Podcasts about antibodies

Most people with elevated thyroid antibodies are told, “Don't worry, your thyroid is fine.” But what does the research actually say?In this episode of Reversing Hashimoto's, Dr. Anshul Gupta explores the hidden impact of thyroid antibodies, including their connection to thyroid tissue destruction, infertility, miscarriage, hormonal imbalances, brain fog, autoimmune disease, and long-term health risks. Learn why normal TSH levels don't always mean optimal thyroid health, how thyroid antibodies affect the entire body, and what current research reveals about their significance.Dr. Gupta also shares practical strategies for lowering thyroid antibodies and a real patient success story that demonstrates what's possible when the root causes of autoimmune thyroid disease are addressed.If you've been told your antibodies don't matter, this episode may change the way you think about your thyroid health.

Bispecific antibodies (BsAbs) are an emerging and fast-developing area of immunotherapy, particularly in the treatment of hematologic malignancies. However, access to this therapy remains limited, particularly for Veterans. Administrative hurdles and challenging adverse events have slowed adoption of BsAbs in the US Department of Veterans Affairs (VA). In this episode, CANCER BUZZ speaks with Nicholas Burwick, MD, hematologist in the Puget Sound VA Health Care System, about how his VA site tackled these challenges and made BsAbs available to its patient population through a collaborative hub-and-spoke model.  Guest: Nicholas Burwick, MD President, Association of VA Hematology/Oncology Hematology and Bone Marrow Transplant Puget Sound VA Health Care System "We set expectations, we came up with a plan, and we didn't have too many bispecific antibody patients at the same time. At least initially, we wanted some control." — Nicholas Burwick, MD  "The collaboration among different VA centers has been something that I've come to appreciate. We have a heme malignancy group, for example, so we can compare notes, work together, and in some cases even collaborate on VA initiative proposals or industry-sponsored clinical trials." — Nicholas Burwick, MD Resources: Addressing Care Disparities for Veterans: Tackling Barriers and Identifying Solutions Bispecific Antibodies Bispecific Antibodies Are Moving Forward; So Are the Implementation Questions Service, Sacrifice, and Survival: Advancing Cancer Care for America's Heroes  

In episode two of our AI & Antibodies mini-series, we speak to Ryan Emerson, Senior Vice President of Data Science at A-Alpha Bio, to discuss AlphaBind, A-Alpha Bio's antibody-antigen binding-affinity prediction model.We discuss how this model was trained, how it operates and how it has enabled researchers to test mutations designed to optimize an antibody candidate for critical quality attributes computationally, assessing their likely impact on binding affinity, before returning to the wet lab. The conversation also explores the future of AI in antibody engineering and the critical role of high-quality data in advancing the field.Contents[02:20] Current challenges in antibody sequence design [04:20] Presenting AlphaBind[08:40] Demonstrating AlphaBind's effectiveness[11:40] Benefits of AlphaBind and it's applications[16:05] How to make the most of AlphaBind[19:25] Current use of AlphaBind [23:00] Predictions for the impact of AI in antibody engineering[25:40] A brief detour into the uses of AI in drug design (See this story for more detail)[26:45] What wish could be granted to improve AI in antibody design? Hosted on Acast. See acast.com/privacy for more information.

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we delve into a series of significant advancements shaping the landscape of our industry. As technology continues to redefine traditional paradigms, the collaboration between Pfizer and Chai Discovery exemplifies this trend. By harnessing artificial intelligence, particularly through custom models like Chai-3, this partnership aims to revolutionize drug discovery. The integration of AI promises not only to accelerate the identification of biologics and antibodies but also to optimize resource allocation in research and development. Such technological integration could pave the way for an enhanced pipeline of innovative treatments, marking a transformative shift in how therapeutic candidates are developed. In the realm of regulatory developments, Lupin's Ranluspec has recently received FDA approval as an interchangeable biosimilar targeting VEGF-A for various retinal conditions. This move underscores the importance of biosimilars in providing cost-effective alternatives to expensive biologics, thereby expanding patient access to essential treatments for conditions like macular degeneration. Additionally, the MHRA's marketing authorization for Aujemflu, an adjuvanted trivalent influenza vaccine for adults aged 50 and over, reflects ongoing efforts to bolster protection against infectious diseases among vulnerable populations. Clinical trial advancements continue to highlight significant progress in therapeutic development. Otsuka Pharmaceuticals' Phase 3 data on Voyxact has shown promising stabilization of kidney function in patients with Immunoglobulin A nephropathy. This protein therapy targets autoimmune pathways, offering new hope for managing this chronic kidney condition. Similarly, Autobahn Therapeutics' Elunetirom has advanced to a pivotal trial following Phase 2 success in treating bipolar depression. This showcases the potential of small molecule therapies targeting thyroid hormone receptors. Meanwhile, Hikma Pharmaceuticals' victory in a landmark patent case regarding skinny labels marks an important development in pharmaceutical intellectual property rights. The unanimous Supreme Court ruling against Amarin supports the legitimacy of using skinny labels to market generic versions of drugs for non-patented indications. This decision could enhance market competition and drive down healthcare costs, setting a precedent for future intellectual property disputes. On the business front, strategic partnerships and mergers continue to shape industry dynamics. Gilead Sciences' acquisition of Ouro Medicines for $1.675 billion strengthens its autoimmune inflammation pipeline. This transaction exemplifies how major deals are reshaping therapeutic portfolios in response to growing demand for treatments targeting rare diseases. Financially, Solix Pharmaceuticals' success in raising $71 million to advance its siRNA pipeline across multiple therapeutic areas demonstrates investor confidence in RNA-based therapeutics as a promising frontier for innovative treatments. Conversely, challenges persist as evidenced by Takeda's $2.5 billion legal provision over an antitrust case related to Amitiza, underscoring ongoing financial risks associated with litigation in the pharmaceutical sector. Corporate restructuring also signals shifts within the industry landscape. Fulcrum Therapeutics' decision to lay off 85% of its workforce following the discontinuation of its sickle cell disease candidate highlights the volatility and high stakes inherent in drug development. Overall, these developments illustrate a dynamic landscape where scientific innovation is propelled by AI-driven approaches and strategic collaborations while regulatory victories and financial maneuvers shape market dynamics. These trends have profound implications for patient care by potentially accelerating the availability of novel therapies and fostering a competitive environment that drives down costs. As we look ahead, stakeholders must navigate these complexities effectively to harness opportunities and address challenges within this rapidly evolving industry landscape. The ability to adapt and capitalize on emerging trends will be crucial as these sectors continue to evolve, ultimately enhancing patient care and advancing therapeutic frontiers globally. Thank you for joining us today on Pharma Daily; stay tuned for more insights into the ever-changing world of pharmaceuticals and biotech.Support the show

Featuring perspectives from Prof Ramez Eskander and Dr Bradley Monk, moderated by Dr Kathleen Moore, including the following topics: Introduction (0:00) Advances in Human Cadherin-6-Targeted Antibody-Drug Conjugates (ADCs) in Ovarian and Other Gynecologic Cancers — Dr Moore (1:30) Leveraging TROP2-Directed ADCs in Advanced Gynecologic Cancers — Prof Eskander (35:39) Tolerability and Other Practical Considerations with Novel Investigational ADCs in Advanced Gynecologic Cancers — Dr Monk (1:04:58) CME information and select publications

We have teamed up with the journal mAbs to cover their article collection on artificial intelligence and machine learning in antibody development. In this, the first episode of the series, we speak to Charlotte Dean, Professor of Structural Bioinformatics in the Department of Statistics at the University of Oxford, about her paper in the collection: Humatch - fast, gene-specific joint humanization of antibody heavy and light chains.Charlotte takes us through a critical issue in the development of antibody therapeutics – humanization – and reveals how new AI-based software can improve our solutions to this long-held problem in the field.Contents[0:47] Please can you tell us a little bit about yourself and your lab?[1:16] You authored a paper in the article collection, Artificial Intelligence and Machine Learning in Antibody Development. What was it that attracted you to that collection? And why did you think it was important to contribute to?[2:36] What other antibody characteristics make for a good drug?[3:36] Why do we need to humanize antibodies? How hard is it to achieve? How many drugs or potential drug candidates are limited by a lack of humanization?[5:43] Can you tell us a bit more about Humatch? How does it work and how does it deliver this sort of humanization?[7:10] Do you have any advice for anyone who might be using Humatch for the first time or is looking to implement it in their own research?[9:18] Your paper was released at the end of 2024. Have you been able to implement this tool in your own research or seen any particularly exciting applications of this platform in the wider research space?[10:20] What are your predictions for the impact of AI in this space in the next five years?[12:20] If there was one thing that you could ask for to help advance the design of antibody therapeutics, what would it be? Hosted on Acast. See acast.com/privacy for more information.

