Podcasts about WNT

HUGE SHOW TONIGHT !Tonight at 9pm EST the boys are back and we'll talk Kyle's trip to @grindtimeprowrestling and air our chats with @thetreymiguel and @realdarrenmccarty from their Grand Opening#cmpunk returns and wins the #wwe undisputed championshipThen last but certainly not least it's the return of #conormcgregor and well give you our picks and predictions for the return of the notorious on at #ufc327 !FOLLOW & SUBSCRIBE – KNOCKOUTS AND 3 COUNTSBringing you the best in Combat Sports and Pro Wrestling – available everywhere!YouTube (Live Tues & Thurs 9PM EST): http://www.youtube.com/c/Knockoutsand3CountsFacebook (Live Tues & Thurs 9PM EST): https://www.facebook.com/knockoutsand3countsApple Podcasts: https://podcasts.apple.com/us/podcast/knockouts-and-3-counts/id1446923286Spotify: https://open.spotify.com/show/3OpvW0QHBe3uRc3D0pbORt?si=33935ad9669146d3Twitter/X: https://twitter.com/ko3cpodInstagram: https://www.instagram.com/ko3cpod/TikTok: https://www.tiktok.com/@ko3cpodMerch, Streams & Videos (Millions): https://millions.co/kyle-collisonIf you love what we do at KO3C, support us by grabbing merch or ordering a personal video at Millions.co.We go LIVE every Tuesday and Thursday at 9 PM EST — bringing you interviews, breakdowns, and the real talk you won't hear anywhere else.Wnt dope podcast clips ? Use our Opus Clip link : https://www.opus.pro/?via=Ko3C

HUGE SHOW TONIGHT !Tonight at 9pm EST the boys are back and we'll talk Kyle's trip to @grindtimeprowrestling and air our chats with @thetreymiguel and @realdarrenmccarty from their Grand Opening#cmpunk returns and wins the #wwe undisputed championshipThen last but certainly not least it's the return of #conormcgregor and well give you our picks and predictions for the return of the notorious on at #ufc329 !FOLLOW & SUBSCRIBE – KNOCKOUTS AND 3 COUNTSBringing you the best in Combat Sports and Pro Wrestling – available everywhere!YouTube (Live Tues & Thurs 9PM EST): http://www.youtube.com/c/Knockoutsand3CountsFacebook (Live Tues & Thurs 9PM EST): https://www.facebook.com/knockoutsand3countsApple Podcasts: https://podcasts.apple.com/us/podcast/knockouts-and-3-counts/id1446923286Spotify: https://open.spotify.com/show/3OpvW0QHBe3uRc3D0pbORt?si=33935ad9669146d3Twitter/X: https://twitter.com/ko3cpodInstagram: https://www.instagram.com/ko3cpod/TikTok: https://www.tiktok.com/@ko3cpodMerch, Streams & Videos (Millions): https://millions.co/kyle-collisonIf you love what we do at KO3C, support us by grabbing merch or ordering a personal video at Millions.co.We go LIVE every Tuesday and Thursday at 9 PM EST — bringing you interviews, breakdowns, and the real talk you won't hear anywhere else.Wnt dope podcast clips ? Use our Opus Clip link : https://www.opus.pro/?via=Ko3C

Joel Rifkin oli New Yorkin Long Islandilla asunut sarjamurhaaja, joka tappoi yhteensä ainakin 17 seksityöntekijää. Joel sai tehdä murhia rauhassa, koska poliisit eivät koskaan edes osanneet epäillä sarjamurhaajan mahdollisuutta seksityöntekijöiden kuolemissa. Osaa Joelin uhreista ei ole koskaan löydetty tai tunnistettu, vaikka hänen rikoksistaan on aikaa jo yli 30 vuotta. * Tiedäthän, että tämä kuuntelemasi jakso on podcastin aiempaa tuotantoa. Podmessa voit kuunnella kaikki Jäljillä-podcastin viimeisten vuosien jaksot. Lisäksi uunituoreita jaksoja julkaistaan Podmessa joka viikko, ja mikä parasta – ilman mainoksia. Eli jos tykkäät kuulemastasi ja haluat lisää, sitä löytyy yllin kyllin osoitteesta podme.com. Uusi throwback-jakso julkaistaan joka perjantai. Ota yhteyttä: jaljillapodcast@gmail.comInstagram: @ jaljillapodcastMusiikki: This work contains Music Track Doug Maxwell Media Right Productions - Heartbeat of the Hood that is licensed under a Creative Commons Attribution license. Source: https://directory.audio/free-music/ambient/5275-doug-maxwell-media-right-productions -heartbeat-of-the-hoodAuthor: Doug Maxwell Media Right Productions LÄHTEET:Kirja: Robert Mladinich: The Joel Rifkin Story: From the Mouth of the Monster (Pocket Books)https://www.youtube.com/watch?v=8hbRRZm6BG8&ab_channel=A%26Ehttps://www.youtube.com/watch?v=Uy2eEjef34g&ab_channel=A%26Ehttps://www.youtube.com/watch?v=v8a2tkTBgbA&ab_channel=CBSNewYorkhttps://www.youtube.com/watch?v=Z6iQHUJEHaU&ab_channel=A%26Ehttps://www.youtube.com/watch?v=8exr1pFIZRc&ab_channel=KatWoundedCougarhttps://www.researchgate.net/publication/354172602_Psychological_Profile_Assessment_of_Serial_Killer_Joel_Rifkinhttps://themillions.com/2013/04/now-she-has-a-name-when-a-serial-killer-visited-my-small-town.htmlhttps://www.oxygen.com/rifkin-on-rifkin-private-confessions-of-a-serial-killer/serial-killer-week/who-were-serial-killerhttps://www.oxygen.com/rifkin-on-rifkin-private-confessions-of-a-serial-killer/crime-news/rifkin-regrets-serial-killingshttps://www.oxygen.com/rifkin-on-rifkin-private-confessions-of-a-serial-killer/crime-news/joel-rifkin-serial-killer-avoided-capture-howhttps://www.oxygen.com/rifkin-on-rifkin-private-confessions-of-a-serial-killer/crime-news/how-joel-rifkins-mom-sisterhttps://web.archive.org/web/20051216082934/http://archives.zinester.com/56505/63063.htmlhttps://abcnews.go.com/blogs/headlines/2013/03/how-police-identified-severed-head-after-24-year-mysteryhttps://abcnews.go.com/WNT/story?id=130048&page=1https://www.crimelibrary.org/serial_killers/predators/rifkin/1.htmlhttps://troopers.ny.gov/joel-rifkin-arrest

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we delve into a series of remarkable advancements and strategic maneuvers that are shaping the future of drug development and patient care. Starting with Roche's breakthrough in oncology, their small molecule inhibitor, Divarasib, has shown promising results in a Phase 3 trial for patients with KRAS G12C-mutated non-small cell lung cancer. This trial demonstrated superior efficacy over competitors like Amgen's Lumakras and Bristol-Myers Squibb's Krazati. Historically, KRAS mutations have been difficult to target, but Divarasib's success underscores the potential of precision medicine in oncology. These findings could lead to more effective treatment options for NSCLC patients, showcasing how targeted therapies are revolutionizing cancer treatment by focusing on specific genetic mutations. In regulatory news, Vertex Pharmaceuticals has made significant strides with Casgevy (exagamglogene autotemcel), a gene therapy that now includes pediatric patients with sickle cell disease and transfusion-dependent beta thalassemia in its FDA-approved label. This marks a pivotal moment for gene therapy applications in blood disorders. Utilizing CRISPR technology, Vertex offers potentially curative solutions for debilitating conditions, signaling a new era where genetic disorders can be addressed at their root cause. Similarly, Novartis has gained European Commission approval for Itvisma to treat 5q spinal muscular atrophy in patients aged two years and older, further cementing gene therapies' role in mainstream medical practice. Strategic partnerships remain essential in driving innovation. Takeda's collaboration with Insilico Medicine on AI-driven drug discovery is a case in point. The $600 million partnership highlights the growing reliance on AI and machine learning to expedite therapeutic development processes. Platforms like Pharma.AI are being leveraged to identify novel drug candidates more efficiently. Additionally, AstraZeneca's alliance with CSPC Pharmaceutical Group to develop siRNA-based therapies for kidney diseases reflects the burgeoning interest in RNA therapeutics as these technologies open new avenues to address complex diseases. On the financial front, BridgeBio's ability to attract $1 billion in convertible preferred equity from Sixth Street and Healthcare Royalty underscores investor confidence in rare disease therapeutics. This funding will bolster its pipeline targeting cardiovascular and rare conditions, emphasizing the profitable potential found within niche markets of the pharmaceutical landscape. Manufacturing is also seeing expansion as Lonza deepens its partnership with an unnamed U.S. drugmaker to enhance biologics programs. Anticipated investments reaching into multi-billion Swiss Francs underscore the critical importance of robust manufacturing infrastructure to meet growing demands for biologics and antibody-drug conjugates. Clinical trials continue to yield promising results. Can-Fite Biopharma's Phase 2a trial for Namodenoson in treating advanced pancreatic ductal adenocarcinoma has shown promising survival data when combined with therapies targeting Wnt/β-catenin signaling pathways. At the same time, Otsuka's Phase 3 data for Voyxact (sibeprenlimab-szsi) demonstrated improved kidney function in patients with immunoglobulin A nephropathy, bolstering traditional FDA approval pathways. On the acquisitions front, GNI Group's acquisition of Ayumi Pharmaceutical for approximately JPY 44.8 billion highlights strategic moves to enhance global biopharma operations focusing on pain management solutions. Yet not all news is positive; Sanofi's Genzyme Ireland unit received an FDA warning letter regarding manufacturing violations related to Altuviiio production, pointing to ongoing regulatory challenges within production practices. Moving on to geopolitical considerations, recent congressional letters to major pharmaceutical CEOs have raised concerns about clinical trials conducted within China due to national security concerns. This tension illustrates the delicate balance between leveraging China's economic potential and safeguarding US interests—a critical issue as international collaborations continue to expand. Meanwhile, AstraZeneca's ongoing collaborations with CSPC Pharmaceutical Group further signify strategic bets on China's capabilities despite geopolitical tensions. Their joint efforts focus on kidney disease treatments while adding to existing agreements addressing obesity and chronic diseases. The FDA remains pivotal as key decisions anticipated this quarter could significantly influence investment strategies and research priorities. This includes revisiting applications previously delayed or rejected—decisions that could reshape industry dynamics. In conclusion, this dynamic landscape is marked by significant scientific breakthroughs and complex global interactions guiding pharmaceutical and biotech sectors toward a transformative era. Gene therapy advancements underscore progress in personalized medicine while geopolitical factors continue influencing strategic industry decisions. As regulatory bodies evolve their approaches alongside increasingly international partnerships, these developments collectively herald profound implications for drug development and patient care globally.Support the show

