensor block. Further, we talk about the Kinefinity VISTA pricing, Apple Immersive Video updates at WWDC26, the ARRI Eurovision documentary, and GoPro's going concern warning. (00:00) Intro (06:00) ZEISS Horizon Anamorphic First Look – 2x Full-Frame Lenses With Internal Motors https://www.cined.com/zeiss-horizon-anamorphic-first-look-2x-full-frame-lenses-with-internal-motors/  (15:04) ZEISS Panoptes 65 Unveiled – Ten Large-Format Primes at T2.2 with LPL Mount and 59.9mm Image Circle https://www.cined.com/zeiss-panoptes-65-unveiled-ten-large-format-primes-at-t2-2-with-lpl-mount-and-59-9mm-image-circle/  (25:36) Sony RIALTO 65 in Development – 65mm Sensor Block for the VENICE 2, Remote Operation, Multiple Recording Modes https://www.cined.com/sony-rialto-65-in-development-65mm-sensor-block-for-the-venice-2-remote-operation-multiple-recording-modes/  (30:41) Cinelux Project SIXTEEN Hybrid Film and Digital Super 16 Camera – First Look https://www.cined.com/cinelux-project-sixteen-hybrid-film-and-digital-super-16-camera-first-look/ (40:30) Bosma Vega H2 First Look – 6K Full-Frame Camera With HVS https://www.cined.com/bosma-vega-h2-first-look-6k-full-frame-camera-with-hvs/  (49:42) SmallRig Steps Into Bags With a 25L Backpack Designed to Secure Your Gear https://www.cined.com/smallrig-steps-into-bags-with-a-25l-backpack-designed-to-secure-your-gear/  (51:15) SmallRig Enters the Storage Market With a Phone-Mounted SSD https://www.cined.com/smallrig-enters-the-storage-market-with-a-phone-mounted-ssd/  (55:02) Why Profoto Is Betting on High-End Cinema Lighting – The Thinking Behind the ProPanel 3×2 https://www.cined.com/why-profoto-is-betting-on-high-end-cinema-lighting-the-thinking-behind-the-propanel-3x2/  (57:20) Strada 2 First Look – Local Drives, Remote Editing https://www.cined.com/strada-2-first-look-local-drives-remote-editing/  (01:02:47) NANLUX Matrix 2500B and Matrix 2500C – First Look https://www.cined.com/nanlux-matrix-2500b-and-matrix-2500c-first-look/  (01:05:18) Eddie AI's Shamir Allibhai on Building an AI Teammate for Editors https://www.cined.com/eddie-ais-shamir-allibhai-on-building-an-ai-teammate-for-editors/  (01:08:45) Tilta Illusion Magnetic Filters Introduced – Modular Polarization and VND https://www.cined.com/tilta-introduces-the-illusion-magnetic-filters-modular-polarization-and-vnd/  (01:10:49) SIRUI IronStar 100mm Anamorphic Macro Lens – A Close Focus First for the Series https://www.cined.com/sirui-ironstar-100mm-anamorphic-macro-lens-a-close-focus-first-for-the-series/ (01:17:20) Cadrage Studio Launches in Early Access – Pre-Production Suite from the Director's Viewfinder Team https://www.cined.com/cadrage-studio-launches-in-early-access-pre-production-suite-from-the-directors-viewfinder-team/  (01:21:42) Kinefinity VISTA Confirmed at $2,499 – Full-Frame 6K Open Gate, 220GB Built-In SSD, 610g Body https://www.cined.com/kinefinity-vista-confirmed-at-2499-full-frame-6k-open-gate-220gb-built-in-ssd-610g-body/  (01:25:00) Apple Immersive Video Gets Live Formats, iPhone Playback, and Static Foveation Streaming at WWDC26 https://www.cined.com/apple-immersive-video-gets-live-formats-iphone-playback-and-static-foveation-streaming-at-wwdc26/  (01:31:40) ARRI, 12 Points – How Eurovision 2026 Was Shot on 24 ALEXA 35 Live Cameras https://www.cined.com/arri-12-points-how-eurovision-2026-was-shot-on-24-alexa-35-live-cameras/  (01:33:19) GoPro Warns It May Not Survive the Year as Auditor Flags Going Concern Doubt https://www.cined.com/gopro-warns-it-may-not-survive-the-year-as-auditor-flags-going-concern-doubt/  (01:35:12) The Chronos Project's Edge Bets on Real Cameras Where Most Long-Term Remote Timelapse Rigs Use Action Cams https://www.cined.com/the-chronos-projects-edge-bets-on-real-cameras-where-most-long-term-remote-timelapse-rigs-use-action-cams/ 

En este episodio: Noticias de Silo T3, Nadie nos va a extrañar T2, el traje de Luthor en Man of Tomorrow, los finales de Hacks y Euphoria, la grata sorpresa que ha sido Nicolas Cage en Spider-Noir y el escandaloso patrocinio de Martin Scorsese y una startup de IA…¡El HYP3 es el podcast de cultura pop y anécdotas gafapasta!Esta es la segunda parte del episodio 636, la primera se subió el viernes pasado. Puedes ver o escuchar este podcast completo y sin anuncios en ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Patreon⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ y ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Membresías YouTube⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠.

In this episode of China Manufacturing Decoded, Adrian is joined by Paul Adams, Head of New Product Development at the Sofeast Group's contract manufacturer Agilian Technology, to discuss one of the most common assumptions hardware founders make before moving into tooling: that tooling will take “8 to 12 weeks.” Paul explains why that figure can be true in very simple cases, but why it is often misleading for real consumer electronics, IoT, and hardware products. Tooling timelines depend on design readiness, DFM review, part complexity, steel selection, toolmaker capacity, customer responsiveness, and the timing of Chinese holidays such as Chinese New Year and Golden Week. They also discuss why the tooling clock does not really start when the purchase order is placed, why T0, T1, and T2 trials need to be planned carefully, and why founders should build schedule buffers before cutting steel. For hardware startups and product teams preparing for injection molding, metal stamping, die casting, or other production tooling, this episode explains how to build a more realistic tooling schedule and avoid costly launch delays.   Podcast sections 00:00:31 – The “8 to 12 week tooling timeline” 00:02:28 – What tooling includes and why it matters 00:04:21 – Tooling cost and why first-time founders get caught out 00:06:08 – Where the 8 to 12 week figure comes from 00:07:23 – Why real consumer electronics products are more complex 00:08:35 – When the tooling timer really starts 00:11:10 – Why design readiness and DFM review are critical 00:13:26 – How part complexity affects tooling lead time 00:13:50 – Steel selection: P20, H13, and tool life 00:15:40 – Responsiveness during T0, T1, and T2 trials 00:16:26 – Why being in China can speed up tooling decisions 00:19:03 – Planning around Chinese New Year, Golden Week, and May Day 00:21:47 – How to create a tooling schedule that works 00:22:05 – Reviewing the DFM report properly before cutting steel 00:24:00 – Building a tooling specification and critical path plan 00:25:34 – Understanding T0, T1, T2, and rework cycles 00:27:45 – Why you should always build in a schedule buffer 00:28:56 – Why many tooling delays come from the customer side 00:30:15 – Final advice: understand the full tooling process   Related content Tooling Management for Plastic Injection Molds in China Plastic Injection Mold Tooling Management & Risk Reduction [Podcast] Common Design For Manufacture Improvements On Plastic Injection Molded Parts Injection Mold Tooling Roadmap: How to Get from Smart Design to T1 Samples What are Plastic Injection Mold Tooling Revisions? (3 examples) How To Make Faster Injection Mold Tooling [7 Tips] Plastic Injection Molding Pilot Runs: What You Need To Know The Four Levels of Plastic Injection Molding Suppliers in China Get in touch with us Connect with us on LinkedIn Contact us via Sofeast's contact page Subscribe to our YouTube channel Prefer Facebook? Check us out on FB

Dr. Bradley Erickson, Director of the Mayo AI Lab, speaks with HexAI podcast host, Jordan Gass-Pooré in advance of the University of Pittsburgh's annual AI Summer School program in Medical Imaging Informatics organized by Pitt's Health and Explainable AI Research Lab (HexAI) and the Computational Pathology and AI center of Excellence (CPACE). The episode simulates two different professional vantage point scenarios to help students visualize the vast, multi-dimensional landscape of artificial intelligence in healthcare and radiology.The first half of the episode drops students directly into the vantage point of an AI expert attending a technical conference, where medical imaging informatics are being contrasted with everyday computer vision. Dr. Erickson explains how medical data often extends into multiple dimensions by incorporating complex spatial matrices and tissue properties like T1 and T2 tracking on MRIs, far surpassing standard 2D photographic pixels. He highlights why generic consumer AI tools like simple heat maps or saliency maps fall short of establishing clinical trust; while they can successfully point to where a brain tumor is, they completely fail to explain what that tumor is or why it is changing texture. Furthermore, Dr. Erickson discusses the profound challenge of "ground truth" uncertainty in medicine, explaining that training predictive algorithms is incredibly difficult because definitive biological labels are frequently masked by biological reactions or a lack of definitive longitudinal data.The second half of the podcast episode places students into the role and vantage point of a hospital administrator, exposing students to the active economic and structural deliberations currently playing out in modern hospital boardrooms. Dr. Erickson underscores the considerations and financial constraints that hospitals contend with and explains that while new narrowly focused diagnostic AI tools are attractive, the most immediate return on investment for hospitals often comes from practical, language-based text summarization and ambient patient recording systems. Crucially, this administrative perspective teaches students that the health industry desperately needs supportive roles beyond traditional doctors and researchers, such as AI project managers, integration specialists, and governance officers who can oversee model confidence and decide exactly when to adapt AI solutions or pull failing applications or algorithms back.Dr. Erickson emphasizes that entering this revolutionary field requires a willingness to learn through iteration, push back on assumptions, and manage the critical intersections of technology, safety, and human care. Through an open exploration of technical hurdles and administrative realities, the episode provides a rich conceptual primer for AI Summer School participants designed to cultivate critical thinking informing views on AI in medical imaging, hands-on project development and coding.

En Capital Intereconomía, el Radar Empresarial pone el foco en Salesforce, que cae en after hours tras decepcionar al mercado con sus previsiones de ingresos pese al impulso general de la inteligencia artificial en el sector tecnológico. En el espacio de IronIA Fintech, Javier Riaño analiza el auge de las carteras modelo y cómo están cambiando la forma en la que los inversores construyen y gestionan sus estrategias de inversión. En el Foro de la Inversión, Iván Plaza, socio director de Aurica Capital, repasa la visión de la firma sobre el mercado de capital privado, la estrategia de inversión en compañías participadas en minoría y el crecimiento mediante operaciones buy & build. La entrevista también aborda casos recientes como la operación con T2ó, la entrada de Reale Seguros en Canitas y la visión de Aurica sobre sectores como el alquiler seguro, además de los próximos pasos estratégicos de la gestora. El programa se completa con el consultorio de fondos junto a Gabriel López, de Inverdif.

Proton-Drive Angebot

Tin tức tối 24-5: Xe đi cao tốc TP.HCM - Long Thành đã bắt đầu đi tuyến T2 để vào cao tốc Biên Hòa - Vũng Tàu; Xử phạt người cha giao con trai 4 tuổi lái ca nô trên sông Tiền; Công an Lào Cai bắt ổ nhóm ma túy ở Tả Van... là những tin tức đáng chú ý.

Are you exhausted, cold, foggy, gaining weight, or feeling “off” even though your thyroid labs look “normal”? In this episode of The Trim Healthy Podcast, Serene and Pearl welcome back special guest Dr. Amie Hornaman, also known as The Thyroid Fixer, to talk about her new book The Thyroid Fix and why so many women are struggling without getting real answers. Dr. Amie shares her own powerful story of being dismissed and misdiagnosed, explains the difference between “normal” and truly optimal thyroid labs, and unpacks why T4-only medications may not be enough for many women. Together, we talk about Hashimoto's, perimenopause, menopause, cortisol, testosterone, birth control, T2, and why thyroid health is deeply connected to energy, metabolism, mood, sleep, weight, and long-term wellness. This conversation is full of straight talk, hope, and practical insight for women who know something is wrong but have been told everything looks fine. In this episode, we discuss: * Why “normal” thyroid labs may still leave women feeling terrible * Dr. Amie's personal journey with thyroid misdiagnosis * The connection between thyroid, sex hormones, cortisol, and metabolism * Why T4-only thyroid medication may not optimize thyroid health * Hashimoto's, autoimmune risk, and low testosterone * How perimenopause and menopause can impact thyroid function * Birth control's effect on thyroid and hormone health * What T2 is and why it may support metabolism and energy * Why thyroid hormone replacement is not “just another medication” Learn more from Dr. Amie at dramie.com Order The Thyroid Fix at thyroidfixbook.com Learn more about your ad choices. Visit megaphone.fm/adchoices

House and Nathan react to Aaron Rai winning the PGA Championship at Aronimink. They break down the top 10 finishes, including Jon Rahm, Justin Thomas, Rory McIlroy, Cameron Smith, and much more. Plus, they react to Bryson DeChambeau missing another major cut, and is Scottie Scheffler still the best golfer in the world?(0:00) Welcome to Fairway Rollin'!(1:40) Aaron Rai (-9) wins the PGA Championship(11:10) Takeaways from Jon Rahm's T2 finish(18:10) Is Justin Thomas back?(19:40) Does Rory have beef with PGA of America?(23:55) Cameron Smith's return to contention(33:15) Does this PGA schedule make sense?(36:05) Thoughts on CBS's coverage(39:30) Is Ludvig Åberg a dog?(45:45) Reacting to Bryson DeChambeau missing the cut again(51:25) Is Scottie Scheffler still the best player in the world?The Ringer is committed to responsible gaming. Please visit https://fanduel.com/playwithaplan to learn more about the resources and helplines.Hosts: Joe House and Nathan HubbardProducers: Tucker Tashjian and Mike Wargon Learn more about your ad choices. Visit podcastchoices.com/adchoices

If you've been told your labs are normal but nothing feels normal - this episode is for you. Dr. Tabatha sits down with Dr. Amie Hornaman, the Thyroid Fixer, to unpack what your labs are missing, why T2 is the forgotten hormone, and what to do about it. Why 'normal' labs do not mean a healthy thyroid.The full thyroid picture: T1, T2, T3, T4 - and why most doctors only test twoT2: the forgotten thyroid hormone and how it supports metabolism without disrupting your natural productionHashimoto's, molecular mimicry, and why gluten removal is not optional for autoimmune thyroid diseaseThe gut-thyroid connection: why healing your gut is required for proper T4-to-T3 conversionThe link between under-optimized thyroid and insulin resistance, heart disease, and Alzheimer'sHow to advocate for yourself and ask for the right labsGet Dr. Amie's book The Thyroid Fix: thyroidfixbook.comSupport your thyroid with Thyro-Lift: shop.fasttofaith.com - use code PODCAST for 20% offScripture: Isaiah 40:29FREE 3-DAY LIVE MASTERCLASS - From Stuck to FreeJoin Dr. Tabatha May 26-28 for three live sessions designed for the woman who has done everything right and still doesn't feel well.Day 1 - Your Body Has Been Waiting Day 2 - Turn Your Healing Into Your Calling Day 3 - Why You're Still Not WellLive at 12PM EST. Same Zoom link all three days. Free to attend. Replay available for registered attendees.Register here: masterclass.fasttofaith.com/fromstucktofree