T-cell-engaging bispecific antibodies represent a major therapeutic and scientific advancement in the treatment of several types of cancer. However, they carry a risk of some unique acute toxicities, such as cytokine release syndrome and neurologic toxicity. This podcast reviews this emerging drug class and strategies for recognition and management of their unique adverse events. The information presented during the podcast reflects solely the opinions of the presenter. The information and materials are not, and are not intended as, a comprehensive source of drug information on this topic. The contents of the podcast have not been reviewed by ASHP, and should neither be interpreted as the official policies of ASHP, nor an endorsement of any product(s), nor should they be considered as a substitute for the professional judgment of the pharmacist or physician.

From Discovery to Delivery: Charting Progress in Gynecologic Oncology, hosted by Ursula A. Matulonis, MD, brings expert insights into the most recent breakthroughs, evolving standards, and emerging therapies across gynecologic cancers. Dr Matulonis is chief of the Division of Gynecologic Oncology and the Brock-Wilson Family Chair at the Dana-Farber Cancer Institute, as well as a professor of medicine at Harvard Medical School, both in Boston, Massachusetts.In this episode, Dr Matulonis was joined by Meghan E. Shea, MD, an attending medical oncologist and ambulatory medical director and disease program leader for medical oncology at Beth Israel Deaconess Medical Center in Boston. Together, they explored the current landscape of cervical cancer, from the urgent need for expanded vaccination and screening to the evolving role of immunotherapy and antibody-drug conjugates (ADCs) across disease settings.Dr Shea opened by addressing the epidemiology of cervical cancer, noting that despite decades of progress, rates are now plateauing and rising among women under 50 years of age. She identified 3 interrelated drivers of this trend: declining rates of routine gynecologic screening, inconsistent uptake of human papillomavirus (HPV) vaccination, and persistent high-risk HPV infections, particularly HPV 16 and 18, which are responsible for most cases. The conversation then turned to the effect of immunotherapy on cervical cancer treatment. Dr Shea traced the evolution of pembrolizumab (Keytruda) from its initial 2018 approval as a single agent in recurrent/metastatic disease to its more recent integration into the frontline setting. The phase 3 KEYNOTE-A18 trial (NCT04221945) demonstrated that adding pembrolizumab to standard weekly cisplatin-based chemoradiation significantly improved outcomes for patients with locally advanced disease. Although responses to immunotherapy, when they occur, are often durable, Dr Shea acknowledged that response rates remain lower than anticipated for a virally driven malignancy, underscoring the need for novel combinations and a deeper understanding of resistance mechanisms. Drs Matulonis and Shea both agreed that immunotherapy combined with ADCs represents one of the most compelling directions for the field, with phase 2 data for sacituzumab tirumotecan plus pembrolizumab generating interest ahead of anticipated phase 3 results.On the ADC front, Dr Shea reviewed the 2 agents in this class that are currently FDA-approved for cervical cancer. Tisotumab vedotin-tftv (Tivdak) offers the advantage of biomarker-independent use, though its requirement for ophthalmologic monitoring at every treatment visit creates real-world access challenges outside major academic centers. Trastuzumab deruxtecan-nxki (Enhertu), approved in the HER2 immunohistochemistry 3+ setting based in part on the results of the phase 2 DESTINY-PanTumor02 trial (NCT04482309), has generated robust response rates but is most likely to benefit patients with adenocarcinoma. Dr Shea also highlighted additional targets under investigation, including Trop-2, Nectin-4, and B7-H4, with multiple phase 3 trials ongoing in both the frontline and recurrent settings.The discussion closed with a look at the locally advanced disease landscape, where the NRG Oncology cooperative group is conducting a phase 3 trial to evaluate whether integrating the neoadjuvant carboplatin/paclitaxel regimen from the INTERLACE trial (NCT01566240) with the pembrolizumab-based regimen from KEYNOTE-A18 can further improve outcomes and reduce the morbidity associated with brachytherapy. Dr Shea expressed optimism about this question, citing preliminary experience suggesting that neoadjuvant chemotherapy may reduce the need for invasive radiation techniques.

Silvia Messina, MD, DPhil / Michael Levy, MD, PhD - Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) or Something Else? How to Tell the Difference

Silvia Messina, MD, DPhil / Michael Levy, MD, PhD - Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) or Something Else? How to Tell the Difference

Dr. Dana Varble, chief veterinary officer for the North American Veterinary Community, joins Lisa Dent to talk all things pets. Lisa explains how her dog, Luna, now has Lyme antibodies and Dr. Varble guides her on what to do next. Later, Dr. Varble takes pet questions from you!

The conversation covers the understanding of Hashimoto's Thyroiditis, the role of the immune system, the impact of iodine, management with diet and supplements, antibody levels, natural auto antibodies, immune system shift, calming the immune system, and the conclusion.TakeawaysUnderstanding the role of the immune system in Hashimoto'sManaging Hashimoto's with diet and supplementsChapters00:00 Understanding Hashimoto's Thyroiditis05:17 The Immune System and Antigens10:24 Understanding Antibody Levels in Hashimoto's

Send us Fan MailWhy are pathology vendors still speaking different image languages when radiology solved that problem decades ago?In this episode of DigiPath Digest #46, I talk through four papers that all point to a bigger issue in digital pathology: we are not only dealing with better algorithms. We are dealing with interoperability, workflow design, explainability, and whether the field is actually ready to use these tools well.I start with DICOM in digital pathology, because I think this is still one of the most important infrastructure questions in the field. Digital pathology has clear value for consultation, image analysis, archival, and workflow, but vendor-specific whole slide image formats still create silos. In the episode, I explain why DICOM matters, why adoption is still low, how the multi-resolution pyramid works, and why this is really about enterprise imaging and future-proofing, not just file conversion. Then I move into kidney transplant rejection, where the paper makes a strong case for multimodal precision diagnostics. Creatinine is late. Antibody testing can miss important biology. Biopsies can miss the area that matters. So the opportunity is not to replace pathology, but to combine biomarkers, biopsy, and machine learning in a way that is more useful than any one signal alone. I also talk about explainability here, because if a model gives a risk score, we need to know what contributed to it. The third paper focuses on perineural invasion in solid tumors, and I liked this one a lot because it shows how AI can help standardize something that is clinically important but still inconsistently detected and reported. Perineural invasion is not just a passive pathway of spread. The biology is more active than that, and the quantification can go far beyond a simple yes-or-no answer. This is a good example of where digital pathology can do something humans cannot realistically do by eye at scale. The last paper is on gastric cancer immunohistochemistry biomarkers and advanced quantification, including HER2, PD-L1, mismatch repair, and CLDN18.2. This section is really about complexity. We are now asking pathologists to visually score biology that is getting harder and harder to summarize consistently, especially when markers, spatial context, and multiplexing all start to matter at once. I make the case that computational pathology is becoming necessary here, not because pathologists are failing, but because the biology is outgrowing purely visual workflows. What ties these four papers together is simple: digital pathology is not only about remote reading anymore. It is about interoperability, quantification, explainable AI, and making pathology more precise in places where the old workflow is reaching its limit. If you are a pathologist, lab leader, or digital pathology trailblazer trying to figure out what actually matters right now, this episode will help you connect the dots.Episode Highlights 07:41 – Why DICOM still matters if we want digital pathology systems to work together. 14:39 – Current adoption of SVS, MRXS, and DICOM, and why DICOM is still lagging. 16:44 – How the DICOM whole slide image pyramid works and why it matters for workflow. 24:29 – Why kidney transplant rejection is still difficult to diagnose with any single marker. 29:18 – Why perineural invasion is clinically important and still inconsistently reported. 34:44 – How AI can quantify tumor-nerve relationships more consistently than visual review alone. 46:39 – Why gastric cancer biomarker scoring is getting too complex for purely visual workflows. 54:55 – Multiplexing, spatial biology, and why explainable AI matters in biomarker interpretation. 01:04:01 – What is really blocking digital pathology adoption: cost, workflow, regulation, or mindset? Resources mentionedDICOM / digital pathology interoperability paper https://pubmed.ncbi.nlm.nih.gov/42093730/Kidney transplant rejection, biomarkers, and artificial intelligence https://pubmed.ncbi.nlm.nih.gov/42073482/Perineural invasion in solid tumors with AI and machine learning applications https://pubmed.ncbi.nlm.nih.gov/42100436/Gastric cancer IHC biomarkers, advanced detection methods, and perspectives https://pubmed.ncbi.nlm.nih.gov/42075555/Digital Pathology Place https://digitalpathologyplace.comDigital Pathology 101 Free PDF book mentioned at the end of the episode through Digital Pathology Place.Support the showGet the "Digital Pathology 101" FREE E-book and join us!

