Podcasts about CK

Tonight, the C3 crew discuss Ikem Ekwonu's shutdown day against Micah Parsons and the likelihood of him getting paid soon, the effectiveness of the offense continuing to run through Rico Dowdle, Preview this week's match up against the Saints, and interview Panthers super fan Carolina_Mic!

Join the C3 crew as they react to the Carolina Panthers traveling north to Lambeau Field to take on the Green Bay Packers in week 9 of the NFL season!

Parce que… c'est l'épisode 0x655! Shameless plug 4 et 5 novembre 2025 - FAIRCON 2025 8 et 9 novembre 2025 - DEATHcon 17 au 20 novembre 2025 - European Cyber Week 25 et 26 février 2026 - SéQCure 2026 14 au 17 avril 2026 - Botconf 2026 28 et 29 avril 2026 - Cybereco Cyberconférence 2026 9 au 17 mai 2026 - NorthSec 2026 3 au 5 juin 2025 - SSTIC 2026 Notes Résilience du cloud Microsoft: DNS outage impacts Azure and Microsoft 365 services Kevin Beaumont: “Yep, just did some testing - A…” - Cyberplace Kevin Beaumont: “If you're wondering what prote…” - Cyberplace Microsoft Services Experience Global Outage Due to Faulty Cloud Configuration Microsoft Azure challenges AWS for downtime crown Kevin Beaumont: “If you're wondering the AWS an…” - Cyberplace IA The glaring security risks with AI browser agents OpenAI's Atlas browser — and others — can be tricked by manipulated web content New Agent-Aware Cloaking Leverages OpenAI ChatGPT Atlas Browser to Deliver Fake Content Ex-CISA chief says AI could mean the end of cybersecurity AI-Generated Code Poses Security, Bloat Challenges AI Trust Paradox: Overcome Fear Auto Cyber Remediation Anthropic's Claude convinced to exfiltrate private data OpenAI unleashes Aardvark security agent in private beta Red New EDR-Redir Tool Breaks EDR Exploiting Bind Filter and Cloud Filter Driver New EDR-Redir V2 Blinds Windows Defender on Windows 11 With Fake Program Files Hackers Exploiting Microsoft WSUS Vulnerability In The Wild - 2800 Instances Exposed Online oss-sec: Questionable CVE's reported against dnsmasq 81% Router Usres Have Not Changed Default Admin Passwords, Exposing Devices to Hackers Sweden's power grid operator confirms data breach claimed by ransomware gang What Is Bring Your Own Vulnerable Driver (BYOVD)? High-Severity OpenVPN Flaw (CVE-2025-10680) Allows Script Injection on Linux/macOS via Malicious DNS Server Beware of Free Video Game Cheats That Delivers Infostealer Malwares New Atroposia malware comes with a local vulnerability scanner New Android Trojan ‘Herodotus' Outsmarts Anti-Fraud Systems by Typing Like a Human Next-gen firewalls, VPNs can increase security risks: At-Bay Tata Motors Data Leak - 70+ TB of Sensitive Info and Test Drive Data Exposed via AWS Keys 9 in 10 Exchange servers in Germany are out of support Cyberpunks mess with Canada's water, energy, farm systems Multiple Jenkins Vulnerability SAML Authentication Bypass And MCP Server Plugin Permissions Blue Mozilla to Require Data-Collection Disclosure in All New Firefox Extensions CISOs Finally Get a Seat at the Board's Table Ransomware Profits Drop As Victims Stop Paying Hackers Making A Virtual Machine Look Like Real Hardware To Malware Open-Source Firewall IPFire 2.29 With New Reporting For Intrusion Prevention System Agent Fatigue Is Real and Your Security Stack Is to Blame ATT&CK v18: The Detection Overhaul You've Been Waiting For How Threat Intelligence Feeds Help Organizations Quickly Mitigate Malware Attacks Passkeys: they're not perfect but they're getting better Google Unveils Guide for Defenders to Monitor Privileged User Accounts Google Chrome Will Finally Default To Secure HTTPS Connections Starting in April CISA Releases Best Security Practices Guide for Hardening Microsoft Exchange Server Russia arrests three suspected Meduza infostealer devs Privacy What brain privacy will look like in the age of neurotech Proton 2025 autumn/winter roadmaps [New Release: Tor Browser 15.0 The Tor Project](https://blog.torproject.org/new-release-tor-browser-150/) Divers EU sovereignty plan accused of helping US cloud giants Red lights flashing at CISPE over Broadcom licensing antics France signs up to the Matrix.org Foundation US declines to join more than 70 countries in signing UN cybercrime treaty International Criminal Court To Ditch Microsoft Office For European Open Source Alternative Everyone Wants to Hack — No One Wants to Think Collaborateurs Nicolas-Loïc Fortin Crédits Montage par Intrasecure inc Locaux réels par Intrasecure inc

Join the C3 crew as they discuss the timetable for injured Panthers O linemen, If Carolina would have beat Buffalo with Bryce Young under center, the Panthers chances against the Green Bay Packers and YOUR catcalls at 252-228-5098!

Why don't Christians talk about the Holy Spirit more often? Have we quietly replaced dependence on God's Spirit with confidence in our own smarts and systems? What starts as a kid's Halloween question about the "Holy Ghost" quickly turns into a bigger conversation about why the church is so divided, whether we'd even notice if the Spirit disappeared from our theology, and how we might learn to let God surprise us again. After all, the Holy Ghost isn't here to haunt us, but to make us alive. 0:00 - Theme Song 0:19 - Sponsor - Dwell - Listen to scripture throughout your day. Go to https://www.dwellbible.com/CK for 25% off! 3:03 - Is the Holy Ghost Real? 6:33 - What Even is the Holy Ghost? 11:18 - How the Holy Ghost Helps Us 16:30 - Sponsor - Hiya Health - Go to https://www.hiyahealth.com/CURIOUSLY to receive 50% off your first order 18:18 - Sponsor - Hello! My Name is Emmanuel - A Heartwarming children's book about a Haitian child learning to trust God by Emmanuel Jean Russell https://a.co/d/8fPoRCL 19:15 - But why a "ghost?" 26:30 - What's the Takeaway? 33:21 - End Credits

Join Lia and Megan as we do 5 minutes (yep, we brought out the timers—Not Today, procrastination!) of hot takes on each member. What have they been up to? What might be Yet to Come? From Dior to medical centers, from CK to Celine...and of course comeback. This episode is pure Dynamite, so get ready to Run with us.Join The BTS Buzz and get access to Afternoona Army's exclusive DISCORD channel, get shout outs on-air in podcast, and receive invitations to quarterly live support groups. Questions? Email afternoonaarmy@gmail.com for more information.Are your family and friends sick of you talking about K-drama? We get it...and have an answer. Check out our sister pod www.afternoonadelight.com for more episodes, book recs and social media goodness. And don't forget about the newest members of our network: Afternoona Asks where diaspora Asians living in the West find ways to reconnect to Asian culture via Asian/KDramas.Want to find more great BTS content? Head over to Afternoona Army for more takes on Bangtan life and links to our social media.

Join the C3 crew as they react to the Carolina Panthers taking on the Buffalo Bills in Bank of America Stadium for week 8 of the NFL season!

The Impact Assessment Agency of Canada has decided not to assess what could happen if the proposed Dresden landfill project moves forward. A defence lawyer in Chatham-Kent says the new federal bail reform package needs more careful thought. CK police have charged a 39-year-old woman following a single-vehicle crash in Tilbury. A Thamesville man is facing multiple impaired driving charges after his vehicle ended up in a ditch over the weekend. Canada's Prime Minister says trade talks were going well with the U.S. until Ontario's anti-tariff ads started running. Financial experts believe the Bank of Canada will lower the interest rate on Wednesday.

Norbert Bolz ist einer der profiliertesten deutschen Medien- und Kulturtheoretiker. Bis zu seiner Emeritierung im Jahr 2018 lehrte er an der Technischen Universität Berlin und prägte Generationen von Studierenden mit seiner scharfsinnigen Kritik an Ideologien, politischer Korrektheit und medialer Manipulation. Bekannt wurde Bolz durch Werke wie „Das konsumistische Manifest“, „Die ungeliebte Freiheit“ und zuletzt „Zurück zur Normalität“. Im Gespräch spricht Norbert Bolz über den Verlust der Normalität, die Ideologisierung der Medien und die Frage, ob es überhaupt ein „Zurück“ geben kann. Er erklärt, warum er den öffentlich-rechtlichen Rundfunk als „Propagandamaschine unserer Zeit“ bezeichnet, weshalb die moderne Linke „geistig obdachlos“ sei und weshalb echte Veränderung nur aus einer Basis gesellschaftlicher Selbstverständlichkeit entstehen kann. Ein Gespräch über Vernunft, Mut und den Preis der Normalität.

Join the C3 crew as they discuss the Panthers chances of beating the mighty Buffalo Bills without Bryce Young. Can Andy Dalton shoulder the load with Bryce Young on the bench? Is this one of the stingiest run defenses in Carolinas history? Are the Panthers proving to be one of the hardest teams to face in the NFC? Is the NFC South ripe for the taking?