Are you doing "all the right things" but still gaining weight, losing hair, feeling exhausted, foggy, anxious, or stuck in your body? Your thyroid may be the missing piece. In this powerful episode of The Girlfriend Doctor Podcast, Dr. Anna Cabeca welcomes Dr. Amie Hornaman—also known as "The Thyroid Fixer," founder of the Advanced Thyroid and Hormone Clinic, host of The Thyroid Fixer podcast, and author of The Thyroid Fix: The No Nonsense Guide to Fix Fatigue, Fogginess and Fat That Won't Budge. Together, Dr. Anna and Dr. Amie unpack why thyroid dysfunction is so often missed in perimenopause and menopause—and why a "normal" TSH may not tell the whole story. They discuss Hashimoto's, weight-loss resistance, hair loss, fatigue, iodine, T2, reverse T3, thyroid antibodies, hormone shifts, stress, environmental toxins, and why women must advocate for a complete thyroid panel. In this episode, you'll learn: Why fatigue, hair loss, depression, constipation, cold intolerance, and stubborn belly fat may point to thyroid dysfunction The full thyroid panel Dr. Amie recommends beyond TSH How perimenopause and menopause can trigger or worsen Hashimoto's Why T4-only medication may not work for every woman The role of iodine, selenium, magnesium, vitamin D, black cumin seed oil, and T2 Why thyroid optimization is a longevity strategy—not just a weight-loss conversation Dr. Amie also shares her personal journey of misdiagnosis, thyroid recovery, PCOS, and navigating endometrial cancer with courage, honesty, and functional medicine wisdom. Listen now and remember: you are your best health advocate—and there is always one next right step. Key Timestamps 00:00 — Why thyroid symptoms often show up in menopause 04:20 — The top symptoms of thyroid dysfunction 08:30 — Hashimoto's, autoimmunity, and hormone shifts 16:40 — The full thyroid panel every woman should know 27:00 — Iodine, thyroid antibodies, and detox reactions 36:30 — Dr. Amie's personal thyroid misdiagnosis story 46:00 — Thyroid dysfunction and weight-loss resistance 55:00 — Optimizing thyroid hormones at every age 1:04:00 — PCOS, progesterone, and endometrial cancer 1:14:00 — T2, metabolism, and mitochondrial support Memorable Quotes "From head to toe, the thyroid runs the show." — Dr. Amie Hornaman "Women are being dismissed when it really is a thyroid problem that can be treated." — Dr. Amie Hornaman "We don't want normal. We want optimal." — Dr. Anna Cabeca "The thyroid is a longevity optimizer, not just an aesthetics conversation." — Dr. Amie Hornaman "You are your best advocate for your health." — Dr. Anna Cabeca Connect With Dr. Amie Hornaman Book: The Thyroid Fix: https://www.simonandschuster.com/books/The-Thyroid-Fix/Dr-Amie-Hornaman/9781668225424 Website: https://dramie.com Supplements: https://betterlifedoctor.com/annacabeca Use code: DRANNA for 10% off Instagram: https://www.instagram.com/dramiehornaman/ YouTube: youtube.com/@DrAmieHornaman Facebook: https://www.facebook.com/AmieHornaman Connect With Dr. Anna Cabeca Website: https://dranna.com Instagram: https://www.instagram.com/thegirlfrienddoctor/ YouTube: https://www.youtube.com/@thegirlfrienddoctor TikTok: https://www.tiktok.com/@drannacabeca Facebook: https://www.facebook.com/thegirlfrienddoctor

Are you doing "all the right things" but still gaining weight, losing hair, feeling exhausted, foggy, anxious, or stuck in your body? Your thyroid may be the missing piece. In this powerful episode of The Girlfriend Doctor Podcast, Dr. Anna Cabeca welcomes Dr. Amie Hornaman—also known as "The Thyroid Fixer," founder of the Advanced Thyroid and Hormone Clinic, host of The Thyroid Fixer podcast, and author of The Thyroid Fix: The No Nonsense Guide to Fix Fatigue, Fogginess and Fat That Won't Budge. Together, Dr. Anna and Dr. Amie unpack why thyroid dysfunction is so often missed in perimenopause and menopause—and why a "normal" TSH may not tell the whole story. They discuss Hashimoto's, weight-loss resistance, hair loss, fatigue, iodine, T2, reverse T3, thyroid antibodies, hormone shifts, stress, environmental toxins, and why women must advocate for a complete thyroid panel. In this episode, you'll learn: Why fatigue, hair loss, depression, constipation, cold intolerance, and stubborn belly fat may point to thyroid dysfunction The full thyroid panel Dr. Amie recommends beyond TSH How perimenopause and menopause can trigger or worsen Hashimoto's Why T4-only medication may not work for every woman The role of iodine, selenium, magnesium, vitamin D, black cumin seed oil, and T2 Why thyroid optimization is a longevity strategy—not just a weight-loss conversation Dr. Amie also shares her personal journey of misdiagnosis, thyroid recovery, PCOS, and navigating endometrial cancer with courage, honesty, and functional medicine wisdom. Listen now and remember: you are your best health advocate—and there is always one next right step. Key Timestamps 00:00 — Why thyroid symptoms often show up in menopause 04:20 — The top symptoms of thyroid dysfunction 08:30 — Hashimoto's, autoimmunity, and hormone shifts 16:40 — The full thyroid panel every woman should know 27:00 — Iodine, thyroid antibodies, and detox reactions 36:30 — Dr. Amie's personal thyroid misdiagnosis story 46:00 — Thyroid dysfunction and weight-loss resistance 55:00 — Optimizing thyroid hormones at every age 1:04:00 — PCOS, progesterone, and endometrial cancer 1:14:00 — T2, metabolism, and mitochondrial support Memorable Quotes "From head to toe, the thyroid runs the show." — Dr. Amie Hornaman "Women are being dismissed when it really is a thyroid problem that can be treated." — Dr. Amie Hornaman "We don't want normal. We want optimal." — Dr. Anna Cabeca "The thyroid is a longevity optimizer, not just an aesthetics conversation." — Dr. Amie Hornaman "You are your best advocate for your health." — Dr. Anna Cabeca Connect With Dr. Amie Hornaman Book: The Thyroid Fix: https://www.simonandschuster.com/books/The-Thyroid-Fix/Dr-Amie-Hornaman/9781668225424 Website: https://dramie.com Supplements: https://betterlifedoctor.com/annacabeca Use code: DRANNA for 10% off Instagram: https://www.instagram.com/dramiehornaman/ YouTube: youtube.com/@DrAmieHornaman Facebook: https://www.facebook.com/AmieHornaman Connect With Dr. Anna Cabeca Website: https://dranna.com Instagram: https://www.instagram.com/thegirlfrienddoctor/ YouTube: https://www.youtube.com/@thegirlfrienddoctor TikTok: https://www.tiktok.com/@drannacabeca Facebook: https://www.facebook.com/thegirlfrienddoctor

Save your seat in the free Thyroid and Hormone class https://fixyourthyroid.com/natalie  If you are a woman in midlife who has been told everything is fine when you know in your body that something is NOT fine, this episode is going to change everything. I have Dr. Amie Hornaman, The Thyroid Fixer, back on the show, and we are going somewhere we have never gone before. One in eight women will develop a thyroid condition in her lifetime. Eighty-eight percent of us are metabolically unhealthy. And yet most doctors run ONE test, look at one number, tell us we are normal, and send us home with an antidepressant. Meanwhile we are gaining weight, losing our hair, can't sleep, can't think, can't lose a pound to save our lives, and being told it is just stress, just aging, just menopause. Today we are tearing that apart. Dr. Amie saw SEVEN doctors before she was finally diagnosed. She is now licensed to prescribe thyroid and bioidentical hormones in all 50 states and most of Canada. She built the Better Thyroid and Hormone Institute, hosts The Thyroid (and Hormone) Fixer Podcast, and has helped thousands of women globally finally get answers. We go DEEP on: Why the standard TSH-only test misses almost everyone, and the six tests you need to ask for by name THYROPAUSE: Dr. Amie's term for what happens when thyroid dysfunction collides with perimenopause and menopause (and why so many women are being treated for the wrong one) The T4-only medication trap: why Synthroid and levothyroxine fail an estimated 98% of patients Reverse T3, the silent saboteur that blocks your active thyroid hormone from getting into your cells Natural desiccated thyroid, the controversy, FDA scrutiny of animal-derived medications, and where Dr. Amie stands T2: the FORGOTTEN thyroid hormone with 30+ years of research that burns fat at the mitochondrial level, does not suppress your own thyroid, does not jack up your heart rate, does not require a prescription, and is showing up in studies as a potential anti-obesity treatment What Ozempic, Wegovy, and Mounjaro are actually doing to your thyroid (and why some women lose ZERO weight on GLP-1s no matter how high they push the dose) The estrogen, progesterone, testosterone, cortisol, and insulin connection: why you cannot fix the thyroid without addressing the whole hormonal system Antibody-support strategies: gluten elimination, black cumin seed oil, low-dose naltrexone, and thymosin alpha Iodine titration cautions, medical gaslighting, and what to say when your doctor refuses to run the full panel The Monday morning action plan: exactly what to do this week if you suspect your thyroid is the missing piece This is not a thyroid 101 episode. This is the conversation I wish every midlife woman was given the day her labs came back normal. You are not broken. You are not crazy. And you are not alone. Sign up for the free Thyroid and Hormone class https://fixyourthyroid.com/natalie    Connect with Dr. Amie: Podcast: The Thyroid (and Hormone) Fixer Instagram: @dramiehornaman Book: https://thyroidfixbook.com/ Live lab-review class https://fixyourthyroid.com/natalie  Better Thyroid and Hormone Institute: dramiehornaman.com   APPROXIMATE TIMESTAMPS: 00:00 — The medical gaslighting that is keeping midlife women sick 06:00 — The full thyroid panel: the six tests to ask for by name 12:00 — Introducing THYROPAUSE: where thyroid meets menopause 20:00 — How estrogen, progesterone, testosterone, and cortisol all impact your thyroid 28:00 — Why T4-only medication (Synthroid, levothyroxine) fails 98% of patients 34:00 — Natural desiccated thyroid, FDA scrutiny, and individualized dosing 40:00 — T2: the forgotten thyroid hormone that burns fat without touching your gland 48:00 — Who should consider T2 (and why it does not require a prescription) 52:00 — What Ozempic and the GLP-1s are actually doing to your thyroid 58:00 — How to protect your thyroid if you are currently on a GLP-1 62:00 — Lifestyle non-negotiables: morning sun, protein, resistance training, sleep, blood sugar 67:00 — Your Monday morning action plan if you suspect your thyroid is the missing piece   Catch the full episode on YOUTUBE HERE: https://bit.ly/MidlifeConversationsYouTube   Learn More About Dr. Amie Hornaman  Instagram ➜ https://www.instagram.com/dramiehornaman Website ➜ https://fixyourthyroid.com/natalie      Thank you to our show sponsors:  MITOQ: Take control of healthy aging and longevity. Get 10% off using code NATALIEJILL at checkout on https://www.mitoq.com/  BIOPTIMIZERS: Get the digestive enzymes I take with every meal here https://www.bioptimizers.com/nataliejill Free Gifts for being a listener of Midlife Conversations! Mastering the Midlife Midsection Guide: https://theflatbellyguide.com/ Age Optimizing and Supplement Guide: https://ageoptimizer.com   Connect with me on social media! Instagram: www.Instagram.com/Nataliejllfit Facebook: www.Facebook.com/Nataliejillfit   For advertising inquiries: https://www.category3.ca/  Disclaimer: Information provided in the Midlife Conversations podcast is for informational purposes only. This information is NOT intended as a substitute for the advice provided by your physician or other healthcare professional. Do not use the information provided in this podcast for diagnosing or treating a health problem or disease, or prescribing medication or other treatment. Always speak with your physician or other healthcare professional before making any changes to your current regimen.  Information provided in this podcast and the use of any products or services related to this podcast does not create a client-patient relationship between you and the host of Midlife Conversations or you and any doctor or provider interviewed and featured on this show. Information and statements may have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent ANY disease. Advertising Disclosure: Some episodes of Midlife Conversations may be sponsored by products or services discussed during the show. The host may receive compensation for such advertisements or if you purchase products through affiliate links. Opinions expressed about products or services are those of the host and/or guests and do not necessarily reflect the views of any sponsor. Sponsorship does not imply endorsement of any product or service by healthcare professionals featured on this podcast.

In this powerful episode, Dr. Fiona Lovely welcomes back her friend and colleague, Dr. Amie Hornaman—known globally as "The Thyroid Fixer." Dr. Amie is a functional medicine expert, host of the top-rated The Thyroid Fixer podcast, and author of the new book The Thyroid Fix: The No-Nonsense Guide to Reclaiming Your Health. Together, they pull back the curtain on why conventional medicine continues to fail women when it comes to thyroid and hormone health. Dr. Amie shares her journey of being misdiagnosed and how that fueled her mission to help women stop wishing on a rainbow for their health to improve. She explains why relying solely on TSH and T4 is a dangerous gamble, revealing that the real story lies in free T3 and reverse T3. Listeners will learn why T4-only medication like Synthroid often falls short and how to advocate for proper testing and treatment. The conversation also explores the forgotten thyroid hormone T2, its role in burning fat without losing muscle, and how GLP-1 medications intersect with thyroid function. Dr. Amie provides scripted, respectful language for women to use with their doctors, including a powerful "nuclear option" to ensure their concerns are documented. Episode Highlights: Why TSH is a misleading marker and which two tests truly matter for thyroid health. The problem with T4-only medication and why it can backfire. How to approach your doctor without overwhelming them—three bullet points, no life stories. The fascinating role of T2 in metabolism and weight loss. A candid discussion on thyroid nodules, unnecessary surgeries, and patient advocacy. Tune in to learn how to become the CEO of your own health, because waiting for your doctor to catch up is no longer an option.   Thank you to our sponsors for this episode: Women in perimenopause and menopause talk about wanting the same things — less bloating, no afternoon crash after eating, steady energy. MassZymes is perfect for helping your body's ability to actually process what you eat. MassZymes uses a full-spectrum blend of 18 enzymes. That means you're getting more out of the food you eat. Plus, it works across different stomach acid levels, which can really matter as we age. Here's what you get when you go to bioptimizers.com/lovely and use code LOVELY: 15% off your entire order AND a free bottle of Masszymes — BiOptimizers' best-selling digestive enzyme — added to your order automatically when you use our exclusive code.

In this episode, Dr. Eric Osansky welcomes back Dr. Amie Hornaman to discuss her new book, The Thyroid Fix. Together, they dive into the most common misconceptions surrounding hypothyroidism and Hashimoto's, including why so many people continue to experience symptoms despite being told their thyroid labs are “normal.” Dr. Amie shares her personal motivation for writing the book and explains how she hopes to empower people to better understand their thyroid health and advocate for themselves.Dr. Amie breaks down what a complete thyroid panel should include, why testing only TSH is often insufficient, and the important roles of free T3 and reverse T3 in thyroid hormone conversion and metabolism. The conversation also explores autoimmune triggers, hormone fluctuations during pregnancy and menopause, the connection between stress and thyroid dysfunction, and why testosterone may play a protective role against autoimmunity. They also discuss T2 supplementation, common nutrient deficiencies, iodine, ashwagandha, and the growing conversation around GLP-1 medications.The episode closes with an encouraging discussion about hope, healing, and the importance of individualized thyroid care. Dr. Amie emphasizes that taking thyroid hormone replacement is not a failure and explains when Hashimoto's may potentially be reversed or put into remission. If you want a clearer, more balanced understanding of Hashimoto's, thyroid hormones, and what optimal thyroid health really looks like, you'll get a lot out of this episode. Free resources for your thyroid healthGet your FREE Thyroid and Immune Health Restoration Action Points Checklist at SaveMyThyroidChecklist.comHigh-Quality Nutritional Supplements For Hyperthyroidism and Hashimoto' s Have you checked out my new ThyroSave supplement line? These high-quality supplements can benefit those with hyperthyroidism and Hashimoto's, and you can receive special offers, along with 10% off your first order, by signing up for emails and text messages when you visit ThyroSave.com. Do You Want Help Saving Your Thyroid?Get free access to hundreds of articles and blog posts: https://www.naturalendocrinesolutions.com/articles/all-other-articles Watch Dr. Eric's YouTube channel: https://www.youtube.com/c/NaturalThyroidDoctor/videos Join Dr. Eric's Graves' disease and Hashimoto's group: https://www.facebook.com/groups/saveyourthyroid Take the Thyroid Saving Score Quiz: https://quiz.savemythyroidquiz.com/sf/237dc308 Read all of Dr. Eric's published books: http://savemythyroid.com/thyroidbooks Work with Dr. Eric: https://savemythyroid.com/work-with-dr-eric/ 

Former BYU horsebeast Carson Lundell medals at the US Open qualifier at Willow Creek by two of four players at T2, all of whom mover on to the Longest Day of Golf second stage qualifier in June. Lundell joins the pod. Sponsored by Goldenwest Credit Union. 

