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Inceptive CEO Jakob Uszkoreit goes Inside the ICE House to challenge the foundational assumptions of modern drug discovery, arguing that AI will enable medicines that work with the body's natural complexity rather than against it. He discusses Inceptive's partnership with Alnylam Pharmaceuticals and why their RNA interference platform and rich data history make them a uniquely powerful AI collaborator. Uszkoreit explains why partnerships are essential for a small company with broadly applicable technology, and why the long-term prize is therapies that are gentler, earlier, and truly personalized.
Welcome to this week's Midlife Minute episode! Statistically, one in three women will die of heart disease. So, today, we're answering some of the many questions I received about lipids and heart health. Although I've done other lipid-focused Midlife Minutes before, this episode is yet another dedicated to Dr. Tom Dayspring, as I've received such a vast number of questions on this particular topic. IN THIS EPISODE, YOU WILL LEARN: Why understanding your ApoB and Lp(a) is an essential part of assessing your cardiovascular risk Why treatments for lipid abnormalities should be individualized to fit each specific abnormality Essential lifestyle measures for supporting overall cardiovascular health How CAC scoring, CT coronary angiography, and Clearly AI-assisted imaging differ, what each test measures, and their limitations How cardiovascular disease can sometimes present differently in women Why are premature atrial contractions and premature ventricular contractions often benign when the heart is structurally normal? How the roles of statins, ezetimibe, PCSK9 inhibitors, GLP-1 medications, and emerging RNA therapies differ, and why they should not be considered interchangeable How declining estrogen impacts cardiovascular health Connect with Cynthia Thurlow Follow on X, Instagram & LinkedIn Check out Cynthia's website. Submit your questions to support@cynthiathurlow.com Join other like-minded women in a supportive, nurturing community: The Midlife Pause/Cynthia Thurlow. Purchase Cynthia's book, The Menopause Gut. Cynthia's Intermittent Fasting Transformation Book The Midlife Pause Supplement Line
Microgravity causes a ton of changes in the human body and there's been a lot of research showing how these changes affect astronauts. One bodily function that hasn't been studied during an active space mission? Menstruation. This episode, Dr. Samantha Yammine is joined by Manju Bangalore, an astronaut-in-training and reproductive scientist aiming to research how the human body menstruates while in microgravity. But there's other space news in the science world so before that, Sam explores what it will take for NASA to build a nuclear reactor on the moon. Later, she looks into how some asteroids contain the raw ingredients for DNA and RNA. Link to Show Notes HERE Follow Curiosity Weekly on your favorite podcast app to get smarter with Dr. Samantha Yammine — for free! Still curious? Get science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. Terms apply. Hosted on Acast. See acast.com/privacy for more information.
The odds of a single living cell assembling by chance are 1 in 10 to the 50,000th power…and evolutionists still won't admit it's over. Kevin Swanson breaks down the staggering complexity of DNA, RNA, and the ATP synthase motor…why "dirt can't write software"…and why Sir Fred Hoyle himself recanted his atheism at the end of his life. Then Bill Jack joins Kevin to talk phrenology, punctuated equilibrium, and why 92% of biology professors now believe gender is a social construct.
What can a few grains of asteroid dust tell us about the origins of life on Earth?In this episode, Host Rick Crandall talks with NASA astrochemist José C. Aponte about the organic chemistry preserved inside asteroid Bennu. From NASA's OSIRIS-REx sample-return mission to amino acids, nucleobases, and the mystery of life's left-handed molecules, Aponte explains how scientists search for clues to our chemical origins. This one is going to be cool!What you'll hear:Why NASA traveled to Bennu: Pristine asteroid material offers evidence that meteorites altered by Earth's environment cannot.How scientists prevent contamination: A fingerprint can contain more organic material than the tiny Bennu samples researchers analyze.What researchers discovered: Bennu contains 14 of the 20 amino acids used to build proteins and all five nucleobases found in DNA and RNA.Why molecular diversity matters: Thousands of nitrogen-bearing compounds reveal the complex chemical environment of the early solar system.How a mass spectrometer works: Aponte explains how scientists use molecular fragments to identify compounds inside asteroid material.The mystery of left-handed amino acids: Life uses almost exclusively one mirror-image form, but scientists still do not know why.The search for tryptophan: Researchers found tentative evidence that could represent the first extraterrestrial detection of this complex amino acid.What Bennu's salts reveal: Minerals formed through evaporating water suggest Bennu's material originated in a different part of the solar system.Learn More:Read the full show notes on the Wings Over the Rockies websiteDonate to Wings Over the Rockies Air & Space MuseumSubscribe and leave a review to support the showThis episode is supported in part by United Airlines.
The odds of a single living cell assembling by chance are 1 in 10 to the 50,000th power…and evolutionists still won't admit it's over. Kevin Swanson breaks down the staggering complexity of DNA, RNA, and the ATP synthase motor…why "dirt can't write software"…and why Sir Fred Hoyle himself recanted his atheism at the end of his life. Then Bill Jack joins Kevin to talk phrenology, punctuated equilibrium, and why 92% of biology professors now believe gender is a social construct.
Welcome to The Daily Wrap Up, an in-depth investigatory show dedicated to bringing you the most relevant independent news, as we see it, from the last 24 hours (8/21/26). As always, take the information discussed in the video below and research it for yourself, and come to your own conclusions. Anyone telling you what the truth is, or claiming they have the answer, is likely leading you astray, for one reason or another. Stay Vigilant. !function(r,u,m,b,l,e){r._Rumble=b,r[b]||(r[b]=function(){(r[b]._=r[b]._||[]).push(arguments);if(r[b]._.length==1){l=u.createElement(m),e=u.getElementsByTagName(m)[0],l.async=1,l.src="https://rumble.com/embedJS/u2q643"+(arguments[1].video?'.'+arguments[1].video:'')+"/?url="+encodeURIComponent(location.href)+"&args="+encodeURIComponent(JSON.stringify([].slice.apply(arguments))),e.parentNode.insertBefore(l,e)}})}(window, document, "script", "Rumble"); Rumble("play", {"video":"v7cb2wc","div":"rumble_v7cb2wc"}); Source Links (In Chronological Order): Sam Husseini Interview - Can A Corrupt System Be Changed From Within? New Tab (20) Brian Cates - Political Columnist & Pundit on X: "@L08818 I slowly came to realize on hanging out with Ron Paul enthusiasts that they don't want to reform the system, drive out the corruption, and restore the country. The want to...and they told me this several times, but back then I didn't really believe them...BURN IT ALL DOWN AND" / X (20) The Last American Vagabond on X: "What an absolutely disingenuous coward you are @L08818. https://t.co/31KRfbLcxZ" / X (20) SheThinksFreely (@L08818) / X (20) SheThinksFreely on X: "@TLAVagabond Bro GTFOH w this stupid sh*t Anarchy is anti American You traitorous piece of excrement" / X (20) SheThinksFreely on X: "
Stacy Horner discusses her work on innate detection of viruses, viral countermeasures, and the role of m(6)A RNA modifications in regulating antiviral immunity. Host: Cindy Leifer Guest: Stacy Horner Subscribe (free): Apple Podcasts, RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Hepatitis virus proteases block host response (J Virol, 2012) Host RNA binds to MAVS (Science, 2024) m6A modifications modify innate response to viruses (Cell Chem Biol, 2024) UFMylation coordinates MAVS assembly for antiviral responses (bioRxiv, 2025) Time stamps by Jolene Ramsey. Thanks! Music by Tatami. Logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv Information on this podcast should not be construed as medical advice.
This week we talk about the liver, viral infections, and the NHS.We also discuss blood scandals, needle usage, and Nobel Prizes.Recommended Book: A World Appears by Michael PollanTranscriptThe term “hepatitis” refers to the inflammation of the liver, which can result from all kinds of things, including environmental toxins, the consumption of alcohol, or autoimmune diseases. It can also result from viral infections, and the most prominent liver-inflaming viruses are called viral hepatitis.There are five types of viral hepatitis, A, B, C, D, and E, and each of these viruses are distinct, not part of the same viral family, they're just similarly named because they impact the same organ.Hepatitis A and E are primarily spread through contaminated food and water, and generally resolve on their own, untreated, and cause relatively mild symptoms. Hepatitis B and C are spread through blood and other bodily fluids, and can linger in a host's body for decades before even showing symptoms. Hepatitis D is a parasite of Hepatitis B, and thus only infects people who carry Hepatitis B.Now again, these are all different conditions that just happen to inflame the liver, so impact and treatment also vary quite a lot. As I mentioned, A and E generally present with mild symptoms and tend to go away on their own, while B and C can stick around a long time. There's a vaccine for B, but no cure; you can treat it, but that treatment involves suppressing it, and keeping it suppressed, forever. Hep C, in contrast, is curable, and has been since 2014 using what are called direct-acting antiviral pills, but these pills, which are taken for 8 to 12 weeks, are expensive—ranging from $22-95k without insurance, though that price is often reduced substantially for those with insurance, down to as low as $5. This category of drug coverage is often rejected by insurance companies, though, in part because they're so expensive, that expense the result of little competition in this space; few companies make this type of drug, so those that do can charge more or less whatever they like.Some people with Hepatitis C clear it on their own; about 30% of people who contract it, in fact, clear it within a few months, medication-free. Which is good, because our understanding of this virus is relatively new. Up until 1989, Hep C didn't even have its own name: it was established as its own thing, not Hep A and not Hep B, back in the 1970s, and doctors knew that something that wasn't those two viruses, that was being spread by transfusions, was causing hepatitis symptoms, but they didn't know any real specifics, so they just called it “non-A, non-B hepatitis,” and that name stuck for more than a decade.In 1989 the virus was cloned using molecular techniques (as opposed to simply growing the virus, which wasn't proving fruitful in trying to isolate and identify the thing), and the folks who managed that cloning, and the person who later proved that the genome they cloned, alone, caused the disease, received a Nobel Prize in Medicine for their efforts in 2020.By 1991, antibody tests were available for Hep C, and many countries began screening donated blood for this virus, to ensure it wasn't working its way into their blood supply.And one instance of that screening process, or I suppose, an event that led up to mass screening, and the consequences that followed, are what I'd like to talk about today. The UK's efforts in trying to eliminate Hep C, and England's recently announced near-success in that pursuit.—Hepatitis C is an RNA virus with high genetic variability that makes developing a reliable vaccine difficult. And though somewhere between a quarter and a third of all cases clear on their own, those that don't clear on their own become chronic, lying in wait for twenty to thirty years, slowly accumulating fibrosis—thick scar tissue in the liver—which eventually results in cirrhosis, which means a liver that's so heavily scarred that the organ is no longer fully functional and the damage is permanent. From there, infected people often experience liver failure or hepatocellular (huh-pah-toe) carcinoma, liver cancer.So this virus is a sleeper, and unless it's caught by accident somewhere along the way, it slowly causes damage over time until the damage is too severe to reverse. About 80% of people who have it don't know they have it, and in some parts of the world medical injections are the most common transmitter, but in higher-income areas, it's usually transmitted by injectable drugs.Pre-2014 treatments for Hep C were pretty horrible, involving a combination antiviral therapy called pegylated interferon plus ribavirin that was injected weekly for six months to a year, and this was terribly tolerated by pretty much everyone, causing anemia, depression, and flu-like symptoms for the duration. It also only cured about 50% of people who received the full treatment, and a lot of people had to stop because it caused such ridiculous side effects.Another antiviral called Sofosbuvir (so-FAS-buh-vir), which kept Hep C from replicating in its host, hit the market in late-2013, and that led to a series of direct-acting antivirals that reduced the treatment period dramatically, allowing most people, 95%, to cure their Hep C entirely by taking generally well-tolerated pills for 8 to 12 weeks.These pills were staggeringly expensive from the get-go, with an entire treatment course initially costing about $84,000, or $1,000 a pill. This led to rationing, and saving these pills for the worst-impacted people who already had severe liver damage. There were also pretty stringent requirements attached to their distribution, including that people who received them could no longer drink alcohol, because it was considered a waste to give these crazy expensive, liver-saving drugs to people who would just go and hurt their liver more, anyway.In the UK, the demand for this treatment type was different than in most other countries, in large part because of something that happened back in the 1970s and 80s.The UK's publicly funded healthcare system, the NHS, was in the midst of a shortage of clotting factor, which are plasma proteins and ions that help blood clot and which are used for medical purposes. So they imported a bunch of plasma products from the US, and those products were sourced from the blood of paid donors—and that donor pool included prisoners and people who used injectable drugs. Just one Hep C contaminated blood donation could contaminate an entire batch of blood, and remember, they only started screening the blood supply for Hep C in 1991, and they didn't start treating their blood supply for Hep C until a little before that, 1985, so this was well before they had any idea what was in those blood products they were importing and administering.Consequently, between 1970 and the early 1990s, more than 30,000 NHS patients received transfusions or other blood product treatments contaminated with Hep B, Hep C, or HIV, and about a tenth of those people, around 3,000 patients, have since died of those conditions.The UK government leaned on denial and a refusal to look into the details of this for years, but in 2017 it announced an independent public inquiry into the matter, and in May of 2024, that inquiry concluded that this whole scandal was avoidable, that patients were knowingly exposed to “unacceptable risks,” and that there was a big cover up by government officials, doctors, and other people working with the NHS.As of mid-2026, only a little over 3,200 people of the more than 18,500 who registered claims, demanding compensation from the government because they were impacted by this scandal, have been paid out. The expected total expense for the UK government is on the order of 12.8 billion pounds, but a lot of people who are probably due a payout, and who are in poor and deteriorating health as a consequence of all this, don't yet have a sense of when they'll receive their payment.Back in 2016, before all that came to a head, the UK set itself an aggressive goal: to eliminate Hep C by the WHO's 2030 target, or before. It then ran a competitive tender for antivirals, inviting medical suppliers to submit competing bids, resulting in the largest single medicine procurement program in the NHS' history. The pharmaceutical companies that won their bids were also obliged, as part of the agreement, to help fund efforts to identify undiagnosed but infected patients, in addition to supplying antiviral pills, and this combination of investment and application led to the deployment of new tests and scanning machines, free postal test kits, the hiring of specialists, and services that focused on prisons and drug users.The impact of all this has been significant: a more than 61% decline in infections from 2015 to 2024, nearly half of all drug users with Hep C had cleared the virus in that time, and deaths from Hep C are down 36% over the past decade.The WHO treatment-coverage target—the percentage of people who are diagnosed getting treatment—was 80%, and England has hit 81.5%, which was recently announced to much fanfare. It hasn't yet hit the diagnosis target, however, which is to diagnose 90% of people who are estimated to have Hep C; they've hit 84.6%, which is still quite a lot of progress, even if they're not yet where they'd like to be. That's all based on models, of course, as are the assumed number of infections among people who use injectable drugs, which is also a spot where England is currently flagging; there's no centralized system in England to monitor needle and syringe provisions, and reinfection rates are around 8.8 per 100 person-years among people who had injected within three years of receiving treatment, and that rate is even higher for people who have ever been to prison, around 9.4 per 100.What that means in practice is that the English government overall has done a pretty astounding and effective job at negotiating their relationships with pharma companies and getting detection on track at that scale, but on more ground-level issues that are, interestingly, a lot cheaper to implement, but at times more politically complicated because of public sentiment about drug use and drug users, they're doing a lot less well—and important to note here is that these outcomes vary a bit across the four programs being run across the UK. Scotland and Wales are doing relatively better and worse in some regards compared to England, for instance.Also worth noting here that while England is broadly doing a great job with Hep C diagnosis and treatment, they aren't the first to achieve those WHO-set goals: Egypt reached Gold tier status according to the WHO's Hep C guidelines in October of 2023, at that point having diagnosed 87% of people who have the virus, and treating 93% of those who were diagnosed. They managed to cut incidence of the virus by 97% in just 8 years, leaning on a system of high-yield testing—they tested more than 60 million people during those 8 years—alongside a production scheme that included local manufacturing of antivirals, making them more available and affordable.All of which are generally good signs about where Hep C testing and treatment is going, at least in these regions. And it paints a optimistic picture for other countries that might want to replicate some of what's working within their own borders.Show Noteshttps://www.bbc.com/news/articles/c75gk620r22ohttps://en.wikipedia.org/wiki/Infected_blood_scandal_in_the_United_Kingdomhttps://en.wikipedia.org/wiki/Hepatitis_Chttps://en.wikipedia.org/wiki/Viral_hepatitishttps://en.wikipedia.org/wiki/Hepatitis_Bhttps://www.healthline.com/health/hepatitis-c/treatment-costshttps://www.who.int/news-room/fact-sheets/detail/hepatitis-chttps://publichealthscotland.scot/publications/surveillance-of-hepatitis-c-in-scotland/surveillance-of-hepatitis-c-in-scotland-progress-on-elimination-of-hepatitis-c-as-a-major-public-health-concern-2025-update/https://www.emro.who.int/media/news/egypt-becomes-the-first-country-to-achieve-who-validation-on-the-path-to-elimination-of-hepatitis-c.htmlhttps://www.gov.uk/government/publications/hepatitis-c-in-england-and-the-uk/hepatitis-c-in-england-2025https://www.england.nhs.uk/2026/08/100000-people-receive-treatment-to-cure-deadly-hep-c-virus-on-nhs-in-just-ten-years/https://www.hepctrust.org.uk/blog/2019/04/hepatitis-c-trust-welcomes-elimination-deal-hepatitis-c-and-calls-government-backed/https://commonslibrary.parliament.uk/research-briefings/cbp-10099/https://www.who.int/teams/global-hiv-hepatitis-and-stis-programmes/hepatitis/reports/global-hepatitis-report-2026 This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit letsknowthings.substack.com/subscribe
On episode #113 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 8/4 – 8/17/26. Hosts: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Two-year durability of MVA-BN vaccine-induced antibodies and the risk of Mpox breakthrough infections among high-risk populations: a prospective, longitudinal study (CMI: Clinial Microbiology and Infection) Notes from the Field: Potential Infant HIV Exposure from Donated Breast Milk Received Through Social Media — Santa Clara County, California, May 2025–January 2026 (CDC: MMWR) Bacterial Associations Between QuantiFERON-TB Gold Plus IFNγ Concentrations and Progression to Symptomatic Tuberculosis in Global High-Burden TB Settings (OFID) Cefadroxil as Oral Transitional Therapy for Gram-Positive Bacteremia With or Without Non-Vertebral Osteomyelitis: A Multicenter Retrospective Cohort Study (OFID) Efficacy of beta-lactam monotherapy versus clindamycin or addition of metronidazole in peritonsillar abscess – an observational cohort study with a focus on Fusobacterium necrophorum (CMI: Clinial Microbiology and Infection) A novel RNA nucleic acid amplification test more accurately distinguishes active Clostridioides difficile infection from colonization (CID) The Clean Margin in Diabetic Foot Osteomyelitis: Conceptual Appeal, Practical Uncertainty (CID) Rising Incidence of New Delhi Metallo-β-Lactamase–Producing Carbapenem-Resistant Enterobacterales, 10 US Sites, 2018–2023 (OFID) Association of anti-anaerobic antibiotics with mortality and the gut microbiome: a sub-study of the BALANCE randomized clinical trial (CID) Fungal The Last of US Season 2 (YouTube) Coccidioidomycosis Testing Among Patients Hospitalized With Community-Acquired Pneumonia (OFID) Parasitic Human Myiasis Resulting from Reemergence of Cochliomyia hominivorax Screwworm, Mexico, 2025–2026 (Emerging Infectious Diseases) The origin, history, and resistance architecture of an invasive urban malaria mosquito in Africa (Science) Clinical, molecular, and in vitro evidence of artemisinin partial resistance in Ethiopian Plasmodium falciparum: a prospective, multisite, surveillance (LANCET: Infectious Diseases) Miscellaneous What's in a Name? Etymology and History of Antibacterials and Antifungal (IOFID) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.