Limb-girdle muscular dystrophies (LGMDs) encompass a group of genetically heterogeneous skeletal muscle disorders. There has been an explosion of newly identified LGMD subtypes in the past decade, and results from preclinical studies and early-stage clinical trials of genetic therapies are promising for future disease-specific treatments. In this episode, Gordon Smith, MD, FAAN, speaks with Teerin Liewluck, MD, FAAN, FANA, author of the article “Limb-Girdle Muscular Dystrophies” in the Continuum® October 2025 Muscle and Neuromuscular Junction 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. Liewluck is a professor of neurology at the Division of Neuromuscular Medicine and Muscle Pathology Laboratory at Mayo Clinic College of Medicine in Rochester, Minnesota. Additional Resources Read the article: Limb-Girdle Muscular Dystrophies 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 Guest: @TLiewluck Full episode transcript available here 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 with Continuum Audio. Today I'm interviewing Dr Teerin Liewluck, a good friend of mine at the Mayo Clinic, about his article on the limb girdle muscular dystrophies. This article appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders, a topic that is near and dear to my heart. Teerin, welcome to the podcast, and maybe you can introduce yourself to our listeners. Dr Liewluck: Thank you very much, Gordon, and I want to say hi to all the Continuum fans. So, I'm Dr Teerin Liewluck, I'm the professor of neurology at Mayo Clinic in Rochester, Minnesota. So, my practice focus on all aspects of muscle diseases, both acquired and genetic myopathies. Glad to be here. Dr Smith: I just had the great pleasure of seeing you at a seminar in Houston where you talked about this topic. And so, I'm really primed for this conversation, which I'm very excited about. I find this topic a little hard, and I'm hoping I can learn more from you. And I wonder if, as we get started, recognizing many of our listeners are not in practices focused purely on muscle disease, maybe you can provide some context about why this is important for folks doing general neurology or even general neuromuscular medicine? Why do they need to know about this? Dr Liewluck: Yes, certainly. So, I would say limb girdle muscular dystrophy probably the most complex category of subgroup of muscle diseases because, by itself, it includes thirty-four different subtypes, and the number's still expanding. So, each subtype is very rare. But if you group together, it really have significant number of patients, and these patients present with proximal weakness, very high CK, and these are common patients that can show up in the neurology clinic. So, I think it's very important even for general neurologists to pick up what subtle clues that may lead to the diagnosis because if we are able to provide correct diagnosis for the patients, that's very important for patient management. Dr Smith: So, I wonder if maybe we can talk a little bit about the phenotype, Terran. I mean, your article does a great job of going over the great diversity. And you know, I think many of us here, you know, limb girdle muscular dystrophy and we think of limb girdle weakness, but the phenotypic spectrum is bananas, right? Rhabdomyolysis, limb girdle distal myopathy. I mean, when should our listeners suspect LGMD? Dr Liewluck: Yes, I think by the definition to all the LGMD patients will have limb girdle of proximal weakness and very high CK. So, these are common phenotypes among thirty-four different subtypes. But if it did take into details, they have some subtle differences. In the article, what I try to simplify all these different subtypes that we can categorize at least half of them into three main group that each group the underlying defect sharing among those subtypes and also translate into similar muscles and extra muscular manifestations. You will learn that some of the limb girdle muscular dystrophy may present with rhabdomyolysis. And we typically think of this as metabolic myopathies. But if you have a rhabdomyolysis patient, the CK remain elevated even after the acute episode, that's the key that we need to think this could be LGMD. That's for an example. Dr Smith: So, I wonder if maybe we can start there. I was going to go in a different direction, but this is a good transition. It's easy to see the opportunity to get confused between LGMD or, in that case, a metabolic myopathy or other acquired myopathies. And I think particularly adult neurologists are more accustomed to seeing acquired muscle disease. Are there particular clues that, or pearls that adult neurologists seeing patients with muscle disease can use to recognize when they should be thinking about LGMD given the diverse phenotype? Dr Liewluck: Yes. What I always tell the patient is that there are more than a hundred different types of muscle diseases, but we can easily divide into groups: acquired and genetic or hereditary. So, the acquired disease is when you encounter the patients who present with acute or subacute cause of the weakness, relatively rapidly progressive. But on the opposite, if you encounter the patient who present with a much more slowly progressive cause of weakness over several months or years, you may need to think about genetic disease of the muscle with also including limb-girdle muscular dystrophy. The detailed exam to be able to distinguish between each type of muscular dystrophy. For example, if proximal weakness, certainly limb girdle muscular dystrophy. If a patient has facial weakness, scapular winking, so you would think about facial scapular hematoma dystrophy. So, the slowly progressive cause of weakness, proximal pattern of weakness, CK elevation, should be the point when you think about LGMD. Dr Smith: So, I have a question about diagnostic evaluation. I had a meeting with one of my colleagues, Qihua Fan, who's a great peripheral nerve expert, who also does neuromuscular pathology. And we were talking about how the pathology field has changed so much over the last ten years, and we're doing obviously fewer muscle biopsies. Our way of diagnosing them has changed a lot with the evolution of genetic testing. What's your diagnostic approach? Do you go right to genetic testing? Do you do targeted testing based on phenotype? What words of wisdom do you have there? Dr Liewluck: Yes, so, I mean, being a muscle pathologist myself, it is fair to say that the utility of muscle biopsies when you encounter a patient with suspects that limb girdle muscular dystrophy have reduced over the year. For example, we used to have like fifteen, seventeen hundred muscle biopsies a year; now we do only thirteen hundred biopsies a year. Yes, as you pointed out, the first step in my practice if I suspect LGMD is to go with genetic testing. And I would prefer the last gene panel that not only include the LGMD, but also include all other genetic muscle disease as well as the conjunctive myopic syndrome, because the phenotype can be somehow difficult to distinguish in certain patients. Dr Smith: So, do you ever get a muscle biopsy, Teerin? I mean you obviously do; only thirteen hundred. Holy cow, that's a lot. So, let me reframe my question. When do you get a muscle biopsy in these patients? Dr Liewluck: Muscle biopsy still is present in LGMD patients, it's just we don't use it at the first-tier diagnostic test anymore. So, we typically do it in selected cases after the genetic testing in those that came back inconclusive. As you know, you may run into the variant of unknown significance. You may use the muscle biopsy to see, is there any histopathology or abnormal protein Western blot that may further support the heterogenicity of the VUS. So, we still do it, but it typically comes after genetic testing and only in the selected cases that have inconclusive results or negative genetic testing. Dr Smith: I'd like to ask a question regarding serologic testing for autoantibodies. I refer to a really great case in your article. There are several of them, but this is a patient, a FKRP patient, who was originally thought to have dermatomyositis based on a low-titer ME2 antibody. You guys figured out the correct diagnosis. We send a lot of antibody panels out. Wonder if you have any wisdom, pearls, pitfalls, for how to interpret antibody tests in patients with chronic myopathies? We send a lot of them. And that's the sort of population where we need to be thinking about limb-girdle muscular dystrophies. It's a great case for those, which I hope is everyone who read your article in detail. What do you have to say about that? Dr Liewluck: Yes, so myositis antibodies, we already revolutionized a few of muscle diseases. I recall when I finished my fellowship thirteen years ago, so we don't really have much muscle myositis antibodies to check. But now the panel is expanded. But again, the antibodies alone cannot lead to diagnosis. You need to go back to your clinical. You need to make sure the clinical antibodies findings are matched. For example, if the key that- if the myocytes specific antibodies present only at the low positive title, it's more often to be false positive. So, you need to look carefully back in the patient, the group of phenotypes, and when in doubt we need to do muscle biopsies. Now on the opposite end, the other group of the antibody is the one for necrotizing autoimmune myopathy; or, the other name, immune-mediated necrotizing myopathy. This is the new group that we have learned only just recently that some patients may present as a typical presentation. I mean, when even thinking about the whole testing autoimmune myopathy, we think about those that present with some acute rapidly progressive weakness, maybe has history of sudden exposures. But we have some patients that present with very slowly progressive weakness like muscular dystrophies. So now in my practice, if I encounter a patient I suspect LGMD, in addition to doing genetic testing for LGMD, I also test for necrotizing doing with myopathy antibodies at the same time. And we typically get antibody back within what, a week or two, but projected testing would take a few months. Dr Smith: Yeah. And I guess maybe you could talk a little bit about pitfalls and interpretation of genetic tests, right? I think you have another case in your article, and I've certainly seen this, where a patient is misdiagnosed as having a genetic myopathy, LGMD, based on, let's say, just a misinterpretation of the genetic testing, right? So, I think we need to think of it on both sides. And I like the fact that the clinical aspects of diagnosis really are first and foremost most important. But maybe you can talk about wisdom in terms of interpretation of the genetic panel?  Dr Liewluck:Yes. So genetic testing, I think, is a complex issue, particularly for interpretation. And if you're not familiar with this, it's probably best to have your colleagues in genetics that help looking at this together. So, I think the common scenario we encounter is that in those dystrophies that are autosomal recessive, so we expect that the patient needs to have two abnormal copies of the genes to cause the disease. And if patients have only one abnormal copy, they are just a carrier. And commonly we see patients refer to us as much as dystrophy is by having only one abnormal copy. If they are a carrier, they should not have the weakness from that gene abnormality. So, this would be the principle that we really need to adhere. And if you run into those cases, then maybe you need to broaden your differential diagnosis. Dr Smith: I want to go back to the clinical phenomenology, and I've got a admission to make to you, Teerin. And I find it really hard to keep track of these disorders at, you know, thirty-four and climbing a lot of overlap, and it's hard to remember them. And I'm glad that I'm now going to have a Continuum article I can go to and look at the really great tables to sort things out. I'm curious whether you have all these top of mind? Do you have to look at the table too? And how should people who are seeing these patients organize their thoughts about it? I mean, is it important that you memorize all thirty-four plus disorders? How can you group them? What's your overall approach to that? Dr Liewluck: I need to admit that I've not memorize all twenty-four different subtypes, but I think what I triy to do even in my real-life practice is group it all together if you can. For example, I think that the biggest group of these LGMD is what we call alpha-dystroglycanopathies. So, this include already ten different subtypes of recessive LGMD. So alpha-dystroglycan is the core of the dystrophin-associated glycoprotein complex. And it's heavy glycosylated protein. So, the effect in ten different genes can affect the glycosylation or the process of adding sugar chain to this alpha-dystroglycan. And they have similar features in terms of the phenotype. They present with proximal weakness, calf pseudohypertrophy, very high CK, some may have recurrent rhabdomyolysis, and cardiac and rhythmic involvement are very common. This is one major group. Now the second group is the limb-girdle muscular dystrophy due to defective membrane repair, which includes two subtypes is the different and on dopamine five. The common feature in this group is that the weakness can be asymmetric and despite proximal weakness, they can have calf atrophy. On muscle biopsy sometimes you can see a myeloid on the muscle tissues. And the third group is the sarcoglycanopathy, which includes four different subtypes, and the presentation can look like we share. For the rest, sometimes go back to the table. Dr Smith: Thank you for that. And it prompts another question that I always wonder about. Do you have any theories about why such variability in the muscle groups that are involved? I mean, you just brought up dystroglycanopathy, for instance, as something that can cause a very distal predominant myopathy; others do not. Do we at this point now have an understanding given the better genetics that we have on this and work going on in therapeutic development, which I want to get to in a minute, that provides any insight why certain muscle groups are more affected? Dr Liewluck: Very good question, Gordon. And I would say the first question that led me interested in muscle disease---and this happened probably back in 2000 when I just finished medical school---is why, why, why? Why does muscle disease tend to affect proximal muscles? I thought by now, twenty-five years later, we'd have the answer. I don't. I think this, you don't know clearly why muscle diseases, some affect proximal, some affect distal. But the hypothesis is, and probably my personal hypothesis is, that maybe certain proteins may express more in certain muscles and that may affect different phenotypes. But, I mean, dysferlin has very good examples that can confuse us because some patients present with distal weakness, some patients present with proximal weakness, that's by the same gene defect. And in this patient, when we look at the MRI in detail, actually the patterns of fatty replacements in muscle are the same. Even patient who present clinically as a proximal or distal weakness, the imaging studies show the same finding. Bottom line, we don't know. Dr Smith: Yeah, who knew it could be so complex? Teerin, you brought up a really great point that I wanted to ask about, which is muscle MRI scan, right? We're now seeing studies that are doing very broad MR imaging. Do you use some muscle MRI very frequently in your clinical evaluation of these patients? And if so, how? Dr Liewluck: Maybe I don't use it as much as I could, but the most common scenario I use in this setting is when I have the genetic testing come back with the VUS. So, we look at each VUS, each gene in detail. And if anything is suspicious, what I do typically go back to the literature to see if that gene defect in particular has any common pattern of muscle involvement on the MRI. And if there is, I use MRI as one of the two to try to see if I can escalate the pathogenicity of that VUS. Dr Smith: And a VUS is a “Variant of Unknown Significance,” for our listeners. I'm proud that I remember that as a geneticist. These are exciting times in neurology in general, but particularly in an inherited muscle disease. And we're seeing a lot of therapeutic development, a lot going on in Duchenne now. What's the latest in terms of disease-modifying therapeutics and gene therapies in LGMD? Dr Liewluck: Yes. So, there are several precritical and early-phase critical trials for gene therapy for the common lymphoma of muscular dystrophies. For example, the sarcoglycanopathies, and they also have some biochemical therapy that arepossible for the LGMD to FKRP. But there are many things that I expect probably will come into the picture broader or later phase of critical tryouts, and hopefully we have something to offer for the patients similar to patients with Duchenne muscular dystrophy. Dr Smith: What haven't we talked about, I mean, holy cow? There's so much in your article. What's one thing we haven't talked about that our listeners need to hear? Dr Liewluck: Good questions. So, I think we covered all, but often we get patients with proximal weakness and high CK, and they all got labeled as having limb-girdlemuscular dystrophy. What I want to stress is that proximal weakness and high CK is a common feature for muscle diseases, so they need to think broad, need to think about all possibilities. Particularly don't want to miss something treatable. Chronic, slowly progressive cause, as I mentioned earlier, we think more about muscle dystrophy, but at the cranial range, we know that rare patients with necrotic autonomyopathy and present with limb good of weakness at a slowly progressive cost. So, make sure you think about these two when suspecting that LGMD patient diabetic testing has come back inconclusive. Dr Smith: Well, that's very helpful. And fortunately, there's several other articles in this issue of Continuum that help people think through this issue more broadly. Teerin, you certainly don't disappoint. I enjoyed listening to you about a month ago, and I enjoyed reading your article a great deal and enjoy talking to you even more. Thank you very much. Dr Liewluck: Thank you very much, Gordon. Dr Smith: Again, today I've been interviewing Dr Teerin Liewluck about his article on limb-girdle muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Please be sure to check out Continuum Audio episodes for this and other issues. And thanks to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Join the C3 crew as they react to the Carolina Panthers taking on the New York Jets on the road in MetLife Stadium in week 7 of the NFL season!