JRAは8日、第31回NHKマイルカップ（GI、東京芝1600m）の枠順を発表した。 重賞2勝のダイヤモンドノットは4枠7番、ニュージーランドT2着のロデオドライブは8枠17番、皐月賞惨敗から巻き返しを期すカヴァレリッツ...The post 【NHKマイルC／枠順】1人気でも「0.0.1.3」の不振…

84% des entreprises du S&P 500 battent les attentes. +27% de croissance des bénéfices. Un record depuis 2021. Sur le papier, tout va bien. Mais quand les valorisations sont déjà tendues et que le marché est sur des sommets, les bons résultats ne suffisent pas toujours à faire monter les indices. Avec Alexandre Baradez d'IG, on fait le point sur le S&P 500, les guidances du T2, l'or, les taux et les risques à surveiller pour les prochains mois. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

PRESENTACIÓN LIBROS 00:01:40 Agatha Raisin y el infierno del amor. Agatha Raisin #11 (M.C. Beaton) 00:04:40 Cómo sobrevivir a tu propio asesinato (Kristen Perrin) 00:07:10 Proyecto Hail Mary (Andy Weir) 00:08:45 Oxígeno (Marta Jiménez Serrano) 00:10:05 La Reina Esther (John Irving) 00:12:25 El club del crimen de Marlow #1 (Robert Thorogood) 00:14:55 Los gritos del pasado, Las hijas del frío, Crimen en directo (Camilla Lackberg) 00:17:55 Carretera maldita (Stephen King) 00:19:10 It's not her (Mary Kubica) 00:21:45 Prisioneros de la geografía (Tim Marshall) 00:24:05 Una luna sin miel (Christina Lauren) 00:25:50 ¿Quién te lo ha contado? (Marian Keyes) 00:28:05 Un rollo académico (Jodi McAlister) 00:29:20 Epidemia ultra (Franco Delle Donne) PELÍCULAS 00:32:15 Cuando Harry encontró a Sally 00:35:15 53 domingos 00:37:55 Turno nocturno 00:40:20 El protector 00:42:10 Proyecto Salvación 00:44:45 Wuthering heights 00:49:15 Te van a matar 00:50:50 Noche de bodas 2 00:52:20 Supermario Galaxy 00:54:00 Outcome 00:56:35 El Diablo viste de Prada 2 00:58:30 Trevor Noah: Joy in the trenches 01:01:00 Deberes: Rental family SERIES 01:03:35 Love Story: John Kennedy Jr y Carolyn Bessette 01:05:20 El asesino de Tik Tok 01:06:25 Juventud robada 01:08:25 Por cien millones 01:10:45 Algo terrible está a punto de suceder 01:12:30 Confía en mí 01:15:30 La edad del amor (T1) 01:18:15 El club del crimen de Marlow (T1) 01:20:15 Scarpetta (T1) 01:23:25 Lo último que me dijo (T2) 01:24:55 The Pitt (T2) 01:26:35 Shrinking (T3) 01:28:25 Deberes: Los Bridgerton (T4) 01:32:30 DESPEDIDA En este programa suenan: Radical Opinion (Archers) / Siesta (Jahzzar) / Place on Fire (Creo) / I saw you on TV (Jahzzar) / Bicycle Waltz (Goobye Kumiko)

Get up to speed on what's fuelling the markets this quarter. Join Mark Verrilli, ETF Strategist, as he breaks down the ETF trends, sector shifts and positioning ideas gaining traction in Q2. From the latest rotations to fresh insights on Fidelity's All‑in‑One ETFs, Mark will highlight the forces driving momentum — and how to use them to stay one step ahead. Recorded on April 22, 2026. At Fidelity, our mission is to build a better future for Canadian investors and help them stay ahead. We offer investors and institutions a range of innovative and trusted investment portfolios to help them reach their financial and life goals. Fidelity mutual funds and ETFs are available by working with a financial advisor or through an online brokerage account. Visit fidelity.ca/howtobuy for more information. For a fifth year in a row, FidelityConnects by Fidelity Investments Canada was ranked #1 podcast by Canadian financial advisors in the 2025 Environics' Advisor Digital Experience Study.   --   Découvrez ce qui propulse les marchés ce trimestre. Joignez-vous à Mark Verrilli, stratège en FNB, qui expliquera les tendances des FNB, les changements sectoriels et les idées de positionnement qui gagneront du terrain au T2. Des plus récentes rotations aux nouvelles perspectives sur les FNB Fidelity Simplié, M. Verrilli mettra en lumière les forces qui influencent le mouvement du marché et comment en tirer avantage pour garder une longueur d'avance. Date : 22 avril 2026 Chez Fidelity, notre mission consiste à aider le public investisseur canadien à se bâtir un meilleur avenir et à rester à l'avant-garde. Nous offrons aux particuliers et aux institutions une gamme de portefeuilles de placement innovants et fiables pour les aider à atteindre leurs objectifs financiers et personnels. Les fonds communs de placement et les FNB de Fidelity sont offerts par l'intermédiaire des conseillers et conseillères en placements et de comptes de courtage en ligne. Pour de plus amples renseignements, visitez fidelity.ca/commentinvestir. Les baladodiffusions DialoguesFidelity se sont classées au premier rang pour une cinquième année consécutive lors du sondage 2025 d'Environics sur l'expérience numérique des conseillers et conseillères en placements au Canada.

In 1991, cinema changed forever.This week on Code Noir, Curtis J François and Jamaal Norman dive into Terminator 2: Judgment Day — the blockbuster that redefined action, revolutionised visual effects, and gave us one of the most unexpected emotional gut-punches in film history.But beneath the explosions, the liquid metal, and the iconic one-liners, T2 is something deeper: a story about control, surveillance, and the terrifying speed of technological progress. It's a film that asks what happens when the systems we build to protect us become the very thing that destroys us.We break down:How James Cameron and Industrial Light & Magic changed cinema foreverThe T-800's evolution from villain to protector — and unlikely father figureSarah Connor as one of the most important action heroes ever put on screenThe T-1000 as a perfect, unstoppable symbol of modern policing and controlWhy Miles Dyson might be the moral centre of the entire storySet against a pivotal year in entertainment, alongside The Silence of the Lambs, Beauty and the Beast, and Boyz n the Hood, Terminator 2 stands as both a technical milestone and a cultural warning.Because in the end, this isn't just a story about machines rising up.It's about the choices we make before they do.No fate. No guarantees. Just consequences.

Kristian joins David to review his huge win at Ironman Texas as well as discuss midseason breaks. (00:00) Introduction(00:28) How is Kristian? (01:40) Hype in the Buildup and its Impact (02:54) Competition vs Weather as a Driver of Fast Times  (04:25) Swim Form (06:33) T1, Calf Sleeves and Big Group(09:29) Bike Groups (13:30) Flat Tyre (15:46) Bike Pack Dynamics and 20m Rule(20:46) Thoughts in T2(22:47) Tactics on the Run (28:00) Crowd and Splits  (30:25) Was the Dynamic on the Run Enjoyable? (31:09) Thoughts on Finish Time (32:14) Did Anything Surprise Kristian About the Race? (33:28) Impact of the PTO on Ironman (34:32) Bike Position (35:26) Learnings from the Racing Block (37:22) What Needs Addressing Going Forward (38:23) Using Spikes  (38:57) Midseason Break (40:13) Pro Series Thoughts (41:38) Race Day Strategy for Kona Thanks to the sponsors of this podcast series:MaurtenTo benefit from the one-time code and get 15% off your next purchase on Maurten.com, simply enter the code “TNMS4” at checkout. The code is applicable once per customer, on all products except the Maurten Bicarb System, valid until 31/12/2026.Maurten WebsiteInstagram: @maurten_officialYouTube: https://www.youtube.com/c/MaurtenOfficialHosted, edited and produced by Dr David LipmanEditing, video and introduction by Roj Ferman

In part two, shop owners on Whangarei's Bank Street say the installation of a priority T2 lane on the street is severely affecting their business. The council says its just teething issues. One of the affected businesses talks to the panel and begs to differ. Then, the history of and the misconceptions around the origin of the ANZAC biscuit. And if that whets your appetite, here's some biscuit recipes for inspiration this ANZAC weekend.