BUFFALO, NY — June 29, 2026 — A new #review was #published in Volume 18 of Aging on May 30, 2026, titled “The love and hate relationship between cellular senescence and stemness.” The review was led by first author Angelos Papaspyropoulos and corresponding author Vassilis G. Gorgoulis from the National and Kapodistrian University of Athens and the Biomedical Research Foundation of the Academy of Athens, Greece. Cellular senescence and stemness have traditionally been viewed as biological opposites. Senescent cells permanently stop dividing in response to cellular stress, helping prevent the spread of damaged cells, while stem cells maintain tissue repair by continuously renewing themselves and generating specialized cells. However, growing evidence suggests that the relationship between these two biological processes is far more complex and depends on the tissue type, physiological conditions, and disease context. In this review, the authors summarize recent research examining how senescence and stemness interact across normal tissues, aging, regeneration, and cancer. Rather than always opposing one another, the two processes can either suppress or reinforce each other depending on the biological setting. Under normal physiological conditions, senescence often limits stem cell activity. The review highlights studies showing that excessive senescence can impair the regenerative capacity of mesenchymal stem cells, muscle satellite cells, dental pulp stem cells, and pancreatic β-cell progenitors. In several experimental models, reducing senescence restored stem cell function and improved tissue regeneration. At the molecular level, multiple signaling pathways contribute to this balance, including the p53/p21 and p16INK4A/RB pathways, mTOR signaling, Wnt/β-catenin signaling, and the senescence-associated secretory phenotype (SASP). These pathways help determine whether cells maintain regenerative potential or enter a stable senescent state. The review also emphasizes that the relationship changes dramatically in cancer. In many tumors, senescent cells can promote the emergence of cancer stem cells through inflammatory signals released as part of the SASP or through cells escaping from the senescent state. This interaction has been reported in several malignancies, including B-cell lymphoma, liver cancer, colon cancer, lung cancer, and breast cancer, where stem cell-like properties may contribute to tumor progression, metastasis, and resistance to therapy. Full press release - https://www.aging-us.com/news-room/cellular-senescence-and-stem-cells-share-a-more-complex-relationship-than-previously-recognized DOI - https://doi.org/10.18632/aging.206387 Corresponding author - Vassilis G. Gorgoulis - vgorg@med.uoa.gr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206387 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, stemness To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Hair loss has many drivers — oxidative stress, aging, medication side effects, and disrupted stem cell signaling among them. A 2026 study published in Aging examined whether methylene blue, a century-old FDA-approved compound, could address several of these simultaneously at the follicle stem cell level.Researchers found methylene blue reduced reactive oxygen species in hair follicle stem cells, activated the Wnt/β-catenin signaling pathway critical for hair regeneration, and accelerated wound closure in follicle cultures. Combined with minoxidil, the two compounds synergistically enhanced stem cell signaling beyond what either achieved alone. The compound also preserved hair follicle stem cell viability under metabolic stress conditions that otherwise caused significant cell death.One notable finding: combining methylene blue with vitamins A or C reduced its regenerative signaling effect — suggesting antioxidant combinations require careful consideration.This was an in vitro study. In vivo and clinical validation are needed before recommendations can be made.

In this solo episode on androgenic alopecia, the host explains that hair loss is slow and progressive, driven largely by genetics and DHT-mediated miniaturization of follicles across the anagen, catagen, and telogen cycle, and stresses early detection using periodic photos of the temples, hairline/vertex, and crown. He frames hair growth as a "battle" between Wnt signaling (promotes growth and anagen entry via stem cell activation) and DHT signaling (suppresses Wnt and increases inhibitors like DKK, TGF-beta, and PGD2), noting advanced loss involves inflammation, fibrosis, and irreversible follicle loss. He reviews contributors like poor scalp blood flow, iron deficiency (most evidence), possible zinc/B12/folate deficiency, thyroid dysfunction, and insulin resistance, then covers treatments: finasteride (oral and topical) and dutasteride as DHT blockers with potential systemic side effects, plus minoxidil and microneedling (home vs professional) as key options, with add-ons like ketoconazole shampoo, PRP, red light, and cautions about anabolic steroids and high-dose testosterone increasing DHT pressure.   Hair loss diagnosis and treatment https://www.aad.org/public/diseases/hair-loss/treatment/diagnosis-treat Androgenetic alopecia https://medlineplus.gov/genetics/condition/androgenetic-alopecia/ DHT and WNT signaling https://pubmed.ncbi.nlm.nih.gov/29549490/ Finasteride https://medlineplus.gov/druginfo/meds/a698016.html Topical finasteride https://pmc.ncbi.nlm.nih.gov/articles/PMC6609098/ FDA warning on compounded topical finasteride https://www.fda.gov/drugs/human-drug-compounding/fda-alerts-health-care-providers-compounders-and-consumers-potential-risks-associated-compounded Post-finasteride syndrome https://pubmed.ncbi.nlm.nih.gov/35983808/ Dutasteride https://medlineplus.gov/druginfo/meds/a603001.html Minoxidil https://www.aad.org/public/diseases/hair-loss/treatment/diagnosis-treat Microneedling for hair loss https://pubmed.ncbi.nlm.nih.gov/23960389/ Ketoconazole shampoo https://pubmed.ncbi.nlm.nih.gov/31858672/ Topical caffeine https://pubmed.ncbi.nlm.nih.gov/39997270/ Pumpkin seed oil https://pubmed.ncbi.nlm.nih.gov/24864154/ PRP for hair loss https://pubmed.ncbi.nlm.nih.gov/30882509/ Red light / low-level light therapy https://pmc.ncbi.nlm.nih.gov/articles/PMC8906269/ Stem cells / exosomes for hair growth https://pmc.ncbi.nlm.nih.gov/articles/PMC12433634/ Iron, zinc, B12, and folate deficiencies https://pmc.ncbi.nlm.nih.gov/articles/PMC6380979/ Thyroid testing https://medlineplus.gov/thyroidtests.html Insulin resistance / metabolic syndrome https://medlineplus.gov/metabolicsyndrome.html Testosterone / TRT https://medlineplus.gov/druginfo/meds/a605020.html Tretinoin https://medlineplus.gov/druginfo/meds/a682437.html Anastrozole / Arimidex https://medlineplus.gov/druginfo/meds/a696018.html Anabolic steroids https://nida.nih.gov/research-topics/anabolic-steroids   Show Notes 00:00 Welcome to the Hart2Heart Podcast 00:56 What Is Androgenic Alopecia 02:17 Hair Follicle Life Cycle 03:55 Miniaturization and Early Detection 06:51 DHT Basics and Other Causes 09:27 WNT Versus DHT Explained 13:10 Nutrients Thyroid and Insulin 16:26 Finasteride Benefits and Risks 19:21 Topical Finasteride and Dutasteride 25:01 Minoxidil Growth Booster 27:19 Microneedling for WNT Activation 30:21 Extra Treatments and Add Ons 37:04 Testosterone TRT and Steroids 40:16 Wrap Up and Key Takeaways   The Hart2Heart podcast is hosted by family physician Dr. Michael Hart, who is dedicated to cutting through the noise and uncovering the most effective strategies for optimizing health, longevity, and peak performance. This podcast dives deep into evidence-based approaches to hormone balance, peptides, sleep optimization, nutrition, psychedelics, supplements, exercise protocols, leveraging sunlight, and de-prescribing pharmaceuticals — using medications only when absolutely necessary. Beyond health science, we explore the intersection of public health and politics, exposing how policy decisions shape our health landscape and what actionable steps people can take to reclaim control over their well-being. Guests range from out-of-the-box thinking physicians such as Dr. Casey Means (author of "Good Energy") and Dr. Roger Sehult (Medcram lectures) to public health experts such as Dr. Jay Bhattacharya (Director of the National Institutes of Health (NIH) and Dr. Marty Mckary  (Commissioner of the Food and Drug Administration (FDA) and high-profile names such as  Zuby and Mark Sisson (Primal Blueprint and Primal Kitchen). If you're ready to take control of your health and performance, this podcast is for you.We cut through the jargon and deliver practical, no-BS advice that you can implement in your daily life, empowering you to make positive changes for your well-being. Connect with Dr. Mike Hart Instagram: @drmikehart Twitter: @drmikehart Facebook: @drmikehart