Welcome to the Oncology Brothers podcast! In this episode, we dived deep into the world of bispecific antibodies approved for multiple myeloma. Joined by myeloma specialists Dr. Hamza Hashmi from Memorial Sloan Kettering and Dr. Cesar Rodriguez from Mount Sinai, they discussed the latest updates, clinical pearls, and practical insights for community oncologists. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers ⁠Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Key topics included: Overview of bispecific antibodies, focusing on GPRC5D and BCMA-targeted therapies. Detailed discussion on talquetamab, teclistamab, elranatamab, and linvoseltamab, including dosing, side effects, and management strategies. Insights on managing cytokine release syndrome (CRS), neurotoxicity, and other side effects like dysgeusia, skin toxicity, and infections. Prophylactic measures, including the use of IVIG and tocilizumab, to enhance patient care and quality of life. Whether you're a healthcare professional or simply interested in the latest advancements in cancer treatment, this episode is packed with valuable information. Don't forget to like, subscribe, and check out our other episodes for more insights into oncology! #MultipleMyeloma, #BispecificAntibody, #ICANS, #CRSmanagement, #OncologyBrothers

In this episode, hear Doris K. Hansen, MD, discuss the management of relapsed/refractory multiple myeloma with bispecific antibodies including: Practical differences among approved bispecific antibodies Toxicity profiles of approved bispecific antibodies When to refer patients for evaluation for immunotherapies Considerations for sequencing bispecific antibodies in the relapsed/refractory setting New findings with combination regimens with bispecific antibodies Program faculty: Doris K. Hansen, MD Assistant Member, Blood and Marrow Transplant and Cellular Immunotherapy H. Lee Moffitt Cancer Center & Research Institute Assistant Professor University of South Florida Morsani College of Medicine Tampa, Florida Link to program page:https://bit.ly/4nufxr2 Get access to all of our new podcasts by subscribing to the Decera Clinical Education Oncology Podcast on Apple Podcasts, YouTube Music, or Spotify. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Dr. Mayank Gandhi, CEO of NEOK Bio, discusses the company's work on bispecific antibody drug conjugates and the limitations of conventional ADCs, which target a single antigen. Using a bispecific antibody to target two unique antigens on a tumor can address the shortcomings of earlier approaches by improving delivery of the toxic payload, overcoming tumor heterogeneity, and reducing off-target toxicity.  NEOK has drugs in development for prostate cancer, and lung, head, neck, and gastrointestinal tumors. The trend for ADCs is toward multi-specific and multi-payload drugs, though Mayank warns it is not a simple task to go from one to many in designing these drug conjugates. Mayank explains, "There have been a lot of advancements in the last couple of decades, and especially the last few years, in various modalities in the treatment of hematological cancers, as well as to a certain degree in solid tumors. However, for many, many solid tumors, there's still a high unmet need given the still significant outcome, poor outcomes that patients experience, particularly with patients having metastatic disease across a variety of solid tumors. Now, if you look at specific modality like ADC or antibody drug conjugates, which is where NEOK Bio is, there's been a renaissance, if you will, with this modality in the last five to six years, particularly after the approval of a drug called Enhertu, which targets HER2 mutation. Now, many ADCs have been approved with different payloads. And so definitely that's made a dent in a variety of tumors, particularly in hematological cancers and select solid tumors as well."   "Conventional ADCs thus far target one antigen or one target on a tumor. So it's an antibody-based approach. The antibody is typically pursuing one specific antigen that's usually an antigen that's expressed on tumors selectively versus normal tissue or normal cells. And then you have a linker and a payload, usually a toxic payload that's conjugated via a linker to the antibody. So that's an antibody drug conjugate construct."   "Thus far, all the ADCs approved have been targeting only one antigen with a couple of different payloads. And so our bispecific approach is targeting two different antigens. If we use a bispecific antibody that targets two unique antigens on the tumor, we have more than one place that a potential antibody can bind and deliver the toxic payload. And then we have made some very significant improvements or changes in the antibody itself." #NEOKBio #DrugDevelopment #Innovation #AntibodyDrugConjugates #ADC #Oncology #Biotech#Oncology #SolidTumors #BispecificADC #CancerResearch #TranslationalResearch #MedicalOncology #HematologyOncology #ClinicalTrials #Biotech #Pharma #DrugDevelopment #PrecisionOncology #TumorMicroenvironment #TargetedTherapy NEOKBio.com Download the transcript here

Dr. Mayank Gandhi, CEO of NEOK Bio, discusses the company's work on bispecific antibody drug conjugates and the limitations of conventional ADCs, which target a single antigen. Using a bispecific antibody to target two unique antigens on a tumor can address the shortcomings of earlier approaches by improving delivery of the toxic payload, overcoming tumor heterogeneity, and reducing off-target toxicity.  NEOK has drugs in development for prostate cancer, and lung, head, neck, and gastrointestinal tumors. The trend for ADCs is toward multi-specific and multi-payload drugs, though Mayank warns it is not a simple task to go from one to many in designing these drug conjugates. Mayank explains, "There have been a lot of advancements in the last couple of decades, and especially the last few years, in various modalities in the treatment of hematological cancers, as well as to a certain degree in solid tumors. However, for many, many solid tumors, there's still a high unmet need given the still significant outcome, poor outcomes that patients experience, particularly with patients having metastatic disease across a variety of solid tumors. Now, if you look at specific modality like ADC or antibody drug conjugates, which is where NEOK Bio is, there's been a renaissance, if you will, with this modality in the last five to six years, particularly after the approval of a drug called Enhertu, which targets HER2 mutation. Now, many ADCs have been approved with different payloads. And so definitely that's made a dent in a variety of tumors, particularly in hematological cancers and select solid tumors as well."   "Conventional ADCs thus far target one antigen or one target on a tumor. So it's an antibody-based approach. The antibody is typically pursuing one specific antigen that's usually an antigen that's expressed on tumors selectively versus normal tissue or normal cells. And then you have a linker and a payload, usually a toxic payload that's conjugated via a linker to the antibody. So that's an antibody drug conjugate construct."   "Thus far, all the ADCs approved have been targeting only one antigen with a couple of different payloads. And so our bispecific approach is targeting two different antigens. If we use a bispecific antibody that targets two unique antigens on the tumor, we have more than one place that a potential antibody can bind and deliver the toxic payload. And then we have made some very significant improvements or changes in the antibody itself." #NEOKBio #DrugDevelopment #Innovation #AntibodyDrugConjugates #ADC #Oncology #Biotech#Oncology #SolidTumors #BispecificADC #CancerResearch #TranslationalResearch #MedicalOncology #HematologyOncology #ClinicalTrials #Biotech #Pharma #DrugDevelopment #PrecisionOncology #TumorMicroenvironment #TargetedTherapy NEOKBio.com Listen to the podcast here

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.