Tackle High-Yield Concepts for USMLE Step 2 CK Cardiology This interactive session, led by Dr. Abraham Titus (Hematology/Oncology Fellow, University of South Alabama) and ScholarRx’s Jeff Downing, focuses on challenging USMLE Step 2 CK cardiology questions that will sharpen your clinical decision-making skills and deepen your understanding of cardiovascular medicine. WHAT YOU’LL LEARN: In this episode, we work through four board-style questions using our proven systematic approach that helps you think like a clinician first, then a test-taker second. You’ll learn how to apply clinical guidelines and make evidence-based management decisions through detailed explanations that go beyond just identifying the correct answer. Topics Covered: Cardiovascular risk management and pharmacotherapy Acute coronary syndrome management strategies Peripheral vascular disease evaluation and treatment Secondary hypertension workup and management Perfect for: Medical students preparing for USMLE Step 2 CK Clinical year medical students on cardiology rotations IMGs studying for board exams Anyone looking to strengthen their cardiology clinical reasoning Review the full test: https://usmle-rx.scholarrx.com/share/1do75erd2wnmg0y Free Resources: Biochemistry Course: https://usmle-rx.com/biochemistry-course/ More Rx Bricks Podcasts: https://usmle-rx.com/podcast Study Planner: https://go.usmle-rx.com/study-schedule/

In this episode of Real Life Pharmacology, we take a deep dive into daptomycin, a lipopeptide antibiotic primarily used for serious Gram-positive infections, including MRSA and VRE. Daptomycin works by binding to bacterial cell membranes in a calcium-dependent manner, causing rapid depolarization and cell death. One key limitation is that daptomycin should never be used for pneumonia because pulmonary surfactant inactivates the drug. Clinically, it's often reserved for bacteremia, endocarditis, or complicated skin and soft tissue infections. From a pharmacokinetic standpoint, daptomycin is given intravenously and primarily eliminated unchanged by the kidneys, so dose adjustments are necessary in renal impairment. Monitoring creatine kinase (CK) levels is crucial, as one of the major adverse effects is myopathy and, rarely, rhabdomyolysis. Patients on statins have a higher risk of muscle toxicity, and clinicians should consider holding or monitoring statin therapy closely. Eosinophilic pneumonia is another rare but serious adverse reaction that can develop after prolonged therapy. Daptomycin has minimal drug interactions, making it an appealing option when other agents pose risks. Overall, it's a powerful antibiotic when used appropriately, but requires careful monitoring for muscle and respiratory-related side effects.

Join the C3 crew as they discuss the emergence of Rico Dowdle as RB 1 for Carolina and how the Panthers will split reps with Chuba Hubbard, what Jalen Coker's return means for Carolina, assess the work Dan Morgan has made thus far, and the Panthers being favorites for the first time all year as they preview this week's matchup against the New York Jets.