This week's stories: *Mud Playgrounds Double Kids' Bacterial Diversity and Spike Immune Genes 30% Finland swapped rubber playground surfaces for natural soil and mud across eight kindergartens — and after just one month, kids in dirt had twice the bacterial species diversity on their skin and a 30% increase in expression of ten immune-related genes. Dave breaks down why your immune system requires microbial exposure to calibrate properly, what the hygiene hypothesis actually means for adults, and the dead-simple weekly habit that primes your innate immunity the same way. Sources: https://creators.yahoo.com/lifestyle/story/finland-replaced-artificial-playground-surfaces-with-natural-elements-like-mud-and-soil--and-the-results-surprised-even-researchers-184318556.html https://www.sciencedaily.com/releases/2026/04/mud-playground-immunity.htm *Mixing Exercise Types Cuts All-Cause Mortality Up to 40% in 170,000-Person Study A 30-year BMJ Medicine cohort study found that people who rotate at least three different types of exercise weekly see 19 to 40% lower all-cause mortality — and that benefit held independent of total training volume. Dave explains why variety is a distinct biological signal, not a motivation trick, and why grinding more of the same thing is leaving longevity gains on the table. Sources: https://bmjmedicine.bmj.com/content/early/2026/04/26/bmjmed-2025-001513 https://www.sciencedaily.com/releases/2026/04/260426012305.htm https://www.theguardian.com/society/2026/apr/26/exercise-diversity-mortality *Facial Aging Rate from Photos Predicts Cancer Survival Better Than Blood Biomarkers AI analysis of serial facial photos in 1,000+ cancer patients found that computed facial aging rate independently predicted five-year survival with a hazard ratio of 2.1 — outperforming CRP and other standard blood markers. Dave covers what the AI is actually reading in those photos, why your face is a more accurate biological ledger than most labs your doctor orders, and the free monthly habit that turns this into an early warning system. Sources: https://medicalxpress.com/news/2026-04-photos-reveal-faster-biological-aging.html https://www.nature.com/articles/s43587-026-00123-4 *Vibration Vest OsteoBoost Mimics Weight-Bearing Exercise to Rebuild Bone Density OsteoBoost raised $8M for a wearable vest delivering 30–50Hz vibrations to the spine and hips, triggering the same Wnt/β-catenin osteoblast pathway activated by mechanical loading — with early trials showing 2–5% bone mineral density gains in six months. Dave makes the case forwhy bone loss is one of the most underrated aging crises in the biohacking community, and who should be watching this category closely. Sources: https://longevity.technology/news/osteoboost-raises-8m-to-scale-bone-wearable/ https://www.crunchbase.com/organization/osteoboost *10+ States Advance Raw Milk Bills as H5N1 Hits 100+ Dairy Herds Legislation expanding raw milk access is moving in Arizona, Iowa, New Hampshire, and elsewhere — while the CDC flags H5N1 in over a hundred dairy herds with documented aerosol transmission concerns. Dave gives an honest read on where the freedom argument, the microbiome argument, and the current risk calculus actually stand in April 2026, and what more rigorous sourcing looks like right now. Sources: https://www.yahoo.com/news/articles/us-med--raw-milk-legislation-120124275.html https://www.cdc.gov/flu/avianflu/dairy.htm This episode is designed for biohackers, longevity seekers, and high-performance listeners who want mechanism-level clarity on immune priming, exercise science, biological age tracking, bone health, and real food risk assessment. Host Dave Asprey connects emerging clinical research, large-scale cohort data, and real-world protocols into actionable frameworks for extending healthspan and sharpening performance. New episodes every Tuesday, Thursday, Friday, and Sunday. Keywords: mud playground immune system microbiome, soil bacteria skin diversity, hygiene hypothesis biohacking, exercise variety longevity, BMJ exercise mortality study, mixed training lifespan, facial aging rate cancer survival, biological age face AI, facial photo biomarker longevity, OsteoBoost vibration vest bone density, whole body vibration osteoporosis, bone mineral density wearable, raw milk H5N1 bird flu, raw milk legislation 2026, raw dairy safety biohacking, biohacking news, longevity research 2026, Dave Asprey weekly roundup Thank you to our sponsors! - KILLSwitch | If you're ready for the best sleep of your life, order now at https://www.switchsupplements.com/and use code DAVE for 20% off - Puori | Go to Puori.com/DAVE or use code DAVE at checkout to get 32% off your Puori Fish Oil subscription. You save more than $18. - iRestore | Reverse hair loss at www.irestore.com/DAVE and get exclusive savings on the iRestore Elite, use code DAVE Resources: • Get My 2026 Clean Nicotine Roadmap | Enroll for free at https://daveasprey.com/2026-clean-nicotine-roadmap/ • Get My 2026 Biohacking Trends Report: https://daveasprey.com/2026-biohacking-trends-report/ • Dave Asprey's Latest News | Go to https://daveasprey.com/ to join Inside Track today. • Danger Coffee: https://dangercoffee.com/discount/dave15 • My Daily Supplements: SuppGrade Labs (15% Off) • Favorite Blue Light Blocking Glasses: TrueDark (15% Off) • Dave Asprey's BEYOND Conference: https://beyondconference.com • Dave Asprey's New Book – Heavily Meditated: https://daveasprey.com/heavily-meditated • Join My Substack (Live Access To Podcast Recordings): https://substack.daveasprey.com/ • Upgrade Labs: https://upgradelabs.com Timestamps: 00:00 – Intro 00:20 – Dirt & Immune Training 02:22 – Exercise Variety & Longevity 04:16 – Facial Aging as a Health Biomarker 05:47 – Bone Loss & Vibration Tech 07:31 – Raw Milk & H5N1 Risk 09:20 – The Wrapup See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

On this episode, Payton dives into the case of Nancy DePriest. What began as a normal shift alone at Pizza Hut quickly spiraled into something far more sinister. Links: Patreon: https://www.patreon.com/murderwithmyhusband Netflix: https://www.netflix.com/murderwithmyhusband NEW MERCH LINK: https://mwmhshop.com Discount Codes: https://mailchi.mp/c6f48670aeac/oh-no-media-discount-codes Twitch: twitch.tv/throatypie Instagram: https://www.instagram.com/paytonmorelandshow/ Discount Codes: https://mailchi.mp/c6f48670aeac/oh-no-media-discount-codes Watch on Youtube: https://www.youtube.com/channel/UCUbh-B5Or9CT8Hutw1wfYqQ Listen on Apple: https://podcasts.apple.com/us/podcast/into-the-dark/id1662304327 Listen on spotify: https://open.spotify.com/show/36SDVKB2MEWpFGVs9kRgQ7 Case Sources: LA Times - https://www.latimes.com/archives/la-xpm-2006-jun-21-me-confess21-story.html   The National Registry of Exonerations - https://exonerationregistry.org/cases/10386  ABC News - https://abcnews.go.com/WNT/story?id=131312&page=1  CATO Institute - https://www.cato.org/regulation/summer-2017/price-injustice#  Innocence Project - https://innocenceproject.org/cases/richard-danziger/  Bluhm Legal Clinic - https://www.law.northwestern.edu/legalclinic/wrongfulconvictions/exonerations/tx/christopher-ochoa.html  WV Innocence Project - https://wvinnocenceproject.law.wvu.edu/innocence-project-blog/our-voices/2018/09/24/the-guilty-plea-problem-by-threat-of-lethal-injection   The Marshall Project - https://www.themarshallproject.org/2017/03/09/facing-her-daughter-s-killer-at-last  Salon - https://www.salon.com/2000/10/31/ochoa/  https://www.salon.com/2000/10/13/texas_10/  Justia U.S. Law - https://law.justia.com/cases/texas/third-court-of-appeals/1991/4881.html   Learn more about your ad choices. Visit podcastchoices.com/adchoices