AI can now read DNA like language, generate working biological sequences, and help scientists identify disease-related mutations. Radical Numerics CEO Eric Nguyen explains how genome language models work, why his earlier model Evo helped scientists design CRISPR systems and bacteriophage genomes, and how the company's newer model, Omnii, combines DNA with RNA, proteins, and other biological signals. The conversation explores personalized medicine, gene therapy, AI-designed biological threats, “deepfake viruses,” and whether the same technology that creates new biology can also defend against it.Learn more about Radical Numerics: https://www.radicalnumerics.ai/
What if your skin could just . . . remember how to act young again? That's essentially the pitch behind Biocogent's new RNActivate W, a next-generation active that doesn't add collagen or push it as peptides do. Instead, it goes upstream and silences a tiny piece of regulatory RNA (the so-called "wrinkle miRNA") that tells your skin cells to stop making collagen and elastin. Join Ella and Maggie for an ingredient deep dive into what microRNAs actually are, why the 2024 Nobel Prize in Medicine matters for your treatment room, what to look for on an INCI list when you see "s-RNA-5," and how to talk about this category with clients without overpromising. Spoiler: This isn't snake oil, but it isn't a retinol replacement either. ASCP Esty Talk with hosts Ella Cressman and Maggie Staszcuk Produced by Associated Skin Care Professionals (ASCP) for licensed estheticians, ASCP Esty Talk is a weekly podcast, hosted by licensed estheticians, Ella Cressman, ASCP Skin Deep Magazine contributor, and Maggie Staszcuk, ASCP Program Director. We see your passion, innovation, and hard work and are here to support you by providing a platform for networking, advocacy, camaraderie, and education. We aim to inspire you to ask the right questions, find your motivation, and give you the courage to have the professional skin care career you desire. About Ella Cressman: Ella Cressman is a licensed esthetician, certified organic formulator, and business owner with more than 20 years of experience in corrective skin care. Known as an "ingredient junkie" and industry cheerleader, she empowers professionals to think beyond products and develop a deeper understanding of skin function and formulation. In addition to her practice, Cressman is the founder of the HHP Collective, a practitioner-led community focused on strengthening clinical reasoning and advancing professional growth within the esthetics industry. Connect with Ella Cressman: Website: www.hhpcollective.com LinkedIn: linkedin.com/in/ella-cressman-62aa46a About Maggie Staszcuk: Maggie Staszcuk serves as the Program Director for ASCP and is the cohost of ASCP Esty Talk podcast. With over 18 years' experience in the esthetics industry, her diverse background includes roles in spa management, spa and med-spa services, and esthetics education. Since becoming a licensed esthetician in 2006, she carries a range of certifications in basic and advanced esthetics. Maggie is dedicated to equipping estheticians with the knowledge and resources they need to thrive in their careers. Connect with Maggie Staszcuk: P: 800.789.0411 EXT 1636 E: MStaszcuk@ascpskincare.com About our Sponsors: Massage Envy is a national franchisor and does not independently own or operate any of the Massage Envy franchised locations nationwide. The Massage Envy franchise network, through its franchise locations, is the leading provider of massage services. Founded in 2002, Massage Envy now has approximately 1,100 franchise locations in 49 states that have together delivered more than 200 million massages and skin care services. Website: www.massageenvy.com/careers/career-areas/esthetician Facebook: @MassageEnvyCareers LinkedIn: @MassageEnvy GlossGenius Gaps in your schedule. Clients who don't rebook. Tight margins. High payment processing fees. Sound familiar? When you're running your own practice, you don't have time to figure out where you could be making more money. Especially when you're stitching together booking, payments, and a clunky EMR that only makes things harder. That's why we love GlossGenius — the business management platform that does the work for you. It fills your calendar, rebooks clients automatically, upsells high-margin services, and has the lowest flat-rate payment processing fees. Plus, all the HIPAA-compliant tools you need for charting, consents, and client records — without the admin chaos. GlossGenius grows your revenue and handles the busywork, so you can focus on your clients. Use code ESTY at GlossGenius.com for 50% off your first two months of their Gold or Platinum plan. GlossGenius. More Growth. Less Busywork. Visit https://glossgenius.com/ascp for more details. About Associated Skin Care Professionals (ASCP): Associated Skin Care Professionals (ASCP) is the nation's largest association for skin care professionals and your ONLY all-inclusive source for professional liability insurance, education, community, and career support. For estheticians at every stage of the journey, ASCP is your essential partner. Get in touch with us today if you have any questions or would like to join and become an ASCP member. Connect with ASCP: Website: www.ascpskincare.com Email: getconnected@ascpskincare.com Phone: 800-789-0411 Facebook: facebook.com/ASCPskincare Instagram: @ascpskincare
BUFFALO, NY — August 12, 2026 — A new #research paper was #published in Volume 18 of Aging on July 27, 2026, titled “Transcriptomic aging clock analysis identifies key genes in opioid dependence.” The study was led by first author Hai Duc Nguyen from the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University. The corresponding author is Woong-Ki Kim, who is affiliated with the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University, and the Department of Microbiology and Immunology at Tulane University School of Medicine. Opioid dependence is a chronic and relapsing condition associated with substantial health and societal burdens. Chronic opioid exposure can affect neuronal signaling, immune function, metabolism, and other biological processes, yet the molecular mechanisms underlying dependence remain incompletely understood. Increasing evidence also suggests that substance use disorders may be associated with molecular changes related to aging, raising questions about how chronic opioid exposure interacts with age-dependent processes in the brain. To investigate these relationships, the researchers conducted an in silico study integrating three complementary approaches: RNA sequencing-based transcriptomic profiling, transcriptomic aging-clock modeling, and analysis of previously published genome-wide association studies (GWAS). The transcriptomic analysis used a publicly available brain RNA-seq dataset containing 42 samples—21 healthy controls and 21 individuals with opioid dependence—while the genetic analysis incorporated findings from six independent GWAS. Full press release - https://www.aging-us.com/news-room/transcriptomic-aging-clock-reveals-age-related-molecular-patterns-in-opioid-dependence DOI - https://doi.org/10.18632/aging.206405 Corresponding author - Woong-Ki Kim - wkim6@tulane.edu Abstract video - https://www.youtube.com/watch?v=7VwU0mFGkbg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206405 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, opioids, GWAS, transcriptomic clock 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
Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we're diving into a landscape marked by remarkable scientific breakthroughs, strategic alliances, and regulatory milestones that are shaping the future of healthcare. Novo Nordisk is making waves with its new partnership with Amazon Web Services, utilizing artificial intelligence to accelerate drug discovery for chronic diseases. By integrating cloud computing and machine learning models, this collaboration highlights the increasing role of digital transformation in drug development. Novo Nordisk's commitment to innovation is further underscored by the launch of a new London Innovation Hub, enhancing research capabilities in the UK and demonstrating how technology can streamline the development of novel therapeutics. In clinical trial news, Silence Therapeutics has achieved a significant milestone with its investigational therapy Divesiran. This small interfering RNA therapeutic met primary endpoints in a Phase 2 trial for polycythemia vera, highlighting the potential of RNA-based therapies in treating complex blood disorders. Meanwhile, AbCellera's monoclonal antibody therapy ABCL635 has shown promising Phase 2 data for alleviating menopause-related hot flashes, surpassing existing treatments and underscoring the potential of targeted biologics in women's health. Regulatory achievements are further advancing personalized medicine. LabCorp received FDA approval for its PGDx elio tissue complete CDx companion diagnostic for BRAF-mutant advanced melanoma. This tool is pivotal for identifying patients who could benefit from targeted therapies, enhancing precision medicine approaches in cancer treatment. Similarly, AstraZeneca's Calquence and Enhertu have received notable endorsements, reinforcing the critical role of regulatory bodies in facilitating access to innovative treatments. The industry's business landscape is vibrant with strategic partnerships and acquisitions aimed at advancing therapeutic pipelines. Sobi's $580 million deal with Innate Pharma to advance lacutamab through Phase III lymphoma trials underscores how combining expertise can accelerate drug development and commercialization efforts. Financially, companies like Denali Therapeutics are surpassing revenue expectations with products like their enzyme replacement therapy Avlayah for Hunter syndrome, while fundraising activities are empowering biopharmaceutical companies to drive forward pain and oncology initiatives. Despite these advances, challenges persist. Sionna Therapeutics' recent clinical setback in cystic fibrosis reinforces Vertex Pharmaceuticals' dominance in CFTR modulator therapies. Additionally, Tenax Therapeutics encountered disappointment with TNX-103 failing to meet primary endpoints in a Phase 3 trial for pulmonary hypertension associated with heart failure. Manufacturing capabilities are also a focal point as Bristol Myers Squibb plans a substantial investment in Houston, reflecting an industry trend towards expanding infrastructure to meet demand and ensure supply chain resilience. However, compliance remains critical, as seen with Scholar Rock's decision to drop Novo Nordisk's Catalent facility following an FDA inspection. In contrast to setbacks, some companies are achieving breakthroughs. Jazz Pharmaceuticals' acquisition of Actio Biosciences aims to enhance their epilepsy treatment portfolio by integrating clinical-stage assets into its pipeline—a strategic move reflecting ongoing consolidation within the industry. The promise of genetic-targeted therapies is vividly illustrated by Biogen's ALS treatment Qalsody, marking a major scientific breakthrough as the first FDA-approved drug targeting a genetic cause of ALS. Patients have reported symptom stabilization and improvement—a significant advancement given ALS's progressive nature. Meanwhile, psychedelics are emerging as transformative agents in psychiatric medicine. As traditional medications often fall short, psychedelics offer hope for innovative mental health therapies supported by growing clinical and policy backing. However, navigating regulatory landscapes remains challenging. The FDA's recent actions illustrate ongoing struggles to balance innovation with oversight amidst leadership transitions. Real-world evidence is increasingly influencing regulatory decisions—reshaping how companies approach market access strategies by integrating patient experiences into evidence-based decision-making. In oncology, Replimune's melanoma drug has finally earned FDA approval after previous setbacks—a testament to persistence and the potential impact of innovative cancer therapies on patient outcomes. These developments underscore a dynamic pharmaceutical and biotech industry where breakthrough technologies like genetic-targeted therapies and psychedelics promise transformative impacts on patient care. Yet, they also highlight the complexities of bringing these innovations to market amidst stringent regulatory standards and competitive pressures. As we continue to track these stories, one thing is clear: the relentless pursuit of novel treatments remains at the forefront of advancing global healthcare.Support the show
Does a woman's sexual history leave lasting biological effects—and could it influence future relationships, pregnancy, or offspring?In this deep-dive conversation, Marquett sits down with a neuroscience graduate to examine controversial claims surrounding body count, microchimerism, epigenetics, semen-derived genetic material, inheritance, fertility, and sexual biology. They also discuss why some scientific claims spread online, how to separate peer-reviewed research from viral interpretations, and why understanding the difference between evidence, hypothesis, and speculation matters.The conversation goes beyond dating culture and into bigger questions surrounding genetics, modern relationships, scientific literacy, social media, education, and the way controversial research is communicated.Topics include: epigenetics, microchimerism, DNA and RNA, sexual history, reproductive biology, genetic inheritance, promiscuity, scientific studies, misinformation, relationships, and modern dating.Watch the full discussion and decide for yourself where the evidence ends—and where the controversy begins.⸻
Η κυβέρνηση του Κουίνσλαντ θα επενδύσει σχεδόν 300 εκατομμύρια δολάρια στην αναβάθμιση των εκθεσιακών χώρων RNA της Βρισβάνης, με νέες εγκαταστάσεις και βελτιωμένη προσβασιμότητα ενόψει των Ολυμπιακών και Παραολυμπιακών Αγώνων του 2032.