Familiarity with the clinical, MRI, CSF, and serologic features of MOGAD can help neurologists recognize this condition in clinical practice. Awareness of the utility and pitfalls of the MOG antibody test is critical. The current therapeutic approach is guided by retrospective studies and the application of immunotherapies used in other autoimmune neurologic disorders. In this episode, Gordon Smith, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, coauthor of the article "Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Flanagan is a professor of neurology and the division chair of the Division of Multiple Sclerosis and Autoimmune Neurology in the Department of Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: So, what neurological disorder can cause bilateral optic neuritis, transverse myelitis, ADEM, or can mimic acute flaccid myelitis, intracranial hypertension, viral encephalitis, or cause seizures? Sounds like the great imitator, perhaps. If you want to know and learn more about this syndrome and how you can treat it---and it is very treatable---keep listening. My name is Gordon Smith, and today I have the great opportunity to talk with Dr Eoin Flanagan from the Mayo Clinic on his article on myelin oligodendrocyte glycoprotein antibody associated disease, or MOGAD, which is in the April 2026 issue of Continuum on Multiple Sclerosis and Related Disorders.  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Eoin Flanagan about his article on myelin oligodendrocyte glycoprotein associated disease, or MOGAD, which appears in the April 2026 Continuum issue on multiple sclerosis and related disorders. Eoin, welcome to the podcast, and please introduce yourself to our audience.  Dr Flanagan: Yeah, thanks so much. I'm Eoin Flanagan. I'm a neurologist at the Mayo Clinic. I'm originally from Ireland. I work in the neuroimmunology lab at the Mayo Clinic, and work and see patients with MS, MOG, and autoimmune disorders here in Rochester, Minnesota.  Dr Smith: Your article is super interesting, I think, and this has been a really rapidly evolving area over the last, you know, many years. We have many more antibodies, and MOG is something that's been around for a while, but we've certainly learned a lot more about it. This is a topic that I think will be familiar to most of our listeners, but I wonder if maybe you can just begin by laying the foundation. Like, what is MOG? What's its typical presentation?   Dr Flanagan: So, MOG is a protein on the surface of the oligodendrocyte or its CNS myelin, and it was always of interest as a potential antibody target, and initially it was investigated in multiple sclerosis. But subsequently, we recognized that the antibodies to MOG have a specific syndrome, of which about a quarter of patients are pediatric and then the remainder are adults. And they can present with a variety of syndromes, probably most commonly optic neuritis, but also acute disseminated encephalomyelitis, or ADEM. Transverse myelitis can also occur, and then some other unusual brain and brainstem cerebellar syndromes can also occur.   Dr Smith: I was really impressed in the very broad phenotypic spectrum of MOG. We'll talk more about that, of course. But I wonder if maybe you can tell us when we should be ordering MOG antibody? Given this broad variability, does anyone who has a CNS demyelinating disease need a MOG assay, only specific phenotypes? What guidance do you have for our listeners?   Dr Flanagan: Yeah. It's a great question. So, I think you have to be a little bit careful because the MOG antibody test is a little bit sticky. So sometimes we can see some low-positive false positives. So, we don't wanna order it in every single patient with classical MS. So, I suppose we'll start with who not to order it in. I think it's also a very optic nerve- and optic neuritis-central disease, so I think you really need to be considering this in a patient with optic neuritis who does not have lesions in the brain suggestive of multiple sclerosis. And then we think about some of the features: if the lesion, the enhancement along the optic nerve is long, if it's bilateral, if there's a lot of optic disc edema accompanying that, we tend to think about MOG antibodies. And then children with demyelinating disease, MOG is over-represented in that cohort, so it accounts for about a third of those. So, if you have a child with CNS demyelinating disease, particularly if they're under twelve, with ADEM presentations or other presentations, you probably want to be ordering the MOG antibody test. And then a longitudinally extensive transverse myelitis in adults, certain types of cerebral phenotypes that we can get into, you would want to consider ordering MOG antibodies too.   Dr Smith: Now, you point out in the article that it's really important that laboratories use the cell-based assay for MOG as opposed to an ELISA, for instance. Is this something folks need to be very attentive to, or are all of the commercial laboratories now using a cell-based assay?   Dr Flanagan: Yeah. I think all of the commercial labs are using cell-based assays, so we don't really get into much of an issue. There are some differences between serum and CSF, so really, serum is the optimal sample to order. There is also some differences between the live cell-based assay and the fixed cell-based assay, where the live cell-based assay may have some advantages in terms of sensitivity. And then CSF is kind of still under evaluation about its role in the condition. So in general, it's a serum test. And then we have to remember that the antibody tends to be highest at the onset, and then it goes down over time. So, if you delay your testing or you're testing a patient long after the condition, it can go negative, for example. So it tends to be highest both around the relapses and particularly at the onset of the condition.   Dr Smith: You mentioned earlier that the test is sticky, which I take to mean that there is some risk for low-titer false positives. How do you navigate that situation? When should we be suspicious about a false positive?   Dr Flanagan: Yeah. I think there's some very useful features that can help you. You know, the main differential diagnosis is going to be multiple sclerosis, particularly in the US, in regions of the northern US where MS is particularly common. So, you really wanna be making sure that if you get a positive result, low positive, that it's not multiple sclerosis. And some of the best discriminating features are CSF oligoclonal bands. They're about 85% in MS and about 15% in MOG, so an easy number to remember, 85 and 15. And then the lesions in MOG, the brain lesions, tend to disappear over time. So, if you have the advantage of that follow-up MRI a year down the line, about 70% of lesions in MOGAD will resolve, while in MS, as we know, the term means multiple scars, so the MS lesions tend to persist over time. So, they are two quite useful features that can help discriminate.   Dr Smith: And how about specific phenotypes or areas of involvement or imaging abnormalities that suggest MOG? One of the things I found really interesting in your article is there are a host of different syndromes that I think had largely been previously described, many of them, that became clear later that these were really tied to MOG antibodies. Presumably, that's helpful in interpreting the antibody assay in that patients who have, perhaps, a borderline low titer, for instance, but have a very typical phenotype are more likely to have MOG than those who have a more clearly MS-type phenotype.   Dr Flanagan: Yeah, absolutely right. Yes. So, there's certain phenotypes that we don't tend to see with MS. The acute disseminated encephalomyelitis, or ADEM, is one that's particularly common in children. And about half of people that have ADEM will be positive for the MOG antibody. So that's a syndrome you need to look out for, which would be often in children, encephalopathy, and they would have multifocal white matter lesions, sometimes involving the gray matter. A second syndrome that was an interesting discovery from a Japanese group was this unilateral cerebral cortical encephalitis, where patients can have this swelling and T2 hyperintensity, often just on one side of the brain. And it's in the cortex, and some of those patients won't have any white matter lesions. And in that situation, it's important to order the MOG antibody, and that seems to be a specific phenotype of MOGAD. But sometimes people don't think about it because the white matter is not involved. So, if you see these patients, they often present with seizures, sometimes they even have fever accompanied by it. And if you see those patients and see this radiological feature, then you really want to consider ordering the MOG antibody too.   Dr Smith: Yeah, I found that really interesting. And I- actually, my next question is perhaps a good follow-up on that, is, what are the diagnostic pitfalls? You give a lot of examples of situations and I think some cases where it's easy to get tripped up and misdiagnose someone who has MOG with another fairly common neurological problem.   Dr Flanagan: Yeah, I think some of the things that can help you when you're determining if the MOG is a true positive or false positive is the level of the antibodies. The super high titers, if it's a clear positive or very strong positive, the likelihood is that that is much more likely to be MOGAD than those low positives just above the cutoff. So that can be useful to help you discriminate from false positives. Those lesions, again, if all the lesions persist over time, that's going to be more suggestive of multiple sclerosis. Other diagnostic pitfalls, I suppose, if it's a syndrome that's not really associated with MOG, like peripheral neuropathy or other syndromes where we'll see some case reports, but usually I would be very cautious about those kind of presentations. So usually, having the antibody at a high level, and then also if they've had other symptoms suggestive of MOGAD, like if a patient has had recurrent optic neuritis and then they have an unusual brain syndrome, or they start out with an unusual brain syndrome and then have recurrent optic neuritis. You know, there are situations that make it more likely if they're having other typical phenotypes of the MOGAD where we can kind of expand the spectrum, but we have to be careful.   Dr Smith: I was really curious about the dynamic imaging findings. And you point this out both in terms of the resolution of imaging findings, but also in that patients who have an acute MOG syndrome often have very rapid evolution of the imaging abnormalities. I'm just curious, you know, why is that, and what do you make of it? Does it have a mechanistic implication, do you think?   Dr Flanagan: I don't think we know for sure. I think there's probably a lot more happening than we see on MRIs sometimes. What sometimes can happen in about 10% of patients is the initial MRI can be normal. We don't tend to see that with multiple sclerosis or NMOSD. Then what we see is it evolving over time. So, at that time, if you do a CSF, you'll often see inflammation, but we don't see the lesions. Now, that might be because the MRI is not very good at picking up cortical involvement. That can be difficult to see in MRI. Or there could be other factors. It could be a functional effect on the MOG but without frank demyelination yet, for example. Or there could be edema that you- myelin edema that you can't see as a lesion yet on MRI. But we do see that if you repeat the MRI, sometimes it'll change a lot. So, you may go from one or two lesions on the first MRI to twenty lesions on the second MRI a week later. So, it does tend to change a lot. And then over time, those lesions also resolve. So, what I say is if it's a very suspicious situation---like a child comes in with new-onset encephalitis, has inflammatory CSF---you might wanna consider repeating that MRI down the line and seeing if it's changing. And then over time, you know, a repeat MRI a year after the onset when there's brain or spinal cord lesions can be very helpful just to make sure you're on the right track, because lots of those lesions will then disappear, and that's a very clear discriminator from multiple sclerosis.   Dr Smith: Yeah, thanks. I mean, I was wondering the same thing about whether that particular feature might imply, you know, a functional abnormality as opposed to more of a structural abnormality. So probably a lot more to learn as we move forward. There are now consensus diagnostic criteria that were published a couple of years ago. I think you've already touched on kind of the general approach, but do you want to speak to those? I found your summary pretty helpful.   Dr Flanagan: Yeah, I think that those criteria are quite useful. They have three main parts to them. The first part is having a characteristic clinical syndrome. So, we talked about ADEM, we talked about cerebral cortical encephalitis, transverse myelitis that's often longitudinally extensive, and optic neuritis being the main syndromes, but sometimes other brainstem or cerebellar involvement can be seen. And then the second part is having a positive MOG antibody. And then there's some caveats there. So, if you have a high positive, then you don't really need any additional supportive criteria. On the other hand, if you're low positive, to get at those sticky antibodies that make sure it's not a false positive, you need some additional supportive clinical or MRI criteria. Or if you're only positive in CSF, you need that additional criteria. You also need to be negative for the aquaporin-4 antibody, because they can overlap clinically. And some of those supportive criteria are things that we talked about a little bit earlier, longer lesions within the optic nerve, bilateral involvement, involvement of the nerve sheath or optic disc edema. This is a situation, MOG antibody disease, where your fundoscope is useful and looking in the back of the eye and seeing swelling, because we don't tend to see that quite as often. It's less common in multiple sclerosis, but we often see prominent edema in MOGAD. And then in the spinal cord, the lesions tend to be central in the cord. Sometimes they form this H sign where it's restricted to the gray matter, and they tend to be longer, sometimes involving the conus. Patients will often have neurogenic bowel or bladder. And then in the brain, deep gray involvement, those large lesions along the cortex with swelling are some of the typical features. And then the final step is exclusion of another diagnosis. Just like with any test that we do in neurology, our final step is going to be to put that into context. So that's just a normal thing that we will always do when we get a group of test results back that we don't know what it means. We have to put it into context. So, make sure it's not multiple sclerosis, everything else does not look like multiple sclerosis, and then you can be on your way to make a diagnosis.   Dr Smith: Definitely encourage listeners to read your article. I guess I say that with every time I- or with everyone I talk to for Continuum Audio, but the images are really fantastic and the cases are fantastic. So, everything you've described is well-illustrated, including really nice schematic sort of diagrams that help differentiate NMO from MOG and MS. So, if you like MRI scans and good imaging frameworks, then this is the article for you.   Dr Flanagan: I think that's true, and the other thing is that the imaging is quite helpful because it takes a while for that antibody to come back. We're lucky at Mayo Clinic, if you work here, it, it comes back faster for you. But for many places, that time of sending it in, so a lot of times you don't know right away. So, looking at scrutinizing that MRI can be very helpful to guide you on your way and to know what you're dealing with and how to approach both the acute treatment and plans to have potentially a steroid taper after the acute treatment and those kind of things that can help guide you in that regard.   Dr Smith: Yeah. So, let's talk about treatment. You know, what's your approach to treating a patient who has an acute demyelinating syndrome related to MOG?   Dr Flanagan: So similar to other things, MOG is very steroid responsive. So, we use high-dose IV methylprednisolone in adults. That would be one gram IV for five days. And then we also will sometimes use oral steroids, twelve hundred and fifty milligrams. That's a bit of a hassle because it's twenty-five fifty-milligram tablets, it doesn't come in a larger tablet version. But it's very helpful to patients because they can get started on it right away. You don't have to set up an infusion center. So, we have used those oral steroids often in people who don't have access to an infusion center, are not in the hospital. And particularly as it's often optic neuritis, some of those patients are seen in the outpatient setting, so we can get in with treatment quickly. In patients where it's more severe, it doesn't recover quickly with steroids, then we would consider escalating to plasma exchange as our second-line treatment, and there's some retrospective data that suggests that plasma exchange can be useful. That's gonna be particularly for those people who don't have that quick response to steroids, or maybe more severe phenotypes like that brain involvement with ADEM or cerebral cortical encephalitis, where those patients might be in the hospital and quite unwell. I will say, we might get on to this, that sometimes MOG can be very, very severe and even fulminant, where there can be increased intracranial pressure, and these patients can be in the ICU, and it can be life-threatening. And so, it's really important to treat those patients aggressively, and some patients have even required hemicraniectomy or additional treatment. Sometimes IL-6 blocking medications have been used in that situation. So, monitoring and treating increased intracranial pressure in those rare patients, probably 2 or 3% that have the very severe attack, is important.   Dr Smith: I think one of the things I found interesting, and then I'd love to get your feedback on this, is that most patients with MOG seem to have a very readily treatable disorder that's monophasic, right? You treat them with steroids, and they do well. On the other extreme, there are these patients that have a much more malignant presentation, and there are some that sound like they benefit from prophylactic or some chronic therapy. What's your approach, right? In MS, we do serial scans to monitor, and obviously, our patients are on, you know, chronic disease-modifying therapy. How do you decide when you're going to provide some sort of prophylactic therapy? How do you monitor it? How long do you continue it?   Dr Flanagan: That's a great point. We don't know for sure yet, but I think for the most part, our approach has been if the patient has a single episode, they recover well from that episode. So, if that's optic neuritis, they're back to twenty/twenty vision. They have recovered well. We don't tend to use chronic maintenance immunotherapy. Sometimes after the first attack, we'll do a little bit of a slow taper, maybe over four, six weeks. We have done longer than that. And then we won't place them on any long-term treatment, because it's about 50% of patients that may have a monophasic disease, so we don't want to treat all those people who are destined never to have another relapse. On the other hand, if a patient had a very severe episode, they're in the ICU, they're intubated, some of those patients then afterwards we will start them at least temporarily on an attack prevention medication for at least a few years to get them through. Some patients will be very fearful of future relapses in that situation. Or if they don't recover well, if they're blind in one eye after an episode and then their other eye is vulnerable, or they're left with some residual deficits neurologically from a myelitis, then we would often sometimes put those patients after the first attack. But most of the time, we're gonna wait and see if they get that second attack, and then once they have the second attack, that is when we would consider a steroid-sparing medication. But I will say that there's no proven medications. We don't have any clinical trial data available yet. So some of those patients with relapsing disease, we'll either try to enroll them in a clinical trial, or we'll use an off-label treatment to try and manage their disease based on what we've learned from neuromyelitis optica or from multiple sclerosis. A few different options seem to be better, and we can maybe get into that too.   Dr Smith: Yeah, let's go there. So, what options are there? You mentioned in more fulminant disease IL-6 inhibitors, and by that I assume you mean tocilizumab, but what are the options when you want to use prophylactic therapy?   Dr Flanagan: So, that tocilizumab can be beneficial in the very acute situation, in that malignant situation. But also as an attack prevention treatment, the IL-6 blockers seem to- some of the retrospective data seems to look like it works reasonably well, so we work and see if we can get that approved. Another medication that can work well is IVIG or subcutaneous immunoglobulin as a maintenance treatment, so we would sometimes give that, like, at least one gram per kilogram once a month. The benefit of that is it doesn't lower your immune system, so there's some advantages there, particularly in people who may be more prone to infections, older people. So, we'll sometimes use that. But we do get into a lot of challenges with insurance coverage, and it can be difficult to get these approved by insurance because we only have retrospective data out there. So then for some patients, if they're in a region where there's a clinical trial available, we might try to enroll them in a clinical trial. And there are some clinical trials underway now, so hopefully in the future we'll be able to have some FDA-approved medications that can have some Class 1 data that we can follow. Because it's hard when you're just following retrospective data or anecdotal reports, it's a little bit difficult to know exactly how well you're doing with your treatments.   Dr Smith: Well, Eoin, I wonder if we could finish up by just looking into the future, right? I mean, it sounds like a fun patient population to take care of because you've got lots of great therapies and can have a durable impact. But sure would be nice to have more evidence-based therapies and an FDA approval. What trials are going on? What's the future look like?   Dr Flanagan: Yep. So, there's some trials going on in the- a couple of worldwide trials. One is on an FCRN blocker called rozanolixizumab, which is kind of like a plasma exchange-type treatment which removes your antibodies, and it's a weekly subcutaneous treatment where adults are enrolled. And the second one is called satralizumab, which is another IL-6 blocking medication. And again, that one's given once monthly under the skin. And the trial for that also includes children down to age eighteen, so for adolescents, too, that can be an option. There are trials, I believe, in Asia for tocilizumab too, and there's one starting in Australia for rituximab. So, the good news is that we're going to have some really good data down the line for lots of different agents, and we'll be able to figure out which treatments work. And this will be really of great benefit to our patients when we get that Class 1 data to kind of guide us on what we should be using and really build on the success of some of the other conditions like neuromyelitis optica spectrum disorder, where we now have four or five approved, medications that work very well.   Dr Smith: Well, Eoin, thank you. This is a great conversation. I will say that it... the topic that I was a little intimidated about. I'm a simple peripheral nerve guy, as you know. But I think moreso than any other Continuum article I've read recently, I'm, like, loaded for bear. I can't wait to go back on the inpatient service and look for some MOG patients, because your article really left me feeling kind of prepared to think through this in a clinical setting. So, thank you for the conversation, and congratulations on a really wonderful piece for Continuum.   Dr Flanagan: Yeah, thanks so much. Always a great honor to be involved in the Continuum, and thanks to all the readers out there.   Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

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Welcome to SHUDDER-ween and to our lovely podcast polygamy, This week Devin and the crew let some groans out as Zyber takes us down his choice of streaming service horror movie starring Eddie Furlong of T2. This month gonna get wild and might even end with a charity stream so be sure to check that out and as always Drink/Smoke and Riff Responsibly!

W/C 6th April 2026As we were driving to Manchester Airport last week we realised we had left the newly-purchased suncream at home. Even though we had only been travelling a few minutes we decided not to turn back, but risk picking some up at the departure lounge, irrespective of the fact it would probably be at an eye-watering supplement.As it turned out it was pretty much the same as buying from Boots on the high street, and another thing I noted was that the coffee and sandwich that I got from Pret was not only the same cost, but I was able to get my Club Pret discount. So kudos to everybody at T2 for not taking advantage of those passing-through.Surprisingly, and in sharp contrast, it cost eleven euros for 2 small cervazas on the way back - which is exactly what I wasn't expecting in GC. This was followed by sixty-five euros for a family Burger King (there really wasn't much more in the way of choice) which really did seem like profiteering.A tale of two departure lounges.Stay safe.Richard Hawley - As The Dawn BreaksTherapy For Me (or TFM as I now refer to it) is a bit of an audio curiosity. It started out as a mechanism for me to clear my head, with the hope that by saying stuff out loud it would act as a little bit of self-help. It's remains loose in style, fluid in terms of content and raw - it's a one take, press record and see what happens, affair.If you want to keep in touch with TFM and the other stuff I do then please follow me on Facebook, Insta, Twitter or Patreon. Thanks for getting this far.