We love to hear from our listeners. Send us a message. On this week's episode of the Business of Biotech, Wyatt McDonnell, Ph.D., cofounder and CEO at Infinimmune, talks about how single-cell biology and computational rigor led to the formation of Infinimmune, and a new way to discover human-derived antibody drugs. Wyatt explains Infinimmune's 'discovered in humans' antibody discovery platform, how the company was launched and initially funded, and how Infinimmune landed a Merck collaboration worth up to $838 million. Access this and hundreds of episodes of the Business of Biotech videocast under the Business of Biotech tab at lifescienceleader.com.  Subscribe to our monthly Business of Biotech newsletter. Get in touch with guest and topic suggestions: ben.comer@lifescienceleader.comFind Ben Comer on LinkedIn: https://www.linkedin.com/in/bencomer/

In this episode, Muhamed Baljevic, MD, FACP, and Johnathan Ticku, MD, discuss various strategies to optimize the use of bispecific antibodies in their practices for the treatment of R/R MM through patient monitoring, dosing in outpatient settings, and using tocilizumab and IVIG, among other management strategies.  Presenters:  Muhamed Baljevic, MD, FACP Associate Professor of Medicine Division of Hematology-Oncology Department of Medicine Director, Multiple Myeloma Program Director, Vanderbilt Amyloidosis Multidisciplinary Program (VAMP) Co-Chair, Scientific Review Committee, VICC Disease Team Lead, Plasma Cell Dyscrasias and Lymphomas Vanderbilt-Ingram Cancer Center Vanderbilt University Medical Center Nashville, Tennessee Jonathan Ticku, MD Medical Oncologist and Hematologist GU Oncology Lead, Mayo Clinic Health System Assistant Professor of Oncology, Mayo Clinic La Crosse, Wisconsin Link to full program: https://bit.ly/4u0xH6q Get access to all of our new podcasts by subscribing to the Decera Clinical Education Podcast on Apple Podcasts, YouTube Music, or Spotify. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

In the second part of this series, Dr. Justin Abbatemarco and Dr. Paulus Rommer discuss how to apply these study results into clinical practice.  Show citation:  Vietzen H, Kühner LM, Berger SM, et al. Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. JAMA Neurol. Published online March 9, 2026. doi:10.1001/jamaneurol.2026.0240  Show transcript: Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco, and we're finishing up our interview with Paulus Rommer on his article on JAMA Neurology, Epstein-Barr Virus Antibodies that differentiate multiple sclerosis from other Neuroinflammatory Diseases. Paulus, can we talk about how we would apply your results into clinical practice right now? Dr. Paulus Rommer: The persistent high apnea antibody responses are a hallmark of multiple sclerosis. And in our micro center study, we found that the singular measurement is not sufficient to differentiate multiple sclerosis from other related disorders like MOGAD or NMOSD, but it's the repeated high levels over time. We see them in about 95% of our MS patients, but really rarely in MOGAD or NMOSD. So this persistent high levels is a good factor, with a high accuracy, to really diagnose multiple sclerosis and to differentiate them from MOGOD or NMOSD. Dr. Justin Abbatemarco: I think these are really helpful and I think a little more evolution in how we interpret these on individual patient level, like we talked about in the podcast, but more to come. Paulus, thank you again for all your work on this topic for coming on and we're excited to have you back in the future. Dr. Paulus Rommer: Thank you.   

In part one of this series, Dr. Justin Abbatemarco and Dr. Paulus Rommer discuss the relationship between Epstein-Barr virus and multiple sclerosis, as well as the questions that still remain unanswered. Show citation: Vietzen H, Kühner LM, Berger SM, et al. Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. JAMA Neurol. Published online March 9, 2026. doi:10.1001/jamaneurol.2026.0240  Show transcript:  Dr. Justin Abbatemarco: Hello and welcome. I just finished interviewing Paulus Rommer on his article published in JAMA Neurology, Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. Paulus, could we maybe talk about this relationship that we've understood about multiple sclerosis and Epstein-Barr virus? And maybe the points that still remain unanswered? Dr. Paulus Romme: There's a very long story behind this because in 1868, Pierre Marie, a student of Charcot was talking about that multiple sclerosis is a sequelae of an infection disorder. By this, we now know that there's a long story. There have been associations between infectious mononucleosis, EBV infection, multiple sclerosis. Also, the migration studies really fits very well in this. So there have been an association, but then, in 2022, there was the US Army study, Bjornevik and Ascherio, who really have shown that there is almost no multiple sclerosis without EBV infection. But still, we do not know why almost all of our patients have EBV infection, but only very small subset have multiple sclerosis. But this is very important to get a deeper understanding, but this is still unknown. Dr. Justin Abbatemarco: This story of EPV and multiple sclerosis continues to evolve. And your work, as we talked about on the podcast, has really helped inform that discussion as well. And we still need to understand, outside of the initiation of the disease, how it drives the pathophysiology years after that initial infection. But it's really helpful to understand this in the larger set and now maybe using it as a biomarker to help us with our other neuroinflammatory diseases, so we'll discuss that the next episode. Again, I was just speaking with Paulas Rommer on his article in JAMA Neurology, Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. Paulus, thank you. 

Dr. Justin Abbatemarco talks with Dr. Paulus Rommer about the evolving understanding of Epstein-Barr virus (EBV) and its role in multiple sclerosis (MS), including recent research on EBV antibodies as diagnostic markers and potential therapeutic targets.  Read the related article in JAMA Neurology.  Disclosures can be found at Neurology.org. 

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.

Join us for a fascinating conversation with choreographer Alexander Whitley about how movement shapes consciousness and how technology transforms our perception of the world and of ourselves.
In this episode, Alexander shares his vision of the body as a site of knowing and self-making. He calls it “auto-fabrication”, meaning we are continually creating ourselves through moving, sensing, perceiving, a process, he asserts, where there is creativity. As Artistic Director of the Alexander Whitley Dance Company, Alexander places live bodies in dialogue with digital systems, staging the tension between our physical, embodied existence and the disembodied way of experiencing the world that modern technologies introduce. He explores how our experience becomes fractured, distributed spatially and temporally, and how social media creates what he calls “jittery, schizoid intervals,” a constant interruption that breaks the flow of attention into fragmented, arrhythmic patterns. In this episode, he walks us through his productions: Antibody, on the transhumanist desire to transcend the body; Overflow, on the emotional impact of social media; Future Rites, a VR reimagining of The Rite of Spring; and his new work Mirror, inspired by Shannon Vallor's The AI Mirror, which asks how much we absorb from what technology reflects back to us. Alex invites us to question the narratives that frame technology as either savior or destroyer, setting us into the grey area, where the real inquiry is. Be prepared to sit with a striking profound reflection: What becomes of the sensitive attunement between humans when screens mediate our bonds? Alexander reminds us that the mind is embodied, shaped by movement, rhythm, and connection. And that dance may be one of our most powerful tools for sensing what it means to be human.

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we delve into some of the most intriguing advancements and strategic moves shaping the future of drug development and patient care. Regeneron has recently ventured into the radiopharmaceuticals market through a substantial $2.1 billion agreement with Australia's Telix Pharmaceuticals. This move marks a significant diversification from Regeneron's traditional focus, such as obesity treatments, to an area that combines radioactive isotopes with targeting molecules for diagnosing and treating diseases like cancer more effectively. The strategic alliance positions Regeneron as a formidable player in this emerging field, promising to expand its therapeutic portfolio and revenue streams. In oncology innovation, GSK is pushing forward with a bold initiative, conducting Phase 3 trials for antibody-drug conjugates (ADCs) in collaboration with Hansoh Pharmaceutical. This effort underscores GSK's commitment to expanding its oncology pipeline, particularly in targeting unmet medical needs through innovative therapies. Antibody-drug conjugates are designed to deliver cytotoxic agents directly to cancer cells, minimizing damage to healthy tissues and offering a precision approach to cancer treatment. Allogeneic CAR-T therapies are also making waves, with Allogene Therapeutics reporting promising early data from their off-the-shelf CAR-T therapy, cema-cel. This therapy effectively eradicated minimal residual disease in lymphoma patients, highlighting the potential of allogeneic approaches to provide accessible cancer treatments without the logistical complexities of autologous methods. In another significant milestone, Ideaya Biosciences, in collaboration with Servier, achieved success with their eye cancer drug candidate meeting its primary endpoint in a crucial Phase 2/3 trial. This success sets the stage for an accelerated FDA approval filing, offering new hope for patients dealing with this challenging condition. Revolution Medicines has made notable progress in oncology as well, with its highly anticipated RAS inhibitor demonstrating improved survival outcomes in a Phase 3 trial for pancreatic cancer. Extending survival by an average of six months compared to chemotherapy could redefine treatment paradigms for one of the most aggressive cancer types. Not every development has been favorable, however. Replimune faced its second FDA rejection for its melanoma candidate RP1, leading to workforce reductions—a testament to the rigorous nature of regulatory approvals and the challenges companies face when bringing novel therapies to market. Meanwhile, BioNTech and Synox Therapeutics are advancing towards FDA approval for their tumor-targeting therapies. These efforts could intensify competition within the oncology space, challenging established giants like AstraZeneca and Daiichi Sankyo. In pain management, AbbVie has expanded its portfolio through a $745 million deal with Haisco Pharmaceutical Group for two non-opioid pain treatment candidates. This move aligns with growing demand for non-opioid alternatives amid the opioid crisis, reflecting a strategic shift towards safer pain management solutions. Spyre Therapeutics has also reported positive Phase 2 results for its ulcerative colitis drug, setting it up as a potential competitor against Takeda's Entyvio. Success here could enhance therapeutic options for patients struggling with this chronic condition, highlighting continued innovation in gastrointestinal disorders. Eli Lilly's recent success with its BTK inhibitor Jaypirca marks a pivotal moment in chronic lymphocytic leukemia (CLL) treatment strategies. Having demonstrated substantial efficacy in a Phase 3 clinical trial—the fourth positive readout—Jaypirca establishes itself as an industry first. Its fixed-duratioSupport the show