Everyone in biotech agrees AI needs more data. Almost no one is willing to pay for it. If you're trying to build or buy a biotech AI model, you've hit the same wall: predictive performance depends on data your budget doesn't cover, and nobody in the field seems willing to close that gap. John Androsavich runs Ginkgo Datapoints, the bio AI data arm of Ginkgo Bioworks. He trained as an RNA scientist, spent years on the pharma side deciding which technologies were worth buying, and now sells the raw biological data everyone claims to want. Ross and John get into why biotech spends a fraction of what tech spends on data, how automation dropped ADME testing to $199 a compound, and what that unlocks for drug discovery pipelines and data science in biotech more broadly. You'll hear why single-cell foundation models don't scale the way the field expected, and how GPT-5 designed its own lab experiments inside an autonomous facility. This one's for data and analytics leaders in biotech who need a clearer read on where to spend on data generation, and where the field is still guessing. It's less useful if you're after a general AI overview with no biotech specifics. Key Takeaways - One Meta investment in a data-labelling vendor outweighs a full year of AI drug discovery venture funding combined, and dwarfs the entire single-cell data market. Biotech's data spend looks nothing like tech's. - Ginkgo's ADME-1 offering runs at roughly a tenth of standard pricing, which is changing when and how much companies test. Teams are now running full tier-one panels earlier instead of triaging molecules before they've generated the negative data models need. - A recent Microsoft Research paper found single-cell foundation model learning saturates at 200,000 to 2 million cells, out of a possible 20 million. Volume alone isn't the lever people assumed it was. - GPT-5 wrote its own experimental protocols for optimising cell-free protein expression, ran them through Ginkgo's autonomous Nebula lab, and hit the lowest price-per-titer ever recorded in the field. Chapter Markers 00:00 Introducing John Androsavich and Ginkgo Datapoints 01:12 Why Ginkgo launched a bio AI data business 05:03 Which companies benefit most from Datapoints 06:31 The paradox: everyone wants data, no one pays 09:00 How automation drives ADME-1's $199 price point 12:59 Testing the Jevons paradox in biotech data buying 16:05 Do we actually know biotech AI's scaling laws? 20:54 Why foundation model builders resist more data 24:59 What an empirical bake-off for bio AI could look like 29:32 The case against sitting on the sidelines 33:26 Inside the Virtual Cell Pharmacology Initiative 41:57 Where VCP fits among other virtual cell projects 44:50 The Antibody Developability Consortium with Apheris 53:57 Autonomous labs and GPT-5 designing its own experiments 59:38 Advice for mid-stage biotech data strategy 01:01:31 Final thoughts on where bio AI investment is heading Useful Links & Resources - Ginkgo Bioworks: [ginkgobioworks.com](https://www.ginkgobioworks.com) - Related episode: Apheris CEO Robin Rohm on federated co-folding (Data in Biotech) - Related episode: Eliza Appel on Lilly's TuneLab and federated learning (Data in Biotech) - CorrDyn: [corrdyn.com](https://www.corrdyn.com) Connect With the Show - Host LinkedIn (Ross Katz): [linkedin.com/in/b-ross-katz](https://www.linkedin.com/in/b-ross-katz/) - Host X: [x.com/brosskatz](https://x.com/brosskatz) - CorrDyn LinkedIn: [linkedin.com/company/corrdyn](https://www.linkedin.com/company/corrdyn/) Where does your organisation sit on the data investment paralysis John describes? Are you waiting for someone else to prove the scaling laws first, or are you buying the data now? Drop your take in the comments. Visit corrdyn.com to learn how CorrDyn can help your organisation extract value from data. #DataInBiotech #BiotechAI #DrugDiscovery #DataScience #GinkgoBioworks
Welcome back to the Jack Westin MCAT Podcast with Mike and Molly! Last episode we covered DNA and RNA structure. Now we put that knowledge to work and answer the question that follows naturally: how do scientists actually study DNA, and how does the MCAT test those techniques?This is the DNA techniques episode, and it connects back to nearly everything you have already learned including amino acids, protein structure, hemoglobin, gel electrophoresis, blotting and central dogma.
Men with non-obstructive azoospermia may undergo microscopic testicular sperm extraction, or mTESE, without knowing whether sperm will be found. Kun Tan, Ph.D., of UC San Diego explains how molecular semen analysis could provide a noninvasive way to predict the procedure's outcome. The assay uses stage-specific germ cell markers identified through single-cell RNA sequencing, then measures those markers in semen with qPCR. Because semen contains germ cells from different stages of sperm development, their molecular signals may reflect what is happening inside the testes. Tan shows how the assay predicts whether sperm retrieval was successful and can identify where sperm development may be blocked. The research could help couples planning IVF or ICSI avoid unnecessary surgery, reduce financial and emotional burdens, and receive more detailed information about male infertility before treatment. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 41630]
In this episode of ASTCT Talks, Dr. Nirali Shah welcomes Crystal Mackall, MD, the Ernest and Amelia Gallo Family Professor at Stanford University and a pioneer in immuno-oncology and cellular therapy, for a conversation in the Titans of Transplant series.Dr. Mackall reflects on her journey into medicine, the mentors who shaped her career, and the evolution of immunotherapy from an emerging concept to a transformative treatment modality. She also shares her perspective on the future of cell and gene therapies, the challenges facing pediatric cancer drug development, and the importance of resilience, mentorship, and innovation in scientific careers.Tune in to hear about:Dr. Mackall's path to becoming a physician-scientist.Lessons learned from mentors and decades of leadership in the field.The evolution of immunotherapy and cellular therapy.Emerging opportunities in RNA-based therapeutics and next-generation treatments.Barriers to advancing pediatric cancer therapies.Advice for trainees and early-career investigators.The role of resilience, collaboration, and curiosity in a successful career.Listen to the episode below or on your favorite podcast app. Subscribe to ASTCT Talks to stay up to date on the latest conversations in transplantation and cellular therapy.
Men with non-obstructive azoospermia may undergo microscopic testicular sperm extraction, or mTESE, without knowing whether sperm will be found. Kun Tan, Ph.D., of UC San Diego explains how molecular semen analysis could provide a noninvasive way to predict the procedure's outcome. The assay uses stage-specific germ cell markers identified through single-cell RNA sequencing, then measures those markers in semen with qPCR. Because semen contains germ cells from different stages of sperm development, their molecular signals may reflect what is happening inside the testes. Tan shows how the assay predicts whether sperm retrieval was successful and can identify where sperm development may be blocked. The research could help couples planning IVF or ICSI avoid unnecessary surgery, reduce financial and emotional burdens, and receive more detailed information about male infertility before treatment. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 41630]
Men with non-obstructive azoospermia may undergo microscopic testicular sperm extraction, or mTESE, without knowing whether sperm will be found. Kun Tan, Ph.D., of UC San Diego explains how molecular semen analysis could provide a noninvasive way to predict the procedure's outcome. The assay uses stage-specific germ cell markers identified through single-cell RNA sequencing, then measures those markers in semen with qPCR. Because semen contains germ cells from different stages of sperm development, their molecular signals may reflect what is happening inside the testes. Tan shows how the assay predicts whether sperm retrieval was successful and can identify where sperm development may be blocked. The research could help couples planning IVF or ICSI avoid unnecessary surgery, reduce financial and emotional burdens, and receive more detailed information about male infertility before treatment. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 41630]
Men with non-obstructive azoospermia may undergo microscopic testicular sperm extraction, or mTESE, without knowing whether sperm will be found. Kun Tan, Ph.D., of UC San Diego explains how molecular semen analysis could provide a noninvasive way to predict the procedure's outcome. The assay uses stage-specific germ cell markers identified through single-cell RNA sequencing, then measures those markers in semen with qPCR. Because semen contains germ cells from different stages of sperm development, their molecular signals may reflect what is happening inside the testes. Tan shows how the assay predicts whether sperm retrieval was successful and can identify where sperm development may be blocked. The research could help couples planning IVF or ICSI avoid unnecessary surgery, reduce financial and emotional burdens, and receive more detailed information about male infertility before treatment. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 41630]
Men with non-obstructive azoospermia may undergo microscopic testicular sperm extraction, or mTESE, without knowing whether sperm will be found. Kun Tan, Ph.D., of UC San Diego explains how molecular semen analysis could provide a noninvasive way to predict the procedure's outcome. The assay uses stage-specific germ cell markers identified through single-cell RNA sequencing, then measures those markers in semen with qPCR. Because semen contains germ cells from different stages of sperm development, their molecular signals may reflect what is happening inside the testes. Tan shows how the assay predicts whether sperm retrieval was successful and can identify where sperm development may be blocked. The research could help couples planning IVF or ICSI avoid unnecessary surgery, reduce financial and emotional burdens, and receive more detailed information about male infertility before treatment. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 41630]
Men with non-obstructive azoospermia may undergo microscopic testicular sperm extraction, or mTESE, without knowing whether sperm will be found. Kun Tan, Ph.D., of UC San Diego explains how molecular semen analysis could provide a noninvasive way to predict the procedure's outcome. The assay uses stage-specific germ cell markers identified through single-cell RNA sequencing, then measures those markers in semen with qPCR. Because semen contains germ cells from different stages of sperm development, their molecular signals may reflect what is happening inside the testes. Tan shows how the assay predicts whether sperm retrieval was successful and can identify where sperm development may be blocked. The research could help couples planning IVF or ICSI avoid unnecessary surgery, reduce financial and emotional burdens, and receive more detailed information about male infertility before treatment. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 41630]
>p>Broadcast from KSQD, Santa Cruz on 7-30-2026: A type of coffee brewed from beans that have been altered by passage through the digestive track of civet cats is a delicacy in Southeast Asia. A Scientific Reports paper using gas chromatography analyzed Kopi Luwak (civet-processed coffee beans) versus fresh-picked beans, finding elevated caprylic and capric acids that carry the characteristic flavor notes found in dairy products. Dr. Manuel Esteller sampled and tested the blood, saliva, urine, and stool of the oldest human Maria Branyas Morera, who died last year at 117. Despite exceptionally short telomeres, she carried anti-inflammatory genetic variants seen in long-lived dogs, worms, and flies, and had unusually high Bifidobacterium levels—likely boosted by her three-daily-servings-of-yogurt habit. Dr. Dawn defends sunscreen use against Environmental Working Group scare campaigns, noting that concerns about absorption of sunscreen ingredients into blood remain theoretical while sunburn's melanoma link is well-established. She argues that a badly sunburned toddler starts a clock that can produce melanoma by the late teens. The FDA advisory committee is reviewing certain short amino acid chains popularly known as "peptides" for potential compounding-pharmacy production, covering proposed to treat ulcerative colitis, wound healing, insomnia, insulin resistance, migraines, and osteoporosis. Dr. Dawn flags that five to seven committee members have industry conflicts of interest, but argues that even flawed approval is preferable to the current gray market, where analysis shows vials contain only 4-28% of labeled content along with endotoxin and toluene contamination. She proposes surveillance tracking of prescribed peptides to catch adverse effects early, citing a foreign melanocortin nasal spray tanning product that caused rare nasal melanomas as a cautionary example. Utah State biochemists working with the Cas12a2 CRISPR enzyme discovered that instead of behaving as a precise gene-editor like Cas9, it goes into an indiscriminate DNA-shredding mode after recognizing its target RNA. By programming it to recognize RNA sequences uniquely activated in cancer cells (embryonic-development genes that shouldn't be running in adults), researchers destroyed only the cancer cells in tissue culture, potentially offering a way to eliminate small metastases without healthy tissue toxicity. Cancer patients who received a COVID-19 mRNA vaccine within 100 days of starting immune checkpoint inhibitor therapy showed dramatically improved outcomes, with median survival in advanced lung cancer rising from 20 to 37 months. Non-mRNA vaccines (flu, pneumonia) showed no such benefit. Lab work suggests the mRNA triggers type-1 interferon release that activates tumor-infiltrating immune cells and drives them to lymph nodes to train other immune cells against the tumor. Researchers redesigned a CD40 agonist antibody to bind multiple receptors simultaneously by clustering with a second antibody, stretching the cell surface and triggering a powerful immune response. In a 12-patient trial, injecting one tumor caused all tumors to shrink in six patients and produced complete remission in two—including a melanoma patient with dozens of leg tumors and a metastatic breast cancer patient whose lung and liver tumors resolved after skin injection. Two small trials of CAR natural killer cells—engineered like CAR T-cells but derived from donor umbilical cord blood and thus potentially available off-the-shelf—showed remarkable results in autoimmune disease. All 27 systemic lupus patients targeting the CD19 protein on autoantibody-producing cells showed improvement, with some remaining in remission at nearly two years. A single Shanghai patient with systemic sclerosis showed restoration of normal skin and blood vessel structure. A paradox has emerged in advanced prostate cancer: while blocking testosterone halts early tumor growth, cancer cells eventually adapt to low-androgen conditions such that flooding tissues with testosterone in advanced disease can actually halt tumor progression by triggering cellular redifferentiation. Separately, Dr. Dawn reviews conflicting evidence on Parkinson's risk from androgen deprivation therapy, singling out enzalutamide (Xtandi) as the most concerning drug due to blood-brain barrier penetration, and recommending darolutamide as the safest alternative with matching prostate efficacy but minimal CNS entry.
Send us Fan MailMitochondrial peptide MOTS-c is a stress-induced signal that reprograms cell metabolism.TOPICS DISCUSSED:Mitochondrial Roles: Not just ATP production, but “speaker of the house” via communication molecules that “talk” to the rest of the cell.Origin of Communication: Mitochondrial peptides were likely co-opted from ancient antimicrobial factors to synchronize nuclear and mitochondrial genomes.MOTC Discovery: Identified in mitochondrial ribosomal RNA regions linked to interferon responses.Stress Induction: MOTS-c is produced in response to exercise, immune activation, and nutrient withdrawal; circulates as a mitokine.Nuclear Regulation: MOTS-c translocates to the nucleus under stress and acts as a nonspecific cofactor that shapes chromatin accessibility and gene expression.Metabolic Effects: Prevents diet-induced obesity and fatty liver in mice without altering baseline weight; engages AMPK and suppresses anabolic pathways.Immune Modulation: Shifts immune cell programs to reduce autoimmune attack in type 1 diabetes models.Aging Phenotypes: Daily or intermittent dosing doubles running capacity and preserves walking ability in old mice.ABOUT THE GUEST: Changhan David Lee, PhD is Associate Professor at the University of Southern California Leonard Davis School of Gerontology. His laboratory investigates mitochondrial communication and microproteins in the biology of aging. RELATED CONTENT:Article | MOTS-c & Cellular Energy HomeostasisSupport the showSupport my work:Good Chemistry: Personalized, science-based health consulting. Work with Dr. Nick Jikomes directly.Affiliate Partners: Visit this link to see my affiliate partners and get discounts codes for products & services to support health.For all the ways you can support my efforts.
Allt fler oinbjudna besökare tar sig in i våra hem. Lyssna på alla avsnitt i Sveriges Radios app. Skadedjur har alltid krupit vid människans sida. Forskare tror att de blodtörstiga vägglössen fanns redan i stenålderns grottboningar. Genom historien har olika typer av ohyra inte bara gett oss kliande bett och förstört våra matförråd, utan också orsakat några av mänsklighetens mest förödande sjukdomsepidemier.Under några decennier på 1900-talet, när en rad nya och kraftfulla bekämpningsmedel gjorde entré, såg det ut som att människan äntligen höll på att vinna den tusenåriga kampen mot krypen.Men segervittringen blev kortvarig. Skadedjuren är tillbaka. De blir fler, de sprider sig till nya platser – och de har blivit allt svårare att bekämpa.Programledare och producent: Anna Lillkung och Wendela AntepohlOrdlistaVektor – en organism, till exempel en råtta eller en kackerlacka, som för över smittämnen mellan varelser.Patogen – ett sjukdomsframkallande smittämne, till exempel ett virus eller en bakterie.Mikrob – en organism som är så liten att den inte syns med blotta ögat, till exempel ett virus eller en bakterie.Resistens – en organisms förmåga att stå emot yttre påfrestningar, till exempel en bakterie som utvecklat motståndskraft mot en eller flera typer av antibiotika.KällförteckningMedverkandeThomas Persson Vinnersten – Biolog och entomolog på AnticimexLisa Sarasohn – Historiker och författare till Getting Under Our Skin: The Cultural and Social History of VerminBobby Corrigan – Skadedjursbiolog med fokus på gnagareÅke Lundkvist – Professor i virologi vid Uppsala universitetTuomas Aivelo – Assisterande professor i biodiversitet och samhälle vid Leiden University i Nederländerna och grundare till Helsinki Urban Rat ProjectJose Pietri – Docent i mikrobiologi och entomologi vid Purdue UniversityBöckerGetting Under Our Skin: The Cultural and Social History of Vermin (Lisa T. Sarasohn, 2021)Rats : A Year With New York's Most Unwanted Inhabitants (Robert Sullivan, 2004)Plagues, Poisons, and Dead Rats: A Multispecies History (Lucinda Cole, ur boken The Palgrave Handbook of Animals and Literature, 2020)Never Home Alone (Rob Dunn, 2020)Artiklar/källor i urvalSkadedjur i byggnader – en kunskapssammanställning (Malmö universitet på uppdrag av Boverket, 2025)Challenges in current pest management practices: Navigating problems and a way forward by integrating controlled release system approach (Singh et al., Chemical Engineering Journal, 2024)How pest control has changed in 100 years (Rentokil, 2025)Studie: Myror lika bra som gifter mot skadedjur (SvD, 2022)“They're always there”: resident experiences of living with rats in a disadvantaged urban neighbourhood (BMC Public Health, 2019)Increasing rat numbers in cities are linked to climate warming, urbanization, and human population (Science Advances, 2025)Reconsidering the “War on Rats”: What We Know From Over a Century of Research Into Municipal Rat Management (Corrigan, Himsworth, Byers, m.fl, Frontiers in Ecology and Evolution, 2022)Surveillance of Emerging Rodent-Borne Pathogens in Wastewater in Taiwan: A One Health Approach (Tropical Medicine and Infectious Disease, 2024)Bedbugs Could Be More Horrifying Than You Think. They might be capable of spreading disease, recent research shows. (The Atlantic, 2024)Anticoagulant rodenticides and resistance development in rodent pest species – A comprehensive review (Journal of Stored Products Research, 2020)Public Health Significance of Urban Pests (World Health Organization, 2008)Rodenticide Toxicity (StatPearls Publishing, 2026)Increasing rat numbers in cities are linked to climate warming, urbanization, and human population (ScienceAdvances, 2025)Public and media interest in bed bugs – Europe 2023 (Current Research in Insect Science, 2024)Large-scale structure of brown rat (Rattus norvegicus) populations in England: effects on rodenticide resistance (PeerJ, 2015)”Hysterisk” ökning av klädesmal (Sveriges Radio, 2015)Second hand–trend bidrar till att fler har problem med pälsmal i hemmen: ”Var extra noga om du köper möbler” (Smålandsposten, 2023)De äter på mattor och kläder – så blir du av med klädmal (Göteborgs-Posten, 2024)Revenge of the clothes moths: as numbers boom, can they be stopped? 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Scientists are investigating new scenarios (Science, 2026)A timeline of the hantavirus outbreak on cruise ship (AP, 2026)Hantavirus outbreak linked to cruise ship travel, Multi-locations (World Health Organization, 2026)Sjukdomsinformation om hantavirusinfektion (Folkhälsomyndigheten)Mjölbaggar erövrar studentboendet: ”Inte mitt hem längre” (SVT, 2025)Silent Carriers: The Role of Rodents in the Emergence of Zoonotic Bacterial Threats (Pathogens, 2025)8 av 10 stockholmare har sett råttor (Anticimex, 2019)Silverfiskar vanligast men inte så farliga (Hem & Hyra, 2017)MusikGeoff Barrow, Ben Salisbury – Dream RealityCristobal Tapia De Veer – Pain SpeedballKid Loco – Theme from the Graffiti ArtistMarcus Bagalà – Duco in Mara's RoomCliff Martinez – I'm in the PinkMarcus Bagalà – Frets: Problem, After ProblemMartin D Fowler – 1 Ships VIIRamin Djawadi – Winter is ComingAlberto Iglesias – TreasureCliff Martinez – Save Some For UsJocelyn Pook – Driving to PrisonCliff Martinez – I'm SickAlice Cooper – PoisonCliff Martinez – Placental RepairJessica Dannheisser, Adele Roberts – Parade of the GeeseCliff Martinez – Speight Lived HereOchre – Midsummer Nice DreamMarcus Bagalà – Wires: WinchimesMichael Andrews – Peter and SylvieK2 – Bexar BexarCliff Martinez – Navy FuneralMike Patton – Murder is WorkMartin D Fowler – 1 Ships XIITrent Reznor, Atticus Ross – Empty Places (Reprise)Cliff Martinez – Same SweatpantsCristobal Tapia De Veer – The PublicJeff Beal – I think I Smell GasTrentemöller – Take Me Into Your SkinTrent Reznor, Atticus Ross – Clue OneKyle Dixon, Michael Stein – ElevenStar Hopper – Through the HeliopausePaul Leonard-Morgan – Anderson's ThemeMartin D Fowler – 1 Ships IIIJon Brion – You LearnThe Mariachis – La Cucaracha
The CEO of New Zealand's biggest independent medical research organisation, the Malaghan Institute, says the ongoing challenge of funding the organisation keeps her up at night. Professor Kjesten Wiig oversees research into groundbreaking cancer treatments and RNA technology, but says it's juggling the institutes' sources of income that remains a constant concern. In 2015, for example, 61 percent of the institutes' income came from government grants, but last year that had fallen to just 26 percent, even as Malaghan brings the game-changing CAR T-cell cancer therapy ever closer to New Zealand patients.