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Novel MRI biomarkers, including cortical lesions, the central vein sign, and paramagnetic rim lesions, are highly specific for MS and can aid diagnosis in select clinical scenarios, particularly early in the disease course or in atypical presentations. When used with appropriate MRI sequences, these markers can improve diagnostic sensitivity while helping prevent misdiagnosis. In this episode, Casey Albin, MD, speaks with Jiwon Oh, MD, PhD, FRCPC, FAAN, author of the article "Diagnostic Neuroimaging Biomarkers for Multiple Sclerosis" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Oh is the medical director of the Barlo Multiple Sclerosis Program at St. Michael's Hospital and an associate professor at the University of Toronto in Toronto, Ontario, Canada. Additional Resources Read the article: Diagnostic Neuroimaging Biomarkers for Multiple Sclerosis Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Full episode transcript available here Dr Albin: Spend any time in a neurology conference, and you are certain to hear about the new central vein sign, which, as I learn, is not actually all that new. But have you heard about cortical lesions or these paramagnetic rim lesions? Because today I have the privilege of talking to Dr Jiwon Oh about her article, and we're going to unpack all these new biomarkers in MS. Dr Jones: This is Dr Lyell Jones, editor in chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Albin: Hello, this is Dr Casey Albin. Today I'm interviewing Dr Jiwon Oh about her article on diagnostic neuroimaging biomarkers for Multiple Sclerosis, which appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast. Thank you so much for being here. I'd love to start by having you introduce yourself to our listeners.  Dr Oh: Thanks, Casey. Hi, everybody. My name is Jiwon Oh and I'm a neurologist, mainly an MS specialist at Saint Michael's Hospital at the University of Toronto, and I'm the medical director of our MS program. Dr Albin: And you have written a really fantastic article that dives deep into some of the nitty gritty about these new diagnostic biomarkers that we find on the MRI that we're getting for our patients with multiple sclerosis. And I think we are going to get into a lot of that nitty gritty. How do we look for them? How do they improve our diagnostic specificity? This is really come a long way in shaping the advances for multiple sclerosis. And I'd kind of like to just start with the big picture. Like why do we need these more specific biomarkers?  Dr Oh: This set of diagnostic criteria in MS, it's actually a huge change in the field, and particularly for people like me who are really interested in developing new MRI measures, we're really, really excited because it's actually the first time since MRI was officially incorporated into the MS Diagnostic criteria, which was way back in 2001. It's the first time that we've actually been able to get newer, more advanced imaging measures beyond just simply detecting, new T2 lesions in the MS diagnostic criteria. So, it's a big moment in the field, and many of us are really excited about it in terms of why we need some of these newer, more specific imaging measures. Well, you know, diagnostic criteria always evolve over time for any disease state, and MS is one that we've recognized over the years. By the time someone actually presents with typical clinical symptoms and has diagnosed, whatever has been happening from a patho-biological standpoint has been happening probably for almost 5 to 10 years before that individual actually presents. And so, because of this recognition in the field and the fact that we're recognizing how important it is to first diagnose MS and then treat MS earlier and earlier, because we know that early treatment helps prevent more clinical outcomes. Diagnostic criteria over time have become much more permissive, meaning that we're doing everything that we can to try to facilitate a diagnosis of MS when we know that someone biologically has MS. But the problem with making diagnostic criteria more permissive, and it's obviously a good thing because you want to capture as many people with MS as early on as possible. The problem with making it permissive is there is this terrible risk of misdiagnosis. As clinicians, we all think we never make mistakes. But it turns out when you actually do studies, you do. And even at MS specialty centers, when studies have been done, 10% to 20% of people with MS are misdiagnosed. So, this is exactly why we need in diagnostic criteria that really help to facilitate a diagnosis. We need things that help us prevent misdiagnosis as well. And these are these specific imaging measures that have now been incorporated into the diagnostic criteria in many settings that will help to facilitate a diagnosis. But the really big perk is if you use them, you can help to prevent misdiagnosis as well.  Dr Albin: Yeah, that really shone through in your article that this was such a big step in towards being more specific about who were diagnosing. Also capturing more people, right? Trying to get those people that we, we don't want to miss because of all the things you say, you know, that allows them to accumulate more disability, have worse outcomes. Early diagnosis is so important. But I really did take away from your article just how critical these are and sharping our diagnostic acumen. And so just to jump right in, and you describe these three new biomarkers, these cortical lesions the central vein sign and paramagnetic rim lesions. And so just to kick things off let's start with cortical lesions I sort of conceptualize multiple sclerosis a disease of white matter. So, what's going on here?  Dr Oh: Yes. MS classically has always been described as a white matter disease. But it turns out when you look at brain and spinal cord tissue, as well as when you use kind of better sequences to actually look for lesions in the gray matter, it actually turns out there's a ton of lesions in the gray matter as well. And in fact, what's interesting is that regardless of whether it's the cortex or the deep gray matter, it's lesions within these areas that seem to have the highest relevance for clinical disability in MS. So, all this to say, of course, MS is a lesion that does affect white matter, but it also affects gray matter a lot. And maybe pathology within the gray matter is even more relevant to clinical disability. So, this is why we're really interested in being able to develop methods using MRI to more accurately visualize the gray matter, particularly the cortex, as well as deep gray matter structures like the thalamus. I should add the caveat that cortical lesions were actually included in the 2017 diagnostic criteria revisions, but they were included together with juxtacortical lesions, which are a typical area that MS lesions form. And so, this imaging measure, despite the fact that it is relatively novel and we consider it advanced, it hasn't been used that much only because it's not that easy to detect lesions within the cortex. And reasons for this include that you usually need higher field magnet platforms. And so, the typical clinical MRI scanners that are available kind of widely, regardless of whether you're at an academic center or a community center, are 1.5 Tesla magnets. And cortical lesions are actually really difficult to detect on those typical scanners. But when you get to like, say, three Tesla or seven Tesla, they're a lot easier to detect. But obviously that's a big hindrance to widespread use. And then you actually need very specialized sequences to adequately visualize cortical lesions. And these are not sequences that are usually collected for clinical purposes. So, it kind of requires convincing your radiologists that you need this additional sequence. And then it actually takes a lot of time and training to be able to adequately, accurately detect cortical lesions. So, despite the fact that it's actually very useful when you do have the appropriate MRI sequences and scanners to detect cortical lesions, even though they were incorporated into the 2017 criteria outside of specialty centers, they're not actually widely used. But when you do have the appropriate sequences, cortical lesions are actually pretty specific for MS. So, very helpful for a diagnosis in certain settings. But there's all these practical limitations that have really limited its widespread use. Dr Albin: That is a beautiful summary. So, it sounds like once we kind of get up to speed in terms of like the protocols for this, having the magnet strength for this, this will be really a game changer in terms of increasing the specificity and also maybe finding things that impact patient's clinical presentation and therefore quite meaningful. But it sounds like for most of us, this is probably not something that they're going to be adopting right away. Is that a fair assessment?  Dr Oh: Yes. And you know, they were included in the last diagnostic criteria revisions. And it really hasn't changed things very much, only because of these difficulties with, you know, requiring higher field magnet strengths and these specialized sequences and then needing training to kind of figure out how you can adequately detect cortical lesions. Dr Albin: Totally. So, the other thing we've heard a lot about, and I have to say, I was in the AAN fall conference not too long ago, and this came up quite a bit, was the central vein sign and the fascination with that, because it tells us a lot about the MS pathophysiology and again, increasing that specificity. And it seems like maybe this is one that we can more easily adopt in clinical practice. So, tell our listeners about what that is, how they detect it. How many do you need to find?  Dr Oh: Sure. And so, this is one of the imaging measures I'm really excited about. So, the central vein sign heard about it recently. And probably in the last ten years particularly in the MS field we're talking about it all the time. But just wanted to emphasize that the central vein sign is not something that is new. Even back in the 1800s, when Charcot described MS lesions in these ancient textbooks, he actually very clearly described that MS lesions form around the central vein. And that makes sense, because we know that these waves of peripherally mediated inflammation somehow get through the blood-brain barrier and cause this cascade of events leading to inflammation in the brain and spinal cord, which is what MS is. But we know that B cells in T cells require veins to get into the central nervous system. And so, it's no surprise, really, that MS lesions form around veins. And so, this is something that's been known pathologically. But the reason we're so excited about it now is because we actually have good enough iron-sensitive MRI sequences that allow us to see a central vein when it is present within a white matter lesion. As a neurologist, we know that there's probably hundreds and hundreds of different things that can cause white matter lesions in the brain. But when you use an appropriate iron-sensitive sequence and you see that many of them, if not most of them, actually have visible central veins, that tells you that this person very likely has MS. And so that's why we're so excited about it, because there have been many studies done in the last ten years. In fact, so much evidence generated in the last ten years that there have been I think it's now four systematic reviews and meta analyzes. Looking at the diagnostic properties of the central vein sign. And, you know, it turns out that when you look at people with MS, most of them have a pretty high proportion of white matter lesions that have visible central veins. And there's a lot of questions about, you know, how to best use the central vein sign. But when 40% or more of the white matter lesions that you see have visible central veins, then the likelihood of a diagnosis of MS is very high. So, this is why we're so excited about it in the MS field because it's a really useful diagnostic tool. You know, again when you have appropriate ion sensitive sequences, if you see someone with white matter lesions and you see that 40% or more of them have visible central veins, this tells you that this person very likely has MS.  Dr Albin: So, Dr Oh, I hear you say, you know, 40% of the lesions. Does that mean the neuro radiologist needs to look at every single lesion and then count how many have the central veins, or is there an easier way to do this? Dr Oh: Great question. Casey, there is definitely an easier way because our neuro radiologists would not be our friends anymore if we made them look at every white matter lesion and make sure that 40% of them had the central vein sign. So, because it's so time-consuming to use that 40% threshold, there's an easier criterion that has actually made it into the diagnostic criteria. And it's called Select Six. And what this means is when you have more than ten lesions, as long as you show that six of them have a visible central vein, you just have to count six with the central vein. Then you're done. So that means you're Select Six positive or central veins nine positive. However, if you have ten or fewer lesions, as long as you show that more than 50% of them show a visible central vein, then you are select six positive, and then you're done. So, as you can see, it's a much simpler criterion to apply, and it seems to perform almost as well as that 40% threshold, which is why that is the criterion that's made it into the new diagnostic criteria.  Dr Albin: Perfect. I love that we definitely do not want to make enemies with our neuro radiology colleagues, but yet they do so much for us. So perfect. I'm glad that we can, make their jobs a little easier without losing any specificity there, or just losing a touch of specificity there. All right. If I am working with a, you know, in a center that maybe doesn't do this all the time, am I just getting a run of the mill SWI sequence? Do I need to ask my radiologist for a special sequence? Or is this just, you know, you can get it from the typical array of what our patients are getting.  Dr Oh: You know, SWI is a widely available commercial sequence that's iron-sensitive, the ones that are typically commercially available, they can detect central veins, but there actually are little tweaks that you can do to make it a little more optimal. With the recent diagnostic criteria publication, which was, led by Xavier Montalban and recently published in Lancet Neurology. There's actually a companion MRI paper that was led by Frederick Barkov and Danny Wright. And the reason I'm specifically citing those papers is in that companion MRI paper, there's a table that has kind of optimal sequence parameters that you can use even with a conventional SWI sequence, to try to best detect the central vein sign. And then there's a wide range of different iron-sensitive sequences, and SWI is one of them, but the one that seems to have emerged as most sensitive to detect the central vein sign is something called the 3D T2*-EPI sequence. But the bottom line is there's a whole bunch of different iron-sensitive sequences that you can use, little tweaks that you can do to make them optimal, to be able to visualize central veins when they're present within white matter lesions. Dr Albin: Incredible. So like partner with your neuro radiologist, there is a great sounds like a field guide almost to this. So, it makes it easy to pick up in your standard of care so that you can make sure that you are detecting them at the optimal level to see that more specific diagnostic biomarker.  Dr Oh: Yes. And you know, in contrast to what we were talking about with cortical lesions, you can actually detect central veins when you use these iron-sensitive sequences at any field magnet. So even at 1.5 Tesla, particularly when you use contrast, which is often given with the diagnostic scan anyway, you can very easily detect a central vein. So that's a huge benefit because it allows for widespread use. As long as you work with your radiologist to get the right iron-sensitive sequences in.  Dr Albin: Yeah, that's incredible. I mean, I think that it really will be practice-changing. And then the last one that I think was honestly new to me, I feel like I had heard a lot about the central vein sign, but the whole new to me term was this paramagnetic rim lesion. So, what does that tell us about the underlying biology of MS? And are there any other things that might also have this finding that we should sort of be aware of? And how specific is it?  Dr Oh: You know, the central vein sign is kind of the main, really new imaging measure that's made it into every part of the MS diagnostic criteria. And then together with that paramagnetic rim lesions or we call them PRL or pearls for short, they've made it as well, but in a much more limited way only because there's not as much evidence that has accumulated over time to support the diagnostic utility of pearls. But first of all, what are pearls? So, people in the MS field are really excited about pearls, because we know that they capture a subset of what we call chronic active lesions. So, MS lesions will form acutely and over time, some of them will become inactive. And then some of them are chronic active lesions, meaning that they have this rim of activated microglia around them. Over time, they continue to slowly expand. And it's almost like this slow burn. And the reason why we focus a lot on chronic active lesions is because we know that they're a driver of progressive disease biology and MS, meaning that in people who have progressive MS or who have pretty severe disability, global disability or cognitive disability, we know that they have a high burden of pearls. And so that's why there's so much excitement in MS about being able to image chronic active lesions. It's because we're always looking for an imaging measure that allows us to accurately predict progression or to, measure progression over time. So that's why there's so much excitement in MS about pearls. But as kind of an added bonus, it turns out pearls are also really specific for MS. And so, when you use the same iron-sensitive sequences, by the way, that's used to detect the central vein sign when you use appropriate iron‑sensitive sequence. And if you see that someone has a pearl, the likelihood of a diagnosis of MS is very high. The one exception to that is Susac syndrome, where pearls have been observed. But other than that, with many other white matter diseases like neuro rheumatology disease, NMOSD, MOGAD, you really don't see pearls. And so, this is why it's made it into the new diagnostic criteria. In contrast to the central vein sign, though, not everybody with MS has a pearl, so the sensitivity isn't as high. However, it's really, really specific in the range of, you know, 90 to 95%. So, this is why it's been added as, an imaging measure in certain settings. It can help facilitate a diagnosis. But the real utility, again, is when you use it, it helps you to prevent misdiagnosis.  Dr Albin: It's fantastic. And hearing you talk about that, this one stands out to me as a biomarker that not only helps increase our diagnostic specificity, but also may really inform if the patient has having progression despite the treatment they're on, that this could play a role in helping you say, look, there probably is something that we need to switch because we can still see this ongoing progression. Dr Oh: Yes. And especially in this new era of treatment in MS. I think, you know, MS as a field, we've been so fortunate to have so many treatments emerge over the years that mainly target relapsing disease. But we hopefully, in the next little while, in short order, I hope we'll have treatments that target these progressive disease biologies. And so, not only is it helpful as a diagnostic marker, but there's a lot of evidence accumulating, showing that it may have a lot of prognostic value and will also help guide treatment decisions, exactly as you said.  Dr Albin: It truly does sound like it's a great time to be an MS doctor there. So, so many new advances in the field. There is so much more that we can do for these patients in our limited time left. I'd love to ask you, what is it that you're most excited about now with the change in the biomarkers, the change in the treatment, what makes you really excited to be a doctor specializing in MS right now? Dr Oh: I feel like we're on the brink of a new era of treatment. I think, you know, in the last two decades, MS care has changed so dramatically. I remember, you know, way back when, as a medical student, when I did my first neurology elective, this was when the first treatments for MS were emerging. And the prognosis that we were talking to patients about at that time is like night and day compared to what we talk to them about now. But we're going to do even better in the next couple of years. And so, there's a number of new treatments that hopefully will be approved soon that, for the first time, have shown an effect in clinical trials where it seems to be decreasing progression that is independent of relapsing activity. And that's really the greatest unmet treatment need that we have. And it seems like we might have some therapies on the horizon that can actually target that aspect of progression. It's really exciting, and even more that we're going to be able to do for our patients to completely change the way, we look at and the way we treat MS in the years to come.  Dr Albin: Dr Oh, this has just been fantastic. To all of our listeners, I really want to point you to the article because obviously, as an imaging biomarker article, there are so many beautiful images. There are great examples. There are some fantastic cases that show how applying these new biomarkers can help get you to the right diagnosis. This is truly a tour de force of how imaging has really shifted the care that we provide patients with MS, and so please go and check it out. It is one that you do not want to miss. And again, today I've been interviewing Dr Jiwon Oh about her article on diagnostic neuroimaging biomarkers for multiple sclerosis, which appears in the April 2026 Continuum issue on multiple sclerosis. Thank you again, Dr Oh, this has just been such a delight.  Dr Oh: Thank you for having me on the show, Casey, and look forward to people reading the article. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Kristian joins David to discuss his record breaking win at IM 70.3 Oceanside. They discuss training leading in, tactics and decision making in race and Kristian thoughts at different stages of the race. They also touch on the 20m draft rule, bike pack dynamics, why so many had a good swim and some thoughts on IM Texas. (00:00) Introduction(01:31) Team Accommodation in Texas (02:33) How is Kristian Feeling? (03:42) Pool Chaos (05:41) New Workout Creation  (06:14) How was the Swim? (07:31) Initial Bike Experience and Thoughts   (09:11) Bike Stress (10:23) Thoughts in T1 (10:49) Bottle Cage Casualty (12:04) How was the Tarmac on the Ride?  (12:50) How was the Military Base and No Speed Limit? (13:38) Fog Issues  (14:18) 20m Draft Zone Thoughts (15:18) Bike Position Thoughts (16:18) Calf Sleeves (17:25) Was Kristian Getting Splits on the Bike?  (18:40) How did Sam Sneak Past Kristian? (19:38) Concerns with Jason West in the Group?  (20:40) Motorbike Issues (23:05) When did Kristian Find Out Sam Long was in Front of Him? (26:40) Picking Jonas Schomburg Last Year  (26:27) Flipping the Cap (27:05) What was Kristian Thinking Coming out of T2? (28:10) Was There a Temptation to Run Without Socks? (28:34) Did Last Year Help This Year's Run? (29:26) Cap Flip (29:58) Thoughts When Passing Sam(30:33) Thoughts When Passing Jonas(31:10) Making the Pass on the Otherside of the Road (31:58) Extra Caffeine (32:58) Thoughts on Run Time(33:38) Thoughts on Tactics of Chasing People on the Run (34:51) Excitement for Texas Field (35:28) Rating the Day and Tactics (38:18) Extra Motivation  (39:30) Why did so Many People Swim Well? (40:17) Was Kristian Trying to Move Quicker Through Transition?  Thanks to the sponsors of this podcast series:MaurtenTo benefit from the one-time code and get 15% off your next purchase on Maurten.com, simply enter the code “TNMS4” at checkout. The code is applicable once per customer, on all products except the Maurten Bicarb System, valid until 31/12/2026.Maurten WebsiteInstagram: @maurten_officialYouTube: https://www.youtube.com/c/MaurtenOfficialHosted, edited and produced by Dr David LipmanEditing, video and introduction by Roj Ferman