We love to hear from our listeners. Send us a message. On this week's episode of the Business of Biotech we speak with Rahul Aras, Ph.D., President and CEO at Iterion Therapeutics, about capital efficient drug development in oncology and progressing a novel therapeutic with relatively small funding amounts. Iterion is a clinical stage company developing cancer therapeutics targeting the Wnt/β-catenin pathway, a known signaling target in oncology, but one that has confounded drug development efforts for decades. Rahul talks about his path from academia to company building and early work in gene therapy, Iterion's partnership strategy, and operating a biotech in the Houston, Texas clinical hub. Access this and hundreds of episodes of the Business of Biotech videocast under the Business of Biotech tab at lifescienceleader.com. Subscribe to our monthly Business of Biotech newsletter. Get in touch with guest and topic suggestions: ben.comer@lifescienceleader.comFind Ben Comer on LinkedIn: https://www.linkedin.com/in/bencomer/

It's Monday, and that means an Extended Newsround! Join Eoin Sheahan, Arthur O'Dea, Stephen Doyle, Tommy Walsh and Ben Symes as they bring you through all the biggest sporting stories from the weekend, including a tough loss for the WNT, a crazy day of 6 Nations rugby, and the beginning of the new F1 season, as well as look ahead to tonight's game between Shelbourne and Shamrock Rovers. Tommy Rooney is with us from 7:30pm to chat through the hurling action from the weekendViagra Connect 50mg film-coated tablets. Contains sildenafil. For adult men with erectile dysfunction. Subject to suitability. Maximum dosage one 50mg tablet per day. Always read the label.

This Biotech CEO Is Creating Advanced & Personalized Therapies To Fight Cancer.Full Name: Thomas JensenTitle: Chief Executive Officer, Allarity Therapeutics Ticker: $ALLRWebsite: https://www.allarity.com/Bio:Thomas Jensen is the Chief Executive Officer of Allarity Therapeutics (NASDAQ: ALLR), a clinical-stage biopharmaceutical company advancing personalized cancer therapies. He was appointed CEO in December 2023 after nearly a decade as Chief Technology Officer, during which he helped pioneer the company's proprietary Drug Response Predictor (DRP®) platform.With over 20 years in the biotech and precision medicine space, Thomas has led Allarity through a focused strategic transformation centered on stenoparib—a first-in-class dual PARP/tankyrase inhibitor currently in Phase 2 trials for advanced ovarian cancer. Under his leadership, Allarity has achieved FDA Fast Track designation, formed key research collaborations, and presented clinical data showing landmark median overall survival of ovarian cancer patients.Company Bio:Allarity Therapeutics (NASDAQ: ALLR) is a clinical-stage biopharma company developing personalized cancer treatments guided by its proprietary DRP® companion diagnostic platform. The company's lead asset, stenoparib, is a novel, orally available dual PARP and WNT pathway inhibitor being evaluated in Phase 2 trials for advanced ovarian cancer. With headquarters in the U.S. and a research facility in Denmark, Allarity is committed to improving patient outcomes through precision oncology. Learn more at www.allarity.com

SDH AM has your Reaction Monday to start your week929TheGame's AbeGordon talks ATLUTD as preseason camp is a week inSoccerforUSPod's Bart Keeler visits on US Soccer (MNT and WNT) plus cards and calls from the weekendKCStar's Daniel Sperry has our preseason look at everything KC- both Sporting and CurrentPlus, the AFCON final, OFC's Pro League begins, and coaches are under fire in England

Welcome to the 33rd episode of The Brain Podcast - the official podcast of the journals Brain and Brain Communications.  This episode features a discussion with first author Dr Courtney R Benoit and senior author Associate Professor Tracy L Young-Pearse of the Brain article entitled: POU3F2 regulates canonical Wnt signalling via SOX13 and ADNP to expand the neural progenitor population We discuss a complex but important topic examining underlying mechanisms of neurodevelopmental and neuropsychiatric disorders, specifically the regulation of canonical Wnt signalling pathway. The authors describe how two autism-related genes, ADNP and POU3F2, are linked through loss-of-function mutations in the transcription factor POU3F2 and how this may contribute to abnormal neurodevelopment. Check out the full article on the Brain website as part of the December 2025 issue: https://doi.org/10.1093/brain/awaf221 This episode was co-hosted, edited and produced by Chaitra Sathyaprakash and Andreas Thermistocleous, edited and produced by Chaitra and Xin You Tai, co-produced by Antonia Johnston, original music by Ammar Al-Chalabi.

Colorectal cancer (CRC) remains the second leading cause of cancer-related deaths globally. While early detection significantly improves outcomes, many patients are diagnosed at advanced stages when treatment options are limited and relapse is common. To address this challenge, researchers are exploring whether existing drugs can be repurposed for cancer therapy, a strategy that could accelerate drug development while reducing associated costs and risks. One class of drugs under investigation is statins, commonly prescribed to reduce cholesterol and prevent cardiovascular disease. Several studies have observed a potential link between elevated cholesterol and increased CRC risk. Cholesterol may support tumor growth by promoting membrane synthesis and energy metabolism in rapidly dividing cells. Building on this connection, researchers from leading Indian institutions, including the Indian Institute of Science Education and Research and the Center of Excellence in Epigenetics at Shiv Nadar Institution of Eminence, investigated how statins influence CRC cells at the molecular level. Their goal was to determine whether these widely used drugs could have a therapeutic role in oncology. The Study: Investigating the Molecular Impact of Statins in CRC Cells The study, titled “Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer,” was published in Oncotarget (Volume 16). Using a combination of lipidomics, transcriptomics, proteomics, and 3D tumor models, the researchers explored how two widely prescribed statins, atorvastatin and simvastatin, affect molecular pathways associated with CRC progression. This integrative, multi-omics strategy enabled tracing statin-induced effects across different layers of cellular function, linking lipid, transcript, and protein changes to pathway-level shifts. Full blog - https://www.oncotarget.org/2025/12/03/repurposing-statins-exploring-anti-tumor-effects-in-colorectal-cancer/ Paper DOI - https://doi.org/10.18632/oncotarget.28755 Correspondence to - Sanjeev Galande - sanjeev.galande@snu.edu.in Abstract video - https://www.youtube.com/watch?v=A95ICULaH3Y Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28755 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, colorectal cancer, statins, SATB1, Wnt/β-catenin signaling, tumor-suppressive phenotype To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

In this episode, LDG interviews with Brooklyn FC + Italy U-23 WNT midfielder Alice Barbieri!Alice talks all about her move to Brooklyn FC, her earliest soccer memories, her experience playing in Serie A Femenile against some of the world's best players as a new professional, and so much more!She also elaborates on what was appealing to her about playing in the Gainbridge Super League, what it means to her to give back to her community by training young soccer players, why she is so proud to represent Italy internationally, how she has acclimated so quickly to the Brooklyn FC system, and her expeirence with Brooklyn FC in the Gainbridge Super League so far.In the rapid-fire section, we get to learn more about Alice and Brooklyn FC off the pitch, such as a match Alice would love to relive, her ideal partner for a TikTok dance with Brooklyn FC, who the team's DJ is in the Brooklyn FC locker room, and so much more!Cover Art Image Credit: Brooklyn FCThank you for listening! Remember to follow us wherever you get your podcasts, on Instagram (@the_womens_soccer_podcast) and Bluesky (@thewomenssoccerpod.bsky.social). In addition, leave a 5-star review and tell all your friends about our show!