Two years after researchers identified ReNU syndrome, where are we now? In 2024, two independent research teams identified the genetic cause of ReNU syndrome, a rare neurodevelopmental condition affecting thousands of people worldwide. The discovery marked the beginning of a new chapter for families searching for answers and opened up exciting new avenues for research. In this episode, host Sharon Jones revisits the story to explore what has happened since that breakthrough. She is joined by: Professor Nicky Whiffin, Associate Professor and Wellcome Career Development Fellow at Big Data Institute and Centre for Human Genetics, University of Oxford Christina Cox, Co-founder of ReNU Syndrome UK and parent of a child with ReNU syndrome Dr Ana Lisa Tavares, Clinical Lead for Rare Disease at Genomics England Together, they discuss how researchers around the world have built on the original discovery to deepen our understanding of ReNU syndrome, why studying the non-coding regions of our DNA is revealing previously unknown rare conditions, and how collaboration between researchers, clinicians and families is accelerating progress. They also explore how the growing ReNU community is supporting newly diagnosed families and what the future could hold for new treatments. Links: Previous episode detailing the discovery of ReNU Syndrome ReNU Syndrome UK's website Original research paper from Nicky's team in Oxford Original research paper from the team based in New York “It's been only two years since our paper came out about this, and in that time, there are now patient family groups that have been set up all around the world. There is the one in the UK led by Christina and the others. There's the one in the US that's led by a group of four women, and there are ones in France, Spain, like, literally all around the world. And all of these groups are also somewhat coordinated. The leads of these groups meet with each other. They've organised meetups. I've been to ones in the US, the UK, and in France. So the fact that they can mobilise all of that and create such a community so quickly is absolutely incredible.” You can download the transcript, or read it below. [00:00:00] Sharon: In 2024, two independent research teams identified a genetic cause of a rare neurodevelopmental condition affecting thousands of people around the world. Since then, that initial groundbreaking discovery has grown into something much bigger, bringing together families, researchers, and clinicians, and building a clearer picture of what we now know as ReNU syndrome. [00:00:26] Sharon: Welcome to Behind the Genes, the podcast that covers everything from cutting-edge research to real-life stories in genomic healthcare. I'm Sharon Jones, and in today's episode, we're looking at what's happened since that discovery, what researchers are continuing to learn, and what the future could hold for people living with ReNU Syndrome and their families. [00:00:46] Sharon: To help us understand more, I'm joined by Professor Nicky Whiffin, Christina Cox, and Dr. Ana Lisa Tavares. So, two papers were published around the same time for this condition. To start us off, Nicky, you worked on one of these papers. Could you explain how this journey first began? [00:01:05] Nicky: Yeah, so this was two years ago now, back in early 2024, where two research teams, so us based in Oxford and a, a group based in New York, were both looking at the data within the National Genomics Research Library, and we both kind of somewhat simultaneously found that there was variance in this very, very small gene, it's called RNU4-2, were found in individuals with previously undiagnosed neurodevelopmental disorders. [00:01:39] Nicky: And this was very, very striking because we initially actually identified the same single DNA change or mutation in 40 or so different individuals within the National Genomics Research Library, and we normally expect to see a whole host of different variants. We don't expect to see the same one. [00:01:59] Nicky: So this was a really, really surprising finding. And it was through a collaboration, large scale collaboration across the world where we started contacting our other collaborators who have similar collections of patients who have been genome sequenced to ask if they had any individuals with DNA changes in this gene. [00:02:17] Nicky: And we found some in the US, some in, in Australia, some in France and Germany. So very, very quickly built up this, this complete picture of variants in this gene, causing this rare neurodevelopmental disorder [00:02:35] Sharon: of people finding it at the same time, what, what did that feel like? [00:02:39] Sharon: Like, give us a ense of, like, that compelling, "We think we found something." What was that like? [00:02:46] Nicky: I didn't believe it initially. You're always told when you're a scientist that if it looks too good to be true, it's, it's not true, and this basically lit up like a beacon. There's this particularly one DNA change that we found in, um, I think it was about 40 different individuals, and we don't really expect that to be the case. [00:03:04] Nicky: We normally expect these genetic variants to be somewhat randomly distributed across the genome. So to find 40 individuals with exactly the same DNA change was very, very surprising. So initially, I didn't believe it. The whole team, including folks at Genomics England, spent a lot of time trying to check that these variants were real and tried to disprove the result, tried to find any other way in which any other reason why we would be seeing this. [00:03:31] Nicky: And after a little while, we had to concede that we couldn't disprove it, so it must be true, and that, that was a very exciting moment. [00:03:38] Sharon Jones: Was it the case that over in the States, the exact same thing was happening? [00:03:42] Nicky: I think we found out when we were both speaking at the same conference, actually. So we didn't actually know that we, that we'd both come across the same result. [00:03:49] Sharon: If you want to check out our previous episode on this initial discovery, you'll find a link to it in the episode description. [00:04:00] Sharon: So Christina, tell us a bit about your situation, your family situation, and for our listeners, what ReNU is. [00:04:05] Christina: So ReNU is, to us, is a family. We got a family when we got diagnosed with ReNU. Beau - Arabella - already had other diagnosises, but people had always said to us, "Oh, there's something else. There's something else. [00:04:20] Christina: We're not sure what it is, but there will be something." And then when we got ReNU, it was like, "Oh, okay, amazing. What do we do? What is it?" Because there was only four lines on Wikipedia when we first got told about it, and there wasn't anything that, ourselves could find. So we kind of went onto Facebook and looked for groups and different people, and there wasn't really anything except for Jess in America. [00:04:46] Christina: And then it grew, and then it kind of, we ended up finding more people in the UK and, like, all over. But for us, it didn't really change how we perceived Beau. It just made life easier. Like, knowing there was other families out there that we could find advice from and support from, and that we kind of knew what we had and going forward then, like, finding researchers and connecting with everybody. [00:05:15] Sharon: Yeah. And for those who don't know, can you talk about what ReNU is? Like, how does it affect Beau? [00:05:20] Christina: So with Beau and ReNU , it affects her with developmental delay. She's non-verbal. She's incontinent. She suffers for walking, so she can do a little bit of walking, but she needs a wheelchair It affects her mood swings. [00:05:38] Christina: It just affects everything. Although she has it, she's still a happy, outgoing, very stubborn, just kind of "keep-going" child. But it affects her in everything, like eating, sleeping. [00:05:51] Sharon: It sounds like life is, you know, very challenging on a day-to-day basis, lots of considerations. How did you feel when you finally got this diagnosis after years of wondering and waiting, not knowing? [00:06:02] Christina: Finding out was, like, really emotional because it was like, "Oh, wow, so we have this diagnosis. Now what? What are we looking for? What's going to happen?" And then we were kind of like, "Oh, but there's not many people that had it." Because we found out in the August, so then it was trying to find people. But it has been life-changing to know that we're not on our own and that there is other people around. [00:06:28] Sharon: Yeah, tell us a bit more about that. How did it feel to get that diagnosis? [00:06:32] Christina: It was quite strange because our pediatrician rang us and said, "Oh, we've got a diagnosis. She's got RNU4-2." And we were like, "Okay, so what's that?" And she's like, "I don't really know. There's four lines on Wikipedia at the moment." [00:06:46] Christina: She goes, "I don't like Wikipedia," but we still kind of... That was it. So then we went on a mission to find and look for where we could find support and find other families. [00:06:58] Christina: At that point, I didn't know of anybody in the UK, and my husband found Jessica in America. What then, kind of, we had somebody to talk to, and then families in the UK kind of started appearing. [00:07:09] Christina: So we ended up getting a whole network of people to bounce ideas off and talk about how it affects their children and what's for the future and things like that. It was really nice. [00:07:22] Sharon: Yeah, yeah, I can imagine. So Ana Lisa, how do these findings contribute to a growing understanding of the condition? [00:07:29] Ana Lisa: So this was an amazing discovery. Although we're finding new rare conditions quite often, not on this sort of scale. It was also an amazing finding because a lot of the genes that we know are associated with rare conditions are genes that encode proteins, and in the 100,000 Genomes Project, we were doing whole genome sequencing, and Nicky and her team were looking in the parts of the genome that don't encode for proteins. [00:08:03] Ana Lisa: And so this was, uh, exciting from that point of view as well. So the vast majority of our genome, more than 98%, does not encode for proteins, but it's relatively unexplored. And if we think about our genome and the letter code that makes it up, which is the manual for how our bodies are built, and grow and function day-to-day. [00:08:30] Ana Lisa: Those 3 billion letters, if you, if you printed them out in a 12 font regular print, it would stretch so far you could fly, I think, from London to Paris several times, maybe three times or something. And so, this actual gene is a very, very small gene, less than 150 of those letters. So again, it was incredible to find that by comparing across many, many different genomes in the National Genomic Research Library. [00:09:00] Ana Lisa: Going back to your question about a growing understanding of a condition, it was a completely new condition, but it also opened up looking at other related genes and actually now more disorders that are being found, like RNU2-2 by colleagues in the US, and that might be one of the most common recessive genetic neurodevelopmental disorders. [00:09:27] Ana Lisa: So it's really, really opened up this understanding about these types of disorders and also those non-coding parts of our genome and the power of collaboration and being able to look across many different whole genomes at the same time. [00:09:44] Sharon: Yeah. And Nicky, you've been involved in much of this research journey. [00:09:50] Sharon: What have been some of the biggest advances or learnings for you so far? [00:09:55] Nicky: I think the biggest one is just how common, or how frequent, these disorders are. So what we discovered recently in terms of new genetic disorders were rarer and rarer conditions, and that's why we hadn't seen them before. But from going from looking at the protein coding genes to looking at these non-coding genes, we found something that was as frequent as disorders that were found in the early 2010s when we first had large-scale sequencing projects that looked at the protein coding genes. [00:10:26] Nicky: So that was really, really surprising. And we now know there's this whole class of disorders. So RN4-2, this gene encodes this -- Well, it produces this small RNA that works in this huge molecular machine that is called the Splicer Zone, that mediates the processing of most of the other genes across the genome. [00:10:50] Nicky: And there are lots of these little RNAs that work in this molecular machine that are called the small nuclear RNAs or the snRNAs And we now know that there are a whole multitude of different disorders associated with different ones of these spliceosomal small nuclear RNAs, and that's really incredible. [00:11:09] Nicky: And for RNU4-2 itself, we also now know that there are, there's not just RENE syndrome, uh, which is a dominant disorder caused by chance de novo variants that are newly arisen in a child, but also a recessive disorder where a child inherits one, uh, gene mutation from each parent. And also another finding that there is a region of the gene where we find DNA changes that cause retinitis pigmentosa, so a retinal phenotype. So we now know a huge amount more about this single gene, but also all of this different class of genes or RNAs that work in the same molecular machine, uh, which is, is really fascinating biologically [00:11:52] Ana Lisa: Vicky, while you were talking, I was thinking about the splicing and how a bit like this podcast recording, you're going to splice out the kind of extreme, the noise that wasn't supposed to be there. [00:12:03] Ana Lisa: And actually, you could make slightly different versions of this podcast, couldn't you? And that's, that's what, what's happening in our bodies for a lot of our genes that, that the kind of output can be varied slightly. [00:12:15] Sharon: So Christina, how has collaboration been involved across the community and with researchers? [00:12:21] Sharon: You know, what sort of things have you been doing? [00:12:23] Christina Cox: So it's amazing to have researchers that are so open and amazing to work with the families. So at the moment, we are just putting together like a panel to discuss questions from families, to then be able to answer families, to work very closely with the researchers for what things are happening and the progress within. [00:12:47] Christina: It's just amazing to be able to work with researchers. They're just fantastic. [00:12:52] Sharon: And from what I understand, like, you, you have a charity, don't you? Can you tell us a bit more about that and how that came about? [00:12:58] Christina: So we have ReNU Syndrome UK, and it came about as there was a group of us parents that were like, we wanted to be able to support other families, knowing what it was like for us when we first started. [00:13:12] Christina: It was very difficult. So we wanted to start a charity that can support families and signpost them, give them the opportunity to have family meetups once or twice a year, so we can work with scientists and specialists to keep everybody in the community, like the ReNU family, up to date. But being able to connect with so many families, because a lot of the doctors don't really know of ReNU Syndrome yet. [00:13:46] Christina: So if we have a problem or a question, we put it in the WhatsApp group, and then somebody can answer it because they've been through it, or they, they've just asked the question. So it's just an amazing resource for everybody [00:14:02] Sharon Jones: That sounds amazing, and it sounds like you've all obviously become experts by experience. [00:14:04] Sharon: So, like you say, you kind of know more, you know, as the science develops, but you're living it every single day [00:14:10] Christina: It's kind of, you go into the hospital and they're like, "Oh, what's ReNU Syndrome?" And then you're like, "Ugh." So, then you just have to say it all. But, and then it's kind of them bringing, teaching new people who don't know about it in the medical professional. [00:14:26] Christina: We always give them the website so that they can go and then find, but being able to put more medical stuff on the website, it just helps everybody, and it's just broadening it out to as many people as possible. Because there's still a lot of people undiagnosed with RNU syndrome. It's, now it's easier to be signposted, but it's just keeping that connection. [00:14:49] Sharon: Yeah. And, and from what I understand, it's got quite an interesting sort of origin of a name, RNU. Where did that... Do you know much more about where that came from? [00:14:57] Christina: So, Nicky is the amazing person who, um, sorted the name and um, the origin. So, I'll pass that over to Nicky to answer that question because she's just amazing [00:15:11] Nicky: Uh, so the name ReNU syndrome is an interesting story. [00:15:13] Nicky: So, a lot of disorders or diseases are named after people. So, we all know Alzheimer's, Parkinson's, etc. And they're often scientists or clinicians that have spent a lot of time working on them. I think that's a little bit odd. I don't think it's the first thing that somebody should know about a disorder, is the name of somebody who's, who's worked on it or studied it. [00:15:36] Nicky: But they're a very, it's very hard to find an alternative. When we were initially doing the press release around our paper, we had a quote from one of the mothers, Nicole Cedar, who has a, a wonderful daughter called Mia Joy, and she said that within their family, they like to refer to RNU, to RNU4-2 as ReNU, which is a really nice play on the RNU in the gene name. [00:16:00] Nicky: So then I had an idea, okay, let's just change the spelling to make the, the kind of big R, little E, large N-U, then it would link to the gene name, but also would be a name that speaks to hope and the renewed hope of being given a diagnosis. [00:16:13] Sharon: Yeah, absolutely, and that's a great, a great story and a great way of kind of making it feel like there is, there is always hope. [00:16:20] Sharon: So, you know, Nicky, you're now part of the patient community. In a way. You know, so how does it feel to be on that other side of it from that sort of research perspective and now kind of, you know, in that, in that community? [00:16:34] Nicky: It's amazing. I've got a new family as well. It's not, not just Christina and everybody. [00:16:39] Nicky: I kind of, I'm a, a basic scientist. I'm not a clinician. Up until this point, we've always been one or two steps removed from actually interacting with the families themselves. Um, so my life has changed an awful lot over the last couple of years, uh, where now, um, I kind of talk to Christina or the folks in the US, really regularly, kind of on a weekly basis. [00:17:02] Nicky: Um, so that's really different. And I just kind of want to highlight just what these families have achieved. So it's been only two years since our paper came out about this, and in that time, there are now patient family groups that have been set up all around the world. There is the one in the UK led by Christina and and the others. [00:17:26] Nicky: Um, there's the one in the US that's led by a group of four women, and there are ones in France, Spain, like, literally all around the world. And all of these groups are also somewhat coordinated. The leads of these groups meet with each other. They've organised meetups. I've been to ones in the US, the UK, and in France. [00:17:46] Nicky: So the fact that they can mobilise all of that and create such a community so quickly is absolutely incredible. And they've got families, they've got so many researchers that are interested in the cause. They're interacting with the pharma companies. They've upskilled themselves to learn so much about genetics. [00:18:04] Nicky: And it's just an absolutely incredible thing to watch. They're so, so inspiring. [00:18:09] Sharon: And from what I understand, Christina, you feel, you know, very passionate about Nicky in the same way, about your paths crossing in this way. [00:18:16] Christina: Oh, my, yes. Every time I see Nicky, I've met her a couple of times, like, in person now, I just cry. [00:18:22] Christina: I literally, we saw her at the UK meetup, and she walked in the door, and that was it. I was done. I was like, it's just meeting somebody who has changed so many lives and brought a community to other families. It's just amazing. And the support that Nicky's giving us weekly, daily, is just amazing. It is just life-changing for all of us. [00:18:49] Sharon Jones: It's such a powerful connection. So Ana Lisa, why is collaboration between researchers, clinicians, and families so valuable in the rare disease research space? You know, and what role do large scale research projects and data sharing play in discoveries like this? [00:19:06] Ana Lisa: Collaboration is completely incredibly valuable and for progress in the rare disease space where there's just so much still to learn. [00:19:16] Ana Lisa: So more than half of patients and families where, uh, they're seeking a potential diagnosis, we're not yet able to, to find one, and there's so much yet that we still need to learn, and collaboration in so many different spaces and directions and across different spheres enables this progress. So for example, the fact that we have a really connected, uh, National Health Service and really close working between the NHS and Genomics England so that we can, for those patients and families that, that consent to their de-identified data being shared in