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common forms of muscular dystrophy, affecting individuals across the lifespan with variable severity. Advances in genetic understanding and therapeutic development have led to an era of promising disease-modifying strategies. In this episode, Katie Grouse, MD FAAN, speaks with Renatta N. Knox, MD, PhD, author of the article “Facioscapulohumeral Muscular Dystrophy” in the Continuum® October 2025 Muscle and Neuromuscular Junction Disorders issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Knox is an assistant professor of neurology in the Division of Pediatric Neurology and Neuromuscular Section at Washington University School of Medicine in St. Louis, Missouri. Additional Resources Read the article: Facioscapulohumeral Muscular Dystrophy 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  Full episode transcript available here 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 Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Knox: Hi Katie, thank you so much for the invitation for the audio interview. I'm looking forward to our conversation. As she mentioned, my name is Renata Knox. It's a pleasure to be here today. Dr Grouse: I'd like to start by asking, what is the key message that you hope your readers will take from your article? Dr Knox: I would say two things. The first is an appreciation and understanding of the unique genetic mechanism that leads to FSHD. And the second is the really exciting therapy landscape that we find ourselves in. So, we're hopeful that there will actually be disease-modifying therapies for FSHD soon. Dr Grouse: We're really looking forward to learning more about that. Now, before we get to that piece, could you just remind us of the clinical manifestations and features that are specific to FSHD? Dr Knox: So, one of the most unique things about FSHD that we see clinically is the pattern of weakness. So, one of the first features is that it's asymmetric. And then there are certain muscle groups that typically are affected, and that's partly where the name comes from. So, we see effects in the face, the limbs, the trunk; and so, those are some of the unique features that we see clinically. Dr Grouse: I'd love it if you could walk us through how you approach diagnosing a patient who presents with proximal weakness where FSHD is in your differential. Dr Knox: Yeah, it's a really great question. So, I would say it depends. So, I actually focus on FSHD in my clinical practice. So, many times patients are referred to me because there's a very high suspicion or there's a known family history of FSHD. So, that's one category of cases. I would say the other category of case is where it's, as you said, maybe more proximal weakness more broadly. Someone that's before me who has a known family history, they really have some of the characteristic physical features---which I'm pretty attuned to, as this is, you know, part of my subspecialty---I'll actually go directly to FSHD genetic testing. And that is one of the unique features of this disease, that the next-generation sequencing panels that are typically used for some of our other muscle diseases, FSHD is not captured on those. So, we actually have to send targeted testing for FSHD to diagnose it. So, that is one category where, again, I have a very high suspicion either based on their clinical presentation and/or a known family history, then I will actually go directly to FSHD-targeted genetic testing. In the second case, where it is one of the conditions that I'm considering among others, I will do more broad testing. So, I will get a CK level to see if there's evidence of muscle breakdown. I'll likely also do one of the next-generation sequencing panels that we have access to, which will allow us to identify, potentially, one to two hundred potential muscle diseases. And then again, if FSHD is higher on my differential in that second group of patients, then I will also send targeted FSHD-specific testing. Dr Grouse: That's really helpful. And I'm wondering if you have any thoughts about common pitfalls that you've seen when providers are trying to work this up? Dr Knox: I don't know if I would say pitfalls. I think I would acknowledge that it's challenging. My subspecialty training in neuromuscular medicine and also gene therapy. And so FSHD is pretty high on my radar. But I would say in neurology in general---and then, you know, the general medical population---,it really isn't something that many people are seeing. So, I would say what patients will communicate to us sometimes is some frustration that maybe it took time to make the diagnosis, but I just have a deep understanding that it's not something that is on many people's radars. And I think, again, it's tricky because it's not picked up on these next-generation sequencing panels, which many of us can send pretty easily. It will be missed. And I will say the biggest pitfall is, again, if you're not thinking about it and you don't send that testing, you actually- it's very difficult to diagnose it. Dr Grouse: Thank you so much for highlighting that. I think there are many people who are not aware that those different panels really aren't picking that up and that they have to test specifically. So, I think that's a great thing for all of us to keep in mind. Are there any tips or tricks to the diagnosis, other than the genetic issues that you mentioned, that sometimes can really bring this diagnosis to the forefront? Dr Knox: I think things that really tip me off to having a higher suspicion for FSHD is facial weakness that we can detect on our exam. Scapular winging---again, there's a small subset of disorders which can impact that. Someone who's presenting with foot drop, you know, with facial weakness, I think definitely about FSHD more. Also, clinically, kind of the presentation or things that they're beginning to have difficulty with is a tip-off. So, if someone is an athlete, like, they're a volleyball player or basketball player and they say, oh, I'm having difficulties, you know, with movements that require them to elevate their arm, which can be a sign of the shoulder weakness that we classically see. Or someone who says, oh, I'm having a harder time shampooing my hair or combing my hair. So those can be tip-offs again, which are basically referencing the type of weakness that they have. Another feature of FSHD which isn't necessarily as broadly appreciated is that pain and fatigue are very common. So, if someone is coming in and saying, actually, I also have a significant amount of fatigue as well or a lot of pain, that's something that can tip me off to it. Hearing loss is something that we can also see in up to 20% of patients with FSHD. So, if they are having those symptoms or saying they're ringing in their ears, these are some things that will make me begin to think about it more. Dr Grouse: Oh, really helpful. I also found it really fascinating reading some of the very FSHD-specific clinical signs, some interesting- some diagrams and pictures as well, that are very specific to the pattern of weakness that develops in FSHD. So, I encourage our listeners to check that out. But are there any highlights from those little clinical pearls that you'd like to point out? Dr Knox: I think the poly-hill sign---so, these are these literal hills that we can see in the shoulders of patients with FSHD---is pretty classic. Popeye arms, which is this older term that we still use that has to do with which muscle groups are preserved versus those that have atrophy. So that's a common feature. And then I would say, really, the asymmetry is something that is a unique feature in FSHD. And again, we did our best to provide good representative images. So again, as you mentioned, Katie, I would really encourage people to look at those images and then think about cases that they may have seen and how similar they are so they can begin to recognize those signs as well. Dr Grouse: Now going back to the genetic topic, the complex genetic underpinnings of FSHD are really well-explained in your article; and again, worth taking a look at to remind ourselves of everything that's of that pathology. Now, I was wondering though, if you could give us a brief overview of how we should approach genetic testing in a suspected case of FSHD? You mentioned some specific panels, but it does sound like there's some more complexity to it as well. Dr Knox: Yes, and I'll just kind of briefly explain that complexity. Part of the thing that we're detecting in the genetic testing is the repeat number. And so, we're actually looking for a contraction in a repeat number. So, not an expansion, which were typical for some of the diseases that we think about, the trinucleotide repeat disorders. And this is why it's not captured in the next-generation sequencing panels, because they do not currently have the ability to do that. And so, again, what the type of testing that I do really depends on my suspicion. So again, if my suspicion is very high for FSHD---they have a family history, they have the classic features---then I will actually go directly to an FSHD-specific testing, which is available from various sources. If, again, it's among different things that I'm thinking about, I will get a CK lab. I typically will also send a next-generation sequencing panel specific for muscle diseases, perhaps muscular dystrophy; again, depending on what I'm thinking about. And then I will also send in a specific FSHD genetic test as well. People are beginning to use whole-genome sequencing, which is capturing some of our true nucleotide repeat disorders and becoming more comprehensive. So, my hope is that as that becomes more standard of care---like, whole-exome sequencing can be gotten pretty routinely now---that it may be easier for us to make some of these diagnoses. Dr Grouse: Well, that's really helpful, and thanks for that overview. Now another thing that you mentioned that I thought was really interesting in your article was that patients with, you know, history of FSHD, perhaps in the family, who are pregnant and want to screen for this disease would not be able to use sort of the more common screening tests like cell-free DNA testing and may have to go to other means to do that. What is generally their route to this type of testing? Dr Knox: Yeah, great question, and really important question for family planning purposes, and it definitely comes up in clinical practice. And so again, because of the unique genetics of FSHD, you actually have to do invasive genetic testing currently to be able to test it. And so that's, you know, amnio or chorio, and then send it to a lab that can perform, again, FSHD-specific testing on the samples that are presented. And there are obviously labs that are capable of doing that and centers that are capable of doing that, but it is not picked up on the cell-free DNA panels that are being very routinely used. You or your provider has to be thinking about it to send that specific testing, similar to our patients that come into clinic and have not yet been diagnosed. Dr Grouse: Once you have the diagnosis, what are our options for therapy? I think it sounds like at this current time, it looks to be mostly supportive. What are some of the supportive care options we should keep in mind? Dr Knox: Yes, so that is definitely accurate. Care today is supportive, but again, we're very excited about the clinical trial and therapy landscape for FSHD. So, I work very closely with my physical therapy colleagues that are in clinic with me. So, we work very closely with physical and occupational therapists to help with supportive measures, adaptive measures, doing assessments, helping our patients to be able to move and exercise safely and effectively. As I mentioned, pain is very common in FSHD and so we can treat that with medications. The most common medication that we use to treat for pain in FSHD are NSAIDs. And then other than that it's really, you know, supportive measures. Do they need to see other subspecialists? There are some surgical options. Those are used very rarely to help with some of the scapular weakness, but typically it's physical therapy, occupational therapy, supportive devices. We treat the pain as we're able to, and then we work with other subspecialists to screen, monitor and support our patients to the best of our ability. Dr Grouse: Well, without further ado, I'd love to hear more about what's coming down the pipeline in clinical trials. What can we look forward to seeing, hopefully, in future years to treat these patients? Dr Knox: Yes. And so, this is actually what got me interested in the neuromuscle space in general is that, because we now for many years have known the genetic cause of many of these disorders as well as some of the underlying mechanisms, we can actually use advances in therapeutics to do what we call targeted therapies. So, rather than treating symptoms or indirect methods or doing kind of broad drug screens---which, again, still do take place and still do have their place---we actually can target mechanisms directly. And so, we know that the underlying biology of FSHD is due to this protein called DUX4 being expressed when it should not be. So, it's what we call a toxic gain of function. And so, the targeted way to address this is to suppress DUX4 expression. And so, kind of broadly speaking, what we're really excited about are a couple of products that are currently in clinical trials right now that actually caused DUX4 suppression to be suppressed. And again, these are targeted pathways. And so, again, the hope is that by doing that, we can hopefully slow the progression of the disease, potentially stop progression of the disease, and potentially reverse. Again, we don't know if that might be possible, but that is one of the hopes. Dr Grouse: Well, that's really exciting, and I know we're all looking forward to more coming down the pipeline soon, and hopefully more things that can really offer some exciting treatments for our patients with this condition. Now, a little more deep-dive into our patients who are diagnosed. You've reviewed some of the treatments currently available and hopefully may someday soon be available. Are there other things that we should be keeping in mind in this population? For instance, screenings that we should be doing for other extramuscular manifestations that we need to be thinking about? Dr Knox: I will answer that question two ways. I think something that's very important to acknowledge is the impact that these diagnoses and these conditions have on our patient practically, psychologically. One of the other unique features of FSHD is, it's autosomal-dominant. So, if it is in a family, you can have many family members who are affected, but the variability is very high. And so, you can have in the same family someone who is wheelchair-dependent, and someone else in the family with the same underlying genetics who has no signs or symptoms or is very mildly affected. And that is something that is definitely challenging for our families and patients to navigate if they're very different than their family members with the same condition. And just navigating the world with a condition that, you know, can be physically debilitating and cause changes to what they're able to do or not able to do, progression is something that's very difficult to handle. So, I think that's one set of things. And we try our best, you know, with my team and my other colleagues in the space, to support our families and patients in the best way that we can. Secondly, there is very important screening that needs to be done for this condition. So, one of the things- and the current guidelines which are actually being updated, the last update was in 2015 is all patients that undergo pulmonary function testing or PFTs. And so that's something we do at baseline and we do at least annually in my practice. Young kids who are presenting very early or patients with certain genetics that we know are more predisposed to extra muscular manifestations, we recommend screening for hearing, which is one of the manifestations, and ophthalmologic exam to look for retinovascular changes, which is one of the manifestations as well. Those are the more common ones that are typically done. There's also some evidence in pediatric patients with very severe manifestations that there may be some cognitive impacts, learning impacts. And so, that is something we're also thinking about screening and supporting our patients in that way. And again, we typically work with these patients in a multidisciplinary team depending on what manifestations and the degrees to which they're impacted by the disorder. Dr Grouse: Thank you so much for that answer. I think a lot of us forget sometimes when we get really focused on what can we do now, that we forget to kind of stop and reflect on sort of the more holistic approach. How is this affecting the patient? How is this affecting the patient's family dynamic, and what other ways are they going through life with this condition that we need to be thinking about? So, I appreciate you bringing that up. I wanted to ask, sort of based on what you're talking about and what you mentioned already, you happened to mention that what initially drew you that to this work was your interest in some of the really exciting breakthroughs in the field. Well, was there anything else that drew you to, specifically, congenital neuromuscular diseases, and FSHD in particular? Dr Knox: I'm a physician scientist by training, and so I would describe myself also as a molecular biologist. So, I love getting into the nitty gritties of disease mechanisms, what genes are doing in bodies, how they function. And so, as I mentioned earlier, in the neuromuscle space, we've known for many years the genetic cause of many of these disorders and have done great, you know, mechanistic work to kind of define why we see the disease. And then now we're at this intersection of that knowledge marrying with these really novel therapeutic approaches, gene therapy approaches, being able to intersect and then in very creative ways actually target diseases very directly. And so, I would say it really is the combination of those two things. FSHD has a really fascinating unique biology, which again, we encourage everyone to read about more in the article. That really drew me to it. I'm very interested in gene regulation, transcription. This is one of the underlying mechanisms that is gone awry in the disorder, and then that being married to advances in therapeutics. So, you could wed those two pieces of information and actually meaningfully impact patient 's lives. And again, that's the real privilege and honor to witness is how these therapies can transform lives. And I saw it happened with this one case for this one disorder when I was a resident where there was no treatment. Young children, unfortunately, would not survive the disease. And then I saw the therapy come be in development and literally change the trajectory. And this is what we're very hopeful for in the FSHD space, that wedding, this wonderful basic science research, translational research, companies working together to develop these therapies that can transform lives. It is just so beautiful to witness and see, and it's something that I get to do. You know, it's a part of my job, so it's a real privilege. Dr Grouse: Well, I have to say, it's really inspiring hearing you talk about it. And I imagine that many neurologists-in-training who are listening to this may be inspired as well and may be convinced to go into this field for that very reason. So, thank you so much for sharing all of this information with us today. I learned a lot, and I think all of our listeners have too. Dr Knox: Thank you. It's really been a pleasure. Dr Grouse: Again, today I've been interviewing Dr Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