Will O'Callaghan is joined by Cathal Mulraney and David Wilson as they take you through today's big news stories from the world of sport following a night where the Republic of Ireland's WNT overcame Belgium on aggregate following a late Abbie Larkin goal and Keith Andrew's Brentford won comfortably in the EFL Cup. Tonight also features more action from the EFL Cup including the high-profile Newcastle United vs Tottenham Hotspur tie and Shamrock Rovers have another chance to win the League of Ireland Premier Division with a win over Galway United in Tallaght Stadium. The Newsround is presented by UPMC #GetBackInAction

In this episode of JCO PO Article Insights, host Dr. Jiasen He summarizes the article, "Somatic Mutation Profiles of Colorectal Cancer by Birth Cohort" by Gilad, et al published October 11, 2025. TRANSCRIPT Jiasen He: Hello, and welcome to the JCO Precision Oncology Article Insights. I am your host, Jiasen He, and today, we will be discussing the JCO Precision Oncology article, "Somatic Mutation Profiles of Colorectal Cancer by Birth Cohort," by Dr. Gilad and colleagues. Early-onset colorectal cancer is defined as colorectal cancer diagnosed before the age of 50. Several reports have suggested that early-onset colorectal cancer has unique characteristics. Compared with late-onset colorectal cancer, early-onset colorectal cancer cases are more commonly found in the distal colon or rectum, tend to be diagnosed at more advanced stages, and may display unfavorable histologic features. Although the overall incidence of colorectal cancer has declined in recent decades, the incidence of early-onset colorectal cancer continues to rise. This increase appears to be driven by birth cohort effects. The reasons behind this rise remain unclear but are likely multifactorial, involving changes in demographics, diet, lifestyle, environmental exposures, and genetic predisposition. At the same time, studies have shown conflicting results regarding whether there are differences in the mutation profiles between early-onset and late-onset colorectal cancer. Therefore, it is crucial to explore whether colorectal cancer somatic mutational landscape differs across birth cohorts, as this could provide important insight into generational shifts in colorectal cancer incidence. To address this question, the authors conducted a retrospective study to characterize the mutation spectrum of colorectal cancer across different birth cohorts. Consecutive colorectal cancer patients who underwent somatic next-generation sequencing at the University of Chicago pathology laboratory between 2015 and 2022 were retrospectively identified. Tumors were tested for 154 to 168 genes and categorized as either microsatellite stable or high according to established thresholds. Patients with hereditary cancer syndromes or inflammatory bowel disease were excluded. Participants were then grouped into birth cohorts by decades, as well as into two major groups: those born before 1960 and after 1960. Genes that were identified in at least 5% of the sample were selected and grouped into 10 canonical cancer signaling pathways. These genes and pathways were then included in the analysis to explore their association with colorectal cancer across different birth cohorts and age groups. A total of 369 patients were included in the study, with a median birth year of 1955 and a median age at colorectal cancer diagnosis of 62.9 years. 5.4% were identified as having microsatellite-high tumors. The median tumor mutational burden was 5 mutations per megabase for microsatellite-stable tumors and 57.7 mutations per megabase for microsatellite-high tumors. Patients with microsatellite-high tumors tended to have earlier birth years and were diagnosed at an older age. However, after adjusting for potential confounders, neither birth year nor age remained statistically significant. Similarly, after controlling for confounders, no significant associations were observed between birth year or age and mutation burden. In this cohort, APC, TP53, and KRAS were the most frequently mutated genes. No statistically significant differences in the prevalence of gene mutations were observed across birth cohorts. Correspondingly, the most affected signaling pathways were the Wnt, TP53, and (RTK)/RAS pathways. Similar to the gene-level finding, no significant differences in the prevalence of these pathways were identified among birth cohorts. When examining patients born before and after 1960, the authors found that the older birth cohorts were diagnosed at an older age and had higher tumor mutational burden. However, no significant differences were observed in any of the genes or pathways analyzed. Among microsatellite-stable tumors, 18.3% were classified as early-onset colorectal cancer, while 81.1% were late-onset colorectal cancer. Consistent with previous reports, early-onset colorectal cancers in this cohort were more likely to be left-sided and more common among more recent birth cohorts. However, no significant differences were identified in any of the examined genes or pathways when comparing early-onset to late-onset colorectal cancer. In this cohort, a higher prevalence of early-onset colorectal cancer was observed among more recent birth cohorts, consistent with previous reports. Still, no distinct mutational signature was identified between the early and late birth cohorts. The authors proposed that the lack of distinct mutational profile by age or birth cohort may be due to the limited number of key molecular pathways driving colorectal cancer. Although environmental exposures likely differ across generations, the downstream effects may have converged on similar biological mechanisms, leading to comparable somatic mutations across cohorts. Alternately, they proposed that the observed birth cohort differences in colorectal incidence may be driven by distinct mutation signatures, epigenetic alterations, or changes in the immune microenvironment rather than variations in canonical gene mutations. As the authors noted, given the retrospective nature of this study, its modest sample size, and the predominance of advanced-stage tumors, larger prospective studies are needed to validate these findings. In summary, this study found no significant differences in the mutational landscape of colorectal cancer across birth cohorts or age groups. The authors proposed that the generational shift in colorectal cancer incidence is unlikely to be driven by changes in the underlying tumor genomics. However, larger prospective studies are needed to validate these findings. Thank you for tuning in to JCO Precision Oncology Article Insights. Do not forget to subscribe and join us next time as we explore more groundbreaking research shaping the future of oncology. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.

Send me a text! I'd LOVE to hear your feedback on this episode!Important Links:To try this breakthrough formulation, go to www.qualialife.com/SANDYK15 or use SANDYK15 at https://www.qualialife.com/Follow me on Instagram:  https://www.instagram.com/sandyknutrition/?hl=enFollow me on Substack:  https://sandykruse.substack.com/Dr. Dan Pardi is the Chief Health Officer at Qualia Life Sciences, where he leads education to advance healthspan and peak performance. He's the founder of humanOS.me and host of humanOS Radio, the official podcast of the Sleep Research Society. Dan has advised elite military units, Fortune 500 companies, and startups through his consultancy, Vivendi Health. He holds a PhD in Cognitive Neuroscience from Leiden University and Stanford, and speaks regularly at events like TEDx, VC Firms, and the Institute for Human Machine Cognition.Think of your body's repair crew as always on call, rarely on stage. Stem cells sit quietly in protective niches until growth factors wake them, chemokines guide them to damaged tissue, and local signals shape them into exactly what's needed. We invited Dr. Dan Pardi, Chief Health Officer at Qualia Life Sciences, to break down that invisible choreography—why it weakens with age and how to support it without pushing the system into overdrive.We start by making stem cells simple: potency tiers, key types like hematopoietic and mesenchymal, and what “exhaustion” really means. Dan explains how inflammation, mitochondrial dysfunction, and epigenetic drift—core hallmarks of aging—distort the niche and blunt self-renewal. From there, we map the full life cycle: quiescence, activation, mobilization, migration, and differentiation guided by ancient pathways like Wnt, Notch, and Sonic Hedgehog. Understanding this sequence clarifies the therapy landscape, from evidence-backed marrow transplants to targeted orthopedic injections, and why unproven IV offerings can be risky.If you care about healthy aging, joint health, recovery, and evidence-based wellness, this conversation offers a grounded roadmap. We keep the science clear, the hype in check, and the focus on balance—protect, pulse, and let biology do its best work. Subscribe, share with a friend who lifts or runs, and leave a review to help others find the show. What would you most want to regenerate first?Support the showPlease rate & review my podcast with a few kind words on Apple or Spotify. Subscribe wherever you listen, share this episode with a friend, and follow me below. This truly gives back & helps me keep bringing amazing guests & topics every week.Instagram: https://www.instagram.com/sandyknutrition/Facebook Page: https://www.facebook.com/sandyknutritionTikTok: https://www.tiktok.com/@sandyknutritionYouTube: https://www.youtube.com/channel/UCIh48ov-SgbSUXsVeLL2qAgRumble: https://rumble.com/c/c-5461001Linkedin: https://www.linkedin.com/in/sandyknutrition/Substack: https://sandykruse.substack.com/Podcast Website: https://sandykruse.ca

After a tricky few weeks for the FAI, their CEO David Courell sat down with OTB's Nathan Murphy on Friday. Together they discussed the future of embattled senior men's manager Heimir Hallgrimsson, the pay dispute involving former WNT boss Eileen Gleeson, and the ongoing row with SIPTU.