the National Genomic Research Library, be able to work with many, many different researchers, uh, whether they're academic, institutions, industry, and try and find all the patients that could benefit from a new diagnosis and, uh, potentially new therapies in future clinical trials. [00:20:21] Ana Lisa: And without that collaboration, it would be really, really hard to find all those people So because we sort of have a clinical research interface where we can go back to clinical teams and therefore to patients and families, even if there's a really, really ultra-rare condition with very few people known to have it that could be under different specialties in different regions, we would be able to contact their clinical team. [00:20:51] Ana Lisa: So I think that, that collaborative working with the NHS is really powerful across researchers worldwide. Like in this example where a group in Oxford and a group in US were able to make this finding and then all the other findings that are coming from it. And really, without being able to compare across thousands of genomes, one wouldn't have been able to see this, this particular signal and see that there were more than 100 patients, and that was really powerful. [00:21:20] Ana Lisa: If you just had one genome, you could never have made this novel discovery. I think the other thing is that, and Nicky will say that, you know, she, she then contacted her collaborators who also had access to, to, to data that had been shared by other families and could compare. And again, it's a whole sort of network across the globe. [00:21:41] Ana Lisa: And we know that there are going to be many more diagnoses to be found. But also, um, I think collaboration will allow us to find new, new treatments. So if we can start to design treatments that target the DNA and RNA at, at source, then actually you could collaborate and say, "Well, this type of genetic mechanism could be targeted in the same way, potentially across even more than one rare condition and reach even more patients." [00:22:13] Ana Lisa: And actually the power of collaboration across the ecosystem is that hopefully we'll end up with a pathway that can actually go from finding a new genetic finding, like Nicky and her team made, to helping all the people who could benefit from a diagnosis, having one, and then can one develop a treatment and get it to as many patients? [00:22:42] Ana Lisa: And, and I think that will really demonstrate the power of collaboration. [00:22:47] Sharon: Yeah. Absolutely, and it can only, you know, benefit those families who have to wait such a incredible amount of time. [00:22:55] Ana Lisa: There's been such a diagnostic odyssey, and as more diagnoses are made, it becomes obvious that there's, uh... [00:23:03] Ana Lisa: and it was, it's already well-described, the therapeutic odyssey. Um, but hopefully these sort of novel understanding of our genome and opening up new biological avenues to treat, um, hopefully will also enable many more new treatments to be developed. [00:23:21] Sharon: Absolutely, and that is the key word there is, is that hope. [00:23:24] Sharon: So, so looking ahead, Nicky, what developments are you most hopeful about over the next few years? [00:23:31] Nicky: That's a difficult question. There's so much, so much happening. One thing is that we are gearing up to do large scale studies across the world to understand more about the progression of ReNU. So you might call them large scale natural history studies or just large scale profiling studies where we can do a range of different tests on ReNU patients and, and monitor them over time. [00:24:02] Nicky: So do those at regular, regular intervals over time so we can see what the progression looks like. And that's really important for trying to think about whether we can treat RNeU syndrome. And on that note, I'm very also excited about the potential for therapeutics. There's lots of people all around the world, both, uh, in academic settings, but also in pharma companies trying to work out whether this is something that we can treat. [00:24:30] Nicky: There's some very promising early data to show that we can selectively remove the RNA containing the mutation from cells, uh, leaving the copy of the RNA that doesn't contain the mutation intact so that can do the correct function. And biologically, we think this should be an effective treatment. [00:24:54] Nicky: Um, so we can do that in cells in a dish. We don't yet know whether we can do that in a patient with ReNU. Uh, but that's really, really promising early data. Um, so I'm very hopeful about where that, those studies might lead. [00:25:08] Sharon: And Ana Lisa, what role will genomics continue to play in improving understanding and care for rare conditions like this? [00:25:15] Ana Lisa: So following on from what Nicky said, I think the really big hope is that we will be able to develop many, many new treatments collaboratively across the world. And whether these are individualised treatments made for one patient but then shared because we can find perhaps other patients who could benefit from the same treatment, whether we understand the genetics better so that we can design treatments from the start that will work for a lot of patients. [00:25:46] Ana Lisa: So I think there will be sort of fancier and fancier ways of targeting rare conditions. And right now we're in a phase where the ecosystem is trying to work out how could we make an end-to-end pathway with initiatives like the Rare Therapies Launchpad in the UK, and that's going to require truly collaborative working. [00:26:08] Ana Lisa: No single organisation can do that. And I think having these incredible use cases will be really powerful for turbocharging the development of these pathways. And the hope is that once you've worked out how to do this across a range of different rare conditions, that one might reach a stage where one could do that a lot faster for many other rare conditions. [00:26:35] Ana Lisa: Because at the moment they're so underserved in terms of treatments available and there's a huge gap between being able to make a genetic diagnosis and then having treatments. The big hope is that understanding the genetics better will help to open up new pathways to treatment. I do hope that we'll also understand other aspects. [00:27:02] Ana Lisa: So for example, it might be that understanding the genetics better also helps us to understand different ways a condition might manifest in somebody, why it may be different from one person to another, why somebody might be more mildly affected and somebody perhaps more severely. And that might, may also help us to understand ways to treat a condition by getting, gaining these insights which are, are useful in and of themselves and may also lead to new therapeutic, uh, possibilities. [00:27:36] Ana Lisa: I think that would be one of my hopes that a lot of these areas overlap and lead to real benefit for patients and families, that we can translate that hope into concrete improvements in treatment for rare conditions. [00:27:57] Sharon: Do you have a sense of time, how long you think this could all take, that amount of collaboration? [00:28:06] Ana Lisa: Yeah, and I think this is actually another reason why sometimes it's quite tricky to make progress in this area because being able to predict those timelines is notoriously difficult when you look back historically. I'd like to hope that we're on the cusp of having an explosion of novel treatments that can target DNA and RNA, for example, or treatments that target something in the underlying biology that we now understand that we didn't before. [00:28:34] Ana Lisa: And I do think that there is going to be a big shift. But I think that the sort of confidence intervals around how big that range of time might be is very hard to predict. And that's why I think Christina and Nicky being able to share these stories and about their collaborative working really shines a spotlight on, on what could be done and how progress can happen. [00:29:02] Ana Lisa: That's really exciting. The other day at a conference, someone from industry stood up and said, "Oh, actually, we set up a clinical trial in the UK because we knew there were patients who could benefit from our work in the National Genomic Research Library," and that was really exciting for us because that's what we want to do; move forwards the opportunities for treatment for patients. [00:29:28] Sharon: And so finally, Christina, as a parent and member of this community, what are your hopes for the future, and what would you say to families who may still be searching for answers today? [00:29:39] Christina: It is a long journey, but there is the support and the help out there. If you have any inclination that you think you might have ReNU, reach out to your paediatrician or your doctor to see if you can get your genetic testing done because it's fighting to get the test, to go to people and say, "I think this is what we may have. Can we look into getting it tested?" And reach out to other families and the website and things because it's all about community and supporting and helping people find that diagnosis. [00:30:16] Sharon: Thank you, Christina, and we'll put the website in the episode description. A huge thank you to Professor Nicky Whiffin, Christina Cox, and Dr. Ana Lisa Tavares for joining me today and sharing their insights and experiences. To learn more about ReNU Syndrome, visit renusyndromeuk.org. If you'd like to hear more stories about the people, research, and discoveries helping to shape the future of healthcare, subscribe to Behind the Genes on your favourite podcast app. [00:30:45] Sharon: Thank you for listening. I've been your host, Sharon Jones. Behind the Genes is produced by Deanna Barac, Florence Cornish, Sophie McLachlan, and Katie Revell at Bespoken Media.
Welcome back to the Jack Westin MCAT Podcast with Mike and Molly! Last episode was hemoglobin. This episode we zoom out even further and ask the question that underlies everything: what is the blueprint that tells your cells what to make in the first place?This is the DNA and RNA episode. And yes, it connects to basically everything you have already studied.
Updated inflation projections are only part of the story when it comes to pharmacy planning. Host Carolyn Liptak is joined by Dr. Jeni Hayes and Dr. Amanda Frick, to discuss Vizient's Summer 2026 Spend Management Outlook and why utilization trends, reimbursement, ambulatory care, and the expanding pipeline of advanced therapies are becoming just as important as inflation when preparing health systems for 2027 and beyond. Guest speakers: Jeni Hayes, PharmD, MS Pharm, BCPS Senior Clinical Manager, Market Insights & Forecasting Vizient Clinical Spend Management Amanda Frick, PharmD, BCPS Senior Clinical Manager, Market Insights and Forecasting Vizient Clinical Spend Management Host: Carolyn Liptak, MBA, BS Pharm Pharmacy Executive Director, Regulatory Compliance Vizient Center for Pharmacy Practice Excellence Show notes: 01:03 Why this year's Spend Management Outlook expands beyond inflation to include utilization, reimbursement, product mix, and operational readiness. How pharmacy leaders can use these broader market signals to make stronger strategic and financial decisions. 01:54 The updated 2027 pharmaceutical inflation projection and why it increased from the previous forecast. Why organizations should pair national benchmarks with their own purchasing data to improve budgeting accuracy. 03:28 Three major trends transforming pharmacy planning, including ambulatory growth, utilization, and enterprise collaboration. Why these consistent themes are changing how health systems approach long term pharmacy strategy. 04:25 How new utilization analyses provide earlier insight into future pharmacy demand than inflation data alone. Examples of shifting trends in oncology therapies and GLP 1 medications that are influencing operational planning. 05:34 Why GLP 1 growth is creating opportunities that extend well beyond pharmacy budgeting. How retail pharmacy, specialty pharmacy, pharmacist led clinics, and medication management can strengthen patient care and organizational performance. 07:10 Why pharmacy has evolved into an enterprise wide capability that impacts access, reimbursement, and financial performance. How stronger collaboration across pharmacy, finance, revenue cycle, and clinical teams supports future readiness. 08:03 Emerging pipeline trends, including continued oncology growth and the rise of advanced therapies. Why cell therapies, gene therapies, and RNA based medicines require organizations to prepare differently than traditional medications. 08:53 How health systems are preparing months before therapy approval by building operational and clinical infrastructure. Why advanced therapies demand coordination across pharmacy, laboratory, nursing, finance, and physician teams. 10:33 The expansion of advanced therapies into autoimmune, neurologic, cardiac, and rare disease treatment. Why organizations must balance planning for both high cost therapies and therapies with growing patient demand. 11:44 How pipeline monitoring has evolved into a strategic planning tool rather than simply tracking approvals. Why early preparation helps organizations identify operational gaps before new therapies reach the market. 12:36 Key takeaways on preparing for the future of pharmacy through utilization data, operational planning, and enterprise collaboration. Resources available through the Spend Management Outlook Insights Hub to support local budgeting and long term strategy. Links and Resources: Vizient Spend Management Outlook Insight Hub Subscribe Today! Apple Podcasts Spotify YouTube RSS Feed
In this episode of Healthcare Beans, James speaks with Ryan Polselli, MD, founder and CEO of MammoLink, about why breast cancer screening remains underused despite decades of awareness, established clinical guidance, and broad insurance coverage. Ryan argues that the core problem is not simply awareness. Screening often conflicts with work, family responsibilities, appointment availability, financial uncertainty, and the natural tendency to postpone preventive care when no symptoms are present. He explains how MammoLink brings mammography and ultrasound directly to workplaces, schools, government sites, and rural communities through patient-centered mobile imaging units. The conversation also explores price transparency, payer quality incentives, direct-pay demand, rural health infrastructure, employer-sponsored screening, nationwide expansion, and the role of data and emerging technologies in the future of breast cancer detection. Episode Timeline 00:00 — Introduction to Ryan Polselli and MammoLinkRyan introduces his background as a board-certified radiologist and breast-imaging specialist and describes his focus on improving access to breast cancer screening. 01:02 — The breast cancer screening paradoxDespite widespread awareness and strong evidence supporting screening, many women still do not receive regular mammograms. Ryan explains why awareness alone has not produced sufficient action. 03:35 — Where the screening process breaks downThe discussion examines the balance between personal responsibility and system responsibility, including the burdens created by work, family obligations, and limited appointment availability. 04:56 — Designing preventive care around human behaviorRyan contrasts urgent medical care with preventive screening. When patients feel healthy, completing screening requires a proactive decision without the emotional urgency that drives emergency care. 06:06 — Making screening compatible with everyday lifeRyan argues that screening must be redesigned around how women actually live rather than requiring patients to navigate numerous scheduling and logistical barriers. 07:12 — Financial barriers and uncertaintyInsurance may cover a routine mammogram, but patients can still face uncertainty involving supplemental imaging, dense breast tissue, diagnostic follow-up, and unexpected bills. 09:23 — Delayed results and lost momentumLong waits for results can increase anxiety and weaken engagement. Ryan explains why faster feedback can restore patient control and encourage better screening habits. 10:39 — From patient experience to systems changeMammoLink began as an effort to improve the individual screening experience but evolved into a broader model connecting patient behavior, economics, employer interests, and payer incentives. 13:04 — How the mobile imaging model worksRyan describes mobile units containing mammography, ultrasound, changing areas, procedure rooms, and other features typically found in an outpatient imaging center. 13:55 — Bringing screening into workplaces and communitiesRecurring visits to schools, employers, municipalities, and government sites allow patients to receive screening where they already spend their time. 14:20 — Social reinforcement and screening adherenceCoworkers can encourage one another to participate, while returning to the same location each year can make regular screening easier to remember and complete. 16:09 — The economics of mobile mammographyMobile screening carries higher capital and operating costs than traditional outpatient imaging, but Ryan describes it as a high-cost, high-yield model capable of reaching populations that might otherwise remain unscreened. 17:00 — Legislative and payer tailwindsCoverage changes involving supplemental breast imaging, along with growing payer interest, may improve the economic viability of comprehensive mobile screening. 18:27 — Access is also about timeRyan emphasizes that patients can be disadvantaged by limited time and flexibility even when they are not financially disadvantaged. 19:54 — Incentives within traditional imaging pathwaysThe conversation considers how fee-for-service payment can encourage separate visits, while a mobile model has stronger operational reasons to complete as much of the episode as possible in one encounter. 21:02 — HEDIS measures and payer motivationRyan explains how quality measures and Medicare Advantage star ratings can create significant incentives for health plans to improve breast cancer screening rates. 22:27 — MammoLink's no-surprise-billing approachRyan describes the company's decision not to send patients an unexpected bill after the visit, even when that means accepting some lost revenue. 25:05 — Technology supporting payment verificationMammoLink is using automated insurance-verification technology to improve up-front accuracy while preserving its principle of no back-end patient billing. 25:30 — Can transparency increase competition?The discussion turns to whether better consumer awareness of price differences between hospitals, outpatient centers, and alternative providers can eventually place downward pressure on costs. 26:46 — Direct pay, privacy, and convenienceRyan discusses the growing number of patients who choose cash payment because they value privacy, simplicity, or freedom from insurance-related friction. 27:51 — Supporting patients after an abnormal findingMammoLink manages diagnostic evaluation up to the point of biopsy and is developing stronger relationships with breast surgeons and health systems to improve downstream handoffs. 29:55 — The rural breast-imaging access gapRyan describes rural communities where mammography may not be available locally and where patients can postpone evaluating a concerning symptom for long periods. 30:40 — Public-sector and community partnershipsMammoLink works with the Florida Department of Health, migrant health organizations, and other partners to bring screening into underserved areas. 31:52 — Rural transformation funding as infrastructure capitalRyan and James discuss whether public funding could cover the initial cost of mobile units while allowing the operating model to become sustainable without permanent subsidy. 33:13 — Expanding beyond FloridaRyan outlines a potential national growth strategy involving grants, outside investment, and targeted entry into cities or states with favorable conditions. 33:55 — Bootstrapping five mobile unitsRyan discusses building the company without outside venture funding and reflects on the effort required to create its existing mobile fleet. 34:22 — The future of patient-centered mobile screeningRyan distinguishes genuinely patient-centered mobile care from simply relocating a traditional service and argues that future expansion will depend on proving outcomes and financial value. 35:30 — Demonstrating employer return on investmentThe conversation explores using clinical, operational, employee, and geospatial data to help employers measure cancers detected, time saved, employee satisfaction, and potential avoided costs. 37:05 — Employers as a preventive-care access channelRyan predicts that employers could play a larger role in providing screening as they seek to strengthen benefits, workforce health, retention, and trust. 37:38 — AI and emerging breast-cancer detection toolsRyan discusses research involving AI, biological markers, RNA-based technologies, and other emerging tools that may complement mammography and genetic screening. 38:39 — No mission without marginThe episode closes with a reflection on why healthcare innovation must be economically sustainable to achieve lasting scale and impact. Godspeed.. James Note: Some statistics and estimates discussed in this episode were provided conversationally by the host or guest and may be approximate. They have not all been independently verified by Healthcare Beans. Listeners should consult current primary sources before relying on specific figures for medical, policy, or business decisions.