Neurologic complications of substance use may be the first symptoms that lead patients with substance use disorders to seek care. Neurologists have a key role in identifying patients with substance use disorders and connecting them to treatment. In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Adeline L. Goss, MD, author of the article "Neurologic Complications of Drug and Alcohol Use" in the Continuum® February 2026 Neurology of Systemic Disease issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Goss is a neurohospitalist and associate chief of neurology for Highland Hospital in Oakland, California. Additional Resources Read the article: Neurologic Complications of Drug and Alcohol Use Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: A big part of neurology is solving mysteries. Patients can show up with all kinds of mysterious symptoms. Sometimes the diagnosis comes from within, some internal disruption of neurophysiology. But sometimes the problem is a complication of drug or alcohol use. Today we have the pleasure of speaking with Dr Adeline Goss, who recently authored an article for Continuum on this exact problem, a topic all neurologists need to be familiar with. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Adeline Goss, who recently authored an article on the neurologic complications of drug and alcohol use for our latest issue of Continuum on the neurology of systemic disease. Dr Goss is a neurohospitalist and the associate chief of neurology at Highland Hospital in Oakland, California. She's also an accomplished writer, broadcaster and podcaster. Dr Goss, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Goss: Great to speak with you, Dr Jones. Yes, I'm Adeline. I also go by Addie Goss. Dr Jones: So, before we get into the discussion, we're going to start off today with something fairly new to the podcast, the Continuum Audio trivia question. So, we all know that alcohol and other substances have many potential complications in that use of these substances fluctuates over time. But this one stood out to me from your article, Dr Goss, just for the sheer size of the change. So, for our listeners, here's the question. Accidental exposures to what substance increased a whopping 1,375% between 2017 and 2021? I'll read that again. Accidental exposures to what substance increased 1,375% between 2017 and 2021? So, stick around to the end of our interview for the answer. And let's get right to it, Dr Goss. If you had a single most important message to our listeners from your article, what would it be? Dr Goss: Well, I mean, many of us went into neurology because of the way that neurologic illnesses can be life-changing for patients. And I work as a neurohospitalist at a public hospital in Oakland, California. Many of my patients are admitted for neurologic conditions related to substance use. And when I see my patients later in the discharge clinic, many tell me that the last day that they used meth or the last day they used cocaine, the last day they smoked, was the day they had their stroke or whatever they came into the hospital for. I think the most important message is that hospitalization for a neurologic condition related to substance use can interrupt use patterns, can motivate change. And therefore, as neurologists, we really have an opportunity to connect to our patients and connect our patients to substance use treatment and make a dramatic difference in people's lives in this regard. Dr Jones: I think that's a fantastic point. I enjoyed a point you made in your article---and I can't remember exactly how you phrased it, I won't say it as well---that you think of the syndromes through which alcohol and drug exposures can present. Those syndromes almost always could end up of other primary neurologic disorders. So, put a different way, when a patient presents with a neurologic problem, most of the time an exposure could be on the differential.  And so, we really do have a responsibility as neurologists to be familiar with these. Dr Goss: To be familiar with these and to know how to connect patients to resources to try to get treatment. Dr Jones: Totally agree. And you touched on the public health aspect of this. It's really hard to talk about drug or alcohol use without acknowledging the public health impact particularly of opioids, which has been a crisis for most of this century. Right? And I think most of our listeners will be familiar with the rapid rise in opioid-related deaths. But there might be a glimmer of optimism there. Is what I've seen true, that opioid-related deaths may have plateaued? Dr Goss: So, yes, it's true that opioid-related deaths, overdose deaths in general, have begun to decline, actually, since 2023. And that's in part because overdose deaths really surged early on in the Covid-19 pandemic, in the setting of all of the social disruption, reduced access to services, and social isolation that occurred with the pandemic. But there were really multiple factors there. So, as you mentioned, there was this really rapid rise in illicitly manufactured fentanyl. Fentanyl became a major driver in overdose deaths starting in the mid-2010s. And by the late 2010s, it overtook heroin and prescription opioids as drivers of overdose deaths. And then this just collided with the pandemic in 2020, causing skyrocketing deaths. So, as we know as neurologists, fentanyl is more potent, it's shorter-acting, and it's also cheaper than heroin. It can cost as little as 50 cents or a dollar a pill. Thankfully, as services have rebooted and also as naloxone has become more widely distributed, there has begun to be a decline in opioid overdose-related deaths. So, we're relying on provisional data from the CDC for the most recent years, but that shows about a 24% decline in annual overdose deaths, comparing late 2023 to late 2024. And that's real. That comes out to 70 lives saved per day. Unfortunately, deaths still remain above prepandemic levels, and we're still talking about 87,000 drug overdoses per year. So, I would agree, a glimmer of hope. But we're still seeing overdose as the leading cause of death among young Americans aged 18 to 44. And there's a very long way to go. Dr Jones: 23% is a big number, and that is certainly exciting to think about, but we're still above that long-term secular trend. So, hopefully whatever is happening to bring that down, hopefully it continues. And we talk a lot about- appropriately, we talk a lot about opioid exposures and some of the neurologic presentations of opioid use and toxicity, but alcohol use disorder is the most common substance use disorder, correct? I learned that from your article. And it has been for some time, and it has well-known acute and chronic toxicities. But I think many of us have been taught something of a myth in the acute treatment of patients who may have thiamin deficiency or Wernicke's encephalopathy. Can you tell us a little more about that? Dr Goss: Yeah, sure. So, boy, what is my favorite vitamin? As a neurologist, I think thiamin is my favorite vitamin. Thiamin is a cofactor in- for several enzymes that are involved in glucose catabolism. And it's necessary to synthesize myelin and several neurotransmitters. And as we know, alcohol use disorder leads to reduced nutritional intake and impaired digestion and absorption of nutrients. And this can lead to deficiencies in water-soluble B vitamins, including thiamin, as well as trace elements. The thing about thiamin is that thiamin deficiency often appears first, because the body's stores of thiamin deplete in about 4 to 6 weeks. You know, we're traditionally taught if a patient presents with symptoms concerning for Wernicke's encephalopathy, that if they're also hypoglycemic or just in general, we have to get glucose into them first, because we don't want to tax these thiamin-dependent glucose catabolism pathways. But really, there's no reported case of a single glucose bolus precipitating some dramatic symptomatic thiamin deficiency. It's thought that harm would come potentially from prolonged carbohydrate administration without thiamin. And so, if a patient in front of you is both thiamin deficient and hypoglycemic, you just treat both. You treat both emergently. But it doesn't really matter in what order you do so. Dr Jones: That's good to know that doing the right thing for the patient can involve using either of those in whatever order. And I agree with you, I don't think I've ever hurt anybody by giving them thiamin. It's an easy one to miss and an important one to remember in the right context. And speaking of, and I think a lot about in your article, Dr Goss, I can see a neurologist seeing a patient in the emergency department or in the hospital or even in the clinic thinking about the wonderful points in your article. But we know that when alcohol or substance use enters our mind on the differential, the next impulse is to test for it. And we also know there are pitfalls of drug screening, doing urine drug screens, etc. How do you approach testing when you think about a potential drug-related complication in their differential? Dr Goss: So, like most people, I would start with a urine drug screen for any patient who's presenting with a possible toxidrome or some substance-related neurological presentation. These urine drug screens, they're rapid, they're inexpensive, they're immunoassays for traditional drugs and their metabolites. So, usually amphetamines, cocaine, opiates, plus/minus cannabis. But I think the first thing to note is that they miss entire categories of drugs, and not just drugs that are not in that list. They miss synthetic opioids, including fentanyl. One group is keeping track of this number. So, I have an update for mid-2025. And that's that 30% of U.S. ED overdose encounters as of mid-2025 included fentanyl testing. Only 30% for patients who are presenting with an overdose syndrome. Dr Jones: And that's for one of the most widely used synthetic opioids. So that's really a striking number. Dr Goss: Yeah, one of the most widely used and one with the greatest rate of complications. So, states can make a difference here. In 2022, California passed a law requiring fentanyl testing on hospital urine drug screens and several states have followed. And so that number is rising, the rate of testing for fentanyl. But that's just a really key thing to know, that that one is often missed. Other just important pitfalls, the timing of the urine drug screen matters because for most substances, it only picks up the drug within 24 to 72 hours after the last use. With amphetamines and cocaine going out a couple more days after that, especially in patients who use repeatedly. And then also, notably, there's a risk of false positives. This is especially true with amphetamine use, and beta blockers are one of the drugs that can lead to false positives on an amphetamine test, on a urine drug screen. So, I'll share that I've had several patients who have presented with intracerebral hemorrhage and who tested positive on the emergency department's urine drug screen and who adamantly stated that they do not use amphetamines, they've never used amphetamines, and they didn't ingest anything that could have contained amphetamines. And when we did serum confirmatory testing, in fact, their amphetamine testing was negative, and all those patients had received esmelol or the labetalol in the ED to treat their blood pressure related to their ICH. So false positives can occur with, you know, other medications like decongestants and certain antidepressants. But beta blockers are a key one to know. And then finally, there are just a number of things outside of that short list of substances that I mentioned, including a huge range of novel psychoactive substances that would not be tested for on a standard urine drug screen. And for those, you'd require serum testing, or at some large academic centers or specialty toxicology labs, you can actually do liquid chromatography high-resolution mass spectrometry, with- which is basically unbiased testing for any substance that's present in the patient sample. So, I guess, you know, you asked about my approach. Start with the urine drug screen, but there's no substitute for good history-taking and close examination of your patient's general examination, not just their neurologic presentation. And if patients are presenting with a toxidrome that I would expect would show up on a urine drug screen but it's negative, there are other confirmatory tests that can be sent, although they're often send-out labs and come back in a very delayed fashion. Dr Jones: So, in other words, it's complicated, which usually means it's humbling. And if I'm understanding it correctly, there's the risk of the false positive on the urine drug screen. And then there's the risk of the false negative if we think we're screening for something that might not even be on that initial screen. So, that's a wonderful reminder that these are clinical diagnoses and we have to keep our clinician hats on while we're thinking about how to establish these diagnoses or exclude them. So, back to opioids, Dr Gross. There are some really peculiar neurologic syndromes associated with opioid overdose. Tell us a little about those. Dr Goss: Well, I mean, some of these were described first with heroin. So, we can start with the one that almost anybody has heard of, heroin-associated spongiform leukoencephalopathy, which we know is associated with a practice known as "chasing the dragon," which is inhaling vapors of heroin heated on foil. But we know now that this syndrome can occur with other opioids, including fentanyl. The clinical features are, you know, apathy, cerebellar signs, quadriparesis, parkinsonism, myoclonus, and some patients progress to coma or even death. But on MRI you're seeing, you know, these confluence symmetric white matter diffusion restriction and T2 hyperintensities in the cerebellar white matter and the posterior limb of the internal capsule that spare the subcortical U-fibers. So, you know, I think this is kind of the classic example of something that's symmetric, that has a very obvious and interesting MRI pattern. But as time is passing, we're seeing more and more similar types of syndromes of leukoencephalopathies, but with different clinical presentations and MRI characteristics. So, another of these is CHANTER syndrome. This is an opioid overdose-related presentation where people have stupor and coma. And on the MRI there, you see bilateral symmetric diffusion restriction in the cerebellar cortex, in the hippocampi, in the basal ganglia. And it spares the cerebral cortex. And notably in these cases, patients can progress to cerebellar edema, to obstructive hydrocephalus. And some require suboccipital craniotomy. I had a week recently at Highland Hospital, where I work, where we had two of these cases in the same week, in just a community hospital. And there's a similar syndrome in children known as POUNCE syndrome with profound cerebellar edema, and many patients require posterior decompression. So that's another different distribution of findings with a different outcome. Fortunately, there's a milder sort of phenotype of opioid-associated amnestic syndrome, is what it's been described, where there's primarily DWI changes in the hippocampi and the globus pallidus. So, patients primarily present with an amnestic syndrome, mostly anterograde amnesia. Seeing these in practice, I'm not sure that patients always fall into one bucket or another. But in general, you'll see some degree of symmetric diffusion restriction or symmetric white matter changes that clearly point to a toxic presentation, a toxic syndrome, as opposed to pure anoxia, for example. And it's important to know that because from a prognostic standpoint, anoxic brain injury, which can occur after cardiac arrest and after opioid overdose, can look different than some of these syndromes. Finally, heroin has been associated with myelopathy, but also that's been reported on with fentanyl. So, I think some of these conditions got their reputation from heroin. But as fentanyl has proliferated---and prior to that as prescription opioid, you know, misuse had proliferated---we're seeing similar syndromes with all of the opiates. Dr Jones: And I think it's a good case in point that you can have multifocal disease and it be a manifestation of an intoxication, and I think that's a really good reminder that we have to have many of these syndromes in our differential, we have to be aware of them, otherwise we might miss them or attribute them to another mechanism. Dr Goss, our last issue of Continuum that was dedicated to the neurology of systemic disease came out in 2023, and here we are in 2026 publishing our latest issue, including your article and this podcast. Since 2023, have there been any emerging patterns or novel agents of abuse or misuse out there? Dr Goss: The short answer is yes, and I would say the reason is just the supply is moving at more and more rapid speed. The relationship between the internet and drug supply has really informed what's out there at any given moment. So, the turnover in the market can change in weeks, not in years. And there's all of this distribution through social media and encrypted apps. And then manufacturers are kind of continuously tweaking chemical structures to evade law enforcement. In the process of researching this article, I came across some, I mean, really wild examples. To be clear, these are not- not all these are common substances, but I think the general phenomenon should be known that people can walk into a vape shop or walk into a gas station or meander around online and buy some really weird stuff. So, in 2024, there was this nationwide recall of a product called Diamond Shrooms that was sold online and in smoke and vape shops, and this was billed as, like, a hemp and mushroom mixture. But it led to multiple- I mean, over 100 cases of seizures and agitation and depressed consciousness and a few possible deaths. And when the contents were analyzed, they included psilocybin analogs and pregabalin. I mean, some weird stuff. And so, those have been pulled. But people are constantly inventing and marketing these different substances. I think another example… we all know about nitrous oxide and its association with B12 myopathy. But the use of nitrous oxide has really changed. Companies are selling large canisters online and in vape shops, and they're flavored, like, in blue raspberry flavor. And unfortunately, there's been a rise of nitrous among youth. So, we're seeing not just increased cases of myelopathy, but also a 2025 study in JAMA found a spike in deaths attributed to actual nitrous oxide overdose. And so nitrous, I think, had not been that commonly used a few years ago, but has become more common in the last couple of years. A final one I'll just mention is ketamine. So, ketamine has certainly appeared in reviews of neurological syndromes related to substance use for a long time, and it's also been studied and used off-label for mood disorders in outpatient infusion clinics for some time. But in the pandemic, there was an expansion in telemedicine, as we know, and an associated proliferation of teleclinics that were prescribing very frequent, even daily oral and lozenge and nasal formulations of ketamine, which has led to increased rates of misuse. So, you know, acutely, the syndrome associated with ketamine intoxication is very brief. And often by the time people come to the emergency department, their symptoms have already worn off. But long-term, frequent use of ketamine is really still being studied. There seems to be an association with persistent neuropsychiatric effects like cognitive impairment, psychosis, persistent depressive symptoms. And so, you know, I think it's just important to realize that while the list of substances may look pretty similar to 2023, the use patterns, the distribution patterns are continuing to change. It's hard to keep up. And while alcohol and opioids and stimulants are by far the most common substances that a neurologist is going to encounter in daily practice, there's this ever-expanding range of possible substances that can trigger neurologic syndromes, both acute and chronic. Dr Jones: And I think that might be the best possible plug to read your article, because it is evolving and we have to stay on top of it. And we really can't be complacent with it. So, thank you for that update. Okay, back to our trivia question. Accidental exposures to what substance increased a whopping 1,375% between 2017 and 2021? Dr Goss, what do you think? Dr Goss: That was THC-infused edibles. Specifically, these would be THC-infused substances that are often marketed as looking like candy or snacks or cereal. Exactly what a kid might want to get their hands on. And unfortunately, accidental cannabis exposures in children under age five went up by 1,375% between 2017 and 2021, and 600 of those patients required critical care admission. Dr Jones: Yeah. So, just a mind-blowing number, and obviously something for us to be on the lookout for, especially if you see children in your practice and someone comes in with CNS depression or stupor, it's one to not miss. So that was something I learned in reading your article, among many other things. And Dr Goss, I want to thank you for joining us. I want to thank you for such a great discussion. I learned a lot from reading your article, I learned a lot just from our conversation today, and I suspect our readers and our listeners will too. Dr Goss: What a pleasure. Thank you so much, Dr Jones. Dr Jones: Again, we've been speaking with Dr Adeline Gross, author of a fantastic article on neurologic complications of drug and alcohol use in our latest issue of Continuum on the neurology of systemic disease. Please check it out, and thank you to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Múineadh na Gaeilge i mbunscoileanna T2 agus Córas na ndíolúintí ag Comhchoiste na Gaeilge

