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In this 2025 spring beekeeping update, Jeff and Becky gather beekeepers from across the country for a timely check-in on seasonal progress, survival rates, and challenges. Joining the table are Ang Roell (MA/FL), Bonnie Morse (CA), Duane Combs (AZ), and Jay Williams (TN), each offering a candid look at their spring buildup after a winter marked by extremes. Topics include overwintering survival—ranging from Duane's 70% losses in Arizona to Jay's impressive 96% survival in Tennessee—and how weather volatility and hive nutrition played pivotal roles. The conversation dives into spring splits, swarm control, queen longevity, and promising new varroa treatments like VarroxSan and RNA-based controls in development. Jay shares the results of using VarroxSan in his operation, while others discuss balancing cost and effectiveness with homemade oxalic pads and breeding practices. The episode also explores instrumental insemination, drone saturation strategies, and queen selection across climates. With thoughtful input from across the country, this roundtable offers insights that every beekeeper—regardless of location—can reflect on as spring rolls into full bloom. Websites from the episode and others we recommend: Honey Bee Obscura Bee Rooms Episode as mentioned by Becky: https://honeybeeobscura.com/225 Honey Bee Health Coalition: https://honeybeehealthcoalition.org The National Honey Board: https://honey.com Honey Bee Obscura Podcast: https://honeybeeobscura.com Copyright © 2025 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! Thanks to Bee Smart Designs as a sponsor of this podcast! Bee Smart Designs is the creator of innovative, modular and interchangeable hive systems made in the USA using recycled and American sourced materials. Bee Smart Designs - Simply better beekeeping for the modern beekeeper. Thanks to Dalan who is dedicated to providing transformative animal health solutions to support a more sustainable future. Dalan's vaccination against American Foulbrood (AFB) is a game changer. Vaccinated queens protect newly hatched honeybee larvae against AFB using the new Dalan vaccine. Created for queen producers and other beekeepers wanting to produce AFB free queens. Retailers offering vaccinated queens and packages: https://dalan.com/order-vaccinated-queens/ More information on the vaccine: https://dalan.com/media-publications/ 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 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; Original guitar background instrumental by Jeff Ott. Beekeeping Today Podcast is an audio production of Growing Planet Media, LLC Copyright © 2025 by Growing Planet Media, LLC
Broadcast from KSQD, Santa Cruz on 5-08-2025: Dr. Dawn examines groundbreaking research on rising rates of early-onset colorectal cancer worldwide, explaining how researchers have identified a bacterial toxin called colibactin produced by specific E. coli strains that appears to cause early genetic mutations in cancer-controlling genes, potentially explaining why younger generations face significantly higher cancer risks. She discusses how modern medical practices like antibiotic overuse and cesarean deliveries may disrupt protective gut microbiomes, while diets low in fiber and high in animal fats create conditions where harmful bacteria thrive and damage the protective mucosal barrier, potentially exposing colon cells to cancer-causing mutations. Dr. Dawn explains fascinating research on transgenerational memory in C. elegans worms and mice, where learned aversions to specific odors are genetically passed down to offspring through epigenetic mechanisms involving methylation and RNA pathways, challenging traditional views on inheritance and suggesting implications for human genetics. Responding to an email about posterior tibial tendon disease (PTTD), she offers comprehensive management strategies including cross-massage with ice, proper footwear selection, careful stretching techniques, and anti-inflammatory approaches while cautioning against invasive procedures like steroid injections that might weaken tendons. She discusses promising research on rosemary's potential in Alzheimer's treatment, explaining how carnosic acid activates the NRF2 pathway that controls antioxidant proteins, with researchers developing a more stable chemical analog that reduced inflammation and improved memory in mouse models of Alzheimer's disease. Dr. Dawn provides updates on vaccination recommendations, noting that egg allergy questions are no longer needed before flu vaccines, pneumococcal vaccines are now recommended for all adults over 50, and explaining the small risk of Guillain-Barré syndrome with RSV vaccines compared to the much larger risk of RSV-related deaths. She shares information about a new hypertension risk calculator called PREVENT that reclassifies many patients to lower risk categories, potentially allowing 2.6 million Americans to manage their blood pressure through lifestyle changes rather than medication, particularly benefiting older women who face different risk profiles than men.