GET HEIRLOOM SEEDS & NON GMO SURVIVAL FOOD HERE: https://heavensharvest.com/wam USE Code WAM to save 25% plus free shipping! USE Code WAM50 for 50% off on select items like the #10 cans & MRE packs! Pledge here! Just a dollar a month can help keep us alive! https://www.patreon.com/user?u=2652072&ty=h&u=2652072 EXCLUSIVE replays of hour plus long live shows are available here at $5 a month or more! BUY GOLD HERE: https://firstnationalbullion.com/schedule-consult/ Avoid CBDCs! GET 10% OFF ON SHILAJIT FROM DR. KAUFMAN WHEN YOU USE CODE WAM10 HERE: https://medauthentica.com/discount/WAM10?redirect=/products/authentica-shilajit%3Fsca_ref=10867124.wrNV3jkYSaMg9 HELP SUPPORT US AS WE DOCUMENT HISTORY HERE: https://gogetfunding.com/help-keep-wam-alive/# Josh Sigurdson reports on the $1.24 billion awarded to Pfizer by the CDC under the Trump Administration for new Covid vaccines. This clipped report comes from WAM's Sunday live show on Rumble. JD Vance recently spoke out on Joe Rogan's podcast about getting sick from getting the covid vaccine in 2021. He pointed to several ways people get seriously sick from the injections claiming he did not get a booster. One might ask why JD Vance would get any injection considering he was being groomed by Peter Thiel who no doubt knew about the vaccine's dangers. Congressman Thomas Massie pointed out that while JD Vance calls out the vaccines years later, the Trump administration has still awarded over a billion dollars to Pfizer for new Covid vaccines. The new head of the CDC has recently claimed that mRNA injections are "safe and effective" despite years of studies that prove otherwise and the FDA is fast tracking self amplifying RNA technology. The EPA is pushing for mRNA pesticides to be sprayed on crops. RFK Jr. has called on children to get Measles vaccines. He has also called for all Americans to have a traceable "wearable" device to track their health at all times. RFK Jr. was of course confirmed by a pharma funded house. So where is the MAHA movement? Was it just one big distraction to keep people apathetic after one of the largest health psyops in history took place? Meanwhile, so often people chirp on about Polio. "What about Polio vaccines?" In this video we also delve into how Polio has been rebranded as countless other paralytic illnesses, all of which actually are known side effects of vaccines. The rate of Polio had almost entirely collapsed in the 1950s before the vaccine even came out for it and the vaccine led to massive lawsuits due to countless injuries. This led to a banning of the initial shot. Stay tuned for more from WAM! GET YOUR WAV WATCH HERE: https://buy.wavwatch.com/WAM Use Code WAM to save $100 and purchase amazing healing frequency technology! Get Your SUPER-SUPPLIMENTS HERE: https://vni.life/wam Use Code WAM15 & Save 15%! Life changing formulas you can't find anywhere else! Get local, healthy, pasture raised meat delivered to your door here: https://wildpastures.com/promos/save-20-for-life/bonus15?oid=6&affid=321 USE THE LINK & get 20% off for life and $15 off your first box! DITCH YOUR DOCTOR! https://www.livelongerformula.com/wam Get a natural health practitioner and work with Christian Yordanov! Mention WAM and get a FREE masterclass! You will ALSO get a FREE metabolic function assessment! GET YOUR APRICOT SEEDS at the life-saving Richardson Nutritional Center HERE: https://rncstore.com/r?id=bg8qc1 Use code JOSH to save money! PayPal: ancientwonderstelevision@gmail.com FIND OUR CoinTree page here: https://cointr.ee/joshsigurdson PURCHASE MERECHANDISE HERE: https://world-alternative-media.creator-spring.com/ JOIN US on SubscribeStar here: https://www.subscribestar.com/world-alternative-media For subscriber only content! BITCOIN ADDRESS: 18d1WEnYYhBRgZVbeyLr6UfiJhrQygcgNU World Alternative Media 2026
What Triggers Age-Related Belly Fat? New Stem Cell Findings and a Nutrition Perspective: Nutritionist Leyla Muedin discusses research from City of Hope (published in Science) on why belly fat increases with age even without major weight gain, emphasizing the health risks of visceral fat as an endocrine organ linked to inflammation, diabetes, heart disease, and accelerated aging. The study suggests aging activates adipocyte progenitor cells (APCs) and produces an age-specific stem cell population called committed preadipocytes (CP-As) that generate new fat cells, with experiments showing older APCs create more fat cells even when transplanted into young mice. Single-cell RNA sequencing identified greater CP-A activity in middle-aged mice and similar cells in higher numbers in middle-aged human tissue. Researchers implicate the LIFR signaling pathway and propose future therapies to block these cells, while Leyla questions root causes and argues metabolic dysfunction—insulin resistance, hyperinsulinemia, high carbohydrate intake, and sedentary behavior—should be addressed nutritionally rather than via a pill.
Sepul Bio recently announced that it completed enrollment of its Phase 2b safety and efficacy clinical trial for ultevursen – an investigational RNA therapy to treat patients who have retinitis pigmentosa (RP) associated with mutations in the USH2A gene.
HEALTH NEWS Analysis of 82 Trials Shows Black Seed May Improve Cardiovascular Risk Markers New Study Reveals Herpesvirus Infection May Accelerate Alzheimer's Disease Favorable lifestyle factors reduce dementia risk across key genetic profiles People are living longer, but spending more years in poor health Imbalances in the oral microbiome linked to symptomatic hand osteoarthritis Analysis of 82 Trials Shows Black Seed May Improve Cardiovascular Risk Markers Shahid Beheshti University of Medical Sciences (Iran), July 21 2026 (Natural News) A pooled analysis of 82 randomized controlled trials involving 5,026 adults has found that supplementation with Nigella sativa, commonly known as black seed or black cumin, is associated with improvements in multiple cardiovascular risk markers. The meta-analysis, published in the journal Pharmacological Research, was conducted by researchers from several Iranian universities. The analysis used a GRADE-assessed, dose-response method to evaluate the effects of black seed compared with placebo or standard care. According to the study, black seed supplementation led to significant reductions in body weight, body mass index, waist circumference, and body fat percentage. The analysis noted that daily amounts used in most trials ranged from 1 to 3 grams of ground black seed or 1 to 3 milliliters of black seed oil. According to the researchers, one teaspoon of ground black seed contains roughly 4 grams, meaning a single daily teaspoon stirred into food falls within the range used in studies. For those who prefer oil, a half teaspoon delivers close to 2 milliliters. The researchers emphasized that consistency, rather than a large single dose, appears to drive positive results. New Study Reveals Herpesvirus Infection May Accelerate Alzheimer's Disease Cardiff University (UK), July 21, 2026 (SciTech Daily) In a new study, researchers found that herpesvirus infection intensified memory problems and other Alzheimer's-related changes in mice already vulnerable to the disease. The damage appeared to be driven not simply by the virus itself, but by the immune system's prolonged attempt to control it. Herpesviruses are a large family that includes viruses associated with cold sores, childhood infections, and glandular fever. After the initial illness passes, some can remain dormant inside the body and reactivate later, repeatedly drawing the immune system into action. Scientists results suggest that T cells, immune cells that identify and attack infected cells, can enter the brain during herpesvirus infection and accelerate cognitive decline. Following infection, large numbers of immune cells moved into the brain. Most were CD8+ T cells that specifically recognized the virus, showing that they had entered the tissue as part of the body's attempt to contain the infection. Similar T cells have previously been found in the brains and spinal fluid of people with Alzheimer's disease, although their exact role has remained uncertain. The results indicate that a virus-driven immune response can actively speed the progression of Alzheimer's-like disease rather than merely appearing alongside it. Favorable lifestyle factors reduce dementia risk across key genetic profiles Kyushu University (Japan), June 5 2026 (News-Medical) With dementia cases expected to nearly triple worldwide by 2050, researchers are increasingly focused on identifying ways to prevent or delay the disease. While lifestyle and health-related factors, such as blood pressure control and physical activity, influence dementia risk, genetics also play a major role. Currently, it is unclear if maintaining a favorable lifestyle reduces dementia risk equally across different genetic backgrounds. A new study led by Kyushu University examines whether favorable modifiable risk factors (mRF)-behaviors or conditions that people can change or control-can lower dementia risk even among individuals with high genetic susceptibility. The researchers analyzed data from 9,605 community-dwelling adults aged 65 and older. They determined each participant's APOE ε4 genotypes, a primary genetic risk factor for Alzheimer's disease, and calculated the mRF score based on lifestyle and health-related factors. This allowed the team to evaluate how genetic predisposition and lifestyle choices jointly interact to influence dementia risk. The results showed that dementia risk rose progressively with the number of APOE ε4 alleles. Notably, among individuals with one or no APOE ε4 alleles, maintaining a healthier profile with lower mRF scores was linked to a significantly lower risk of dementia. In contrast, among individuals with two APOE ε4 alleles, dementia risk did not differ significantly between those with lower and higher mRF scores. These findings suggest that maintaining favorable lifestyle and health conditions can effectively mitigate dementia risk, even among individuals carrying a single APOE ε4 allele. This underscores the importance of population-based prevention strategies focused on managing vascular and lifestyle risk factors. People are living longer, but spending more years in poor health Institute for Health Metrics and Evaluation (US), July 21 2026 (Eurekalert) People are living longer, but spending more years in poor health The morbidity gap—the number of years people live in poor health—widened in nearly all countries, with wealthier nations facing the largest gaps. The US has the largest morbidity gap, closely followed by Australia and Canada. Women consistently live longer but spend more years in poor health than men. Musculoskeletal disorders, mental health conditions, hearing loss, and falls and other unintentional injuries are driving most years lived in poor health worldwide. Within a generation, the global morbidity gap widened by nearly two years, increasing from 8.8 years in 1990 to 10.7 years in 2023. Globally, people spent an average of 14.5% of their lives in poor health in 2023, up from 13.6% in 1990. Instead of occurring only in the final years of life, the widening morbidity gap was observed across the adult lifespan, suggesting that people are spending more years living with disease and disability throughout adulthood. Between 1990 and 2023, global life expectancy at birth increased from 64.6 years to 73.8 years, while healthy life expectancy rose from 55.9 years to 63.1 years. In 2023, the United States had the largest national morbidity gap at 14 years, followed by Australia at 13.9 years and Canada at 13.7 years. Imbalances in the oral microbiome linked to symptomatic hand osteoarthritis Central South University (China), July 21 2026 (Medica Xpress) A study published RMD Open has linked specific imbalances and disruptions in the oral microbiome to symptomatic hand arthritis. Its findings suggest that the microbial environment of the mouth may influence the disease process of hand arthritis, which is associated with pain, stiffness and reduced grip strength and can severely impair quality of life. The oral microbiome plays a role in systemic inflammation and interacts closely with the gut microbiome, which is significantly associated with symptomatic hand arthritis. To assess the role of the oral microbiome, saliva samples from 52 people with symptomatic hand arthritis recruited from a community-based osteoarthritis study and 712 people without the condition were analyzed using ribosomal RNA gene sequencing. Compared with samples taken from participants without hand arthritis, samples from participants with symptomatic hand arthritis showed significantly lower oral microbial richness and altered composition. Specifically, the abundance of Trichococcus bacteria was significantly higher in the symptomatic hand arthritis samples and positively associated with the severity of hand arthritis symptoms. Trichococcus abundance in the oral microbiome was also positively associated with the gut microbial tyrosine metabolism pathway—a metabolic pathway previously implicated in hand arthritis. Samples from participants with symptomatic hand arthritis also displayed reduced oral-gut microbiome correlations compared with controls, suggesting the balance between these two microbial communities was disrupted.
Episode 2860 - In this episode, Ted and Austin Broer connect Moderna's RNA cancer shot trial dangers, COVID vaccine memory issues and hospital whistleblower claims, acai berry antioxidant benefits, Berberine's blood sugar and body fat management superiority, the trades career opportunity versus student loan default crisis, EV market collapse and hybrid technology promise, and the Andrew and Tate arrest for dating scams into a broadcast that delivers both urgent health warnings and sharp economic and cultural commentary.