Kristian joins David to discuss his win at IM 70.3 Geelong, including a tactical breakdown and a quick look forward to Oceanside and travel. They discuss the course, Kristian's mindset in the race and much more. (00:00) Introduction(01:07) How has Training in Geelong Been? (03:44) Training in Carbon Shoes (04:48) Recovery Post IMNZ(06:08) Did Kristian Feel Overlooked Pre-Race? (07:50) How was the Swim? (10:30) What was Kristian Thinking in T1?  (11:15) Bike Focus for the Day (12:37) Falling off the Back of the Pack  (13:34) Bike Course Thoughts  (16:45) Challenges with Fog  (17:39) Thoughts in T2  (19:35) Run  (22:40) Thoughts When Passing Jelle  (25:00) Thoughts Passing Hayden  (25:50) Was it Helpful Having People Between the Leader and Kristian? (26:27) Flipping the Cap (26:48) Sunglasses (27:33) Did Kristian Want to Ease Off with an Eye on Oceanside? (29:10) Is the Rolling Course Enjoyable? (30:06) The Mentality To Catch Hayden and Jelle (32:54) Kristian's Thoughts on His Race Tactically(35:40) Training Week Upcoming Pre-Oceanside (37:28) Oceanside Thoughts Thanks to the sponsors of this podcast series:MaurtenTo benefit from the one-time code and get 15% off your next purchase on Maurten.com, simply enter the code “TNMS4” at checkout. The code is applicable once per customer, on all products except the Maurten Bicarb System, valid until 31/12/2026.Maurten WebsiteInstagram: @maurten_officialYouTube: https://www.youtube.com/c/MaurtenOfficialHosted, edited and produced by Dr David LipmanEditing, video and introduction by Roj Ferman

Today we talk about how to think about riding the trainer so you can be more prepared for the reality of the course. We talk about hills, wind, aero, cadence, and much more. We take a look at the last hour of your race and how you can work on being stronger as you come into T2. Do we all complicate specific workouts when the reality is we just have to be stronger both physically and mentally to deal with the demands of certain courses. We look at flat and windy along with the continually changing demands of a hilly course. Put a little more reality into your trainer rides.  Topics: Ramp rides Cadence and power Body shots and how to make them less impactful Your ability to close out a climb  Simulating headwinds and tailwinds Training your body to handle long rides Preparing for the real demands of the bike  Moving your ceiling Staying within yourself Making yourself more uncomfortable on a trainer Fighting through the wrong gear Putting your mind on the course while on the trainer Mike Tarrolly - mike@c26triathlon.com Robbie Bruce - robbie@c26triathlon.com 

Welcome to Bumppp! FM Episode 169 w/ T2 & Tyra The Zombie Join us live @ Eaton DC while we provide the best music across all genres to turn your Sunday up! Instagrams: @thegoodguysdc @bumppprecords @tazz.hq @tyrathezombie Tracklist: Coming soon

SEE THE BOYS LIVE - https://punchup.live/samtallent     Sponsors: HIMS - Support the show & get simple, online access to personalized, affordable care with HIMS @ http://hims.com/CHUBBY     Ridge - Take advantage of Ridge's once-a-year anniversary sale & get UP TO 40% OFF by going to https://www.Ridge.com/CHUBBY #Ridgepod #sponsored #ad     PATREON EPISODES: https://www.Patreon.com/chubbybehemoth     This week the boys are all together in Boston! Sam had to wear a dress so he'd fall asleep in his bosom, told a friend he wants to shrink them down to make them walk his city, and likes when Lund does Scorpion-esque attacks. Nathan woke up terrified on the plane, wants to watch T2, and was just thinking outloud when he said that.     00:00 Imagine Wiping It Once 01:18 Getting A Little Taste 04:58 Inside Stuff 06:43 Missing Every Time 07:48 Reverse Wahlberg 08:36 I Hope I Sleep Through It 10:22 Parks And Promenades 12:07 Death Waves 14:23 Bathing With Bottled Water 16:43 Not Molting 18:06 Traffic In Salem 19:46 Last Time I Was Here 21:28 Nasty Little Worm People 23:15 Buried Under Submissions 25:13 She's Around You Lots 27:35 Yeah I Hate It 29:34 Everybody Smells Like Pears 33:02 Cash Only 36:07 Allowed Me To Think More 38:29 I'm The King 41:45 It Was Probably Your Mom 42:24 Hurt People Hurt People 46:44 Armadillo That Worked At Hot Topic 47:56 Chubby Chess 51:48 The Sunset Ride 53:36 To The Airport Boys 57:15 Thank God You're Here 01:00:57 Burning Out And Fading Away     Nathan Lund and Sam Tallent are Chubby Behemoth   MORE WIDE WORLD: @SamTallent   Pre-Order Sam's New Book - https://www.amazon.com/dp/0593978897/ref=sr_1_1?crid=3I4LOBQ02YIGW&dib=eyJ2IjoiMSJ9.k5eCApJdjwVfn7hSelWi5VdRMlVrzKa4zf68ficcjcg.tZZOiI0nB0n3kkWiGAbidMQy5yUS_MkvmEIaXp-LXjo&dib_tag=se&keywords=sam+tallent+brut&qid=1769522903&sprefix=sam+tallent+,aps,181&sr=8-1&dplnkId=90401c83-a6a0-4ad4-999e-ece570a5d320&nodl=1

Kristian and David sit down to debrief Kristian's day at Ironman New Zealand and how to debrief races more generally. (00:00) Introduction(00:31) How is Kristian(01:02) How has Kristian Found New Zealand? (02:50) Has Kristian Been Sick? (03:24) How did Kristian Find the Swim? (05:58) How Was Kristian Feeling Coming out of the Swim?(07:08) Was Kristian Holding Back Early on the Bike? (09:00) What Happened with Krsitian's Aero bar?(12:19) What Went Through Kristian's Mind when the Aero Bar Came Loose? (13:20) How do you Stay Positive and Switch Your Mindset When Something Goes Wrong? (15:49) How Did Kristian Decide not to DNF?(17:38) Did Kristian Have a Second Mechanical? (18:04) Tactical Thoughts on the Bike(18:32) How was the Run? (20:21) How was T2?(20:56) What Happened with Kristian's Vomiting? (22:02) Why Were Kristian's Run Splits Yo-Yo'ing? (22:45) How Does Kristian Review a Race? (25:47) How Does Kristian Deal with Bike Mechanic Needs on the Road?  (28:03) Why Was IMNZ so Tough for Kristian?(28:59) What Does Kristian Think of his Tactics Today? (30:10) Do Today's Results Change How Kristian Thinks about Kona? (31:44) Training Plans Coming up(33:57) Travel Plans Upcoming(34:55) Does IMNZ Change the Year's Plan? (36:00) Why Did Kristian Decide to do Roth? Thanks to the sponsors of this podcast series:MaurtenTo benefit from the one-time code and get 15% off your next purchase on Maurten.com, simply enter the code “TNMS4” at checkout. The code is applicable once per customer, on all products except the Maurten Bicarb System, valid until 31/12/2026.Maurten WebsiteInstagram: @maurten_officialYouTube: https://www.youtube.com/c/MaurtenOfficialHosted, edited and produced by Dr David LipmanEditing, video and introduction by Roj Ferman

In this Terminator 2: Judgment Day Review, the Born to Watch crew dives headfirst into what many consider the greatest sequel ever made. James Cameron didn't just follow up the original Terminator… he reinvented the blockbuster. Released in 1991, Terminator 2: Judgment Day changed action movies forever with groundbreaking visual effects, unforgettable characters, and one of Arnold Schwarzenegger's most iconic roles.This week the full team is back, and the discussion kicks off with a simple but loaded question, is Terminator 2 the greatest sequel of all time? From the opening future-war battlefield to the legendary showdown between the T-800 and the liquid-metal T-1000, the boys break down why this film still holds up more than three decades later.Arnold Schwarzenegger returns as the Terminator, but this time the formula is flipped. Instead of hunting Sarah Connor, he's protecting her son, John Connor, the future leader of the human resistance. It's a twist that audiences in 1991 didn't see coming, and it gives the film its emotional core.The crew digs into Schwarzenegger at the absolute peak of his powers. After dominating the 80s with films like Predator, The Running Man and the original Terminator, Arnie was arguably the biggest movie star on the planet when T2 arrived. The famous bar scene, the sunglasses moment, and of course the immortal line "Hasta la vista, baby" all get the Born to Watch treatment.Linda Hamilton also gets her flowers in this episode. Her transformation from the vulnerable Sarah Connor of the first film into the hardened warrior of Judgment Day is one of the most dramatic character evolutions in action movie history. The boys discuss her intense performance, the physical transformation she underwent, and why her portrayal still feels authentic today.Edward Furlong's debut as John Connor sparks plenty of debate, too. Some love his rebellious street-kid energy, others question whether he's the most annoying teenager ever put in charge of humanity's future. Either way, he plays a crucial role in the film's emotional arc, and the developing bond between John and the T-800 is one of the movie's biggest surprises.Then there's Robert Patrick's T-1000. With his cold stare, relentless pursuit, and shape-shifting liquid metal body, he created one of the most terrifying villains of the 1990s. The guys break down why the T-1000 works so well and how the visual effects still look incredible today.Of course, no discussion of Terminator 2 would be complete without talking about the action set pieces. The LA River chase, the motorcycle-and-truck pursuit, the hospital escape, and the steel mill finale are all analysed in classic Born to Watch fashion. These scenes helped redefine what audiences expected from blockbuster filmmaking.The episode also dives into the film's massive cultural footprint. From the Guns N' Roses track "You Could Be Mine" to the revolutionary CGI that brought the T-1000 to life, Terminator 2 pushed cinema technology forward and influenced action movies for decades.But the big question remains: Does Terminator 2 actually surpass the original?That's the debate the Born to Watch crew finally settles.So slide into your leathers, fire up the Harley, and join the boys as they revisit one of the biggest and most influential action films ever made.JOIN THE CONVERSATIONIs Terminator 2 the greatest sequel of all time?T-800 or T-1000 — which Terminator wins the showdown?Does Judgment Day beat the original Terminator?Drop us a voicemail at https://www.borntowatch.com.au and be part of the show!Listen now on Spotify, Apple Podcasts, or wherever you get your podcasts.#BornToWatch #Terminator2 #JudgmentDay #ArnoldSchwarzenegger #JamesCameron #90sAction #MoviePodcast #SciFiMovies #T1000 #HastaLaVistaBaby

Here's a cheeky preview of our latest Take Ultra video episode in which Mark and Simon look ahead to this week's Oscars and assess the state of the race.  Ultra-Vanguardistas get these live streams every other week, our weekly T2 episodes in video and loads more. You can join them here: https://www.patreon.com/c/kermodeandmayo/membership   Learn more about your ad choices. Visit podcastchoices.com/adchoices

Comenzamos el episodio con la tertulia sobre la T3 de Strange New Worlds que, para nosotros, sigue en buena forma y, a pesar de sus excesos humorísticos, la hemos disfrutado tanto como la T2. Hasta tal punto que casi calcamos la duración de las tertulias, fueron 1h32m para la T2, y han sido 1h33m para la T3, que os podéis saltar si queréis evitar spoilers e ir directamente al episodio de TNG. En ‘Force of Nature', tenemos un episodio ecologista, con acciones estilo Greenpeace, de denuncia de la contaminación producida por los vehículos de combustión, representado en este caso por el motor de curvatura. El resultado final, una limitación a Warp 5, equivalente a la zona verde, pero un episodio muy flojo, especialmente si lo comparamos con el resultado de Star Trek IV, con una temática también ecologista, pero una ejecución excelente.