In this SRNA "Ask the Expert" episode moderated by Krissy Dilger, Dr. John Chen of the Mayo Clinic answered audience questions about MOG antibody disease (MOGAD). He discussed diagnosis and the importance of titers and live cell-based assays given possible false positives [00:02:42]. Dr. Chen reviewed acute management with early high-dose steroids, prolonged tapers, and escalation to plasma exchange for severe or steroid-refractory attacks, as well as evolving long-term options including IVIG/subcutaneous IG and IL-6 blockade [00:04:14]. Audience questions covered relapse prediction, vision recovery timelines, fatigue, pregnancy, heredity, symptom interpretation, and whether to stop immunotherapy when antibodies become undetectable [00:12:13]. Finally, Dr. Chen described current and upcoming research, including a trial that is currently enrolling participants, and future prospects for optic nerve regeneration while cautioning against unproven stem cell clinics [00:41:37].John J. Chen, MD, PhD attended the University of Virginia for his undergraduate and combined MD/PhD degrees and completed his Ophthalmology residency and Neuro-Ophthalmology fellowship training at the University of Iowa. He then took a position at the Mayo Clinic in 2014 where he specializes in Neuro-Ophthalmology. Currently, he serves as a Consultant and Professor of Ophthalmology and Neurology, and Neuro-Ophthalmology Fellowship Director at the Mayo Clinic. Among Dr. Chen's awards and honors are the AAO Senior Achievement Award, Top Doctors in Minnesota, the Heed Fellowship, Real World Ophthalmology Inspiring Academic Leader Award, Ophthalmology Teacher of the Year Award four times leading to induction to the Educators Hall of Fame, and the Mayo Clinic Distinguished Educator Award – awarded to the top educator at Mayo Clinic in Rochester. He is an Associate Editor for Ophthalmology and the Journal of Neuro-Ophthalmology, has authored more than 250 peer-reviewed publications, and focuses his research on ophthalmic imaging, idiopathic intracranial hypertension, and optic neuritis, particularly NMOSD and MOG antibody–associated disease.00:00 Welcome and Introductions01:08 What Is MOGAD?02:42 Causes and Triggers03:23 How MOGAD Is Diagnosed04:14 Acute Attack Treatments06:35 Steroid Side Effects08:13 Testing During Treatment09:09 Long Term Therapies12:13 Interpreting MOG Positivity16:51 Eye Symptoms and Vision Fluctuations20:12 Antibody Titers and Severity21:19 Relapse Risk After First Attack23:09 Seizures and Encephalitis24:17 Vision Recovery After Optic Neuritis25:13 Acute Treatment Window25:57 Hereditary Risk Questions26:35 Stopping Azathioprine Safely29:56 Managing Post Attack Pain30:16 Steroids IVIG and Plasma Exchange32:08 Infections as Triggers33:01 Retesting MOG Antibodies35:01 Fatigue and Workup36:23 Prognosis and Life Expectancy37:45 Tinnitus and Brain Pressure39:05 Pediatric and Pregnancy Concerns41:37 Trials and Future Regeneration46:05 Research Resources and Wrap Up

In this episode, Dr Matthew Gubens and Dr Helena Yu discuss the evolving role of TROP2-directed therapies in non-small-cell lung cancer, with a focus on how antibody–drug conjugates (ADCs) fit into current treatment strategies, including The mechanism of action and clinical trial outcomes of TROP2-directed ADCs like datopotamab deruxtecan and sacituzumab tirumotecan Use of these therapies in EGFR-mutant disease and how they fit into a changing treatment landscape Practical advice on associated adverse events and additional considerations, A look at future directions on the horizon, such as first-line studies and predictive biomarkers Get access to all of our new podcasts by subscribing to the Decera Clinical Education Oncology Podcast on Apple Podcasts, YouTube Music, or Spotify. Presenters: Matthew Gubens, MD, MS, FASCO​ Medical Director, Thoracic Medical Oncology​ University of California, San Francisco​ San Francisco, California Helena Yu, MD​ Professor of Medicine​ Thoracic Oncology Service​ Memorial Sloan Kettering Cancer Center​ New York, New York Link to full program:https://bit.ly/41vAnfH Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Did you know that antibody-drug conjugates (ADCs) targeting Trop2 have demonstrated significant clinical potential for patients with TNBC? Credit available for this activity expires: 4/8/27 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/front-antibody-drug-conjugates-shifting-paradigm-metastatic-2026a1000a9z?ecd=bdc_podcast_libsyn_mscpedu

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we delve into a series of dynamic changes and strategic shifts reshaping these industries, driven by scientific advancements and regulatory updates. Let's start with Biogen, which recently resolved an investor lawsuit concerning its Alzheimer's drug, Aduhelm. Approved under controversial circumstances by the FDA, Aduhelm faced scrutiny for its efficacy and costs. This settlement is a critical reminder of the importance of transparent communication with investors, especially when navigating high-stakes therapeutic areas like Alzheimer's. The broader implication for pharmaceutical companies is the need to balance innovation with accountability and transparency—a challenge that resonates across the industry. Meanwhile, Pfizer's decision to vacate office space in South San Francisco exemplifies a significant trend toward remote work, accelerated by the COVID-19 pandemic. This shift suggests that traditional workplace models are being reassessed in favor of flexibility and cost efficiency, a change likely to influence real estate investments and organizational structures across biotech firms. Amgen stands out with its notable financial growth highlighted by CEO Robert Bradway's $24.7 million compensation package in 2025. This success underscores Amgen's strategic prowess in maintaining robust performance amidst competitive pressures. Their approach could serve as a blueprint for other firms aiming to achieve sustained growth through innovation and strategic management. On the clinical trial front, Insmed's decision to halt development of Brinsupri after underwhelming mid-stage results illustrates the inherent risks in drug development. This highlights the need for rigorous trial designs and adaptive strategies within development pipelines to address potential setbacks efficiently. Turning to Gilead Sciences, there's a strategic pivot from mergers and acquisitions towards strengthening its internal research pipeline, now described as stronger than ever. This shift away from external acquisitions reflects an industry trend prioritizing internal R&D capabilities, potentially leading to breakthrough therapies that enhance patient care while ensuring sustained business growth. In regulatory developments, GSK's Exdensur received new approval in China, showcasing the ongoing globalization of pharmaceutical markets. Navigating diverse regulatory environments becomes crucial for maximizing drug accessibility worldwide. Another trend is seen through Invivyd's “Antibodies for Any Body” campaign featuring Olympic skier Lindsey Vonn. Leveraging public figures can significantly raise awareness about innovative treatments, playing a crucial role in educating the public about medical advancements. There's also significant financial movement within the sector as Jeito Capital announced a record $1.2 billion fundraising for an independent biopharma-focused European fund. This capital influx is poised to accelerate research and development activities across Europe, potentially leading to new therapeutic breakthroughs. Vivtex Therapeutics' $2.1 billion deal with Novo Nordisk illustrates the power of strategic collaborations in advancing therapeutic solutions and enhancing drug delivery systems—key components for improving patient outcomes. Sidewinder Therapeutics is making strides with a $137 million funding round to develop antibody-drug conjugates (ADCs), highlighting investor confidence in technologies that integrate precision medicine approaches to offer potent cancer treatments with reduced side effects. Astellas Pharma's collaboration with Dyno Therapeutics marks another milestone in gene therapy advancements. A $15 million agreement aims at utilizing engineered adeno-associated virus (AAV) capsids for muscle disorders, proSupport the show