Millions of people are told their thyroid labs are "normal" even though they continue to struggle with fatigue, brain fog, weight gain, depression, and hormone imbalances. In this episode, Dr. Jen sits down with Dr. Daryl Turner to discuss why conventional thyroid testing often misses subclinical thyroid dysfunction and how his patented Thyroflex System measures thyroid function at the cellular level. They explore Hashimoto's disease, Graves' disease, reverse T3, DNA and RNA interventions, iodine, adrenal health, and why symptoms—not just lab values—should guide treatment. This conversation challenges conventional thyroid care while offering a fascinating look at emerging approaches to personalized endocrine medicine.Dr. Daryl Turner is a hormone and thyroid specialist, medical researcher, and founder of Nitek Medical. With more than two decades of research and clinical innovation, he developed the patented Thyroflex System to assess thyroid function beyond conventional blood testing. His work focuses on cellular endocrinology, autoimmune thyroid disease, hormone optimization, and personalized approaches to treating Hashimoto's disease, Graves' disease, and complex thyroid dysfunction. Dr. Turner lectures internationally on advanced thyroid care and has appeared on numerous national television programs, including The Dr. Phil Show, The Doctors, Today, and the Discovery Channel. Website: https://www.nitekmedical.com Facebook: https://www.facebook.com/NitekMedical YouTube: https://www.youtube.com/user/NiTekMedicalInc PODCAST: Thank you for listening please subscribe and share! Shop supplements: https://healthybydrjen.shop/CHECK OUT a list of my Favorite products here: https://www.healthybydrjen.com/drjenfavoritesFOLLOW ME:Instagram: https://www.instagram.com/integrativedrmom/Facebook: https://www.facebook.com/integrativedrmomYouTube: https://www.youtube.com/@integrativedrmomFTC: Some links included in this description might be affiliate links. If you purchase a product through one of them, I will receive a commission (at no additional cost to you). I truly appreciate your support of my channel. Thank you for watching! Video is not sponsored.DISCLAIMER: This podcast does not contain any medical or health related diagnosis or treatment advice. Content provided on this podcast is for informational purposes only. For any medical or health related advice, please consult with a physician or other healthcare professionals. Further, information about specific products or treatments within this podcast are not to diagnose, treat, cure or prevent disease.
Bet on informationIf test loss flatlines after 1.5B parameters while training loss continues to drop as you scale, that tells you that your model is limited by the amount of information in your data.Training on a single, smallish data set exposed an information gap: the 3.1B model falls off the scaling trend. Neither parameters nor compute will improve performance past this wall. For predicting changes to gene expression, you need more information rich data.This is what Chu and Bo's teams have done, and here is what ~30x the information buys you:Now we can scale with parameters and training compute! We don't know how much this effort costed, but we can guess that data collection experiments and infrastructure was a few tens of millions, and compute + headcount + research was a few million. The budget looks like a RL rollout budget, rather than a data rich pre-training one.We were lucky enough to have the two central figures in this story on our podcast. Taking the lead from Ci Chu and Bo Wang, Xaira Therapeutics is betting that information rich data is the key to AI-driven drug development. Chu was recently promoted to Chief Discovery Officer and Bo to Chief AI Scientist, underscoring just how strategic Xaira considers this bet.Reverse engineering the human cellIf you had to figure out how a human cell works, what would you do? A good place to start might be by documenting what genes are expressed (e.g. what RNA is floating around) in different kinds of cells, in different circumstances.That is CELLxGENE, a database of 168M cells built by Chan Zuckerberg Institute that maps each cell to a count of how many times 20K-30K genes were detected in that cell, plus detailed metadata about every cell. A ~4 trillion-entry matrix.If the Protein Data Bank (PDB) unlocked structural biology models (Boltz Episode, ESM/BioHub Episode), CELLxGENE has done the same thing for Virtual Cell models. Like PDB, CELLxGENE has inspired a zoo of AI models of RNA expression; so much so that RNA expression models have become synonymous with Virtual Cell models. Bo Wang built one of the most influential, scGPT, that became the starting point for Xaira's new model.RNA expression ≠ Virtual CellModels trained on CELLxGENE describe the relationship between cell types and cell states, but they are not good at predicting what will happen if we make changes to RNA expression. Changes in gene expression are highly correlated, and its is difficult (impossible) to figure out what causes what in most cases.If you could “turn the dial down” on one gene at a time, however, then you would be able to observe what is upstream and downstream of a given gene. You could tell if A → B & C or B → A & C or B → A, C → B → … If you did this for all of the genes, then maybe you could train a model that could predict what would happen to a cell if you change a gene (e.g. with a drug or a gene edit). Or maybe you could figure out the least invasive way to change a particular gene's expression.X-Atlas → X-CellThis is exactly what Chu and Bo's teams have done. The data set is called X-Atlas and the model is called X-Cell.In this episode, we discuss:* Why the team abandoned autoregression for diffusion* The CRISPR-based experiments that run millions of tests in parallel, and generate the raw data for X-Atlas and X-cell* Generalization to real lab experiments in real human cells* Beating the linear baseline that has outperformed previous models* Justifying a kitchen-sink of priors, and how that stacks up vs. data and architectureBo also shared with us some of the (major) advantages he has as an academic vs. industry leader, and how his labs keep up with the breakneck pace of AI innovation.Check out the full episode on YouTube, or your favorite podcasting platform! This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.latent.space/subscribe
1912 stirbt ein zweijähriges Mädchen in Berlin an den Masern. Ihre Lunge wird konserviert, beschriftet – und dann vergessen. Bis Forscher sie über ein Jahrhundert später wiederentdecken. In dieser Folge sprechen Laura und Kai darüber, wie es den Forschern gelingt, das Virus aus dem Präparat zu sequenzieren, was das über den Ursprung der Masern verrät und warum das alles ein neues Kapitel in der Virenforschung eröffnet.
In this episode we speak with Alon Goren from UC San Diego about his work at the intersection of genomic technology development and chromatin biology. We discuss how his lab studies how the epigenome is regulated, how disruption of that regulation contributes to disease, and how technology can be improved to make results more robust and reproducible. We talk about his early interest in biology, how that developed through medical research training, and how a molecular biology lab shaped the direction of his career. He explains how curiosity about how cells and organisms work led him toward genomics and chromatin research. We then discuss several methods from his career, including early direct sequencing approaches for small amounts of DNA and RNA, ChIP-based methods for chromatin regulators, and work on improving ChIP-seq workflows. He explains why antibody choice matters, why monoclonal antibodies can improve reproducibility, and how automation helped scale the process. We also cover his work on spike-in normalization, including the risks of using exogenous chromatin incorrectly and the need for better safeguards in genome-wide comparisons. He describes a newer approach that uses two spike-ins to provide multiple checks on normalization. Finally, we discuss his work on short tandem repeats, zebrafish heart regeneration, and SIRT6-related polymerase pausing, as well as a newer platform that converts molecular interactions into sequencing-readable barcodes. He closes by stressing the importance of validation, careful protocol design, and methods that can be used reliably by multiple people. References Ram, O., Goren, A., Amit, I., Shoresh, N., Yosef, N., Ernst, J., Kellis, M., Gymrek, M., Issner, R., Coyne, M., Durham, T., Zhang, X., Donaghey, J., Epstein, C. B., Regev, A., & Bernstein, B. E. (2011). Combinatorial patterning of chromatin regulators uncovered by genome-wide location analysis in human cells. Cell, 147(7), 1628–1639. https://doi.org/10.1016/j.cell.2011.09.057 Busby, M., Xue, C., Li, C., Farjoun, Y., Gienger, E., Yofe, I., Gladden, A., Epstein, C. B., Cornett, E. M., Rothbart, S. B., Nusbaum, C., & Goren, A. (2016). Systematic comparison of monoclonal versus polyclonal antibodies for mapping histone modifications by ChIP-seq. Epigenetics & chromatin, 9, 49. https://doi.org/10.1186/s13072-016-0100-6 Patel, L. A., Cao, Y., Mendenhall, E. M., Benner, C., & Goren, A. (2024). The Wild West of spike-in normalization. Nature biotechnology, 42(9), 1343–1349. https://doi.org/10.1038/s41587-024-02377-y Ben-Yair, R., Butty, V. L., Busby, M., Qiu, Y., Levine, S. S., Goren, A., Boyer, L. A., Burns, C. G., & Burns, C. E. (2019). H3K27me3-mediated silencing of structural genes is required for zebrafish heart regeneration. Development (Cambridge, England), 146(19), dev178632. https://doi.org/10.1242/dev.178632 Patel, L., Cao, Y., Xu, T., Modolo, E., Dishon, T., Zhang, L., Mendenhall, E., Heinz, S., Simon, I., Benner, C., & Goren, A. (2025). Improved spike-in normalization clarifies the relationship between active histone modifications and transcription. Genomics. https://doi.org/10.1101/2025.11.25.690627 Xu, T., Wang, J., Shin, Y., Cao, Y., Zhang, L., Modolo, E., Dishon, T., Fisher, J., Norton, M., Fry, C. J., Farjoun, Y., Mendenhall, E., Heinz, S., Benner, C., & Goren, A. (2026). Multiplexed measurements of protein-protein interactions and protein abundance across cellular conditions using Prod&PQ-seq. Genomics. https://doi.org/10.64898/2026.01.01.697286 Related Episodes Taking ChIP from Yeast to ENCODE to Enable Genome-Wide Regulatory Protein Mapping (Peggy Farnham) Comparing CUT&Tag to ENCODE ChIP-Seq in Alzheimer's Disease Samples (Sarah Marzi) Chromatin Profiling: From ChIP to CUT&RUN, CUT&Tag and CUTAC (Steven Henikoff) Contact Epigenetics Podcast on Mastodon Epigenetics Podcast on Bluesky Dr. Stefan Dillinger on LinkedIn Active Motif on LinkedIn Active Motif on Bluesky Email: podcast@activemotif.com
Cardiologist Dr. Peter McCullough on mRNA Persistence, Nattokinase, and the Fight Over COVID-19 Treatment" Six years after standing before the US Senate and calling out the pandemic response in real time, Dr. Peter McCullough returns with new evidence on where the spike protein came from, how long it persists in the body after infection or vaccination, and what's being done to break it down. This episode traces the science from a 2015 gain-of-function paper to a patient still showing circulating spike protein 3.6 years after vaccination. Get Dr. McCullough's free spike protein guide: myfreespikeguide.com Host Dave Asprey sits down with Dr. Peter McCullough, a physician trained in internal medicine, cardiology, and epidemiology, and one of the most published and most censored voices of the COVID-19 pandemic. He authored the first multi-drug treatment protocol for COVID-19, testified before the US Senate in 2020 and again in 2025, and has published extensively in the peer-reviewed literature on vaccine safety, spike protein biology, and early treatment. His book Courage to Face COVID-19 and his most recent New York Times bestseller, Vaccines, Mythology, Ideology and Reality, examine the history and science behind vaccine policy. Dave and Dr. McCullough trace the origins of the spike protein back to 2015 and 2016 research papers describing a lab-created, SARS-like coronavirus explicitly labeled "poised for human emergence," and discuss the funding, institutions, and researchers involved. They break down why synthetic mRNA vaccines resist the body's normal RNA breakdown process, what a patient case revealed about spike protein circulating 3.6 years after vaccination, and how nattokinase, a natural enzyme, has shown the ability to break the spike protein down. They also cover the suppression campaigns against ivermectin and hydroxychloroquine, the wartime propaganda origins of terms like "misinformation" and "anti-vaxxer," and what Dr. McCullough says he would do differently if he ran HHS. The conversation closes with new research on cognitive superagers, the small percentage of people who reach 100 with intact memory and health. You'll Learn: Why 2015 and 2016 research papers described a lab-created coronavirus as "poised for human emergence" years before the pandemic Why synthetic mRNA in COVID-19 vaccines resists the body's natural RNA breakdown process What one patient's case revealed about spike protein still circulating 3.6 years after vaccination How nattokinase, a natural enzyme, has been shown to break down the spike protein Why the FDA and FTC targeted ivermectin, hydroxychloroquine, and companies selling nasal sprays during the pandemic The wartime propaganda origins of terms like "misinformation," "disinformation," and "anti-vaxxer" What Dr. McCullough says he would do first if he were running HHS What research on cognitive superagers reveals about the small number of people who reach 100 with intact health Thank you to our sponsors! - TrueDark | Visit truedark.com and use code DAVEASPREY15 (discount applies to all frames except Aegis) - ZenBud | Dave's Nervous System Biohack. Visit zenbud.health and use code DAVE15 at checkout for a discount. - Qualia | Go to qualialife.com/ASPREY for 50% off, and use code ASPREY for an additional 15% off. - ENERGYbits | If you want a simpler, smarter way to support your body… this is it. Head to ENERGYbits.com and use code ASPREY for 20% off your order. Dave Asprey is a four-time New York Times bestselling author, founder of Bulletproof Coffee, and the father of biohacking. With over 1,000 interviews and 1 million monthly listeners, The Human Upgrade brings you the knowledge to take control of your biology, extend your longevity, and optimize every system in your body and mind. Each episode delivers cutting-edge insights inhealth, performance, neuroscience, supplements, nutrition, biohacking, emotional intelligence, and conscious living. New episodes are released every Tuesday, Thursday, Friday, and Sunday (BONUS). Dave asks the questions no one else will and gives you real tools to become stronger, smarter, and more resilient. Keywords: spike protein detox, how long does spike protein last in your body, nattokinase spike protein, mRNA vaccine side effects, is the spike protein still in my blood, gain of function research explained, where did COVID come from, Wuhan lab leak evidence, ivermectin banned, why was hydroxychloroquine banned, vaccine injury compensation act, mRNA vaccine shedding, spike protein detox protocol, how to live to 100, cognitive superagers, Peter McCullough, Dave Asprey Resources: • Learn More About Dr. McCullough's Work At: https://www.twc.health/pages/focal-points • Get My 2026 Clean Nicotine Roadmap | Enroll for free at https://daveasprey.com/2026-clean-nicotine-roadmap/ • 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 – Trailer 00:43 – Intro 02:10 – 2020 Public Health Failures 05:07 – Vaccine History & Mythology 07:19 – Vaccine Hesitancy as Disease 13:12 – Masks & Lockdown Absurdity 18:03 – War on Hydroxychloroquine 23:56 – Ivermectin Suppression 28:58 – FTC Misinformation Crackdown 31:18 – Propaganda Terms Explained 39:55 – McCullough's Confidence & Career 43:08 – Spike Protein Origins 57:10 – Nattokinase & Spike Clearance 58:50 – mRNA Persistence in Body 1:11:50 – Fixing the System 1:17:32 – Political Divisiveness 1:22:41 – Secrets to Longevity See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
Dr. Bill Andrews is the Founder and CEO of Sierra Sciences; a company focused on finding ways to extend human lifespan and health span. Bill has been featured in Popular Science, The Today Show, The Doctor's TV Show, and numerous documentaries on the topic of life extension. Bill co-stars with Dr. Aubrey de Grey in the documentary “The Immortalists” that made it to the “Top-10-List” to receive an Oscar in 2014Bill is also an ultramarathon runner with over 100 ultramarathons under his belt. Bill believes that consistent and fun endurance exercise is one of the best ways to reduce inflammation and slow aging.Speaking at the Cell Surgical Conference 2024Bill's areas of research have included Dwarfism, Cancer, CardiovascularDisease, Inflammation, Osteoporosis, Anemia, Multiple Sclerosis,Aging, and many others. Before founding Sierra Sciences Bill was aMedical Researcher at Armos Corporation, Codon Corporation, BerlexBiosciences, Geron Corporation, and EOS Biotech. Bill played key rolesin the discoveries and inventions of:Human Growth Hormone (hGH), Prorennin (Prochymosin), Tissue Plasminogen Activator(tPA), Osteo-Inductive Factor (OIF), Thrombomodulin, Erythropoietin (EPO), Beta-Seron, HTSite Specific Mutagenesis, Various Cancer Treatments (Rytelo, Telomelysin, GV1001, UV1,mutant hTR, and others), Telomerase, TRAPeze, TA-65, hTERT mRNA RT-PCR HTS,Telomerase Gene Therapy, C0314818 (TAM818), TeloSMRT, Isagenesis (Product B), Premere, Telo-Vital, Rytelo, and many more.In 1997 Bill was awarded 2nd Place as National Inventor of the Year for his cancer research. In the early-to-mid 1990s, while at Geron Corporation, Bill led the research to discover both the RNA and protein components of human telomerase, the enzyme responsible forpreventing telomeres from shortening in our reproductive cells. He has determined that the only real definite “hard-stop” to lifespan and health span, that is true for all humans, as well as non-human primates, cats, dogs, horses, sheep, pig, and deer, is “Telomere Shortening”. No matter what else we do to treat aging, aging will neverbe cured and/or reversed unless we also solve the telomere shortening problem.Presently, the primary focus of Sierra Sciences is to find ways toproduce telomerase and lengthen telomeres in all cells of the humanbody, not just our reproductive cells, and eliminate this key hard-stop tosuper-longevity. But Bill is aware that the war against aging is not goingto be won with just one battle.Contact Dr. Bill Andrews:website: https://sierrasci.com/https://www.facebook.com/telomere.bill.andrewshttps://www.facebook.com/profile.php?id=61551532301673linkedin.com/in/billandrewsphdhttps://www.youtube.com/@billandrewsphdhttps://www.youtube.com/@sierrasciences1625https://www.instagram.com/yonderssi/Dr. Kimberley LinertSpeaker, Author, Broadcaster, Mentor, Trainer, Behavioral OptometristEvent Planners- I am available to speak at your event. Here is my media kit: https://brucemerrinscelebrityspeakers.com/portfolio/dr-kimberley-linert/To book Dr. Linert on your podcast, television show, conference, corporate training or as an expert guest please email her at incrediblelifepodcast@gmail.com or Contact Bruce Merrin at Bruce Merrin's Celebrity Speakers at merrinpr@gmail.com702.256.9199Host of the Podcast Series: Incredible Life Creator PodcastAvailable on...Apple: https://podcasts.apple.com/us/podcast/incredible-life-creator-with-dr-kimberley-linert/id1472641267Spotify: https://open.spotify.com/show/6DZE3EoHfhgcmSkxY1CvKf?si=ebe71549e7474663 and on 9 other podcast platformsAuthor of Book: "Visualizing Happiness in Every Area of Your Life"Get on Amazon: https://amzn.to/4cmTOMwWebsite: https://linktr.ee/DrKimberleyLinertThe Great Discovery eLearning platform: https://thegreatdiscovery.com/kimberleyl