Episode 190: Measles BasicsFuture Dr. Kapur explained the basics of measles, including the pathophysiology, diagnosis and management of this disease. Dr. Schlaerth added information about SPPE and told interesting stories of measles. Dr. Arreaza explained some statistics and histed the episode. Written by Ashna Kapur MS4 Ross University School of Medicine. Comments by Katherine Schlaerth, MD, and Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Introduction.According to the CDC, as of April 24, 2025, a total of 884 confirmed measles cases were reported by 30 states, including California, and notably Texas. This is already three times more cases than 2024. There are 3 confirmed deaths so far in the US. What is measles?Measles is a disease that's been around for centuries, nearly eradicated, yet still lingers in parts of the world due to declining vaccination rates. Let's refresh our knowledge about its epidemiology, clinical features, diagnosis, management, and most importantly — prevention.Definition.Measles, also known as rubeola, is an acute viral respiratory illness caused by the measles virus. It's a single-stranded, negative-sense RNA virus belonging to the Paramyxoviridae family. It's extremely contagious with a transmission rate of up to 90% among non-immune individuals when exposed to an infected person.EpidemiologyBefore the introduction of the measles vaccine in 1963, nearly every child got measles by the time they were 15 years old. With the introduction of vaccination, cases and deaths caused by measles significantly declined. For example, in 2018, over 140,000 deaths were reported in the whole world, mostly among children under the age of 5.Measles is still a common disease in many countries, including in Europe, the Middle East, Asia, and Africa. Measles outbreaks have been reported recently in the UK, Israel, India, Thailand, Vietnam, Japan, Ukraine, the Philippines, and more recently in the US. So, let's take prevention seriously to avoid the spread of this disease here at home and abroad. How do we get measles, Ashna?Mode of Transmission:● Air: Spread primarily through respiratory droplets.● Surfaces: The virus remains viable on surfaces or in the air for up to 2 hours. (so, if a person with measles was in a room and you enter the same room within 2 hours, you may still get measles)● Other people: Patients are contagious from 4 days before until 4 days after the rash appears.PathophysiologyThe measles virus first infects the respiratory epithelium, replicates, and then disseminates to the lymphatic system.It leads to transient but profound immunosuppression, which is why secondary infections are common. It affects the skin, respiratory tract, and sometimes the brain, leading to complications like pneumonia or encephalitis.Clinical PresentationThe classic presentation of measles can be remembered in three C's:● Cough● Coryza (runny nose)● ConjunctivitisCourse of Disease (3 Phases):1. Prodromal Phase (2-4 days)○ High fever (can peak at 104°F or 40°C)○ The 3 C's○ Koplik spots: Small white lesions on the buccal mucosa.2. Exanthem Phase○ Maculopapular rash begins on the face (especially around the hairline), then spreads from head to toe. The rash typically combines into 1 big mass as it spreads, and the fever often persists during the rash.3. Recovery Phase○ Rash fades in the same order it appeared.○ Patients remain at risk for complications during and after rash resolution.Complications:● Pneumonia (most common cause of death in children)● Otitis media (most common overall complication)● Encephalitis (can lead to permanent neurologic sequelae)● Subacute sclerosing panencephalitis (SSPE): A rare, fatal, degenerative CNS disease that can occur years after measles infection.High-risk groups for severe disease include:● Infants and young children● Pregnant women● Immunocompromised individualsDiagnosisClinical diagnosis is sufficient if classic symptoms are present, especially in outbreak settings.Ashna: Laboratory confirmation:● Measles-specific IgM antibodies detected by serology.● RT-PCR from nasopharyngeal, throat, or urine samples.Notify public health authorities immediately upon suspicion or diagnosis of measles to limit spread. ManagementThere is no specific antiviral treatment for measles. Management is supportive:● Hydration (by mouth and only IV in case of severe dehydration)● Antipyretics (e.g., acetaminophen) for fever● Oxygen if hypoxicVitamin A supplementation:● Recommended for all children with acute measles, particularly in areas with high vitamin A deficiency. It has shown to reduce morbidity and mortality.Hospitalization may be necessary for:● Severe respiratory compromise● Dehydration● Neurologic complicationsPrevention: We live in perilous times and vaccination is under scrutiny right now. Before the measles vaccine, about 48,000 people were hospitalized and 400–500 people died in the United States every year. Measles was declared eradicated in the US in 2000, but the vaccination coverage is no longer 95%. How do we prevent measles?Vaccination is the cornerstone of prevention.● MMR vaccine (Measles, Mumps, Rubella):○ First dose at 12-15 months of age.○ Second dose at 4-6 years of age.○ 97% effective after 2 doses.The Advisory Committee on Immunization Practices (ACIP) has noted that febrile seizures typically occur 7 to 12 days after vaccination with MMR, with an estimated incidence of 3.3 to 8.7 per 10,000 doses. The Centers for Disease Control and Prevention (CDC) states that febrile seizures following MMR vaccination are rare and not associated with any long-term effects. The risk of febrile seizures is higher when the MMR vaccine is administered as part of the combined MMRV (measles, mumps, rubella, and varicella) vaccine compared to the MMR vaccine alone.Post-exposure prophylaxis:● MMR vaccine within 72 hours of exposure (if possible).● Immunoglobulin within 6 days for high-risk individuals (e.g., infants, pregnant women, immunocompromised).Herd immunity requires at least 95% vaccination coverage to prevent outbreaks.Key Takeaways● Measles is a highly contagious viral illness that can lead to severe complications.● Diagnosis is often clinical, but lab confirmation helps with public health tracking.● Treatment is mainly supportive, with Vitamin A playing a critical role in reducing complications.● Vaccination remains the most effective tool to eliminate measles worldwide.While measles might seem like a disease of the past, it can make a dangerous comeback without continued vigilance and vaccination efforts.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Centers for Disease Control and Prevention (CDC). Measles (Rubeola), Clinical Overview, July 15, 2024. Accessed on May 1, 2025. https://www.cdc.gov/measles/hcp/clinical-overview/index.html.World Health Organization (WHO). Measles, November 14, 2024. https://www.who.int/news-room/fact-sheets/detail/measlesGans, Hayley and Yvonne A. Maldonado, Measles: Clinical manifestations, diagnosis, treatment, and prevention, UpToDate, January 15, 2025. Accessed on May 1, 2025. https://www.uptodate.com/contents/measles-clinical-manifestations-diagnosis-treatment-and-preventionTheme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