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Join the C3 crew is as they react to the Carolina Panthers taking on the Dallas Cowboys at home at Bank of America Stadium for week 6 of the NFL season!

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She sold her advertising agency to write stories about the fierce, overlooked women who built America. CK Van Dam's debut novel, Proving Her Claim, has already won two Spur Awards and immerses readers in a frontier romance as bold and expansive as the Dakota plains themselves. In this episode, CK shares the inspiration behind her “On the Dakota Frontier” series, why she chose to spotlight unconventional heroines like Anna Olson, and how historical fiction can challenge the myths we've been told about the American West. If you're looking for adventure, romance, and action all woven into a powerful story of resilience and reinvention, you won't want to miss this conversation. Quotes: “History is full of women who were strong, resourceful, and too often forgotten.” “Romance on the frontier wasn't just about love—it was about survival.” “Fiction lets us reimagine the past and reclaim voices that history left out.” Resources: Follow CK Van Dam on Facebook Connect with CK Van Dam on LinkedIn On the Dakota Frontier

Tonight the C3 crew discusses how the Panthers will split reps between Rico Dowdleand Chuba Hubbard, if Carolina will pick up Bryce Young's 5th year option, the return of Jalen Coker to practice, the emergence of Nic Scourton, and previewing this Sunday's matchup against the Dallas Cowboys!

