Podcasts about inhibition

TWiV explains studies which reveal that Inhibition of CXCL10 and IFN-γ mitgates myocarditis associated with SARS-CoV-2 mRNA vaccination, and identification of a bacteriophage T7 protein that antagonizes the DNA restriction system of the host by mimicking B form DNA. Hosts: Vincent Racaniello and Jolene Ramsey Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode Support science education at MicrobeTV ASV 2026 Understanding mRNA vaccine-associated myocarditis (Sci Transl Med) T7 protein overcomes DNA restriction of host (J Mol Biol) Structure of T7 protein that mimics DNA (Mol Cell) Letters read on TWiV 1283 Timestamps by Jolene Ramsey. Thanks! Weekly Picks Jolene – Book series Dinosaur Therapy, Dinosaur Philosophy, & Dinosaur Friendship Vincent – One Plus One Equals One: Symbiosis and the evolution of complex life by John Archibald Listener Picks Terry – Arcadia by Tom Stoppard Greg – Charctic Interactive Sea Ice Graph | National Snow and Ice Data Center Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv Content in this podcast should not be construed as medical advice.

This Editor's Special Episode of The HemOnc Pulse features Paul G. Richardson, MD, of Dana-Farber Cancer Institute, discussing treatment strategies for relapsed/refractory multiple myeloma and where selinexor-based regimens fit in today's evolving landscape. Drawing from real-world cases, Dr. Richardson explores care for patients before CAR T, after CAR T relapse, and in between—highlighting how selinexor can be used flexibly across multiple lines, including as a bridge to future immunotherapies. The conversation emphasizes individualized, dynamic treatment planning to balance disease control, tolerability, and long-term goals in an increasingly complex era of myeloma care.

Carla M. Nester, MD, MSA, FASN - 2025 Congress Highlights From Houston, Texas: Translating C3G and IC-MPGN Trials to Treatment in an Era of Complement Inhibition

Commentary by Dr. Pilar Martin.

Carla M. Nester, MD, MSA, FASN - 2025 Congress Highlights From Houston, Texas: Translating C3G and IC-MPGN Trials to Treatment in an Era of Complement Inhibition

Carla M. Nester, MD, MSA, FASN - 2025 Congress Highlights From Houston, Texas: Translating C3G and IC-MPGN Trials to Treatment in an Era of Complement Inhibition

Carla M. Nester, MD, MSA, FASN - 2025 Congress Highlights From Houston, Texas: Translating C3G and IC-MPGN Trials to Treatment in an Era of Complement Inhibition

The management of hidradenitis suppurativa (HS) is evolving, but many patients still face significant hurdles in achieving optimal outcomes with current therapies. In this episode, "JAK Inhibition and the Future of HS Treatment," expert dermatologists, Hadar Lev-Tov, MD, and Jennifer L. Hsiao, MD discuss: Increasing Awareness: Debunking common myths and misconceptions about HS. Building Trust: Strategies for overcoming diagnostic delays and insufficient management. Comprehensive Care: Adopting a holistic approach, including addressing common comorbidities. The Road Ahead: Exploring the future of the HS treatment landscape, including JAK inhibition.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/TEA865. CME/MOC/NCPD/AAPA/IPCE credit will be available until December 10, 2026.Taking a New Look at Psoriatic Arthritis and Its Comorbidities Through the Lens of TYK2 Inhibition In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/TEA865. CME/MOC/NCPD/AAPA/IPCE credit will be available until December 10, 2026.Taking a New Look at Psoriatic Arthritis and Its Comorbidities Through the Lens of TYK2 Inhibition In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/TEA865. CME/MOC/NCPD/AAPA/IPCE credit will be available until December 10, 2026.Taking a New Look at Psoriatic Arthritis and Its Comorbidities Through the Lens of TYK2 Inhibition In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/TEA865. CME/MOC/NCPD/AAPA/IPCE credit will be available until December 10, 2026.Taking a New Look at Psoriatic Arthritis and Its Comorbidities Through the Lens of TYK2 Inhibition In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/TEA865. CME/MOC/NCPD/AAPA/IPCE credit will be available until December 10, 2026.Taking a New Look at Psoriatic Arthritis and Its Comorbidities Through the Lens of TYK2 Inhibition In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/TEA865. CME/MOC/NCPD/AAPA/IPCE credit will be available until December 10, 2026.Taking a New Look at Psoriatic Arthritis and Its Comorbidities Through the Lens of TYK2 Inhibition In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