BUFFALO, NY - May 9, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on May 8, 2025, titled “METTL3 promotes oral squamous cell carcinoma by regulating miR-146a-5p/SMAD4 axis." In this study, researchers Jayasree Peroth Jayaprakash, Pragati Karemore, and Piyush Khandelia from the Birla Institute of Technology and Science, India, discovered that a molecule called METTL3 contributes to the development and spread of oral squamous cell carcinoma (OSCC). The study shows that METTL3 increases the levels of a small RNA molecule called miR-146a-5p, which blocks SMAD4, a key tumor-suppressing gene. These findings help explain why oral cancers are difficult to treat and may offer a new target for more effective therapies. Oral squamous cell carcinoma is a common and aggressive cancer affecting the mouth and throat. It has a high death rate, mainly due to late detection, treatment resistance, and the cancer's ability to invade nearby tissues. In this study, the researchers focused on METTL3, an enzyme that adds chemical tags known as m6A marks to RNA, which change how genetic information is used by cells. They found that METTL3 is unusually active in OSCC cells, causing an increase in miR-146a-5p. This molecule, in turn, blocks the function of SMAD4, which helps control how cells grow and die in our bodies. “METTL3, the primary m6A RNA methyltransferase, is significantly upregulated in OSCC cells leading to increased global m6A levels.” When METTL3 was reduced or chemically blocked, miR-146a-5p levels dropped and SMAD4 levels increased. This shift slowed the growth of cancer cells, increased their death, and made them less likely to spread. When researchers reintroduced miR-146a-5p or lowered SMAD4 levels again, the cancer-promoting behavior returned. These results show that the METTL3–miR-146a-5p–SMAD4 pathway plays a key role in OSCC. The findings open up new possibilities for treatment. Drugs that block METTL3 or miR-146a-5p or that restore SMAD4 could slow or stop tumor growth. One such drug, STM2457, which targets METTL3, has already shown promise in lab studies. As research progresses, targeting this molecular pathway may offer a new strategy in treating OSCC. This discovery improves our understanding of how OSCC develops and avoids the body's defenses. By interfering with this newly discovered pathway, future treatments may become more successful, improving survival rates and quality of life for people with this disease. DOI - https://doi.org/10.18632/oncotarget.28717 Correspondence to - Piyush Khandelia - piyush.khandelia@hyderabad.bits-pilani.ac.in Video short - https://www.youtube.com/watch?v=o5XuDlcIma8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28717 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
A great idea isn't enough to build a thriving business—execution depends on how well a team works together. Miscommunication, misalignment, and unspoken tension can quietly stall progress, no matter how innovative the product is. The best founders aren't just visionaries; they know how to bring people together, translate ideas into action, and create an environment where momentum doesn't fade. Success often has less to do with the idea itself and more to do with the people making it happen. Dr. Kevin Scanlon has built a diverse career in academic medicine, pharmaceuticals, and biotech. He authored The Hybrid Entrepreneur, a guide to startup success, and has contributed to RNA research while mentoring university startups and investment groups. With a background in teaching entrepreneurship, he brings a deep understanding of business innovation and team dynamics. Today, he explores the challenges of turning scientific breakthroughs into business success. He emphasizes the need for clear communication, adaptable teams, and bridging the language gap between scientists, business leaders, and investors. Stay tuned! Resources: Connect with Kevin Scanlon on LinkedIn
In May 2025, we attended IMMUNOLOGY2025™, the annual meeting of the American Association of Immunologists in Honolulu, and recorded daily episodes discussing highlights of the previous 24 hours. Here is the second of five special episodes from the meeting. Brenda and Jason discuss highlights from sessions on tumor-infiltrating lymphocyte and T-cell receptor therapies, unconventional functions of Tregs, and advances in single-cell RNA sequencing.
What is measles - a refresher? Measles is a serious, highly contagious and potentially deadly viral infection. It is caused by an RNA paramyxovirus. It is spread by contact with droplets from an infected person's nose, mouth or throat. Sneezing and coughing can aerosolize the droplets and increase the range of infectious spread. Symptoms usually develop 8 to 10 days following exposure to an infected individual. A sick individual is contagious for 4 days before and 4 days after symptom onset. The reproductive rate is very high at 12+ meaning that 1 person will infect 12 and those 12 will get 12 more sick (144) and then 144 X 12 = 1728 X 12 = 20,736 and you are off to the exponential races....Plus, The Shock of a New Diagnosis: A Stoic Path Through the Storm. Enjoy, Dr. M
According to LinkedIn, half of all workers are considering a career change in 2025. As government employees continue to experience layoffs in this volatile job market, they face an uncertain career future. Finding a new role in an oversaturated job market requires more than just updating a resume, it demands a strategic pivot. With more than 20 years in career strategy, Patrice Lindo, CEO of Career Nomad has helped more than 3,500 professionals pivot successfully by identifying their transferable skills and by leveraging her RNA framework. RNA stands for rebrand, network and achieve recognition. We discuss how laid off government employees can reposition their skill set to secure jobs in the private sector; the hidden job market and how networking and not online applications unlock career breakthroughs and why the traditional job search does not work in a saturated market. She shares what to do instead.