While genetic testing has replaced muscle biopsy in the diagnosis of many genetic myopathies, clinical assessment and the integration of clinical and laboratory findings remain key elements for the diagnosis and treatment of muscle diseases. In this episode, Casey Albin, MD, speaks with Margherita Milone, MD, PhD, FAAN, FANA, author of the article “A Pattern Recognition Approach to Myopathy” in the Continuum® October 2025 Muscle and Neuromuscular Junction Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Milone is a professor of neurology and the director of the Muscle Pathology Laboratory at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: A Pattern Recognition Approach to Myopathy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Albin: Hello, this is Dr Casey Albin. Today I'm interviewing Dr Margherita Milone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, Dr Milone. Thank you so much for joining us. I'll start off by having you introduce yourself to our listeners. Dr Milone: Hello Casey, thank you so much for this interview and for bringing the attention to the article on muscle diseases. So, I'm Margherita Milone. I'm one of the neuromuscular neurologists at Mayo Clinic in Rochester. I have been interested in muscle disorders since I was a neurology resident many years ago. Muscle diseases are the focus of my clinical practice and research interest. Dr Albin: Wonderful. Thank you so much. When I think about myopathies, I generally tend to think of three large buckets: the genetic myopathy, the inflammatory myopathies, and then the necrotizing myopathies. Is that a reasonable approach to conceptualizing these myopathies? Dr Milone: Yeah, the ideology of the myopathies can be quite broad. And yes, we have a large group of genetic muscle diseases, which are the most common. And then we have immune-mediated muscle diseases, which include inflammatory myopathies as well as some form of necrotizing myopathies. Then we have some metabolic myopathies, which could be acquired or could be genetic. And then there are muscle diseases that are due to toxins as well as to infection. Dr Albin: Wow. So, lots of different etiologies. And that really struck me about your article, is that these can present in really heterogeneous ways, and some of them don't really read the rule book. So, we have to have a really high level of suspicion, for someone who's coming in with weakness, to remember to think about a myopathy. One of the things that I like to do is try to take us through a little bit of a case to sort of walk us through how you would approach if someone comes in. So, let's say you get, you know, a forty-year-old woman, and she's presenting with several months of progressive weakness. And she says that even recently she's noted just a little bit of difficulty swallowing. It feels to her like things are getting stuck. What are some of the things when you are approaching the history that would help you tease this to a myopathy instead of so many other things that can cause a patient to be weak? Dr Milone: Yes. So, as you mentioned, people who have a muscle disease have the muscle weakness often, but the muscle weakness is not just specific for a muscle disease. Because you can have a mass weakness in somebody who has a neurogenic paralysis. The problem with diagnosis of muscle diseases is that patients with these disorders have a limited number of symptom and sign that does not match the large heterogeneity of the etiology. So, in someone who has weakness, that weakness could represent a muscle disease, could represent an anterior horn cell disease, could represent a defect of neuromuscular junction. The clinical history of weakness is not sufficient by itself to make you think about a muscle disease. You have to keep that in the differential diagnosis. But your examination will help in corroborating your suspicion of a muscle disease. Let's say if you have a patient, the patient that you described, with six months' history of progressive weakness, dysphagia, and that patient has normal reflexes, and the patient has no clinical evidence for muscle fatigability and no sensory loss, then the probability that that patient has a myopathy increases. Dr Albin: Ah, that's really helpful. I'm hearing a lot of it is actually the lack of other findings. In some ways it's asking, you know, have you experienced numbness and tingling? And if not, that's sort of eliminating that this might not be a neuropathy problem. And then again, that fatigability- obviously fatigability is not specific to a neuromuscular junction, but knowing that is a hallmark of myasthenia, the most common of neuromuscular disorders. Getting that off the table helps you say, okay, well, it's not a neuromuscular junction problem, perhaps. Now we have to think more about, is this a muscle problem itself? Are there any patterns that the patients describe? I have difficulty getting up from a chair, or I have difficulty brushing my hair. When I think of myopathies, I historically have thought of, sort of, more proximal weakness. Is that always true, or not so much? Dr Milone: Yeah. So, there are muscle diseases that involve predominantly proximal weakness. For example, the patient you mentioned earlier could have, for example, an autoimmune muscle disease, a necrotizing autoimmune myopathy; could have, perhaps, dermatomyositis if there are skin changes. But a patient with muscle disease can also present with a different pattern of weakness. So, myopathies can lead to this weakness, and foot drop myopathies can cause- can manifest with the weakness of the calf muscles. So, you may have a patient presenting to the clinic who has no the inability to stand on tiptoes, or you may have a patient who has just facial weakness, who has noted the difficulty sealing their lips on the glasses when they drink and experiencing some drooling in that setting, plus some hand weakness. So, the muscle involved in muscle diseases can vary depending on the underlying cause of the muscle disease. Dr Albin: That's really helpful. So, it really is really keeping an open mind and looking for some supporting features, whether it's bulbar involvement, extraocular eye muscle involvement; looking, you know, is it proximal, is it distal? And then remembering that any of those patterns can also be a muscle problem, even if sometimes we think of distal being more neuropathy and proximal myopathy. Really, there's a host of ranges for this. I really took that away from your article. This is, unfortunately, not just a neat way to box these. We really have to have that broad differential. Let me ask another question about your history. How often do you find that patients complain of, sort of, muscular cramping or muscle pain? And does that help you in terms of deciding what type of myopathy they may have? Dr Milone: Many patients with muscle disease have muscle pain. The muscle pain could signal a presence of inflammation in skeletal muscle, could be the result of overuse from a muscle that is not functioning normally. People who have myotonia experience muscle stiffness and muscle pain. Patients who have a metabolic myopathy usually have exercise-induced muscle pain. But, as we know, muscle pain is also very nonspecific, so we have to try to find out from the patient in what setting the pain specifically occurs. Dr Albin: That's really helpful. So, it's asking a little bit more details about the type of cramping that they have, the type of pain they may be experiencing, to help you refine that differential. Similarly, one of the things that I historically have always associated with myopathies is an elevation in the CK, or the creatinine kinase. How sensitive and specific is that, and how do you as the expert sort of take into account, you know, what their CK may be? Dr Milone: So, this is a very good point. And the elevation of creatine kinase can provide a clue that the patient has a muscle disease, but it is nonspecific for muscle disease because we know that elevation of creatine kinase can occur in the setting of a neurogenic process. For example, we can see elevation of the creatine kinase in patients who have ALS or in patients who have spinal muscular atrophy. And in these patients---for example, those with spinal muscular atrophy---the CK elevation can be also of significantly elevated up to a couple of thousand. Conversely, we can have muscle diseases where the CK elevation does not occur. Examples of these are some genetic muscle disease, but also some acquired muscle diseases. If we think of, for example, cases where inflammation in the muscle occurs in between muscle fibers, more in the interstitium of the muscle, that disease may not lead to significant elevation of the CK. Dr Albin: That's super helpful. So, I'm hearing you say CK may be helpful, but it's neither completely sensitive nor completely specific when we're thinking about myopathic disorders. Dr Milone: You are correct. Dr Albin: Great. So, coming back to our patients, you know, she says that she has this dysphasia. How do bulbar involvement or extraocular eye movement involvement, how do those help narrow your differential? And what sort of disorders are you thinking of for patients who may have that bulbar or extraocular muscle involvement? Dr Milone: Regarding dysphagia, that can occur in the setting of acquired myopathies relatively frequent; for example, in inclusion body myositis or in other forms of inflammatory myopathy. Your patient, I believe, was in their forties, so it's a little bit too young for inclusion body myositis. Involvement of the extraocular muscles is usually much more common in genetic muscle diseases and much less frequent in hereditary muscle disease. So, if there is involvement of the extraocular muscles, and if there is a dysphagia, and if there is a proximal weakness, you may think about oculopharyngeal muscular dystrophy, for example. But obviously, in a patient who has only six months of history, we have to pay attention of the degree of weakness the patient has developed since the symptom onset. Because if the degree of weakness is mild, yes, it could still be a genetic or could be an acquired disease. But if we have a patient who, in six months, from being normal became unable to climb stairs, then we worry much more about an acquired muscle disease. Dr Albin: That's really helpful. So, the time force of this is really important. And when you're trying to think about, do I put this in sort of a hereditary form of muscle disease, thinking more of an indolent core, something that's going to be slowly progressive versus one of those inflammatory or necrotizing pathologies, that's going to be a much more quick onset, rapidly progressive, Do I have that right? Dr Milone: In general, the statement is correct. They tend, acquired muscle disease, to have a faster course compared to a muscular dystrophy. But there are exceptions. There have been patients with immune mediated necrotizing myopathy who have been misdiagnosed as having limb-girdle muscular dystrophy just because the disease has been very slowly progressive, and vice versa. There may be some genetic muscle diseases that can present in a relatively fast way. And one of these is a lipid storage myopathy, where some patients may develop subacutely weakness, dysphagia, and even respiratory difficulties. Dr Albin: Again, I'm hearing you say that we really have to have an open mind that myopathies can present in a whole bunch of different ways with a bunch of different phenotypes. And so, keeping that in mind, once you suspect someone has a myopathy, looking at the testing from the EMG perspective and then maybe laboratory testing, how do you use that information to guide your work up? Dr Milone: The EMG has a crucial role in the diagnosis of muscle diseases. Because, as we said earlier, weakness could be the result of muscle disease or other form of neuromuscular disease. If the EMG study will show evidence of muscle disease supporting your diagnostic hypothesis, now you have to decide, is this an acquired muscle disease or is this a genetic muscle disease? If you think that, based on clinical history of, perhaps, subacute pores, it is more likely that the patient has an acquired muscle disease, then I would request a muscle biopsy. The muscle biopsy will look for structural abnormalities that could help in narrowing down the type of muscle disease that the patient has. Dr Albin: That's really helpful. When we're sending people to get muscle biopsies, are there any tips that you would give the listeners in terms of what site to biopsy or what site, maybe, not to biopsy? Dr Milone: This is a very important point. A muscle biopsy has the highest diagnostic yield if it's done in a muscle that is weak. And because muscle diseases can result in proximal or distal weakness, if your patient has distal weakness, you should really biopsy a distal muscle. However, we do not wish to biopsy a muscle that is too weak, because otherwise the biopsy sample will result just in fibrous and fatty connected tissue. So, we want to biopsy a muscle that has mild to moderate weakness. Dr Albin: Great. So, a little Goldilocks phenomenon: has to be some weak, but not too weak. You got to get just the right feature there. I love that. That's a really good pearl for our listeners to take. What about on the flip side? Let's say you don't think it's an acquired a muscular disease. How are you handling testing in that situation? Dr Milone: If you think the patient has a genetic muscle disease, you pay a lot of attention to the distribution of the weakness. Ask yourself, what is the best pattern that represent the patient's weakness? So, if I have a patient who has facial weakness, dysphagia, muscle cramping, and then on examination represent myotonia, then at that point we can go straight to a genetic test for myotonic dystrophy type one. Dr Albin: That's super helpful. Dr Milone: So, you request directly that generic test and wait for the result. If positive, you will have proof that your diagnostic hypothesis was correct. Dr Albin: You're using the genetic testing to confirm your hypothesis, not just sending a whole panel of them. You're really informing that testing based on the patient's pattern of weakness and the exam findings, and sometimes even the EMG findings as well. Is that correct? Dr Milone: You are correct, and ideally, yes. And this is true for certain muscle diseases. In addition to myotonic dystrophy type one, for example, if you have a patient who has fascial scapulohumeral muscular weakness, you can directly request a test for FSHD. So, the characterization of the clinical phenotype is crucial before selecting the genetic test for diagnosis. Dr Albin: Wonderful. Dr Milone: However, this is not always possible, because you may have a patient who has just a limb-girdle weakness, and the limb-girdle weakness can be limb-girdle muscular dystrophy. But we know that there are many, many types of limb-girdle muscular dystrophies. Therefore, the phenotype is not sufficient to request specific genetic tests for one specific form of a limb-girdle muscular dystrophy. And in those cases, more complex next-generation sequencing panels have a higher chance of providing the answer. Dr Albin: Got it, that makes sense. So, sometimes we're using a specific genetic test; sometimes, it is unfortunate that we just cannot narrow down to one disease that we might be looking for, and we may need a panel in that situation. Dr Milone: You are correct. Dr Albin: Fantastic. Well, as we wrap up, is there anything on the horizon for muscular disorders that you're really excited about? Dr Milone: Yes, there are a lot of exciting studies ongoing for gene therapy, gene editing. So, these studies are very promising for the treatment of genetic muscle disease, and I'm sure there will be therapists that will improve the patient's quality of life and the disease outcome. Dr Albin: It's really exciting. Well, thank you again. Today I've been interviewing Dr Margarita Malone on her article on a pattern recognition approach to myopathy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining us today. And thank you, Dr Milone. Dr Milone: Thank you, Casey. Very nice chatting with you about this. 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.