Broadcast from KSQD, Santa Cruz on 7-09-2026: Researchers refined a technique to reverse skin cell aging by about 30 years while preserving cellular identity. Exposing adult fibroblasts to Yamanaka factors—stopping before full reversion to pluripotent stem cells,reset the epigenetic clock and gene expression patterns to resemble much younger cells. The rejuvenated fibroblasts produced significantly more collagen, migrated faster to close artificial wounds, and showed reversal of gene expression patterns associated with Alzheimer's and cataracts. Since long-term epidemiologic data doesn't yet exist, Dr. Dawn follows up on last week's vaping question by exploring cancer mechanisms. Vaping aerosols impair DNA repair fidelity while triggering IL-6, IL-8, and TNF-alpha secretion. Nicotine-derived nitrosamines, reactive carbonyls (formaldehyde, acetaldehyde, acrolein) are generated when propylene glycol and vegetable glycerin are heated. Upregulated cytochrome P450 enzymes convert precarcinogens like benzopyrene into carcinogens. Mice exposed for 54 weeks developed lung adenocarcinomas in 22% and precancerous bladder hyperplasia in 57%, with markers matching those show predict lung cancer years before diagnosis. The Mexican Biobank—which includes over 40,000 samples from all 31 Mexican states revealed dramatic regional variation in drug-metabolism genes driven by Indigenous ancestry. In Chiapas, nearly 40% of the population carries two copies of a CYP2D6 variant reducing fentanyl metabolism, versus just 10% in Sinaloa. The SLCO1B1 variant hindering statin metabolism is found in over 15% of Yucatán residents., where 8 million Mexicans take statins. Dr. Dawn discusses both the promise and potential dark side of population genetic testing, including UK plans to genotype all children at birth for inborn errors of metabolism. Dr. Dawn briefly revisits the recent Indian study showing conch-shell blowing reduces sleep apnea by 34%, comparing it to earlier didgeridoo research, both of which strengthen airway muscles through forced-blowing exercises. A caller from Capitola recovering from non-Hodgkin's lymphoma near the L5 nerve asks about Japanese Kampo medicine formulas (Goshajinkigan, Yokukansan) for post-treatment nerve pain. Dr. Dawn suggests the pain likely originates from scar tissue tethering the nerve, and recommends consulting the Oriental Medicine Doctor program at Five Branches in Santa Cruz where faculty can advise on herbal formulas that trace back thousands of years through cultural exchange between China and Japan. Dr. Dawn explains Lp(a):lipoprotein(a), a small protein string attached to LDL particles that promotes clumping and clotting, is a genetically-determined coronary artery disease and stroke risk factor invisible to standard lipid panels. Levels of 250 particles double coronary risk and 350 particles triple it. Less than 75 is normal. Two new pharmaceutical strategies are in development to reduce Lp(a) : antisense oligonucleotides (single-stranded RNA that recruits RNase H to cleave target mRNA) and small interfering RNA (double-stranded RNA that triggers destruction of matching mRNA). Pelacarsen, a monthly injection in Phase 3 trials, reduces Lp(a) by 80%. These gene-silencing platforms open therapeutic possibilities for previously undruggable orphan diseases. Vitamin K2 is produced in the gut microbiome. MK-4 is most common in humans. Dr. Dawn recommends MK7 for stabilizing coronary calcium plaques and directing calcium into bone. A study of hepatitis B and C patients found MK4 to be protective in hepatocellular carcinoma. HCC developed in 2 of 21 MK-4-treated patients versus 9 of 19 controls, with a risk ratio of 0.2. MK-4 activates protein kinase A in vitro, inhibits HCC invasiveness, and restores apoptosis signaling that cancer cells normally block. Dr. Dawn recommends a couple milligrams of MK-4 daily for anyone with cirrhosis or prior hepatitis B or C infection.
Randomized evidence suggests that routinely used mucoactive therapies may no longer have a role in mechanically ventilated ICU patients, while a large comparative effectiveness study indicates GLP-1 receptor agonists may offer superior cardiovascular and atrial fibrillation outcomes compared with SGLT2 inhibitors in patients with both AF and type 2 diabetes. We also highlight a promising blood-based RNA biomarker panel that may predict Alzheimer's symptom onset several years before cognitive decline, potentially improving patient selection for emerging disease-modifying therapies.
Honey bee nutrition is more complex than simply providing protein. In this episode, Jeff Ott and Dr. Becky Masterman welcome Dr. Vincent Ricigliano to discuss emerging research exploring algae-based supplemental diets, functional feeds, RNA interference technologies, and new approaches to supporting colony health. Vincent explains how microalgae such as spirulina and chlorella may help improve supplemental feeding by providing highly bioavailable proteins, amino acids, lipids, vitamins, and micronutrients that more closely resemble natural pollen. The discussion explores how modern nutritional science can help create more complete diets for honey bees. The conversation also examines RNA interference (RNAi) technologies, including approaches designed to suppress viral pathogens and potentially manage Varroa mites. Vincent shares insights into ongoing research involving antiviral RNA delivery systems, sustainable production methods, and future biotechnology tools that may complement integrated pest management strategies. Along the way, the discussion touches on pollinator health, commercial beekeeping collaborations, miticide resistance, and the continuing search for practical tools that improve colony resilience under modern beekeeping conditions. Websites from the episode and others we recommend: Honey Bee Health Coalition: https://honeybeehealthcoalition.org Project Apis m. (PAm): https://www.projectapism.org The National Honey Board: https://honey.com Honey Bee Obscura Podcast: https://honeybeeobscura.com Copyright © 2026 by Growing Planet Media, LLC ______________ Betterbee is the presenting sponsor of Beekeeping Today Podcast. Betterbee's mission is to support every beekeeper with excellent customer service, continued education and quality equipment. From their colorful and informative catalog to their support of beekeeper educational activities, including this podcast series, Betterbee truly is Beekeepers Serving Beekeepers. See for yourself at www.betterbee.com This episode is brought to you by Global Patties! Global offers a variety of standard and custom patties. Visit them today at http://globalpatties.com and let them know you appreciate them sponsoring this episode! As a beekeeper, you want products that benefit you and your bees. When you choose Premier Bee Products, you choose hive components that are healthier for bees and more productive for you. Because we believe that in beekeeping, details make all the difference. Premier Bee Products: Better for bees. Better for beekeepers. Use promo code PODCAST for 10% off your next online order. Thanks to Strong Microbials for their support of Beekeeping Today Podcast. Find out more about their line of probiotics in our Season 3, Episode 12 episode and from their website: https://www.strongmicrobials.com HiveIQ is revolutionizing the way beekeepers manage their colonies with innovative, insulated hive systems designed for maximum colony health and efficiency. Their hives maintain stable temperatures year-round, reduce stress on the bees, and are built to last using durable, lightweight materials. Whether you're managing two hives or two hundred, HiveIQ's smart design helps your bees thrive while saving you time and effort. Learn more at HiveIQ.com. We'd like to thank Vita Bee Health for supporting the podcast. Vita provides proven tools for controlling Varroa—from Apistan and Apiguard to the new VarroxSan extended-release oxalic acid strips—helping beekeepers keep stronger, healthier colonies. Thanks for Northern Bee Books for their support. Northern Bee Books is the publisher of bee books available worldwide from their website or from Amazon and bookstores everywhere. They are also the publishers of The Beekeepers Quarterly and Natural Bee Husbandry. _______________ We hope you enjoy this podcast and welcome your questions and comments in the show notes of this episode or: questions@beekeepingtodaypodcast.com Thank you for listening! Podcast music: Be Strong by Young Presidents; Epilogue by Musicalman; Faraday by BeGun; Walking in Paris by Studio Le Bus; A Fresh New Start by Pete Morse; Wedding Day by Boomer; Christmas Avenue by Immersive Music; Red Jack Blues by Daniel Hart; Bolero de la Fontero by Rimsky Music; Perfect Sky by Graceful Movement; I'm Not Running Away This Time by Max Brodie; Original guitar background instrumental by Jeff Ott. Beekeeping Today Podcast is an audio production of Growing Planet Media, LLC ** As an Amazon Associate, we may earn a commission from qualifying purchases Copyright © 2026 by Growing Planet Media, LLC
Broadcast from KSQD, Santa Cruz on 7-02-2026: Dr. Dawn devotes the first half of the show to a nuanced defense of GLP-1 receptor agonists, arguing the polarized debate treats obesity as a moral failure rather than a physiological one. She recounts the "Marilyn Monroe dress" moment that transformed semaglutide from diabetes drug into elite cosmetic tool, and pushes back on the puritanical framing that behavior change must be earned rather than pharmacologically enabled—noting we don't apply this logic to antihypertensives or statins. Dr. Dawn catalogs visceral fat as a genuine endocrine organ producing over 17 hormones, most of which drive self-perpetuating growth: leptin (this satiety hormone at high levels disables it's own brain receptor), IL-6, TNF-alpha (blocks insulin), resistin (increases insulin resistance and inflammation), PAI-2 (blocks clot breakdown, raising cardiovascular risk), retinol-binding protein 4 (impairs muscle glucose uptake), chemerin (recruits macrophages and directs fat to the belly), and visfatin. Only adiponectin declines with rising visceral fat. It improves insulin sensitivity, suppresses hepatic gluconeogenesis, and blocks IL-6 . Dr. Dawn describes GLP-1's neurobiological action: receptors in the hypothalamus, brainstem, hippocampus, and mesolimbic reward system, with the drugs quieting the brain's salience network so food loses its intrusive pull. Taste buds shift, sweet and salty become muted, and reward circuits stop firing on cheat foods—creating a window during which behavioral change becomes possible. Dr. Dawn frames group support through self-determination theory (autonomy, competence, relatedness), arguing GLP-1s create the cognitive bandwidth for behavioral programs to succeed. A Tufts study of patients discontinuing after 10% weight loss found those enrolled in behavioral support programs regained about three times less weight than usual-care controls, outperforming even medically-tailored meal plans. Group engagement doubled the time patients stayed on the medication. A November 2025 Nature study piggybacked on deep brain stimulation research at Penn. Electrodes implanted in the nucleus accumbens of post-bariatric patients recorded low-frequency brain activity surges during food-noise episodes on drug free patients. A third participant who started tirzepatide showed complete silencing of that signature—the first direct electrical confirmation that GLP-1s suppresses compulsive food thoughts in the reward center. RNA sequencing of adipose tissue from 25 obese patients before and after bariatric surgery, compared to 24 lean controls, revealed persistent epigenetic changes even after weight loss. Lipid-associated inflammatory macrophages drop but retain some of their pro-inflammatory epigenetics, explaining the well-known slippery slope back to obesity—and why Dr. Dawn suggests GLP-1s may work best as intermittent tools when behavioral maintenance starts slipping. An emailer asks about long-term smoking versus vaping data. Dr. Dawn notes there is no long-term data yet, but short-term evidence shows e-cigarettes contain nicotine, propylene glycol, reactive oxygen species, and nitrosamines, producing spirometry readings similar to mild COPD in otherwise-healthy vapers. Vaping over a year raises stroke relative risk by 1.62 and nearly doubles MI risk, and combining smoking and vaping produces a multiplicative rather than additive harm. Data on cancer will take decades to emerge. Researchers built a functioning underwater breathing apparatus for cockroaches with electrodes attached to brain and sensory organs allowing remote-controlled direction while preserving natural obstacle-navigation autonomy. The 10mm × 10mm sponge-based oxygen tank uses magnesium dioxide catalyzing hydrogen peroxide breakdown, delivering oxygen through silicone tubes to the roach's spiracles for up to three hours underwater. Deployemenet will improve search-and-rescue in flooded and collapsed structures where dogs cannot reach. A Science Advances paper from Yong Lin Kong's lab at Rice University describes 3D-printing electronic circuits directly onto living tissue. Researchers achieved microwave-focused annealing at sub-200-micrometer resolution. By selectively heating only conductive ink particles (copper, silver, gold) without damaging surrounding tissue, the technique enables printing circuits onto 3D-printed heart valves, tracheas, and ear scaffolds, potentially creating combined graft-and-sensor implants, ingestible diagnostic devices, and perhaps even decorative electronic tattoos. A single-shot reformulation of zanamivir (originally the inhaled flu drug Relenza) provided 76.1% flu protection in a 5,000-participant trial—far exceeding the roughly 40-45% offered by annual flu vaccines. Because zanamivir targets neuraminidase in a way that inactivates it if the virus tries to mutate around the drug, trapping newly-made viral copies inside their host cells, this approach works across all flu strains and could bypass the annual guessing game of trivalent vaccine formulation.
Sean Carroll's Mindscape: Science, Society, Philosophy, Culture, Arts, and Ideas
Messenger RNA (mRNA) plays a literally central role in the functioning of life as we know it, shuttling information back and forth between the DNA where it is stored to the ribosome where it is used to produce proteins. RNA may even have been the first molecule to kick-start the origin of life. Today, scientists are learning how to manipulate mRNA to cure and prevent diseases, whether through vaccination or literally editing one's DNA. Jeff Coller explains how it all works and how mRNA is revolutionizing medicine as we know it. Blog post with transcript: https://www.preposterousuniverse.com/podcast/2026/06/15/357-jeff-coller-on-mrna-vaccines-and-bespoke-therapeutics/ Support Mindscape on Patreon. Jeff Coller received his Ph.D. in cell and molecular biology from the University of Wisconsin-Madison. He is currently Bloomberg Distinguished Professor of Biomedical Engineering and Director of the RNA Innovation Center at Johns Hopkins University. He is co-founder of Tevard Biosciences and the Alliance for mRNA Medicines, and leads the REPAIRx consortium. He is a fellow of the American Association for the Advancement of Science. Web site Johns Hopkins web page Google Scholar publications "This May Be the Most Important Medical Story of the Decade," New York Times, April 9, 2026
Jake Becraft is the CEO and co-founder of Strand Therapeutics, a company building one of the most advanced programmable genetic medicine platforms in biotechnology. Under his leadership, Strand is redefining what RNA medicines can do by enabling cell-selective targeting and therapeutic payload delivery inside the body, unlocking a new class of precision genetic therapies.This episode is brought to you by:Helix Sleep premium mattresses: HelixSleep.com/Tim (20% off any purchase) Incogni, which automatically removes your personal data from the web, helping shield you from fraud, scams, and identity theft: Incogni.com/Tim (use code TIM at checkout and get 60% off an annual plan)*For show notes and past guests on The Tim Ferriss Show, please visit tim.blog/podcast.For deals from sponsors of The Tim Ferriss Show, please visit tim.blog/podcast-sponsorsSign up for Tim's email newsletter (5-Bullet Friday) at tim.blog/friday.For transcripts of episodes, go to tim.blog/transcripts.Discover Tim's books: tim.blog/books.Follow Tim:Twitter: twitter.com/tferriss Instagram: instagram.com/timferrissYouTube: youtube.com/timferrissFacebook: facebook.com/timferriss LinkedIn: linkedin.com/in/timferrissSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
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