SJ Show Notes:Please support Shannon's independent network with your donation HERE:https://www.paypal.com/donate/?hosted_button_id=MHSMPXEBSLVT6Support Our Sponsors:You can get 20% off your first order of Blackout Coffee! Just head to http://blackoutcoffee.com/joy and use code joy at checkout.Be ready before you need it! Stock up now and protect your family. Go to https://www.allfamilypharmacy.com/JOY and use code JOY10 for 10% off your order.The Satellite Phone Store has everything you need when the POWER goes OUT. Use the promo code JOY for 10% off your entire order TODAY! www.SAT123.com/JoyThe 100% toxin free P600 sizzle set is 55% OFF for the SJ audience!! Go to https://www.chefsfoundry.com/joy today to claim the limited time discount!Get 45% OFF Native Path HYDRATE today! Special exclusive deal for the Joy audience only! Check it out HERE: www.nativepathhydrate.com/joyColonial Metals Group is the company Shannon trusts for all her metals purchases! Set up a SAFE & Secure IRA or 401k with a company who shares your values! Learn more HERE: https://colonialmetalsgroup.com/joyPlease consider Dom Pullano of PCM & Associates! He has been Shannon's advisor for over a decade and would love to help you grow! Call his toll free number today: 1-800-536-1368Or visit his website at https://www.pcmpullano.comTune in LIVE Today ——> https://rumble.com/v6srwiz-100-day-shocker-trump-is-deporting-fewer-illegal-immigrants-than-biden.htmlWatch LIVE TODAY and follow the SJ Show on Rumble HERE: https://rumble.com/c/TheShannonJoyShowShannon's Top Headlines April 30, 2025:BE PATIENT!!!: Trump's Economy Shrinks, Prices Soar, and the Blame Game Begins: https://croakycaiman.substack.com/p/be-patient-trumps-economy-shrinks?utm_source=post-email-title&publication_id=2855663&post_id=162537358&utm_campaign=email-post-title&isFreemail=false&r=fuu7w&triedRedirect=true&utm_medium=emailNumbers show no mass deportation of migrants, despite Trump immigration crackdown: https://x.com/Docjohnc/status/1894819606058922176Arcturus Therapeutics Receives U.S. FDA Fast Track Designation Self Amplifying RNA: https://www.biospace.com/press-releases/arcturus-therapeutics-receives-u-s-fda-fast-track-designation-for-the-starr-mrna-vaccine-candidate-arct-2304-for-pandemic-influenza-a-virus-h5n1The Reckless Gamble of Self-Amplifying RNA: A Runaway Experiment with No Off Switch: https://x.com/Docjohnc/status/1894819606058922176Is Self-Amplifying RNA a Synthetic Disease? https://therealcdc.substack.com/p/is-self-amplifying-rna-a-syntheticCLICK HERE To Stop The #DrDeath Bill In NYS: https://www.votervoice.net/AUTISMACTION/Campaigns/115959/Respond?unregistered=_ttc9anYD9aeEliyHNSITQYou really can't make this up …"Frankly I was shocked. They're lower, their daily average is simply 10 percent lower." This was according to Sue Long, a researchers who analyzed Trump's deportation statistics in the first 100 days of his presidency, comparing them to Biden era levels.This is another example of how the reality of Trump's first 100 days is drastically different than what Con Inc. & MAGA propagandists are pimping to their audiences.Meanwhile, as Trump gaslights his base on deportations, he is also fast tracking self amplifying mRNA shots to combat ‘bird flu' which is not only a continuation of Biden era health policies but an acceleration of potentially catastrophic biotechnology.Meet the new boss … same as the old boss. #UNIPARTYToday we are joined by two experts on the matter of emerging sa-RNA, the dangers of mRNA shots and government kill protocols, John Beaudoin Sr. and Jessica Rose. They will help us understand how this attempted merging of technology with biology is so dangerous and what we need to do to stop it.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
You're likely familiar with the genetic revolution — the discovery that physical structures in the cell, including DNA and RNA, shape every organism. But we are now overdue for another and more profound revolution in science, one you've likely heard very little about. Recent findings reveal that genetic and even epigenetic sources alone cannot account for the rich dynamism of life — not even close. Some other informational source is required. On this ID The Future, science writer and Discovery Institute Senior Fellow David Klinghoffer speaks with host Andrew McDiarmid about his new book Plato's Revenge: The New Science of the Immaterial Genome. It's a little book about a very big idea. It also tells the story of the scientist, Dr. Richard Sternberg, who has spent the last two decades bringing together cutting-edge molecular biology, higher mathematics, and commonsense reasoning to flesh out this potentially revolutionary new idea. Source
"If you are that person, if you feel like you can't find your box and you're off doing these random things that no one else seems to find interesting, it's okay. Embrace it. It's who you are and it's going to be your superpower someday." In this episode of The Biotech Startups Podcast, host Jon Chee sits down with Rabia Khan, founder and CEO of Serna Bio, to discuss her journey from Sensyne Health to building a data-driven biotech company pioneering RNA-targeted drug discovery. Rabia shares how she overcame scientific and operational hurdles, navigated contract research limitations, and boldly moved Serna Bio from the UK to San Francisco. She also reveals her intentional approach to company culture, frugality, and long-term impact—emphasizing her vision to create a biotech business built for enduring innovation, not just acquisition.
Discover the smallest motor in the universe—an astonishing molecular machine that powers all living cells with atomic precision. Explore why ATP synthase, with its near-perfect efficiency, challenges human engineering and evolutionary explanations. Dr Jonathan Sarfati explains how DNA’s replicating, repair, and detangling machines are vital for life. They are all encoded in the DNA, but the DNA can’t be decoded without these machines. This presents a “chicken-and-egg” paradox for naturalistic theories. DNA is also very unstable. Its presence in dinosaur bones undermine millions of years. RNA is 100× less stable than DNA, so could not be the first life. Evolutionists claim LUCA (Last Universal Common Ancestor) lived 4.2 billion years ago and already had 2.5 million DNA letters encoding 2,500 proteins. Life needed to start “very good” as Genesis 1:31 says. Otherwise, it would have crashed via error catastrophe.
Ochre Bio co-founder and CSO Quin Wills spoke with In Vivo about the UK-based company's novel approach to finding and validating RNA therapies for chronic liver diseases.
Desde hace décadas, los científicos estudian qué genes a lo largo de la evolución han sido los más importantes para que los humanos hablemos. Hasta ahora, el principal candidato era el gen llamado FOXP2. Los humanos poseemos una variante del gen FOXP2 que no poseen otros animales relacionados con nosotros, en particular no la poseen chimpancés o gorilas. Esta aparente exclusividad humana hizo creer en un principio que esa variante de FOXP2 era la que nos capacitaba para hablar. Gracias a los progresos en la secuenciación del DNA se ha podido obtener y comparar la secuencia de especies humanoides, como neandertales y denisovanos, así como de gorilas, chimpancés, orangutanes y bonobos. A partir de la comparación de esos genomas, se han identificado 61 genes cuyas variantes aparecen exclusivamente en la especie humana. Una de estas variantes génicas ha atraído mucho la atención de los científicos. Se trata de una variante del gen NOVA1, que produce una proteína que interacciona con el RNA en las neuronas y modula su función.