CK and Carmen On Demand....EVERYTHING you missed on this morning show. Get caught up NOW!!!!

Join the C3 crew as they react to the Carolina Panthers taking on the Miami Dolphins at home in week five of the NFL season!

CK and Carmen On Demand....EVERYTHING you missed on this morning show. Get caught up NOW!!!!

CK vs. Mr. Pizza by Ethan by 826 Valencia

Tonight the C3 crew ask if the Carolina Panthers are the most untalented team in the NFL? How Miami losing Tyreek Hill for the season affects Carolinas defense on Sunday, are the Panthers to blame for Bryce Young deficiencies, Carolina cutting DJ Johnson, and is Dave Canales on the hot seat?

If you've been doomscrolling and need a break, skip to the next episode. A lot is going on in the world and on US soil. It's crazy times we're living in, and while we try to keep things lighthearted, we're tired.  Rest in Peace, Assata Shakur, a Black Liberation Activist and revolutionary. Assata Shakur Passes Away via PBS: https://www.pbs.org/newshour/nation/assata-shakur-fugitive-black-activist-who-escaped-life-sentence-for-killing-police-officer-dies-in-cuba   The Free Black Women's Bookstore PDF of Assata's Biography - https://linktr.ee/thefreeblackwomenslibrary?fbclid=PAQ0xDSwNGJ-NleHRuA2FlbQIxMQABp1bSxJNCcPtRZeEkb0pxmL5bhvR8WjMtkSUx-MH4XeLcBFUcIb0w7D-dgvj3_aem_mOIfRUHFWI0gYk2ipflzvQ   Workers Penalized for CK comments - https://www.theguardian.com/us-news/2025/sep/19/workers-disciplined-charlie-kirk-shooting  

This week, Kaitlyn tackle a kid's big question: “I know there's one true God, but are there little gods beneath him?” From Psalm 82 to Job and Paul, the Bible's language about gods, angels, demons, and spiritual powers is stranger than most of us realize. Kaitlyn unpacks what these passages mean, why scripture sometimes blurs the line between human rulers and spiritual beings, and how it all points back to the hope that the one true God reigns above every power.   Holy Post Plus: My Hill to Die On: Red Letter Bibles: https://www.patreon.com/posts/my-hill-to-die-138522925   0:00 - Theme Song   0:58 - Are There Little gods in the Bible?   3:26 - Psalm 82 mentions “gods?”   10:28 - Are these gods extensions of rulers?   12:13 - Sponsor - Dwell - Listen to scripture throughout your day. Go to https://www.dwellbible.com/CK for 25% off!   13:25 - Sponsor - No Small Endeavor - Award-winning podcast where theologians, philosophers, and best-selling authors talk about faith with Lee C. Camp. Start listening today: https://pod.link/1513178238   14:28 - Book of Job   22:50 - Why Isn't This All Clearer?   27:01 - Evil's Real, but God's Stronger   31:45 - End Credits

CK and Carmen On Demand....EVERYTHING you missed on this morning show. Get caught up NOW!!!!

Join the C3 crew as they react to the Carolina Panthers taking on the New England Patriots in week 4 of the NFL season!

In this episode, Steve and Adam dive into one of Milwaukee's most beloved annual traditions - Doors Open Milwaukee - celebrating its 15th anniversary this September 27th and 28th. They're joined by Grace from Historic Milwaukee, who coordinates this incredible event that opens more than 150 locations across the city for free public tours, from private clubs like the Wisconsin Club to neighborhood gems you'd never normally see inside. They also chat with Jeff from Milwaukee Fashion Week about how their fashion showcase is partnering with Doors Open at City Hall's rotunda, and CK from Villa Arco, the stunning former funeral home turned event space and art gallery. Whether you're interested in historic architecture, local fashion, or discovering the hidden stories behind Milwaukee's most intriguing buildings, this episode has something for everyone ready to explore our city.For more information on Doors Open Milwaukee: https://historicmilwaukee.org/doors-openExperience Milwaukee is presented by Habush Habush & Rottier, VISIT Milwaukee, the Milwaukee Admirals, nvisia, Summerfest, and Crescent 9 THC Seltzers and our official beer partner is New Barons Brewing Cooperative.Thanks for listening.Love you, Milwaukee.

On this week's episode: The White House finds the connections between JC and CK ... Rumor has it that Ryan Walters fucked a pile of flour during a board of education zoom call? ... And Don Ford will be here to read Paul's homophobic letter to the Romans. --- To make a per episode donation at Patreon.com, click here: http://www.patreon.com/ScathingAtheist To buy our book, click here: https://www.amazon.com/Outbreak-Crisis-Religion-Ruined-Pandemic/dp/B08L2HSVS8/ If you see a news story you think we might be interested in, you can send it here: scathingnews@gmail.com To check out our sister show, The Skepticrat, click here: https://audioboom.com/channel/the-skepticrat To check out our sister show's hot friend, God Awful Movies, click here: https://audioboom.com/channel/god-awful-movies To check out our half-sister show, Citation Needed, click here: http://citationpod.com/ To check out our sister show's sister show, D and D minus, click here: https://danddminus.libsyn.com/ Report instances of harassment or abuse connected to this show to the Creator Accountability Network here: https://creatoraccountabilitynetwork.org/ --- Headlines: At Kirk Service, an Extraordinary Fusion of Government and Christianity: https://www.nytimes.com/2025/09/21/us/politics/kirk-memorial-service-christianity-religion.html https://www.nytimes.com/interactive/2025/09/21/us/politics/kirk-memorial-photos.html White House's Karoline Leavitt appears to connect earthquake to Charlie Kirk's death and Biblical prophecy: https://www.independent.co.uk/news/world/americas/us-politics/charlie-kirk-death-karoline-leavitt-prophecy-earthquake-b2828284.html Trump links autism to Tylenol use during pregnancy: https://www.cnn.com/2025/09/22/health/trump-autism-announcement-cause-tylenol https://www.nytimes.com/2025/09/23/us/trump-tylenol-autism-vaccines-fact-check.html https://www.npr.org/sections/shots-health-news/2025/09/22/nx-s1-5550153/trump-rfk-autism-tylenol-leucovorin-pregnancy Pope nixes 'virtual pope' idea, explains concerns about AI: https://www.ncronline.org/vatican/vatican-news/pope-nixes-virtual-pope-idea-explains-concerns-about-ai The rapture was supposed to happen:  https://www.nytimes.com/2025/09/23/us/rapture-tiktok-sept-23.html https://substack.com/home/post/p-174218365 Oklahoma's Supreme Court blocks Ryan Walters' Bible-heavy Social Studies standards: https://www.friendlyatheist.com/p/oklahomas-supreme-court-blocks-ryan

Raider talk at its best with CK and Your Boy Q w CK On Sports

Join the C3 crew as they discuss the Panthers' DOMINANT defensive performance against the Atlanta Falcons, preview the week 4 match up with the New England Patriots, discuss the injury of Ja'Tavion Sanders and its implications for the TE Mitchell Evans, and YOUR Cat Calls at 252-228-5098!

Send us a textWhat happened last week to CK can be written a number of ways... But the bottom line is this:  Either we shut up, get back in line, do what we are told and comply with the new tyranny... Or we stand up, we speak up, we KEEP our VOICE and make it HEARD, and we DECIDE that they have finally gone TOO FAR!!!  The choice is yours.  The choice is ours.  Let's make it count.  Listen now. We are forming a NEW GROUP!  Join the current group to stay up to date on the move and to get your personal invitation to join!Contact US:  Rumble/ YouTube/ IG: @powerofmanpodcastEmail: powerofmanpodcast@gmail.com.Twitter: @rorypaquetteLooking for Like-Minded Fathers and Husbands? Join our Brotherhood!"Power of Man Within" , in Facebook Groups:https://www.facebook.com/groups/490821906341560/?ref=share_group_linkFree Coaching Consultation call whenever you are ready... Message me!Believe it!

Joseph in NYC called Mark to let him know that people should always remember CK as "Charlie Kirk". Vincent in Brooklyn, NY, calls Mark to let him know that Democrats didn't get the message at yesterday's speeches during Charlie Kirk's memorial. See omnystudio.com/listener for privacy information.

Joseph in NYC called Mark to let him know that people should always remember CK as "Charlie Kirk". Vincent in Brooklyn, NY, calls Mark to let him know that Democrats didn't get the message at yesterday's speeches during Charlie Kirk's memorial.

"Jack Riccardi breaks the news about Jimmy Kimmel's ABC reinstatement, announcement from Trump on autism/Tylenol and reaction to the CK memorial."

Join the C3 crew as they react to the Carolina Panthers taking on the Atlanta Falcons in their home opener for week 3 of the NFL season!