Starting with von Békésy's traveling wave and the cochlea's +80 mV biological battery, we move millisecond-by-millisecond through the auditory brainstem response (ABR Waves I–V), auditory nerve, cochlear nucleus, superior olivary complex, inferior colliculus, thalamic reticular nucleus, and finally primary auditory cortex (A1). The Endocochlear Potential (EP) is the highest DC voltage in the human body. As signals travel, excitation-inhibition attempts to balance that. When intact, brains can filter noise and locate meaningful sound. In Autism, reduced GABAergic sculpting (parvalbumin, somatostatin, and VIP interneuron dysfunction) plus lower myelination and a delayed Wave V — already detectable on the newborn hearing screen — turn ordinary environments into an unfiltered flood. The result is listening dissonance: a moment-to-moment perceptual struggle that collapses 40-Hz gamma, recruits massive frontal effort and emotional regions of the brain, frequently ends in sensory overload, shutdown, or literal pain. We close with the exact equation the pathway reveals: Low Inhibition + High Excitation = Sensory Overload.Daylight Computer Company, use "autism" for $50 off at https://buy.daylightcomputer.com/autismChroma Light Devices, use "autism" for 10% discount at https://getchroma.co/?ref=autismFig Tree Christian Golf Apparel & Accessories, use "autism" for 10% discount at https://figtreegolf.com/?ref=autismCognity AI for Autistic Social Skills, use "autism" for 10% discount at https://thecognity.com0:00 Chroma Light Devices and Daylight Computer Company01:56 Audition & Autism; von Békésy Traveling Wave & Tonotopy; Hair Cells & Cochlear Amplifier04:20 Endocochlear Potential (+80 mV Battery); Bioelectric Currents06:30 Stria Vascularis, Melanin, & Water Role08:15 Auditory Nerve – ABR Wave I (1.6 ms)08:36 ABR Wave II (2.7 ms)09:00 Cochlear Nucleus & Early E:I12:10 ABR Wave III – Superior Olivary Complex (3.8 ms)12:13 Binaural Processing & Calyx of Held15:00 ABR Wave V – Inferior Colliculus (5.6 ms)15:42 Inferior Colliculus Gamma & Cell Types18:00 Thalamus MGN & TRN Noise-Canceling21:30 2021 Newborn ABR Study – Prolonged Wave V Biomarker24:30 Listening Dissonance Explained28:30 Auditory Cortex Gamma Collapse in Autism32:30 Primary Auditory Cortex A1 Mini-Columns36:00 Parvalbumin, Somatostatin & VIP Interneurons39:00 Formula: Low GABA + High Excitation = Overload & PainX: https://x.com/rps47586YT: https://www.youtube.com/channel/UCGxEzLKXkjppo3nqmpXpzuAemail: info.fromthespectrum@gmail.com

Mike Sharma, MD, MSc, FRCPC - Challenging the Status Quo in Secondary Stroke Prevention: Current Perspectives on the Potential of Factor XIa Inhibition

Mike Sharma, MD, MSc, FRCPC - Challenging the Status Quo in Secondary Stroke Prevention: Current Perspectives on the Potential of Factor XIa Inhibition

Mike Sharma, MD, MSc, FRCPC - Challenging the Status Quo in Secondary Stroke Prevention: Current Perspectives on the Potential of Factor XIa Inhibition

Mike Sharma, MD, MSc, FRCPC - Challenging the Status Quo in Secondary Stroke Prevention: Current Perspectives on the Potential of Factor XIa Inhibition

Mike Sharma, MD, MSc, FRCPC - Challenging the Status Quo in Secondary Stroke Prevention: Current Perspectives on the Potential of Factor XIa Inhibition

Mike Sharma, MD, MSc, FRCPC - Challenging the Status Quo in Secondary Stroke Prevention: Current Perspectives on the Potential of Factor XIa Inhibition

In this episode of Tea with Dr D, host James Q. Del Rosso, DO, is joined by Christopher Bunick, MD, PhD, and later Lisa Swanson, MD, for a deep look at phosphodiesterase-4 (PDE4) inhibition in dermatology, with a special focus on topical roflumilast.  Dr Bunick opens with a primer on the science of PDE4, an enzyme that degrades cyclic AMP (cAMP), an intracellular messenger that regulates anti-inflammatory pathways. In conditions such as atopic dermatitis (AD) and psoriasis, overactive PDE4 leads to reduced cAMP and amplified inflammation. By “gumming up” PDE4, roflumilast restores a more balanced, anti-inflammatory state.  He explains why PDE4 inhibition is relevant across multiple inflammatory pathways, including Th1, Th2, and Th17, and why roflumilast has demonstrated stronger efficacy than earlier inhibitors like crisaborole. Molecularly, roflumilast mimics cyclic AMP's binding to PDE4 across 3 key sites, producing far tighter binding than apremilast and crisaborole, which translates to superior clinical potency.  Dr Bunick illustrates this with a case of palmoplantar pustular psoriasis that cleared dramatically within 8 weeks on topical roflumilast after multiple biologic and corticosteroid failures, highlighting its durability and barrier-restoring properties. He and Dr Del Rosso contrast this with the limitations of chronic steroid use, noting that roflumilast supports long-term control without barrier compromise.  The discussion also touches on vitiligo, where Dr Bunick shares an early case of repigmentation following roflumilast treatment, suggesting possible cAMP-mediated stimulation of melanogenesis. They highlight the molecule's innovative aqueous-based formulation, optimized for skin-compatible pH and excellent tolerability.  In Part 2, Dr Swanson joins to discuss pediatric use. She reviews the 0.15% cream for AD in patients ≥6 years and the 0.05% cream for ages 2–5, both once-daily, steroid-free options that minimize burning and stinging compared with earlier PDE4 inhibitors. They review clinical data that demonstrate rapid itch relief, strong efficacy across IGA and EASI end points, and sustained control with twice-weekly maintenance.  Tune in to hear how PDE4 inhibition, and particularly topical roflumilast, is redefining nonsteroidal therapy across age groups and disease states in dermatology. 