Desde hace décadas, los científicos estudian qué genes a lo largo de la evolución han sido los más importantes para que los humanos hablemos. Hasta ahora, el principal candidato era el gen llamado FOXP2. Los humanos poseemos una variante del gen FOXP2 que no poseen otros animales relacionados con nosotros, en particular no la poseen chimpancés o gorilas. Esta aparente exclusividad humana hizo creer en un principio que esa variante de FOXP2 era la que nos capacitaba para hablar. Gracias a los progresos en la secuenciación del DNA se ha podido obtener y comparar la secuencia de especies humanoides, como neandertales y denisovanos, así como de gorilas, chimpancés, orangutanes y bonobos. A partir de la comparación de esos genomas, se han identificado 61 genes cuyas variantes aparecen exclusivamente en la especie humana. Una de estas variantes génicas ha atraído mucho la atención de los científicos. Se trata de una variante del gen NOVA1, que produce una proteína que interacciona con el RNA en las neuronas y modula su función.
JCO PO author Dr. Timothy Showalter at Artera and University of Virginia shares insights into his JCO PO article, “Digital Pathology–Based Multimodal Artificial Intelligence Scores and Outcomes in a Randomized Phase III Trial in Men With Nonmetastatic Castration-Resistant Prostate Cancer” . Host Dr. Rafeh Naqash and Dr. Showalter discuss how multimodal AI as a prognostic marker in nonmetastatic castration-resistant prostate cancer may serve as a predictive biomarker with high-risk patients deriving the greatest benefit from treatment with apalutamide. TRANSCRIPT Dr. Rafeh Naqash: Hello and welcome to JCO Precision Oncology Conversations where we'll bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, podcast Editor for JCO Precision Oncology and assistant professor at the OU Health Stephenson Cancer Center at the University of Oklahoma. Today, we are excited to be joined by Dr. Timothy Showalter, Chief Medical Officer at Artera and professor of Radiation Oncology at the University of Virginia and author of the JCO Precision Oncology article entitled, “Digital Pathology Based Multimodal Artificial Intelligence Scores and Outcomes in a Randomized Phase 3 Trial in Men with Non-Metastatic Castration Resistant Prostate Cancer.” At the time of this recording, our guest's disclosures will be linked in the transcript. Dr. Showalter, it's a pleasure to have you here today. Dr. Timothy Showalter: It's a pleasure to be here. Thanks for having me. Dr. Rafeh Naqash: I think this is going to be a very interesting discussion, not just from a biomarker perspective, but also in terms of how technologies have evolved and how we are trying to stratify patients, trying to escalate or deescalate treatments based on biomarkers. And this article is a good example of that. One of the things I do want to highlight as part of this article is that Dr. Felix Feng is the first author for this article. Unfortunately, Dr. Felix Feng passed away in December of 2024. He was a luminary in this field of prostate cancer research. He was also the Chair of the NRG GU Committee as well as Board of Directors for RTOG Foundation and has mentored a lot of individuals from what I have heard. I didn't know Dr. Feng but heard a lot about him from my GU colleagues. It's a huge loss for the community, but it was an interesting surprise for me when I saw his name on this article as I was reviewing it. Could you briefly talk about Dr. Feng for a minute and how you knew him and how he's been an asset to the field? Dr. Timothy Showalter: Yeah. I'm always happy to talk about Felix whenever there's an opportunity. You know, I was fortunate to know Felix Feng for about 20 years as we met during our residency programs through a career development workshop that we both attended and stayed close ever since. And you know, he's someone who made an impact on hundreds of lives of cancer researchers and other radiation oncologists and physicians in addition to the cancer patients he helped, either through direct clinical care or through his innovation. For this project in particular, I first became involved soon after Felix had co-founded Artera, which is, you know the company that developed this. And because Felix was such a prolific researcher, he was actually involved in this and this research project from all different angles, both from the multimodal digital pathology tool to the trial itself and being part of moving the field forward in that way. It's really great to be able to sort of celebrate a great example of Felix's legacy, which is team science, and really moving the field forward in terms of translational projects based on clinical trials. So, it's a great opportunity to highlight some of his work and I'm really happy to talk about it with you. Dr. Rafeh Naqash: Thanks, Tim. Definitely a huge loss for the scientific community. And I did see a while back that there was an international symposium organized, showcasing his work for him to talk about his journey last year where more than 200, 250 people from around the globe actually attended that. That speaks volumes to the kind of impact he's had as an individual and impact he's had on the scientific side of things as well. Dr. Timothy Showalter: Yes. And we just had the second annual Feng Symposium the day before ASCO GU this year with, again, a great turnout and some great science highlighted, as well as a real focus on mentorship and team science and collaboration. Dr. Rafeh Naqash: Thank you so much for telling us all about that. Now going to what you guys published in JCO Precision Oncology, which is this article on using a biomarker approach to stratify non-metastatic prostate cancer using this artificial intelligence based H&E score. Could you tell us the background for what started off this project? And I see there is a clinical trial data set that you guys have used, but there's probably some background to how this score or how this technology came into being. So, could you superficially give us an idea of how that started? Dr. Timothy Showalter: Sure. So, the multimodal AI score was first published in a peer reviewed journal back in 2022 and the test was originally developed through a collaboration with the Radiation Therapy Oncology Group or Energy Oncology Prostate Cancer Research Team. The original publication describes development and validation of a risk stratification tool designed to predict distant metastasis and prostate cancer specific mortality for men with localized prostate cancer. And the first validation was in men who were treated with definitive radiation therapy. There have been subsequent publications in that context and there's a set of algorithms that have been validated in localized prostate cancer and there's a test that's listed on NCCN guidelines based on that technology. The genesis for this paper was really looking at extending that risk stratification tool that was developed in localized prostate cancer to see if it could one, validate in a non-metastatic castrate refractory prostate cancer population for patients enrolled on the SPARTAN trial. And two, whether there was a potential role for the test output in terms of predicting benefit