Bonjouuur ! Petit débriefing de lectures en vrac de ce début d'année :DOn espère que ça vous plaira, n'hésitez pas à nous donner vos avis, par mail : entrenospages@gmail.com ou via les réseaux sociaux que vous pouvez retrouver sur notre linktree ⁠⁠⁠⁠⁠⁠https://linktr.ee/entrenospages⁠⁠⁠⁠⁠⁠.Bonne écoute !Les livres abordés dans l'épisode (bonus inclus) sont : - Les derniers jours de l'apesanteur, Fabrice Caro- Le château des animaux, Xavier Dorison et Félix Delep- Vingt-quatre heures de la vie d'une femme, Stefan Zweig- A la vie !, L'homme étoilé- Fenêtre sur frousse, Michaël La Monnaie- Echecs, Victor L. Pinel- 9 secondes : La civilisation du poisson rouge, Bruno Patino et Morgan Navarro- Les enfants indociles T2, Seanan McGuire- Dungeon Crawler Carl, Matt Dinniman- Flatland, Edwin A. Abbott et Dani Collaterale- Le trône de fer, George R. R. Martin- Catalogue exposition Disney 100- Les enquêtes de Renoir et Monet, Léonie VilbertMusique : "La Pompe Du Trompe" de Shane Ivers - https://www.silvermansound.com

Today we look into your race day logistics. Things to think about beforehand so they are not taking up space in your brain on race day. We get into realistic race goals and how to give yourself the best chance for a good race. We talk about how to deal with brick legs off the bike. Is it something you can train more for or is it something you have to get used to. We dive into transition preparation and time saving techniques, some which are guaranteed to save you several minutes if you're not already doing them. And we look at having to go to the bathroom during the race. I know, but it is definitely another area that can cost you a ton of time. We also discuss the recent Barkley Marathons and here's a link to the mini-documentary we referenced..  Barkley Marathons mini-doc. - https://www.youtube.com/watch?v=eXi4xHj4SfU&t=19s Come join us at one of our awesome Camps: Nashville, May 13-17 - https://runsignup.com/Race/TN/Nashville/2026Camp Madison, Wisconsin, July 30-Aug 2 - https://c26triathlon.com/camps/triathlon-camp-wisconsin-2026/ Topics: What is a realistic goal time for a first-time Ironman, and how should I pace each leg Shoot for a wide window… it's like a long putt… trying to make it when you don't need to is risky business….. Fake Fresh What should I put in my bike and run "Personal Needs" bags? How can I manage the "jelly legs" sensation when I start the marathon? What is the best strategy for minimizing time in the transition areas (T1 and T2)? What's the protocol for using the restroom (or peeing) during the race?   Mike Tarrolly - mike@c26triathlon.com Robbie Bruce - robbie@c26triathlon.com

Dr. Amie Hornaman to discuss one of the most underdiagnosed and misunderstood health issues affecting millions—especially women over 35. Dr. Amie shares her personal journey from being a misdiagnosed fitness competitor who gained 25 pounds despite extreme dieting and exercise, to becoming a leading thyroid hormone specialist.Discover why 95% of hypothyroidism is actually Hashimoto's disease, why standard TSH testing fails most patients, and why T4-only medications like Synthroid don't work for the vast majority. Learn about the "forgotten hormone" T2 and its potential as a game-changer for metabolism and weight loss, the critical role of iodine, and what comprehensive thyroid testing should actually include.Whether you're struggling with unexplained weight gain, crushing fatigue, hair loss, or have been told "everything is normal" despite feeling terrible, this episode provides the roadmap to proper thyroid diagnosis and treatment.Contact Dr. Amie Hornaman: DrAmie.comSend Dr. Ovadia a Text Message. (If you want a response, you must include your contact information.) Dr. Ovadia cannot respond here. To contact his team, please send an email to team@ifixhearts.com Pre-Order Stay Off My Kitchen Table at Amazon. Like what you hear? Head over to IFixHearts.com/book to grab a copy of my book, Stay Off My Operating Table. Ready to go deeper? Talk to someone from my team at IFixHearts.com/talk.Stay Off My Operating Table on X: Dr. Ovadia: @iFixHearts Jack Heald: @JackHeald5 Learn more: Stay Off My Operating Table on Amazon Take Dr. Ovadia's metabolic health quiz: iFixHearts Dr. Ovadia's website: Ovadia Heart Health Jack Heald's website: CultYourBrand.com Theme Song : Rage AgainstWritten & Performed by Logan Gritton & Colin Gailey(c) 2016 Mercury Retro RecordingsAny use of this intellectual property for text and data mining or computational analysis including as training material for artificial intelligence systems is strictly prohibited without express written consent from Dr. Philip Ovadia.

Terminator 2D: No Fate (2025) synopsis: “Play through the events of Terminator 2 in pixel perfect 16bit graphics!”Available on: PC, PlayStation, XBox, and SwitchOn this bonus episode of Podcasting After Dark, Corey reviews the new Terminator 2 video game by Mike Tucker at Bitmap Bureau! If you're a fan of old school side-scrollers and/or T2 this game might be for you! Listen to the review to find out what works and what might be lacking.Leave a comment on Spotify and let us know what you thought of this bonus mini-review!— SUPPORT PODCASTING AFTER DARK —PATREON - Two extra shows a month including Wrap-Up After Dark and The Carpenter Factor, plus other exclusive content!MERCH STORE - We have a fully dedicated merch store at TeePublic with multiple designs and products!INSTAGRAM / FACEBOOK / LETTERBOXD - Follow us on social media for updates and announcements!This podcast is part of the BFOP Network

We're cracking open 1991 like a fresh VHS rental and drafting the very best films the year had to offer. Rob, Dave, and Kurt will go head to head, assembling their dream rosters from a cinematic moment that still hums with electricity. This was the year of Terminator 2: Judgment Day rewriting the rules of the blockbuster, The Silence of the Lambs turning prestige drama into a pop culture event, and comedies lodging themselves permanently in the brain. What About Bob?, with Bill Murray at peak controlled chaos, sat right alongside Hot Shots!, proving 1991 could swing from psychological tension to perfectly timed lunacy without breaking stride. The draft unfolds across six categories, including comedy, blockbuster, big budget, and drama, forcing tough calls right out of the gate. Do you lock in T2 or Robin Hood: Prince of Thieves for sheer scale, grab Boyz n the Hood or Thelma & Louise for dramatic weight, or roll the dice on something like Point Break, where surf culture, skydiving, and philosophy collide? Strategy matters, nostalgia runs hot, and no one leaves without defending at least one hill they're willing to die on. By the end, we'll have three very different blueprints of 1991, built from quotable lines, seismic action, and films that still feel permanently etched into moviegoing memory Apple: https://podcasts.apple.com/us/podcast/totally-80s-and-90s-recall/id1662282694    Spotify: https://open.spotify.com/show/11dk5TUoLUk4euD1Te1EYG?si=b37496eb6e784408    Amazon: https://music.amazon.com/podcasts/1960c8f9-158d-43ac-89a6-d868ea1fe077/totally-80s-and-90s-recall    YouTube Podcasts: https://youtube.com/playlist?list=PLH9lGakNgCDZUkkHMUu88uXYMJu_33Rab&si=xo0EEVJRSwS68mWZ   Contact Us: Website: https://totally80s90srecall.podbean.com/  Email: 80s90srecall@gmail.com LinkTree:https://linktr.ee/80s90srecall  Voicemail #: (509) 426-4542 

This week we're joined by Mike Tucker and Quang DX from Bitmap Bureau to talk about the making of Terminator 2D: No Fate. We hear how their lifelong love of Terminator 2 turned into a three-year obsession, why so many classic T2 games missed the mark, and how this project set out to put that right. From painstakingly recreating iconic film moments in pixel art, to difficulty balancing, licensing hurdles, hidden Easter eggs, and expanding the Future War beyond the film, this is the story of how the Terminator game fans always wanted finally became reality.  Powerhoof games: https://www.powerhoof.com/Contents:00:00 - The Week's Retro News Stories 55:33 - Terminator 2D: No Fate Interview Please visit our amazing sponsors and help to support the show:Bitmap Books - https://www.bitmapbooks.comLeeds Gaming Market: https://leedsgamingmarket.com/Check out PCBWay at https://pcbway.com for all your PCB needsTake your business to the next level today and enjoy 3 months of Shopify for £1/month: https://shopify.co.uk/retrohourWe need your help to ensure the future of the podcast, if you'd like to help us with running costs, equipment and hosting, please consider supporting us on Patreon:https://theretrohour.com/support/https://www.patreon.com/retrohourJoin our Discord channel: https://discord.gg/GQw8qp8Website: http://theretrohour.comFacebook: https://www.facebook.com/theretrohour/X: https://twitter.com/retrohourukInstagram: https://www.instagram.com/retrohouruk/Bluesky: https://bsky.app/profile/theretrohour.comTwitch: https://www.twitch.tv/theretrohourShow notesSonic Lands on the Amiga: https://tinyurl.com/4rckwhvwCelebrate 50 Years of Jaws: https://tinyurl.com/348uw48eCES Retro Tech: https://tinyurl.com/3fwpynyhModder Creates Switch-Style Dock for the Nintendo 3DS: https://youtu.be/Kqn9QqYMQOMThe Iconic QuickShot II Joystick Returns in 2026: https://tinyurl.com/2p9pr8k9Support for the Sega Dreamcast Web Browser Ends After 25 Years: https://tinyurl.com/4c9ppapcStreets of Rage 2 New Era v3 Out Now: https://tinyurl.com/3xd8jrx3

Want to drop 8-12 lbs before summer without crash dieting or losing muscle? Join the Get Lean in 45 Days Workshop on January 20th. Includes replay, fat loss workout program, custom macros, and complete 45-day protocol.—Are you lifting weights, tracking macros, and still stuck with stubborn fat? What if your labs look “normal” but your metabolism feels broken?Body recomp is supposed to feel simpler when you train hard and eat well, yet many people chasing weight loss and muscle building feel stuck. I brought on Dr. Amie Hornaman, known as the Thyroid Fixer, to challenge the way we think about metabolism, hormone health, and strength training. We explored T2, a lesser-known thyroid hormone that acts directly at the mitochondria to help burn fat, boost energy, and protect lean mass.This conversation matters if you care about nutrition and fitness, longevity, and strength training over 40, especially for women's fitness and anyone frustrated by slow progress despite doing “everything right.” We connected evidence-based fitness, evidence-based nutrition, and smart supplementation, without hype or shortcuts.Today, you'll learn all about:0:00 – Why metabolism feels broken4:20 – The forgotten thyroid hormone9:45 – T2 vs T3 and T415:30 – Fat loss without muscle loss22:10 – Mitochondria and metabolism28:40 – Appetite vs energy expenditure35:55 – Strength training and thyroid health44:30 – Hashimoto's and lab myths52:20 – Practical next stepsEpisode resources:Thyroid Fixxr T2 Supplement - get 10% off with code WITSThe Thyroid Fixer Podcast - follow to get Philip's episode soon!Free 7-Day Thyroid Healing KickstarterJust Fix Your THYROID Facebook GroupWebsite: dramie.com Support the show

Dr. Zohaib Siddiqi talks with Dr. Catarina Bernardes about a case involving a 35-year-old woman presenting with personality changes and gait impairment.  Show citation:  Bernardes C, Lemos JM, Santo GC. Clinical Reasoning: A 35-Year-Old Woman With Personality Change and Gait Impairment. Neurology. 2025;104(2):e210252. doi:10.1212/WNL.0000000000210252  Show transcript:  Dr. Zohaib Siddiqi: Hi, everyone. My name is Zohaib Siddiqi and I'm a fifth-year neurology resident and a part of the Neurology® Resident and Fellow Section Editorial Board. I just finished interviewing Catarina Bernardes about her article, Clinical Reasoning: A 35-year-old Woman with Personality Change and Gait Impairment. Catarina, can you tell us the main points of the article? Dr. Catarina Bernardes: So in this article, we discussed the case of a 35-year-old woman who presented with a three-year history of walking difficulties. On examination, she had signs of a frontal temporal dysfunction, a dorsal lateral myelopathy, optic atrophy, and pes cavus. Her brain and spinal cord MRI was completely normal, but her son's brain MRI was being studied for spastic paraparesis showed signs of hypomyelination involving the subcortical U fibers. Given the suggestive inheritance pattern, we considered an X-linked leukoencephalopathy and central nervous system hypomyelination points to Pelizaeus-Merzbacher disease. Important learning points. When differentiating leukoencephalopathies, remember that hypomyelinating disorders often have less pronounced hypointensity on T2 and hypointensity on T1, and in demyelinating disorders, there is very prominent hyperintensity on T2 and hypointensity on T1. Also, Pelizaeus-Merzbacher is a hypomyelinating disorder affecting the subcortical U fibers, while X-linked adrenoleukodystrophy presents a demyelinating pattern sparing the subcortical U fibers and involving mainly the parietooccipital regions. Dr. Zohaib Siddiqi: Thanks so much for that summary, Catarina. A lot of learning points there. For those of you who want to learn more about the case, you can listen to the full-length podcast available now on all streaming platforms and find the article titled, Clinical Reasoning: A 35-year-old Woman with Personality Change and Gait Impairment on the Neurology® Resident Fellow Website. Thanks so much for joining today, and see you next time. 

Episode 2725 - Vinnie Tortorich and Chris Shaffer discuss Vinnie's recent vacation, questioning the narratives throughout the years, magnesium, and more. https://vinnietortorich.com/2025/11/questioning-the-narratives-episode-2725 PLEASE SUPPORT OUR SPONSORS Pure Vitamin Club Pure Coffee Club NSNG® Foods VILLA CAPPELLI EAT HAPPY KITCHEN YOU CAN WATCH THIS EPISODE ON YOUTUBE - @FitnessConfidential Podcast Questioning the Narratives Vinnie just returned from vacation. (3:00) They discuss how the climate change debate has developed over the years. (10:00) The conversation shifts to panda behavior and their lack of reproductive interest. (21:00) Regenerative farming and preserving topsoil are essential, whether you eat meat or not. They also talk about celebrity children making speeches about environmental and health issues. (25:00) "Fat: A Documentary" includes the story of Dr. Gary Fettke and how he learned to help T2 diabetics avoid amputations of their damaged limbs. (28:00) Vinnie shares an encounter he had with a guy about vitamins. (43:00) He specifically talks about magnesium and choosing the proper forms and ratios. (46:00) They also discuss business at Pure Vitamin Club. Vinnie finally shares his experience with his first pina colada. (1:00:00) Don't forget to sign up for the NSNG VIP group. Vinnie's video workouts will be free to all members! (1:05:00) You can get on the wait list -https://vinnietortorich.com/vip/ Also, you'll want to join as soon as it opens, because once it closes again, it will be closed indefinitely. You can book a consultation with Vinnie to get guidance on your goals. https://vinnietortorich.com/phone-consultation-2/ More News Serena has added some of her clothing suggestions and beauty product suggestions to Vinnie's Amazon Recommended Products link. Self Care, Beauty, and Grooming Products that Actually Work! Don't forget to check out Serena Scott Thomas on Days of Our Lives on the Peacock channel. "Dirty Keto" is available on Amazon! You can purchase or rent it here.https://amzn.to/4d9agj1 Please make sure to watch, rate, and review it! Eat Happy Italian, Anna's next cookbook, is available! You can go to https://eathappyitalian.com You can order it from Vinnie's Book Club. https://amzn.to/3ucIXm Anna's recipes are in her cookbooks, website, and Substack — they will spice up your day! https://annavocino.substack.com/ Don't forget you can invest in Anna's Eat Happy Kitchen through StartEngine. Details are at Eat Happy Kitchen. https://eathappykitchen.com/ PURCHASE DIRTY KETO (2024) The documentary launched in August 2024! Order it TODAY! This is Vinnie's fourth documentary in just over five years. Visit my new Documentaries HQ to find my films everywhere: https://vinnietortorich.com/documentaries Then, please share my fact-based, health-focused documentary series with your friends and family. Additionally, the more views it receives, the better it ranks, so please watch it again with a new friend! REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter! PURCHASE BEYOND IMPOSSIBLE (2022) Visit my new Documentaries HQ to find my films everywhere: https://vinnietortorich.com/documentaries REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter! FAT: A DOCUMENTARY 2 (2021) Visit my new Documentaries HQ to find my films everywhere: https://vinnietortorich.com/documentaries FAT: A DOCUMENTARY (2019) Visit my new Documentaries HQ to find my films everywhere: https://vinnietortorich.com/documentaries