Endocrinologist Joy Wu says that osteoporosis can affect more than half of women and a quarter of men over 50 – often without symptoms until a fracture changes everything, leading to a loss of mobility and independence. Wu explains why bones weaken with age and how to strengthen them through exercise and smart medicine. Her lab is exploring innovative drugs and turning skin cells into new bone-forming osteoblasts. We're delving into the great mystery of building new bone and making old bones stronger, Wu tells host Russ Altman on this episode of Stanford Engineering's The Future of Everything podcast.Have a question for Russ? Send it our way in writing or via voice memo, and it might be featured on an upcoming episode. Please introduce yourself, let us know where you're listening from, and share your question. You can send questions to thefutureofeverything@stanford.edu.Episode Reference Links:Stanford Profile: Joy WuConnect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>> Twitter/X / Instagram / LinkedIn / FacebookChapters:(00:00:00) IntroductionRuss Altman introduces guest Joy Wu, a professor of endocrinology at Stanford University.(00:03:06) Path into Bone ResearchJoy shares her path from endocrinology training to studying bone biology.(00:04:10) Calcium and Vitamin D in Bone HealthHow these nutrients build strong bones and prevent fractures.(00:05:13) Why Bones Heal ThemselvesWhy bones can regenerate so effectively compared to other tissues.(00:06:26) Can We Feel Our Bones?The mystery of weather-related aches at old fracture sites.(00:07:23) Understanding OsteoporosisThe prevalence of osteoporosis in the elderly, especially in women.(00:08:34) Diagnosing OsteoporosisWhy osteoporosis often goes undetected until fractures appear.(00:09:36) Risk Factors Beyond AgingThe risk factors outside of aging that can lead to osteoporosis.(00:10:48) Steroids, Exercise, and Bone HealthThe impact of systemic steroids and exercise on bone health.(00:12:40) Height Loss and Spine FracturesHow shrinking height in older adults can signal vertebral fractures.(00:14:46) Cancer and Bone HealthHow cancers spread to bone and how therapies affect bone health.(00:17:09) Medications for OsteoporosisThe complexities of using certain medications in cancer patients with bone loss.(00:20:10) Hormones and Bone GrowthUsing SERMs to protect bone while reducing breast cancer risk.(00:21:45) Stem Cells and Building BoneResearch on reprogramming skin cells into bone-forming osteoblasts.(00:23:31) Why Treatments PlateauWhy bone-building drugs stop working after two years.(00:24:49) Challenges in Bone RegenerationThe potential of Wnt signalling and stem cells in lasting bone regeneration.(00:28:09) Validating Osteoblasts in the LabTesting whether reprogrammed cells behave like natural osteoblasts.(00:29:11) Future Outlook for Bone BiologyThe limits of bone cell replication and what it means for future therapies.(00:30:10) Advice for Strong BonesPractical do's and don'ts for optimizing bone health.(00:32:41) Conclusion Connect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>>Twitter/X / Instagram / LinkedIn / Facebook

Aiden Deacon from the University of Minnesota-Twin Cities, Minneapolis, discusses a research paper he co-authored that was published in Volume 16 of Oncotarget, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.” DOI - https://doi.org/10.18632/oncotarget.28758 Correspondence to - Justin Hwang - jhwang@umn.edu Video interview - https://www.youtube.com/watch?v=OXKhWWU1gnY Abstract This study investigates the R-spondin family of genes (RSPO1/2/3/4), a group of secreted proteins that act as Wnt regulators, and their subsequent role in advanced prostate cancer (PC). When evaluating transcriptomic data from primary and metastatic PC patients, we found that alterations in RSPO2 were more prevalent than in other RSPO family members or Wnt-regulating genes APC and CTNNB1. Further, we found that RSPO2 alterations in PCs were significantly associated with worse disease-free survival. Through our in silico modeling, RSPO2 exhibited strong positive associations with genes regulating epithelial-mesenchymal transition (EMT) and double-negative prostate cancer (DNPC), but had negative correlations with androgen receptor (AR) and AR-associated genes. Furthermore, 3D modeling of RSPO2 revealed structural differences between itself and other RSPOs. In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1. Conversely, this was not observed when CTNNB1 was overexpressed in the same models. These findings highlight that, in PC, RSPO2 functions as a unique member of the R-spondin family by promoting genes and signaling pathways associated with aggressive PC, and RSPO2 amplifications are associated with poor outcomes in PC patients. Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28758 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – August 11, 2025 – A new #researchpaper was #published in Volume 16 of Oncotarget on July 25, 2025, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.” In this study, researchers led by first author Aiden Deacon and corresponding author Justin Hwang from the University of Minnesota-Twin Cities investigated a group of genes known as the R-spondin family (RSPO1/2/3/4) in advanced prostate cancer (PC). The RSPO gene family regulates Wnt signaling, a pathway involved in cancer progression. Prostate cancer is the most common cancer among men in the United States and becomes especially dangerous when it spreads beyond the prostate. Most patients are treated with hormone therapies that target the androgen receptor; however, many tumors eventually become resistant. The research team analyzed thousands of tumor samples and found that RSPO2 alterations were more common than changes in other R-spondin genes or even some well-known cancer-related genes like CTNNB1 and APC. RSPO2 amplification occurred in over 20% of metastatic prostate cancer. Patients with these alterations showed signs of more aggressive disease, including higher mutation rates and greater tumor complexity. Using laboratory models, the team discovered that RSPO2 increases cancer cell growth and triggers a biological process called epithelial-mesenchymal transition (EMT). EMT is known to promote tumor spread and resistance to standard treatments. Unlike other genes in the same pathway, RSPO2 also appeared to reduce the activity of androgen receptor genes, suggesting it drives a type of prostate cancer that no longer relies on hormones for growth. “In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1.” Importantly, RSPO2 showed structural differences from other R-spondin proteins, which may allow researchers to design drugs that specifically block its activity. Current therapies targeting the Wnt pathway are limited, and there are no approved drugs that inhibit RSPO2. However, this study highlights RSPO2 as a promising therapeutic target, especially for patients who do not respond to existing hormone-based treatments. This research adds critical knowledge about how aggressive prostate cancers develop and persist despite therapy. The identification of RSPO2 as a key driver of disease progression opens new possibilities for treatment strategies aimed at improving outcomes for patients with advanced prostate cancer. DOI - https://doi.org/10.18632/oncotarget.28758 Correspondence to - Justin Hwang - jhwang@umn.edu Video short - https://www.youtube.com/watch?v=iyu5D_c1dbY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28758 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – July 22, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 21, 2025, titled “Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer.” In this work, led by first author Sneha Tripathi from the Indian Institute of Science Education and Research and corresponding author Sanjeev Galande from the Center of Excellence in Epigenetics at Shiv Nadar University, researchers discovered that statins, widely used to lower cholesterol, may also suppress colorectal cancer growth. This finding highlights a potential new role for these common drugs in cancer prevention and therapy. Colorectal cancer is one of the leading causes of cancer-related deaths worldwide, and new strategies are urgently needed to improve treatment results. Statins, originally developed to lower cholesterol levels, have gained attention for their possible anti-cancer properties. The study investigated how statins affect the Wnt/β-catenin signaling pathway, a critical driver in colorectal cancer development and progression. The researchers discovered that statins disrupt the Wnt/β-catenin signaling pathway, leading to lower levels of tumor-promoting proteins and to cancer-suppressing cellular behaviors. Experiments in both colorectal cell cultures and mouse models confirmed that statins reduced tumor growth without causing noticeable side effects. This study further revealed that statins downregulate SATB1, a protein linked to aggressive tumor behavior, while increasing SATB2, a protein with tumor-suppressing effects. These changes made the cancer cells less able to grow and spread. “This reciprocal regulation shifts cellular phenotypes between epithelial and mesenchymal states in 3D spheroid models.” Overall, the findings suggest that statins could be repurposed to complement existing colorectal cancer treatments or even be used in preventive strategies for high-risk individuals. By targeting the molecular machinery that drives colorectal tumor development, statins offer a promising, accessible, and well-understood option for further research in cancer therapy. This research opens the door to larger clinical studies to explore how best to integrate statins into cancer care. If successful, this approach could provide a cost-effective strategy for reducing the global burden of colorectal cancer, which remains a significant health challenge. DOI - https://doi.org/10.18632/oncotarget.28755 Correspondence to - Sanjeev Galande - sanjeev.galande@snu.edu.in Video short - https://www.youtube.com/watch?v=A95ICULaH3Y Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28755 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, colorectal cancer, statins, SATB1, Wnt/β-catenin signaling, tumor-suppressive phenotype To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Dan Casey was back with another installment of the Big Red Bench. Plenty to get through including hearing from Pat Ryan and John Kiely ahead of next Saturday's Munster final. We also hear from Cork's Megan Connolly ahead of the WNT clash vs Slovenia on Tuesday

TW - SA of a minor May 24th: Jesse Dirkhising Born (1986) Not everyone deserves your trust. On May 24th 1986 a young boy was born. A boy whose parents trusted two grown men with him. A deadly decision. https://en.wikipedia.org/wiki/Murder_of_Jesse_Dirkhising, https://www.allgaylong.com/blog/murder-jesse-dirkhising/, https://www.oddmurdersandmysteries.com/the-murder-of-jesse-dirkhising/, https://www.arkansasonline.com/news/2019/jun/08/judge-denies-new-dna-tests-for-child-ra/, https://abcnews.go.com/WNT/story?id=131125&page=1 Learn more about your ad choices. Visit megaphone.fm/adchoices

On Friday's Football Daily, Phil Egan brings you a full preview of this evening's League of Ireland action. We'll have live and exclusive coverage of St. Pats' Dublin derby with Shelbourne on tonight's Off The Ball, with coverage starting on Newstalk from 7pm. We hear from Pat's boss Stephen Kenny, Galway captain Greg Cunningham, Shamrock Rovers manager Stephen Bradley, Waterford forward Trae Coyle, Derry boss Tiernan Lynch and Sligo assistant Ryan Casey on tonight's top flight games. The FAI have strongly hit back at Kerry's claims of being 'bullied into silence'. Cobh Ramblers have moved to allay fears around their financial future. The Republic of Ireland. WNT have an afternoon appointment in Greece. And David Moyes responds to death threats aimed at Everton defender James Tarkowski.