from apalutamide for patients with non-metastatic prostate cancer. For patients who are enrolled on the SPARTAN study, almost 40% of them had H&E stain biopsy slide material available and were eligible to be included in this study. Dr. Rafeh Naqash: Going a step back to how prostate cancer, perhaps on the diagnostic side using the pathology images is different as you guys have Gleason scoring, which to the best of my knowledge is not necessarily something that most other tumor types use. Maybe Ki-67 is somewhat of a comparison in some of the neuroendocrine cancers where high Ki-67 correlates with aggressive biology for prognosis. And similarly high Gleason scores, as we know for some of the trainees, correlates with poor prognosis. So, was the idea behind this based on trying to stratify or sub-stratify Gleason scoring further, where you may not necessarily know what to do with the intermediate high Gleason score individual tumor tissues? Dr. Timothy Showalter: Well, yeah. I mean, Gleason score is a really powerful risk stratification tool. As you know, our clinical risk groupings are really anchored to Gleason scores as an important driver for that. And while that's a powerful tool, I think, you know, some of the original recognition for applying computer vision AI into this context is that there are likely many other features located in the morphology that can be used to build a prognostic model. Going back to the genesis of the discovery project for the multimodal AI model, I think Felix Feng would have described it as doing with digital pathology and computer vision AI what can otherwise be done with gene expression testing. You know, he would have approached it from a genomic perspective. That's what the idea was. So, it's along the line of what you're saying, which is to think about assigning a stronger Gleason score. But I think really more broadly, the motivation was to come up with an advanced complementary risk stratification tool that can be used in conjunction with clinical risk factors to help make better therapy recommendations potentially. So that was the motivation behind it. Dr. Rafeh Naqash: Sure. And one of the, I think, other important teaching points we try to think about, trainees of course, who are listening to this podcast, is trying to differentiate between prognostic and predictive scores. So, highlighting the results that you guys show in relation to the MMAI score, the digital pathology score, and outcomes as far as survival as well as outcomes in general, could you try to help the listeners understand the difference between the prognostic aspect of this test and the predictive aspect of this test? Dr. Timothy Showalter: So let me recap for the listeners what we found in the study and how it kind of fits into the prognostic and the predictive insights. So, one, you know, as I mentioned before, this is ultimately a model that was developed and validated for localized prostate cancer for risk stratification. So, first, the team looked at whether that same tool developed in localized prostate cancer serves as a prognostic tool in non-metastatic castrate-refractory prostate cancer. So, we applied the tool as it was previously developed and identified that about 2/3 of patients on the SPARTAN trial that had specimens available for analysis qualified as high risk and 1/3 of patients as either intermediate or low risk, which we called in the paper ‘non-high risk'. And we're able to show that the multimodal AI score, which ranges from 0 to 1, and risk group, was associated with metastasis free survival time to second progression or PFS 2 and overall survival. And so that shows that it performs as a prognostic tool in this setting. And this paper was the first validation of this tool in non-metastatic castrate-refractory prostate cancer. So, what that means to trainees is basically it helps you understand how aggressive that cancer is or better stratify the risk of progression over time. So that's the prognostic performance. Dr. Rafeh Naqash: Thank you for trying to explain that. It's always useful to get an example and understand the difference between prognostic and predictive. Now again, going back to the technology, which obviously is way more complicated than the four letter word MMAI, I per se haven't necessarily done research in this space, but I've collaborated with some individuals who've done digital pathology assessments, and one of the projects we worked on was TIL estimation and immune checkpoint related adverse events using some correlation and something that one of my collaborators had sent to me when we were working on this project as part of this H&E slide digitalization, you need color deconvolution, you need segmentation cell profiling. Superficially, is that something that was done as part of development of this MMAI score as well? Dr. Timothy Showalter You need a ground truth, right? So, you need to train your model to predict whatever the outcome is. You know, if you're designing an AI algorithm for Ki-67 or something I think you mentioned before, you would need to have a set of Ki-67 scores and train your models to create those scores. In this case, the clinical annotation for how we develop the multimodal AI algorithm is the clinical endpoints. So going back to how this tool was developed, the computer vision AI model is interpreting a set of features on the scan and what it's trying to do is identify high risk features and make a map that would ultimately predict clinical outcomes. So, it's a little bit different than the many digital pathology algorithms where the AI is being trained to predict a particular morphological finding. In this case, the ground truth that the model is trained to predict is the clinical outcome. Dr. Rafeh Naqash: Sure. And from what you explained earlier, obviously, tumors that had a high MMAI score were the ones that were benefiting the most from the ADT plus the applausive. Is this specific for this androgen receptor inhibitor or is it interchangeable with other inhibitors that are currently approved? Dr. Timothy Showalter: That's a great question and we don't know yet. So, as you're alluding to, we did find that the MMAI risk score was predictive for benefit from apalutamide and so it met the statistical definition of having a significant interaction p value so we can call it a predictive performance. And so far, we've only looked in this population for apalutamide. I think you're raising a really interesting point, which is the next question is, is this generalizable to other androgen receptor inhibitors? There will be future research looking at that, but I think it's too early to say. Just for summary, I think I mentioned before, there are about 40% of patients enrolled on the SPARTAN study had specimens available for inclusion in this analysis. So, the SPARTAN study did show in the entire clinical trial set that patients with non-metastatic castrate-refractory prostate cancer benefited from apalutamide. The current study did show that there seems to be a larger magnitude of benefit for those patients who are multimodal AI high risk scores. And I think that's very interesting research and suggests that there's some interaction