André, The Impulsive Thinker™, takes a practical look at inhibition and impulsivity in the ADHD Entrepreneur's daily life, reflecting on his discussion with Dr. Russell Ramsay. Ever wondered why hitting pause before reacting feels tough? It's not a flaw—it's just how your brain works. André shares real strategies that help tackle quick reactions, impulsive decisions, emotional triggers, and distractions. This episode breaks down inhibition as a skill you can build, not something you're missing. If you're ready to shift from reacting to responding in your life and business, tune in to find clarity and tools for ongoing progress, not perfection.  

Intravenous dihydropyridine calcium channel blockers can quietly worsen oxygenation by blunting hypoxic pulmonary vasoconstriction. In this episode, we break down the bedside mechanism, which agents are implicated, who's at highest risk (post-op atelectasis, obesity, pneumonia, focal ARDS, COPD), how soon it happens, and exactly what to do.The Vasopressor & Inotrope HandbookAmazon: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://amzn.to/47qJZe1⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ (Affiliate Link)My Store: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://eddyjoemd.myshopify.com/products/the-vasopressor-inotrope-handbook⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ (Use "podcast" to save 10%)Citations:Weir EK, López-Barneo J, Buckler KJ, Archer SL. Acute oxygen-sensing mechanisms. N Engl J Med. 2005 Nov 10;353(19):2042-55. doi: 10.1056/NEJMra050002. PMID: 16282179; PMCID: PMC2803102.Weir EK, Olschewski A. Role of ion channels in acute and chronic responses of the pulmonary vasculature to hypoxia. Cardiovasc Res. 2006 Sep 1;71(4):630-41. doi: 10.1016/j.cardiores.2006.04.014. Epub 2006 Apr 27. PMID: 16828723.Lumb AB, Slinger P. Hypoxic pulmonary vasoconstriction: physiology and anesthetic implications. Anesthesiology. 2015 Apr;122(4):932-46. doi: 10.1097/ALN.0000000000000569. PMID: 25587641.Timour G, Fréderic V, Olivier S, Shango DN. Nicardipine-induced acute respiratory failure: Case report and literature review. Clin Case Rep. 2023 May 1;11(5):e7186. doi: 10.1002/ccr3.7186. PMID: 37143457; PMCID: PMC10151601.McMurtry IF, Davidson AB, Reeves JT, Grover RF. Inhibition of hypoxic pulmonary vasoconstriction by calcium antagonists in isolated rat lungs. Circ Res. 1976 Feb;38(2):99-104. doi: 10.1161/01.RES.38.2.99. PMID: 1245025.Simonneau G, Escourrou P, Duroux P, Lockhart A. Inhibition of hypoxic pulmonary vasoconstriction by nifedipine. N Engl J Med. 1981 Jun 25;304(26):1582-5. doi: 10.1056/NEJM198106253042606. PMID: 7231503.Kennedy T, Summer W. Inhibition of hypoxic pulmonary vasoconstriction by nifedipine. Am J Cardiol. 1982 Oct;50(4):864-8. doi: 10.1016/0002-9149(82)91246-2. PMID: 7124646.Chrétien B, Decros JB, Suard F, Dolladille C, Fischer MO, Alexandre J, Descamps R. Hypoxia Associated With Dihydropyridine Calcium Channel Inhibitors: A Pharmacovigilance Study in VigiBase. Clin Pharmacol Ther. 2023 Sep;114(3):686-692. doi: 10.1002/cpt.2970. Epub 2023 Jun 29. PMID: 37309986.Burghuber OC. Nifedipine attenuates acute hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease. Respiration. 1987;52(2):86-93. doi: 10.1159/000195309. PMID: 3671896.Suard F, Mombrun M, Fischer MO, Hanouz JL, Decros JB, Derville S, Gakuba C, Al Issa G, Menard C, Chretien B, Descamps R. Oxygenation Effects of Antihypertensive Agents in Intensive Care: A Prospective Comparative Study of Nicardipine and Urapidil. Clin Pharmacol Ther. 2025 Mar;117(3):742-748. doi: 10.1002/cpt.3509. Epub 2024 Nov 27. PMID: 39604146.