In this episode of Tiny Show and Tell Us, we explore the strange world of camelid antibodies—tiny, heavy-chain-only immune molecules that turned out to be incredibly useful for research and medicine. Then we chat about archaeochemistry and how pristine white Greco-Roman statues were once "garishly" painted. Using modern chemical techniques, scientists are revealing traces of vivid pigments like Egyptian blue. But how definitive are these reconstructions? Drama!Check out Wow if True here or wherever you listen to podcasts!We need your stories — they're what make these bonus episodes possible! Write in to tinymatters@acs.org *or fill out this form* with your favorite science fact or science news story for a chance to be featured.A transcript and references for this episode can be found at acs.org/tinymatters.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Of all the scares and scandals around meat farming practices in the UK, few have been as persistent as been bovine TB. While we're nowhere near the 1930s estimate of the number of cattle infected, it's never really gone away. Why is that?Dr. Neil Watt of MV Diagnostics joins us to cover where bovine TB has been hiding between outbreaks, how changes in testing may help pin it down, and why now might be the turning point on the management, maybe even eradication, of bovine TB in the UK.Read the original paper: https://doi.org/10.1002/vetr.4241Read more : https://www.mvdiagnostics.co.uk/

Antibody–drug conjugates (ADCs) are rapidly evolving from experimental hybrid molecules into mature, platform-driven therapeutics, with the global market projected to reach $36 billion by 2029. As pipelines expand and molecular designs grow more complex, developers are rethinking how ADCs are designed, characterized, and manufactured. In this episode of Off Script, we spoke with Lonza's Sandro Holzer, PhD, director and head of development bioconjugates, and Anette Sommer, PhD, head of bioconjugates research, about how the ADC field has changed over the last several years and what is driving the next wave of innovation. The conversation explores the industry's shift toward standardized linker–payload platforms, site-specific conjugation, higher drug-to-antibody ratios, and emerging dual-payload ADCs aimed at overcoming tumor heterogeneity and drug resistance. Holzer and Sommer discuss how rising molecular complexity is reshaping CMC strategy, analytics, and downstream processing, and why early integration of biology, chemistry, and manufacturability is essential to de-risk development and enable scale-up. The episode also examines how ADC manufacturing paradigms are now informing adjacent bioconjugate modalities signaling a broader move toward integrated, multi-component therapeutics beyond oncology.

In this episode, we welcome Kirollos Hanna, PharmD, BCPS, BCOP, a recognized leader in oncology pharmacy practice and research. Dr. Hanna shares insights into the evolving landscape of antibody-drug conjugates (ADCs) and the unique challenges they present in managing chemotherapy-induced nausea and vomiting (CINV).  As ADC use expands, oncology teams are observing new and sometimes underrecognized patterns of nausea and vomiting, particularly with HER2-directed therapies and delayed-phase symptoms that extend beyond the traditional monitoring window. This discussion highlights how these patterns differ from conventional chemotherapy and what that means for clinical practice.  Dr. Hanna also reviews emerging pharmacokinetic data and clinical trial evidence supporting the use of NK1 receptor antagonist–based antiemetic strategies. The conversation emphasizes practical, actionable approaches for optimizing supportive care, improving patient quality of life, and ensuring proactive symptom management within the medically integrated oncology team.  Learning Objectives:  Describe emerging patterns of chemotherapy-induced nausea and vomiting (CINV) associated with antibody–drug conjugates (ADCs), with emphasis on HER2-directed ADCs and delayed-phase nausea beyond day 5  Discuss pharmacokinetic and clinical trial evidence on NK1 receptor antagonist–based antiemetic strategies when optimizing CINV prevention for patients receiving ADC therapy.  This episode offers 0.5 CE credit hours to pharmacists and pharmacy technicians. Claim CE credit here. Guest: Kirollos Hanna, PharmD, BCPS, BCOP, Director of Pharmacy, Minnesota Oncology, Assistant Professor of Pharmacy, Mayo Clinic College of Medicine, Associate Editor, Journal of the Advanced Practitioner in Oncology (JADPRO)  Disclosures: Speaker: BeOne, BMS, Exelixis, Pfizer Consulting Fees: BeOne, BMS, Exelixis, Pfizer, Astrazeneca

Antibody drug conjugates (ADCs) are transforming cancer research — but how do they actually work, and what does it take to bring them safely to patients?In this episode of Moving Medicine Forward, we speak with scientist Lidia Blasco about the science and promise of antibody drug conjugates (ADCs) in cancer research. Lidia shares her journey from pharmacy and forensic analysis to oncology research, explaining in clear terms how ADCs work, why they're transforming treatment, and what it means to develop them responsibly. The conversation also highlights the human side of clinical trials and the patients who make medical progress possible.01:18 – Lidia Blasco's background and path into ADC research02:30 – Balancing PhD work with hands‑on industry lab experience03:40 – Antibody drug conjugates explained simply04:45 – Why ADCs are a promising cancer treatment approach06:26 – The goal and impact of Lidia's PhD research platform07:30 – Improving dosing decisions and patient safety in clinical trials08:06 – Emerging trends and innovations in ADC development09:27 – Advice for those considering a career in oncology research10:43 – Honoring the patients behind the research samples12:53 – Closing reflections and final takeaways

Up to 50% of homes are at risk of mold exposure, and knowing the warning signs could protect you from the harmful effects of black mold and mycotoxins. In this episode, I share the latest research and my personal experiences with mold symptoms and testing to help you identify hidden mold in your home — including how to choose the right testing option for your situation. I also cover the most common mold mistakes to avoid, so you can find mold, test for it, and confidently take the right next steps.  

Cincinnati Children's study reveals that many newborns are protected from serious bacterial infections by antibodies passed from mother before birth.

Broadcast from KSQD, Santa Cruz on 3-12-2026: Dr. Dawn discusses Michael Pollan's critique of MAHA dietary recommendations, agreeing that ultra-processed foods should be avoided but noting the lack of science supporting high saturated fat intake. She acknowledges extra virgin coconut oil as an exception that doesn't raise LDL, and pushes back on the social Darwinism embedded in anti-vaccine, anti-welfare MAHA thinking. Dr. Dawn expresses serious concern about Surgeon General nominee Casey Means, a Stanford-trained physician who dropped out of residency to become a wellness influencer. She objects to Means hawking supplements and glucose monitors for personal profit—conduct she considers unethical for a physician giving medical advice. An emailer from Switzerland shares success managing histamine intolerance by avoiding aged meats, shellfish, fermented foods, and cross-reactive pollens during hay fever season. The game-changer was taking DAO (diamine oxidase) supplements before meals to break down histamine in the gut. Researchers found that blood from pediatricians who worked in children's hospitals for over a decade contains powerful antibodies against RSV—up to 25% more effective than existing treatments—built up through years of constant exposure. Dr. Dawn critiques a study finding 2.5 times more microplastics in prostate tumor tissue than surrounding healthy tissue, noting that fast-growing cancers develop extra blood vessels and would naturally incorporate more circulating plastics. She attributes the 6% rise in late-stage prostate cancer to discontinued PSA screening rather than microplastics. An emailer asks what to do about microplastics already in our bodies. Dr. Dawn says there's no way to remove them, and advises avoiding microwaving in plastic, limiting breaded processed foods, and rinsing well after brushing teeth with plastic bristles. AI analysis of mammograms can now detect breast artery calcification as a marker for cardiovascular disease risk, with severe calcification indicating 3.3 times greater risk of heart attack, stroke, or death. This could identify high-risk women years before cardiac events. Dr. Dawn questions a non-peer-reviewed study presented at an orthopedic meeting found five years of GLP-1 drug use associated with 30% higher osteoporosis risk, 150% higher osteomalacia risk, and increased tendon ruptures—likely from reduced food intake and vitamin D consumption. Twin studies now estimate genetics account for 55% of lifespan variation when separating internal biological causes from external factors. Separately, fathers who showed warmth and responsiveness to 10-month-old babies had children with lower inflammation and better blood sugar regulation at age 7—an effect not seen with mothers' parenting. Grandparents actively involved in childcare showed slower cognitive decline than non-caregiving grandparents. Dancing emerged as the standout physical activity for dementia prevention—combining aerobic exercise, social interaction, music, and motor coordination—with three hours weekly showing observable benefits.