there. But I certainly would want to emphasize that we have not shown that patients with intermediate or low risk don't benefit from apalutamide. I think we can say that the original study showed that that trial showed a benefit and that we've got this interesting story with multimodal AI as well. Dr. Rafeh Naqash: Sure. And I think from a similar comparison, ctDNA where ctDNA shows prognostic aspects, I treat people with lung cancer especially, and if you're ctDNA positive at a 3 to 4-month period, likely chances of you having a shorter disease-free interval is higher. Same thing I think for colorectal cancers. And now there are studies that are using ctDNA as an integral biomarker to stratify patients positive/negative and then decide on escalation/de-escalation of treatment. So, using a similar approach, is there something that is being done in the context of the H&E based stratification to de-intensify or intensify treatments based on this approach? Dr. Timothy Showalter: You're hitting right on the point in the most promising direction. You know, as we pointed out in the manuscript, one of the most exciting areas as a next step for this is to use a tool like this for stratification for prospective trials. The multimodal AI test is not being used currently in clinical trials of non-metastatic castrate-refractory prostate cancer, which is a disease setting for this paper. There are other trials that are in development or currently accruing where multimodal AI stratification approach is being taken, where you see among the high-risk scores, at least in the postoperative setting for a clinical trial that's open right now, high risk score patients are being randomized to basically a treatment intensification question. And then the multimodal AI low risk patients are being randomized to a de-intensification experimental arm where less androgen deprivation therapy is being given. So, I think it's a really promising area to see, and I think what has been shown is that this tool has been validated really across the disease continuum. And so, I think there are opportunities to do that in multiple clinical scenarios. Dr. Rafeh Naqash: Then moving on to the technological advancements, very fascinating how we've kind of evolved over the last 10 years perhaps, from DNA based biomarkers to RNA expression and now H&E. And when you look at cost savings, if you were to think of H&E as a simpler, easier methodology, perhaps, with the limitations that centers need to digitalize their slides, probably will have more cost savings. But in your experience, as you've tried to navigate this H&E aspect of trying to either develop the model or validate the model, what are some of the logistics that you've experienced can be a challenge? As we evolve in this biomarker space, how can centers try to tackle those challenges early on in terms of digitalizing data, whether it's simple data or slides for that matter? Dr. Timothy Showalter: I think there's two main areas to cover. One, I think that the push towards digitalization is going to be, I think, really driven by increasing availability and access to augmentative technologies like this multimodal AI technology where it's really adding some sort of a clinical insight beyond what is going to be generated through routine human diagnostic pathology. I think that when you can get these sorts of algorithms for patient care and have them so readily accessible with a fast turnaround time, I think that's really going to drive the field forward. Right now, in the United States, the latest data I've seen is that less than 10% of pathology labs have gone digital. So, we're still at an early stage in that. I hope that this test and similar ones are part of that push to go more digital. The other, I think, more interesting challenge that's a technical challenge but isn't about necessarily how you collect the data, but it certainly creates data volume challenges, is how do you deal with image robustness and sort of translating these tools into routine real-world settings. And as you can imagine, there's a lot of variation for staining protocols, intensity scanner variations, all these things that can affect the reliability of your test. And at least for this research group that I'm a part of that has developed this multimodal AI tool can tell you that the development is sophisticated, but very data and energy intensive in terms of how to deal with making a tool that can be consistent across a whole range of image parameters. And so that presents its own challenges for dealing with a large amount of compute time and AI cycles to make robust algorithms like that. And practically speaking, I think moving into other diseases and making this widely available, the size of data required and the amount of cloud compute time will be a real challenge. Dr. Rafeh Naqash: Thank you for summarizing. I can say that definitely, you know, this is maybe a small step in prostate cancer biomarker research, but perhaps a big step in the overall landscape of biomarker research in general. So definitely very interesting. Now, moving on to the next part of the discussion is more about you as a researcher, as an individual, your career path, if you can summarize that for us. And more interestingly, this intersection between being part of industry as well as academia for perhaps some of the listeners, trainees who might be thinking about what path they want to choose. Dr. Timothy Showalter: Sure. So, as you may know, I'm a professor at the University of Virginia and I climbed the academic ladder and had a full research grant program and thought I'd be in academia forever. And my story is that along the way, I kind of by accident ended up founding a medical device company that was called Advaray and that was related to NCI SBIR funding. And I found myself as a company founder and ultimately in that process, I started to learn about the opportunity to make an impact by being an innovator within the industry space. And that was really the starting point for me. About four years ago, soon after Felix Feng co-founded Artera, he called me and told me that he needed me to join the company. For those who were lucky to know Felix well, at that very moment, it was inevitable that I was going to join Artera and be a part of this. He was just so persuasive. So, I will say, you know, from my experience of being sort of in between the academic and industry area, it's been a really great opportunity for me to enter a space where there's another way of making an impact within cancer care. I've gotten to work with top notch collaborators, work on great science, and be part of a team that's growing a company that can make technology like this available. Dr. Rafeh Naqash: Thank you so much, Tim, for sharing some of those thoughts and insights. We really appreciate you discussing this very interesting work with us and also appreciate you submitting this to JCO Precision Oncology and hopefully we'll see more of this as this space evolves and maybe perhaps bigger more better validation studies in the context of this test. Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcast. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.