In today's episode, we had the pleasure of speaking with Kevin Kalinsky, MD, MS, FASCO, about the evolving treatment paradigm for hormone receptor (HR)–positive breast cancer post-CDK4/6 inhibition, as well as the need for more advanced therapies to improve patient outcomes in this setting. Dr Kalinsky is a professor and director in the Division of Medical Oncology of the Department of Hematology and Medical Oncology at Emory University School of Medicine, as well as the director of the Glenn Family Breast Center and the Louisa and Rand Glenn Family Chair in Breast Cancer Research at Winship Cancer Institute in Atlanta, Georgia. In our exclusive interview, Dr Kalinsky discussed combination therapies that have shown promise for the management of HR-positive breast cancer following endocrine therapy, factors influencing treatment selection for patients who have received prior CDK4/6 inhibition, best practices for genomic testing in this population, and breast cancer research highlights from the 2025 ESMO Congress.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

Brad McGregor joins us on the heels of his #ESMO25 discussion of these important data in the NMIBC landscape.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-Inhibitors-Safety-and-Tolerability-Profiles/37338/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/The-Future-of-PI3K-Inhibition-in-HR-HER2-Breast-Cancer/37339/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Case-in-Point-Applying-PI3K-Combinations-in-Early-Recurrent-HR-HER2-mBC/37336/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Understanding-Endocrine-Resistance-in-HR-HER2-mBC/37323/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-inhibition-in-HR-HER2-mBC-Mechanistic-Insights/37329/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Comprehensive-Biomarker-Testing-in-mBC-Informs-Clinical-Decision-Making/37332/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Double-Take-Pivotal-Data-Evaluating-PI3K-Inhibitor-Endocrine-Therapy-Regimens-in-mBC/37333/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Triple-Threat-Key-Data-on-Simultaneous-Estrogen-CDK4-6-and-PI3K-Inhibition-in-mBC/37335/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/The-Future-of-PI3K-Inhibition-in-HR-HER2-Breast-Cancer/37339/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Understanding-Endocrine-Resistance-in-HR-HER2-mBC/37323/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-inhibition-in-HR-HER2-mBC-Mechanistic-Insights/37329/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Comprehensive-Biomarker-Testing-in-mBC-Informs-Clinical-Decision-Making/37332/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Double-Take-Pivotal-Data-Evaluating-PI3K-Inhibitor-Endocrine-Therapy-Regimens-in-mBC/37333/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Triple-Threat-Key-Data-on-Simultaneous-Estrogen-CDK4-6-and-PI3K-Inhibition-in-mBC/37335/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Case-in-Point-Applying-PI3K-Combinations-in-Early-Recurrent-HR-HER2-mBC/37336/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.

In today's episode, we had the pleasure of speaking with Asad Dean, MD, about treatment selection for patients with chronic lymphocytic leukemia (CLL) in the second-line setting. Dr Dean is a physician at the Texas Oncology-Fort Worth Cancer Center. In our exclusive interview, Dr Dean discussed the roles of covalent BTK inhibitors and BCL-2 inhibitors in the management of CLL. He highlighted the importance of molecular profiling for treatment rechallenge decisions and the potential for resistance mutations in this disease. He also noted the role of pirtobrutinib (Jaypirca) in overcoming treatment resistance, along with clinical signs indicating that patients may need a therapy change. Dr Dean also mentioned the high response rates seen with CAR T-cell therapy in patients with CLL and explained the possibility for combination regimens in CLL. Additionally, he expressed optimism about BTK degraders and bispecific antibodies.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on IL-1 Pathway Inhibition in Recurrent Pericarditis Management: Real-World Adoption of Corticosteroid Sparing in RESONANCE.

As we continue to learn more and more about arthrogenic muscle inhibition after ACL reconstruction surgery, we can continue to build better rehabilitation programs for our athletes.In this episode, the team discusses a recent review article on AMI and its impact on postoperative rehabilitation and return to sport decision-making.To see full show notes and more, head to: https://mikereinold.com/management-of-arthrogenic-muscle-inhibition/ Click Here to View My Online CoursesWant to learn more from me? I have a variety of online courses on my website!Disclaimer: This post contains affiliate links. If you make a purchase, I may receive a commission at no extra cost to you.Support the show_____Want to learn more? Check out my blog, podcasts, and online coursesFollow me: Instagram | Twitter | Facebook | Youtube