Epidemiologist Yvonne “Bonnie” Maldonado is an expert in vaccine research and public health. Look back centuries, and the story is always the same, she says: Death rates from viruses have plummeted, especially in children and the elderly. And yet, millions of children die each year from vaccine-preventable diseases. Vaccines need a return of public confidence, and that starts with better messaging and greater support of nongovernmental messengers like herself. The bottom line is that vaccines are safe, she says. Vaccines work and we have saved many lives because of them, Maldonado reminds host Russ Altman on this episode of Stanford Engineering's The Future of Everything podcast. Have a question for Russ? Send it our way in writing or via voice memo, and it might be featured on an upcoming episode. Please introduce yourself, let us know where you're listening from, and share your question. You can send questions to thefutureofeverything@stanford.edu. Episode Reference Links: Stanford Profile: Yvonne Maldonado Connect With Us: Episode Transcripts >>> The Future of Everything Website Connect with Russ >>> Threads / Bluesky / Mastodon Connect with School of Engineering >>> Twitter/X / Instagram / LinkedIn / Facebook Chapters: (00:00:00) Introduction Russ Altman introduces guest Yvonne “Bonnie” Maldonado, a professor of pediatrics, epidemiology and population health at Stanford University. (00:03:01) Career in Vaccines Bonnie shares what led to her career in vaccine research. (00:04:53) How Vaccines Work How vaccines train the immune system to recognize and fight pathogens. (00:06:46) Why Vaccine Responses Vary The variability in immune responses and breakthrough infections. (00:09:22) Risk vs. Benefit in Vaccines How researchers evaluate side effects versus disease severity. (00:11:53) How Viruses Evolve The evolutionary dynamics that shape viral behavior. (00:13:59) Vaccine Boosters Why some vaccines last for life while others require multiple doses. (00:17:14) Herd Immunity How community protection works and why vaccination rates matter. (00:21:22) Vaccine Controversy The controversy surrounding vaccines and what led to it. (00:24:27) Global Vaccine Hesitancy How declining trust and past outbreaks influence vaccination globally. (00:27:07) The Future of Vaccines Why vaccines are essential and how outbreaks shape public response. (00:29:08) Preparing for Future Pandemics How healthcare systems prepare for new threats after COVID-19. (00:30:43) Future In a Minute Rapid-fire Q&A: hope, public trust, and the future of health. (00:32:54) Conclusion Connect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>>Twitter/X / Instagram / LinkedIn / Facebook Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

It's an era of breakthroughs in Alzheimer's research, yet for many clinicians, it's also a time of profound uncertainty. We are currently navigating competing definitions of the disease, multiple new biomarkers coming on market seemingly every week, and the clinical rollout of new amyloid antibodies. How do we translate this rapid-fire science into daily practice? On this week's GeriPal podcast, we sit down with dementia experts Halima Amjad, Barak Gaster, and Heather Whitson. We dive deep into: The evolving definitions of Alzheimer's disease.  Does someone have Alzheimer's disease if you have only an abnormal biomarker as defined by the Alzheimer's Association, or is amyloid pathology necessary but not sufficient to define Alzheimer's as per the International Working Group (IWG) recommendations? Where do blood-based biomarkers for Alzheimer's fit into the diagnostic workup, and should they be used at all in primary care?  FYI - here is my take on that question in a recent JAMA IM article titled "The Limited Role of Alzheimer's Disease Blood-Based Biomarkers in Primary Care." What's the role of amyloid antibodies in the care of individuals with Alzheimer's disease, including who to use them on? We covered a lot and discussed some of these resources that you can do a deeper dive on: Blood-based biomarker resources JAMA article on Blood-Based Biomarkers for Alzheimer's Disease: Preventing Unintended Consequences  Alzheimer's Dementia article on Blood-based biomarkers for detecting Alzheimer's disease pathology in cognitively impaired individuals within specialized care settings: A systematic review and meta-analysis JAMA IM article on The Limited Role of Alzheimer Disease Blood-Based Biomarkers in Primary Care Appropriate use recommendations for amyloid antibodies Donanemab: Appropriate use recommendations  Lecanemab: Appropriate Use Recommendations Primary Care Resources Cognition in Primary Care program A JAGS article on "Large Health System Quality Improvement Intervention Providing Training and Tools to Improve Detection of Cognitive Impairment in Primary Care" Other resources AGS's new online curriculum for Alzheimer's Disease By Eric Widera  

Dr. Alex Marson, MD, PhD, is a professor of medicine at the University of California, San Francisco. We discuss the biology of the immune system and cancer, and everyday choices that can increase or decrease your cancer risk, several of which are surprising but all of which are actionable. We also discuss immunotherapy, including how engineered T-cells can be used to defeat childhood and adult cancers. Dr. Marson explains CRISPR and gene editing to cure diseases, and we address the ethical questions surrounding gene editing in embryos, children and adults. This discussion is for anyone interested in avoiding cancer and/or seeking to understand the science and practical applications of immune- or gene-therapy. Read the show notes at hubermanlab.com. Thank you to our sponsors AG1: https://drinkag1.com/huberman BetterHelp: https://betterhelp.com/huberman Helix Sleep: https://helixsleep.com/huberman LMNT: https://drinklmnt.com/huberman Function: https://functionhealth.com/huberman Timestamps (00:00:00) Alex Marson (00:02:21) Diseases & Current Biological Landscape; AI & Computational Tools (00:05:56) Immune System, Innate vs Adaptive Immune System (00:10:55) Thymus, T Cell Selection; B Cells & Antibodies (00:13:23) Sponsors: BetterHelp & Helix Sleep (00:16:11) Immune System Health, Sleep, Diet; Genes (00:20:56) Childhood Exposure & Allergy Prevention; Autoimmune Reactions (00:25:27) Whole Body Immune Response, Cytokines & Fever; Antibiotics (00:30:51) Cancer; Mutations & Cell Regulation; Smoking, BRCA Mutations, Sunlight (00:38:27) BRAC Mutations, Mutagens, Pesticides (00:42:33) Sponsor: AG1 (00:43:57) X-Rays & Airport Scanners, Carcinogen vs Mutagen, Charred Meat, Food Dye (00:49:34) Immune-Based Cancer Treatment, Checkpoint Inhibitors, CAR T-Cell Therapy (00:59:04) CRISPR, Immunotherapies (01:02:52) Age & Cancer Risk; CAR T-Cells, Targets & Side Effects; Ketogenic Diet (01:08:27) CRISPR Discovery & Mechanism (01:17:06) CRISPR Precision, Risk & Benefit; CRISPR Technology Evolution (01:20:57) Sponsor: LMNT (01:22:17) CRISPR Cell Delivery, Clinical Trials; Treating Early Cancers & Prevention (01:33:47) Liposomes, Engineered Viruses, Lipid Nanoparticles (LNPs), Vaccines (01:39:57) COVID Pandemic & Trust in Science, mRNA Vaccine (01:47:51) Sponsor: Function (01:49:39) Drug Delivery to Cancer, Immunotoxins, T-Cell Engagers; AI Protein Targets (01:55:45) CRISPR Embryo Modification, Ethics; Heritable Gene Editing, Diversity (02:05:42) Deep Sequencing Embryos, Diversity; Overcoming Adversity & Resilience (02:10:44) Upcoming Therapeutics, Autoimmunity & CAR T-Cells, CRISPR & Gene Function (02:17:55) Banking T Cells or iPSCs?, Future of Cell Programming (02:24:41) Zero-Cost Support, YouTube, Spotify & Apple Follow, Reviews & Feedback, Sponsors, Protocols Book, Social Media, Neural Network Newsletter Disclaimer & Disclosures Learn more about your ad choices. Visit megaphone.fm/adchoices