On Friday's Football Daily, Phil Egan brings you a full preview of this evening's League of Ireland action. We'll have live and exclusive coverage of St. Pats' Dublin derby with Shelbourne on tonight's Off The Ball, with coverage starting on Newstalk from 7pm. We hear from Pat's boss Stephen Kenny, Galway captain Greg Cunningham, Shamrock Rovers manager Stephen Bradley, Waterford forward Trae Coyle, Derry boss Tiernan Lynch and Sligo assistant Ryan Casey on tonight's top flight games. The FAI have strongly hit back at Kerry's claims of being 'bullied into silence'. Cobh Ramblers have moved to allay fears around their financial future. The Republic of Ireland. WNT have an afternoon appointment in Greece. And David Moyes responds to death threats aimed at Everton defender James Tarkowski.

On Thursday's Football Daily, Phil Egan brings you all the reaction worth airing from the Merseyside derby. Liverpool skipper Virgil van Dijk speaks to OTB about their Premier League dreams, while David Moyes claims last night's winner should not have stood. PGMOL have reacted to James Tarkowski's contentious challenge on Alexis MacAllister. Amber Barrett discusses a potential 50th WNT cap. And the Women's World Cup is coming to Belfast.

On Thursday's Football Daily, Phil Egan brings you all the reaction worth airing from the Merseyside derby. Liverpool skipper Virgil van Dijk speaks to OTB about their Premier League dreams, while David Moyes claims last night's winner should not have stood. PGMOL have reacted to James Tarkowski's contentious challenge on Alexis MacAllister. Amber Barrett discusses a potential 50th WNT cap. And the Women's World Cup is coming to Belfast.

BUFFALO, NY - March 25, 2025 – A new #review was #published in Oncotarget, Volume 16, on March 13, 2025, titled “Signaling pathway dysregulation in breast cancer." In this review article, Dinara Ryspayeva and colleagues from Brown University provide a detailed look at how breast cancer cells change the way they communicate and grow—helping tumors survive, spread, and resist treatment. The review highlights how certain gene mutations and disrupted signaling pathways influence therapy response across different types of breast cancer. It also outlines current treatment strategies and clinical trials, offering insights that could improve care for patients with aggressive or hard-to-treat cancers. Breast cancer is the most common cancer in women and a major cause of cancer-related deaths worldwide. While many patients respond to treatment at first, some cancers return or stop responding. The review explores how signaling disruptions inside tumor cells are often behind these setbacks. The authors discuss several major pathways involved in breast cancer, including PI3K/Akt/mTOR, RAS/RAF/MEK/ERK, HER2, Wnt/β-catenin, Notch, NF-κB, and the DNA damage response (DDR). These pathways help control cell growth, division, DNA repair, and survival. When altered by mutations or other changes, they can promote tumor progression and resistance to treatment. One of the most disrupted pathways is PI3K/Akt/mTOR. It plays a central role in cell growth, but in many breast cancers—especially hormone receptor-positive and HER2-positive types—it becomes overactive due to gene mutations, or the loss of a tumor-suppressing protein called PTEN. “Up to 25–40% of BC cases exhibit variations that hyperactivate the PI3K/Akt/mTOR pathway, underscoring its critical role in oncogenesis.” Another key pathway, RAS/RAF/MEK/ERK, can also promote tumor growth. Even without mutations, it may become active when primary pathways are blocked, particularly in HER2-positive and triple-negative breast cancers. The review also highlights several new and emerging treatments aimed at blocking down these signaling pathways. Some drugs are already approved, while others are in clinical trials. The authors suggest that combining different treatments may help stop multiple pathways at once, making it harder for cancer cells to adapt. Matching treatments to each tumor's unique genetic changes could also improve patient outcomes. This comprehensive review gives researchers and clinicians a clearer understanding of how breast cancer resists treatment and where future therapies should focus. A better understanding of these disrupted signaling systems could lead to more personalized and effective treatments for patients facing aggressive or recurring disease. DOI - https://doi.org/10.18632/oncotarget.28701 Correspondence to - Dinara Ryspayeva - dinara_ryspayeva@brown.edu Video short - https://www.youtube.com/watch?v=ppFVGwdztHI Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Welcome to Wednesday's OTB Breakfast Bite - your FREE bitesize taster of this morning's full Off The Ball Breakfast. On a packed show this morning, former Ireland defender Méabh de Búrca reviewed a disastrous evening for the WNT in Slovenia. GAA referee David Coldrick discusses the new rules in Gaelic football.Former Munster hooker Mike Sherry joins to talk Six Nations and more.And we were joined by Watford's on-loan defender James Abankwah. And that's where we take our Bite this morning, but not until after Ger and Colm address Ireland's terrible Women's Nations League result in Koper. Catch Off The Ball Breakfast LIVE weekday mornings from 7:30am or just search for Off The Ball Breakfast and get the podcast on the Off The Ball app. SUBSCRIBE at OffTheBall.com/join

Welcome to Wednesday's OTB Breakfast Bite - your FREE bitesize taster of this morning's full Off The Ball Breakfast. On a packed show this morning, former Ireland defender Méabh de Búrca reviewed a disastrous evening for the WNT in Slovenia. GAA referee David Coldrick discusses the new rules in Gaelic football.Former Munster hooker Mike Sherry joins to talk Six Nations and more.And we were joined by Watford's on-loan defender James Abankwah. And that's where we take our Bite this morning, but not until after Ger and Colm address Ireland's terrible Women's Nations League result in Koper. Catch Off The Ball Breakfast LIVE weekday mornings from 7:30am or just search for Off The Ball Breakfast and get the podcast on the Off The Ball app. SUBSCRIBE at OffTheBall.com/join

On Friday's Football Daily, Phil Egan helps preview tonight's Women's Nations League clash of the Republic of Ireland and Türkiye at Tallaght Stadium. Ahead of that game, Katie McCabe has blasted the FAI's treatment of Colin Healy as 'not good enough', we speak to the skipper. And new WNT manager Carla Ward's view of the domestic game seems to be at odds with MNT counterpart Heimir Hallgrimsson. Nathan catches up with Stephen Bradley following Shamrock Rovers Conference League exit. And we hear from Stephen Kenny, Greg Cunningham and Tiernan Lynch ahead of tonight's Premier Division fixtures. Don't forget, Galway United's clash with St. Pat's is LIVE & EXCLUSIVE on tonight's Off The Ball.

On Friday's Football Daily, Phil Egan helps preview tonight's Women's Nations League clash of the Republic of Ireland and Türkiye at Tallaght Stadium. Ahead of that game, Katie McCabe has blasted the FAI's treatment of Colin Healy as 'not good enough', we speak to the skipper. And new WNT manager Carla Ward's view of the domestic game seems to be at odds with MNT counterpart Heimir Hallgrimsson. Nathan catches up with Stephen Bradley following Shamrock Rovers Conference League exit. And we hear from Stephen Kenny, Greg Cunningham and Tiernan Lynch ahead of tonight's Premier Division fixtures. Don't forget, Galway United's clash with St. Pat's is LIVE & EXCLUSIVE on tonight's Off The Ball.