Send us a textSummary:Matilda Medium discusses the concept of spiritual bypassing in metaphysical work, emphasizing the importance of addressing unresolved trauma and emotions rather than avoiding them through spiritual practices. She highlights the dangers of bypassing for both practitioners and clients, advocating for a more integrated and compassionate approach to spirituality.Matilda also talks about criticism based on other peoples judgement and discussions regarding her input on the Assassination of CK.Matilda also discussed the weekly spiritual ability in depth for those wanting to catalogue different abilities.At the end of this episode Matilda talks about what she sees coming in globally over the coming weeks or months.Chapters:Introduction to Spiritual BypassingThe Impact of Bypassing on PractitionersBalancing Spirituality and PracticalityReview Rant :-) NSFWPredictions and moving forwardYouTUBE Licence AZE9OIW8PZJAFG3CMatilda's Links and Events WebsiteLearn to connect to your spirit guides workshopPatreon2026 Charts and Channeling Event with Laurie Rivers

In this episode, James Maude sits down with Kevin E. Green, Chief Security Strategist at BeyondTrust, whose 25+ year career stretches from configuring Nokia firewalls in basements to shaping federal research initiatives. Kevin recalls how crashing systems during penetration tests at Ernst & Young was once considered a win - a “capture the flag” moment - and how he crossed paths with future industry leaders like Stuart McClure and George Kurtz, who went on to found Cylance. He shares his pivotal work in mapping NIST 800-53 controls to the MITRE ATT&CK framework, transforming static security catalogs into threat-informed heat maps that show which defenses light up against real-world attacks. Blending technical depth with cultural insight, Kevin also draws unexpected parallels between cybersecurity and hip-hop — from how attacker techniques echo rapper “signatures” to why his alter ego "Kevtorious" and his "Secure Coding by Nature" brand reflect the creativity and pattern recognition needed in both fields.

In this episode, host Jeremy Almond sits down with Mike Peterson, the founder of Bitcoin Beach in El Salvador, and CK Snarks from the Human Rights Foundation to explore how Bitcoin is transforming lives at the community level and beyond.Mike shares the Bitcoin Beach perspective on how a small grassroot project in El Zonte grew into a movement that helped shape El Salvador's decision to make Bitcoin legal tender. What started with paying local youth in Bitcoin for community work turned into a living example of financial inclusion and a circular economy built on digital currency. For many who had no access to banking, Bitcoin became the first tool to save, plan, and participate in the global economy.CK adds the human rights lens, showing how activists around the world are using Bitcoin when traditional financial systems fail. From Venezuela to Ukraine, digital currency has provided a way to fund movements, access money across borders, and resist dictatorships. Together, the stories show that Bitcoin is not just an asset but a tool that empowers people where it is needed most.If you want to understand Bitcoin adoption from the ground up, this conversation gives you the Bitcoin Beach perspective: real people, real communities, and a clear look at how financial inclusion can begin with one small project. Subscribe, share with a friend, and let us know in the comments how you see Bitcoin shaping the future. And yes, surfing in El Zonte might just be part of the story.-Bitcoin Beach TeamConnect and Learn more about Jeremy Almond and CK SnarksJeremy Almond - https://x.com/jeremyalmondJeremy Almond - https://www.youtube.com/@redefinedpodcast CK Snarks – https://primal.net/ckCK Snarks - https://x.com/ck_SNARKs Support and follow Bitcoin Beach:X: @BitcoinBeachIG: @bitcoinbeach_svTikTok: @livefrombitcoinbeachWeb: bitcoinbeach.comBrowse through this quick guide to learn more about the episode: 00:00 Why Bitcoin matters for communities in El Salvador00:27 Is Bitcoin just for trading or a real paradigm shift?01:17 What does a circular Bitcoin economy look like?02:18 How Bitcoin Beach began in El Zonte03:02 Why the Human Rights Foundation turned to Bitcoin06:03 Why most of the world is excluded from banking10:59 How Bitcoin changes saving habits and education12:45 How Bitcoin helps activists survive under dictatorships19:33 Are banks starting to embrace Bitcoin adoption?21:39 Is Bitcoin the next major monetary paradigm shift?25:53 How can people get involved in Bitcoin adoption?Live From Bitcoin Beach

Patrick addresses Jimmy Kimmel’s suspension for callous remarks, candidly discusses the ethics of de-platforming, and shares Frank Turek's wrenching eyewitness account from the scene of Charlie Kirk’s death while listeners chime in with raw stories of grief, faith, and the grind of reconnecting with church after trauma. Conversations move fast, swinging from somber to candid, confronting division, online fury, and the search for hope, all while Patrick keeps the focus on faith and discernment. Arlo (email) - My daughter told me the other day about these dark web sites relating to subcultures that are influencing and manipulating people. (00:49) Jimmy Kimmel fired (05:13) “Jimmy Kimmel Live” will be replaced Friday by a Charlie Kirk tribute special on Sinclair's ABC affiliate stations Audio: Jimmy Kimmel says unvaccinated people should be discriminated against by hospitals. Audio: Kimmel on Tucker Carlson getting fired Audio: You think it’s wrong that you should lose your job because of what you said, but what you said was CK should lose his life for what he said Audio: AOC gloating over Tucker Carlson being fired – “Deplatforming works” Audio: Frank Turek on what happened to CK – Charlie was like a son to me (19:10) Vincent - Have you heard of the book, Vatican Secret Archives, and what do you think about it? (27:56) Lisa - You were talking about miscarriages. I found that naming the baby really helps heal. That way you don't forget. (30:56) Betty Jane (email) - I've been a listener for about a year, but things have changed, and I think it's time for a name change. The show should be called Patrick Madrid MAGA radio. His shows are now far more politics than Jesus. (32:49) Charles - I think Charlie Kirk would have had a great impact if he had become Catholic. (35:24) Jennifer - Can I receive the Eucharist after not going to Church? (40:36) Mark - Patrick, you give me clarity and that is what we need. As Catholics, I feel we are remorseful. Have you heard on how any of the bishops have responded? (48:23)

CK

Patrick shares Pastor Rob McCoy’s moving words on grief, humility, and the need for prayer over self-promotion. He challenges listeners to seek out full context before judging, especially as cherry-picked soundbites and heated rhetoric fan confusion and division online. Callers struggle with discerning truth from spin, while Patrick insists that Christians ground themselves in charity and honest dialogue, always returning to what Christ would have them do amid the noise. Audio: Charlie Kirk’s Pastor Rob McCoy speaks out “This is not the time to get clicks” (02:54) Audio: Minister talking about what happens when you demonize political opponents (20:42) Elizabeth (email) - He is the “alleged killer” or can be referred to as “the one police say killed Charlie Kirk.” (22:06) Marvin - How can we fact check what we see and hear online when it comes to Charlie Kirk? (25:08) Audio: What Charlie Kirk really said about the Civil Rights Act (28:03) Cindy - We need to help others have Jesus in their heart through Charlie's death (35:01) Audio: Roadmap to CK assassination – montage of government officials saying there is a rise of fascism that needs to be stopped (38:57) Audio: Senator Eric Schmitt OBLITERATES the “both sides” nonsense – if we want to get to unity, let’s be honest (47:03) Addison - How can I respond charitably to those of my friends who insist that Charlie was bad guy? (49:07)

"Jack Riccardi wonders if we are one people speaking two different languages on either CK killing or other things, gushing over the killer's text messages, kash patel hearing and Charlie Kirks voice in tik tok believers."

Patrick unpacks the public reaction to Charlie Kirk’s murder, focusing on the moral backlash against those celebrating the tragedy and the wave of firings and exposure that followed. He fields questions about Kirk’s approach and challenges perceptions, weaving in raw perspectives from callers, many reflecting on race, online culture, forgiveness, and how real-world consequences ripple out from digital outrage. Voices from the black community add truth and tension, sharpening the episode’s call for clarity, dialogue, and deeper humanity in a fractured society. Patrick comments on the people who celebrated Kirk’s murder on their social media are being fired from their jobs (00:25) Audio: Scott Jennings on backlash against anti-CK rhetoric (03:24) Terry (email) - I don’t understand why you so wholeheartedly supported Charlie Kirk. I’ve watched several of his debates, and to me, he comes across as self-righteous, confrontational and condescending, not very Christ-like. (05:47) Miss Williams - I do agree with you about most of the things you say. I'm not a republican or democrat. Charlie Kirk's views are his views. What happened to him is sad because it happened to him in front of his family. I think of the Kennedy assassination. We need to do something about guns. Where was his security? We Americans need to do better. (11:15) Audio: Charlie Kirk Didn't Even Believe In Race (25:29) Anthony - Want to thank Patrick for what he does best. I've been listening for years. Such good values and such an awesome person. (30:30) Don - A lot of people who didn't like Charlie Kirk didn't like him because he liked Trump. (31:53) James (email) - H.G. Wells had a poignant message in his book. When the man Griffin loses his body (becomes invisible) he loses his conscience and becomes a sociopath-murderer. So, with Social Media, when we lose our face-to-face interactions, we are being trained to be sociopathic. The smartphone has magnified these interactions and put them in our pocket, and they are displacing actual human interaction. (36:26) Dee Dee - Concerning the murder of Charlie Kirk: I just wanted to bring the fact that as Catholics, we should be an example of how to behave. (40:20) Heidi - I hope this troubled young man gets life in prison instead of the death penalty. He needs God's mercy. I fear if he's given the death penalty, some will see him as a martyr. (47:44) Mary - When I discussed Charlie Kirk with my sister, she said there are extremists on both sides. (49:29)

091625 2nd Guest Dallas Hyland A Former Weekly Guest And Your Calls About Facts on CK! by Kate Dalley

The Boyz talk CK's assination, JP's neighborhood drug raid, the UPS pension trap, and much more.