Interview with Hannes Vietzen, PhD, author of Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases. Hosted by Cynthia E. Armand, MD. Related Content: Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases

In today's episode, we spoke with Eric K. Singhi, MD. Dr Singhi is an assistant professor in the departments of general oncology and thoracic/head and neck medical oncology at The University of Texas MD Anderson Cancer Center in Houston.Antibody-drug conjugates (ADCs) are rapidly emerging as one of the most exciting therapeutic advances in lung cancer. In this episode, Singhi explored how TROP2-directed ADCs are beginning to reshape treatment strategies across both non–small cell and small cell lung cancer.Singhi discussed where these agents currently fit within the treatment algorithm for EGFR-mutant non–small cell lung cancer, including the recent accelerated approval of datopotamab deruxtecan-dlnk (Datroway; Dato-DXd) and the evolving clinical data supporting its use after progression on targeted therapy and platinum-based chemotherapy. He also examined emerging evidence for other TROP2-targeting agents such as sacituzumab tirumotecan (sac-TMT) and what early trial results suggest about response rates and future treatment sequencing.Beyond efficacy, Singhi highlighted the practical considerations oncologists must navigate as ADCs enter routine practice, from managing chemotherapy-like toxicities to monitoring for unique adverse effects such as stomatitis, ocular effects, and interstitial lung disease.In our exclusive interview, Dr Singhi discussed where agents like dato-DXd and sac-TMT may fit in evolving treatment algorithms, the clinical data driving their momentum, and what oncologists should consider as these therapies move closer to routine practice in lung cancer.

The killer mutant snowman plagued by antifreeze RETURNS for one more go at being a carrot or whatever the hell he feels like doing. Antifreeze, Asahi, Antibodies. What? NEXT EPISODE ➟ The Strangers chapter who fucking cares PATREON (BONUS EPISODES, VIDEO CONTENT, AND MORE!) ➟ https://patreon.com/screampodcast SCREAM! SOCIALS: Instagram ➟ https://z-p42.www.instagram.com/screampodcast/ Facebook ➟ https://www.facebook.com/thescreampod/?ref=py_c HORRORMOVIEREQUESTS@YAHOO.COM SCREAMPODCAST@YAHOO.COM HORROR SOUP SOCIALS: Instagram ➟ https://www.instagram.com/horrorsoup/?hl=en YOUTUBE ➟ https://www.youtube.com/c/HorrorSoup LETTERBOXD (MOVIE REVIEW APP) ➟ https://letterboxd.com/horrorsoupcaleb/ ~Music Credits~ ETHAN HURT – WWW.ETHANHURT.COM KYLE HERMAN - @iamkyleherman on Instagram Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

In this Q&A episode, Dr. Eric answers listener-submitted questions all about thyroid antibodies—what they are, why they matter, and how they impact both Graves' disease and Hashimoto's thyroiditis. He begins by clarifying the three main thyroid antibodies—TPO, TSI/TRAB, and thyroglobulin antibodies—and explains why understanding these markers is critical when assessing true remission.Throughout the episode, Dr. Eric addresses common concerns such as: Can you be in remission if antibodies are still positive? How often should antibodies be tested? Can diet alone normalize them? He also explores the role of environmental triggers, gut health, gluten, iodine, and even supplements like selenium, black seed oil, and low-dose naltrexone (LDN). You'll hear practical guidance on why antibodies fluctuate, what “optimal” really means (not just “within range”), and why many conventional endocrinologists don't routinely monitor these markers.If you're confused about your antibody results—or wondering why you relapsed after being told you were “in remission”—this episode will help you connect the dots. If you want a clearer, more balanced understanding of thyroid antibodies and what they really mean for your recovery, you'll get a lot out of this episode.If you want to subscribe to my free Healing Graves' Naturally newsletter visithttps://savemythyroid.com/GravesNewsletter 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/

Featuring perspectives from Dr Hope S Rugo and Dr Sara M Tolaney, including the following topics: Introduction: Long-Term Outcomes with Antibody-Drug Conjugates (0:00) HER2-Positive Breast Cancer (8:02) HER2-Negative Breast Cancer (32:41) CME information and select publications

In this week's Principles of New Biology webinar, Tom read Chapter 2 of his developing booklet: “Then Something Happened.” He explores the idea that humanity experienced a profound shift in consciousness beginning in the 1600–1700s—moving from a vitalistic, ether-based understanding of life to a mechanical, reductionist worldview.This chapter dives into:– Lost ancient knowledge and hidden history– Electromagnetism and the four elements– What “the catastrophe” was and how we chose it– Healing with ether, light, and sound– How to reclaim meaning, coherence, and true vitalityThe session also included Q&A on:– Trauma and where it's stored– Sick sinus syndrome and restoring heart rhythm– Antibodies, blood types & Rhesus factor– Vitality, frozen shoulder, and modern vehicles– Chemotherapy recovery, Rife machines & scalar healing– Healing approaches to Crohn's and animal careSupport the showWebsites:https://drtomcowan.com/https://www.drcowansgarden.com/https://newbiologyclinic.com/https://newbiologycurriculum.com/Instagram: @TalkinTurkeywithTomFacebook: https://www.facebook.com/DrTomCowan/Bitchute: https://www.bitchute.com/channel/CivTSuEjw6Qp/YouTube: https://www.youtube.com/channel/UCzxdc2o0Q_XZIPwo07XCrNg

Year in Review: Clinical Investigator Perspectives on the Most Relevant New Datasets and Advances in Antibody-Drug Conjugates for Breast Cancer | Faculty Presentation 2: Current and Emerging Role of TROP2-Directed ADCs — Sara M Tolaney, MD, MPH CME information and select publications

Thank you for joining us for our 2nd Cabral HouseCall of the weekend!   I'm looking forward to sharing with you some of our community's questions that have come in over the past few weeks…   Sami: Hi Dr. Cabral! I am currently doing your 21 day detox. I am loving every second of it. For one of my meals I decided to have red beats as my carb/veggie. I had this for two dinner meals in a row and noticed the redness in my stool showed up the next morning after my second meal and then 48 hours after my second meal. I read online that eating red beats can help display gut transit time. I know red beats normally turn your stool a red/pink color in general. Are red beats a good natural/home remedy to decide gut transit time? Or would something like the blue poop test work best?                                              Larissa: Hello! My patient recently tested positive for EBV VCA IgM antibodies with positive EBV IgG antibodies but negative early EBV antigen and EBNA levels. She is experiencing fatigue. Would you consider this an acute or reactivated infection? Could it be a false positive? Would you treat this? Thank you in advance!      Katrina: As I explore your protocol options and tests, how would having gastric bypass, 22 years ago affect the results to achieve optimal health. Will the products be effective due to potential absorption issues?     Ateba: Hello Dr.Cabral, I've had some bony growth behind my teeth over the last decade. I believe it's called Mandibular Tori. It seems to have grown quite a bit the last few years. My dentist says it's from jaw clenching, which I had during sleep for quite some time, but I've also heard other things (nutrition deficiencies/toxicity's etc). Don't have parasites according to my stool test, just excessive stress. Wondering if you have any recommendations for this condition. God Bless.      Lisa: Hi Dr Cabral! I listen to you daily, thank you for your knowledge and swear by your functional detox a few times a year! I have been waking up recently (about the last year now) with a mouth full of saliva and I'm forced to get up to spit. I sleep really well - straight through the night, yet this is a bit concerning to me. Any ideas?    Thank you for tuning into this weekend's Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! - - - Show Notes and Resources: StephenCabral.com/3663 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

This week, we discuss a new antibody-based nasal spray that protects against the flu: how does it work? Plus, the tiny self-replicating molecule that may give clues to the origins of life on Earth, whether we should regulate "mirror life" research, and how bacteria protect oak trees from drought and other stresses... Like this podcast? Please help us by supporting the Naked Scientists