BUFFALO, NY – February 14, 2025 – A new #review was #published in Oncotarget, Volume 16, on February 12, 2025, titled “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.” Authors Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, and Antonin Marchais from the Gustave Roussy Cancer Campus analyzed recent studies on a gene called SETDB1, which may play a key role in osteosarcoma, a type of bone cancer that mostly affects teenagers and young adults. Their review highlights how SETDB1 helps cancer cells grow, resist treatment, and avoid the immune system. Because of this, blocking SETDB1 could be a promising new way to treat osteosarcoma. Osteosarcoma is a fast-growing bone cancer that is usually treated with surgery and chemotherapy. However, if the cancer spreads or returns, treatment options are very limited. Scientists are searching for new ways to stop this disease, and recent studies have found that osteosarcoma cells often have extra copies of the SETDB1 gene. This seems to make the cancer more aggressive and harder to treat. “Whole exome sequencing of osteosarcoma samples from both diagnosis and relapses has highlighted several factors, including SETDB1, that are amplified in the most aggressive forms of the disease.” SETDB1 is involved in epigenetics, meaning it affects how genes are turned on and off without changing the DNA itself. The review explains that SETDB1 helps tumors hide from the immune system, making it difficult for the body to fight the cancer naturally. The researchers believe that blocking SETDB1 could help the immune system recognize and attack osteosarcoma cells. Some experimental drugs that target SETDB1 are already being tested in the lab. The review also describes how SETDB1 influences key cancer pathways, such as Wnt signaling, which helps cancer cells grow, and epithelial-mesenchymal transition (EMT), a process that allows cancer to spread. The authors suggest that combining SETDB1-blocking drugs with immunotherapy or radiation could be an effective new strategy for treating osteosarcoma. Another key finding is that SETDB1 may help cancer cells become resistant to chemotherapy, making treatment less effective. This means that drugs targeting SETDB1 could not only slow cancer growth but also make existing treatments work better. While more research is needed, this review brings attention to SETDB1 as a potential treatment target. Scientists hope that a deeper understanding of SETDB1 will lead to new therapies that improve survival rates for osteosarcoma patients. DOI - https://doi.org/10.18632/oncotarget.28688 Correspondence to - Antonin Marchais - antonin.marchais@gustaveroussy.fr, and Maria Eugenia Marques Da Costa - jenny.marquescosta@gustaveroussy.fr Video short - https://www.youtube.com/watch?v=f9WgaDoEubs About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

On Wednesday's Football Daily, Phil Egan brings you details of Mason Melia's blockbuster move to Tottenham, and what it means for St. Pat's. Denise O'Sullivan has strongly criticised the FAI's treatment of former WNT assistant Colin Healy. Bohemians are weighing up a move for former Premier League striker Lys Mousset, and we hear from another of their arrivals - Connor Parsons. Arne Slot discusses Conor Bradley replacing Trent Alexander-Arnold for Liverpool in the Carabao Cup. And Adam Idah is ready to take on more responsibility at Celtic.

On Wednesday's Football Daily, Phil Egan brings you details of Mason Melia's blockbuster move to Tottenham, and what it means for St. Pat's. Denise O'Sullivan has strongly criticised the FAI's treatment of former WNT assistant Colin Healy. Bohemians are weighing up a move for former Premier League striker Lys Mousset, and we hear from another of their arrivals - Connor Parsons. Arne Slot discusses Conor Bradley replacing Trent Alexander-Arnold for Liverpool in the Carabao Cup. And Adam Idah is ready to take on more responsibility at Celtic.

In case you missed it, here is episode one from our Settle In Series, as a bonus listen for all of our GAA Fans!Former Ireland international and coach Linda Gorman joined Eoin Sheahan to discuss how she's tackling ageism in sport by encouraging more people to take up walking football and she also discussed how much support for the women's game in Ireland has changed since she played on the first ever WNT over 50 years ago.‘Settle in' in partnership with Guinness 0.0.

In case you missed it, here is episode one from our Settle In Series, as a bonus listen for all of our GAA Fans! Former Ireland international and coach Linda Gorman joined Eoin Sheahan to discuss how she's tackling ageism in sport by encouraging more people to take up walking football and she also discussed how much support for the women's game in Ireland has changed since she played on the first ever WNT over 50 years ago.‘Settle in' in partnership with Guinness 0.0.

Former Ireland international and coach Linda Gorman joined Eoin Sheahan to discuss how she's tackling ageism in sport by encouraging more people to take up walking football and she also discussed how much support for the women's game in Ireland has changed since she played on the first ever WNT over 50 years ago.‘Settle in' in partnership with Guinness 0.0.

On Friday's Football Daily, Phil Egan brings you reaction to Shamrock Rovers' invaluable point in the Conference League, as we hear from Stephen Bradley. Ruben Amorim admits his Manchester United players are giving him anxiety. Eileen Gleeson and Denise O'Sullivan speak ahead of tonight's vital Euro playoff for Ireland's WNT in Cardiff. And we hear from new Coventry manager Frank Lampard.

On Friday's Football Daily, Phil Egan brings you reaction to Shamrock Rovers' invaluable point in the Conference League, as we hear from Stephen Bradley. Ruben Amorim admits his Manchester United players are giving him anxiety. Eileen Gleeson and Denise O'Sullivan speak ahead of tonight's vital Euro playoff for Ireland's WNT in Cardiff. And we hear from new Coventry manager Frank Lampard.

Former Ireland international and coach Linda Gorman joined Eoin Sheahan to discuss how she's tackling ageism in sport by encouraging more people to take up walking football and she also discussed how much support for the women's game in Ireland has changed since she played on the first ever WNT over 50 years ago.‘Settle in' in partnership with Guinness 0.0.

On this episode of the Modern Facilities Management Podcast, Griffin Hamilton interviews Yaron Dycian from Wint.AI, discussing the critical issues of water management in buildings. They explore the significant waste of water, the financial implications of leaks, and how Wint leverages AI for anomaly detection and predictive analytics to optimize water usage. The conversation also touches on proactive measures facilities managers can take and the future of water management technology in buildings.Chapters00:00Introduction to Wnt and Water Management03:01The Impact of Water Waste05:55Leveraging AI for Water Management09:00Insights and Analytics in Water Usage12:04Proactive Measures for Water Management14:59Future of Water Management in Facilities17:57Career Influences and Closing ThoughtsInterested in closing the skills gap? Check out our friends at Interplay Learning!

Vitamin D is not a vitamin; it's a hormone intimately involved in 10% of our genes. If you don't have enough vitamin D, it can interfere with the genes responsible for hair growth. There is also a very high concentration of vitamin D receptors in the hair follicle. Without enough vitamin D, your immune system is at risk of autoimmune conditions, including alopecia. Vitamin D supports the T cells that help combat autoimmune diseases. Psoriasis, dandruff, and dermatitis are also related to low vitamin D. Magnesium is the most potent regulator of calcium and is involved with enzymes important for hair health. It's also essential for the proper function of vitamin D. There are 2 systems of vitamin D: one that controls calcium and one that has several functions, including hair growth and hair restoration. This form of vitamin D has a 24-hour half-life, so you need daily sun or supplements to prevent a hair loss problem. There is a worldwide vitamin D deficiency epidemic! Several factors contribute to this massive vitamin D deficiency problem, including genetics, skin color, insulin resistance, diabetes, obesity, and air pollution. Your blood vitamin D levels should be at least 70 to 100 ng/mL. You need at least 20,000 IU of vitamin D daily and 50 mg of magnesium to support hair growth. Zinc, iron, vitamin B12, and omega-3 fatty acids are also essential for hair restoration. Key genes involved in hair growth: 1. Sonic Hedgehog (SHH) gene 2. WNT genes 3. BMP (Bone Morphogenetic Protein) genes 4. FGF (Fibroblast Growth Factor) genes 5. TGF-β (Transforming Growth Factor-Beta) genes 6. LEF1 (Lymphoid Enhancer-Binding Factor 1) 7. PDGF (Platelet-Derived Growth Factor) 8. Dkk (Dickkopf WNT Signaling Pathway Inhibitor) genes 9. CTNNB1 (Beta-Catenin)

Bart drops by to talk all the NT talk- USYNT and the U20 loss in Mexico, the USMNT losing in the knockouts in Paris and the WNT continuing to chase a medal under Emma Hayes

Ryan and Graham are here to deliver an update on the US teams at Paris 2024! It's the end of the road for the men, whose limitations were exposed by Morocco, while the WNT survived a technical battle with Japan to progress! JOIN THE TSS+ PATREON! Check out our Patreon, which houses bonus podcasts, access to our exclusive Discord, blog posts, videos, and much more. Become a member today at patreon.com/totalsoccershow! Learn more about your ad choices. Visit megaphone.fm/adchoices

Ryan and Graham are here to deliver an update on the US teams at Paris 2024! It's the end of the road for the men, whose limitations were exposed by Morocco, while the WNT survived a technical battle with Japan to progress!JOIN THE TSS+ PATREON!Check out our Patreon, which houses bonus podcasts, access to our exclusive Discord, blog posts, videos, and much more.Become a member today at patreon.com/totalsoccershow! Hosted on Acast. See acast.com/privacy for more information.

Belz, Vince and Tara recap the 2-1 win over Australia. Not as cathartic as the win over Germany, but still lots to celebrate, plenty to nitpick. The WNT and Emma Hayes have given us a nine-point window! So we had to dust off an old number for the intro to this episode. Subscribe to Scuffed on Patreon! Patrons get a private ad-free feed for all episodes that go out on the public feed, plus the Monday Review every week with Watke and Vince. Patrons also get access to our private Discord server, live call-in shows, and the full catalog of historic recaps we've made: https://www.patreon.com/scuffed