Dr Matthew Wilson, Postdoctoral Fellow at the Centre for Human Genetics, KU Leuven, joins hosts Silvia Radenkovic and Rodrigo Starosta to discuss a scintillating selection of CDG papers in our first ever research round-up. The papers discussed include: A pseudoautosomal glycosylation disorder prompts the revision of dolichol biosynthesis. Wilson et al Clinical and biochemical footprints of congenital disorders of glycosylation: Proposed nosology. Ng et al Rft1 catalyzes lipid-linked oligosaccharide translocation across the ER membrane. Chen et al Molecular characterization of Rft1, an ER membrane protein associated with congenital disorder of glycosylation RFT1-CDG. Hirata et al Genome and RNA sequencing were essential to reveal cryptic intronic variants associated to defective ATP6AP1 mRNA processing. Morales-Romero et al N-glycoproteomic and proteomic alterations in SRD5A3-deficient fibroblasts. Garapati et al In vitro treatment with liposome-encapsulated Mannose-1-phosphate restores N-glycosylation in PMM2-CDG patient-derived fibroblasts. Shirakura et al Liposome-encapsulated mannose-1-phosphate therapy improves global N-glycosylation in different congenital disorders of glycosylation. Budhraja et al D-mannose as a new therapy for fucokinase deficiency-related congenital disorder of glycosylation (FCSK-CDG). Starosta et al Glycoproteomics in Cerebrospinal Fluid Reveals Brain-Specific Glycosylation Changes. Baerenfaenger et al Neural and metabolic dysregulation in PMM2-deficient human in vitro neural models. Radenkovic et al
What does it take to go from humble beginnings to billionaire status while revolutionizing health and technology? In this episode of The Thrive State Podcast, Dr. Kien Vuu sits down with Naveen Jain, the visionary entrepreneur behind Viome, Moon Express, and other billion-dollar companies, to discuss mindset, health, AI, and longevity. Episode Highlights: From rags to billionaire – Meet Naveen Jain The #1 mindset shift that makes success inevitable Why entrepreneurs should never compete—only disrupt How AI is transforming healthcare (Detecting disease before symptoms appear!) The gut-brain connection and how it impacts mental health
This episode explores the critical role of tryptophan, an aromatic amino acid, in forming tubulin—the key protein building microtubules, which act as cellular "train tracks" for structure and movement. We delve into how microtubules drive mitosis, the process of cell division essential for growth and repair, and discuss tryptophan's unique biochemical significance, including its single codon (UGG) and contributions to DNA methylation.We connect these cellular mechanisms to Autism, examining how microtubule disruptions may affect neuron proliferation and migration during prenatal development, potentially leading to sensory processing issues and altered connectivity. The episode highlights the intricate dance of cells in neural tube formation and emphasizes the need for deeper research into these upstream processes to uncover Autism's developmental roots.YT video of tryptophan and microtubules https://youtu.be/AY6GmS_AePk?si=K_ZTy5RjLGkm1hGdInner Cell Life video https://youtu.be/RrS2uROUjK4?si=DCHs927yteOZ00dWSee Stuart Hameroff, Martin Picard, Michael Levin, Jack Kruseuse "autism" for $25 off athttps://buy.daylightcomputer.com/RYAN03139use "autism" for 10% discount athttps://getchroma.co/?ref=autism00:00 Daylight Computer Company, use "autism" for $25 discount04:22 tryptophan, aromatic amino acid, microtubules, mitosis; human biology, autism04:44 tryptophan, UGG codon, methionine, SAM, MTHFR, folate, DNA methylation; upstream biology, RNA, DNA06:04 microtubules, train tracks, mitosis, cell division, spindle, DNA separation; skin repair06:55 tryptophan, tubulin, microtubules, mitosis, intracellular transport, cell shape; Autism research, upstream processes9:25 Chroma Light Devices- Lights Designed for Humans, use "autism" for 10% discount12:27 tryptophan fluorescence, mitosis, prophase, prometaphase, metaphase, anaphase, telophase, cytokinesis; microtubules, chromosome movement, cell division, tissue repair15:58 mitosis, neural tube, embryonic development, neuron proliferation, migration; Autism, brain size, connectivity20:33 sensory processing, hyperconnectivity, synaptic pruning, microtubules; Autism, sensory sensitivities, cortical connections25:06 excitation-inhibition imbalance, microtubules, environmental toxins, light exposure, fertilization, blastocyst; Autism, prenatal development, cell polarity31:09 microtubules, neural tube, gastrulation, neurogenesis, synaptogenesis, ectoderm, mesoderm, endoderm; Autism, cell migration,37:18 outro, reviewsX: https://x.com/rps47586Hopp: https://www.hopp.bio/fromthespectrumYT: https://www.youtube.com/channel/UCGxEzLKXkjppo3nqmpXpzuAemail: info.fromthespectrum@gmail.com
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! HELP SUPPORT US AS WE DOCUMENT HISTORY HERE: https://gogetfunding.com/help-wam-cover-history/ GET NON-MRNA FREEZE DRIED MEAT HERE: https://wambeef.com/ Use code WAMBEEF to save 20%! GET HEIRLOOM SEEDS & NON GMO SURVIVAL FOOD HERE: https://heavensharvest.com/ USE Code WAM to save 5% plus free shipping! GET YOUR APRICOT SEEDS at the life-saving Richardson Nutritional Center HERE: https://rncstore.com/r?id=bg8qc1 Josh Sigurdson reports on the FDA fast tracking the new "Self Amplifying mRNA Vaccine Candidate" for Bird Flu as RFK Jr. refuses to shut down Covid injections and the dangerous schedule. "Self Amifying mRNA Vaccines" (sa-RNA) which has been studied heavily in Japan in the past few years turns your body into a deadly mRNA vaccine factory for the rest of your life as the poisons regularly regenerate themselves. As the Bird Flu fear mongering continues, the eugenicists are planning a major depopulation event targeting the food supply. From modRNA in the food supply that survives the digestive system to forced food rations on a digital ID and the destruction of health following sa-RNA mandates, this plandemic hoax isn't going away any time soon. All the while, Measles fear mongering continues with RFK Jr. telling people to inject themselves with the Measles MMR vaccine. Flu shots have also recently been found to make recipients 27 percent more likely to "catch the flu" though that just sounds in general like a destroyed immune system from injecting yourself with poison. 122 million Americans are also drinking water contaminated with cancer causing chemical trihalomethanes. They're targeting you. Prepare yourselves and don't fall for the fear. Simply withdraw from their control. Stay tuned for more from WAM! 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! SIGN UP FOR HOMESTEADING COURSES NOW: https://freedomfarmers.com/link/17150/ Get Prepared & Start The Move Towards Real Independence With Curtis Stone's Courses! GET YOUR WAV WATCH HERE: https://buy.wavwatch.com/WAM Use Code WAM to save $100 and purchase amazing healing frequency technology! GET ORGANIC CHAGA MUSHROOMS HERE: https://alaskachaga.com/wam Use code WAM to save money! See shop for a wide range of products! GET AMAZING MEAT STICKS HERE: https://4db671-1e.myshopify.com/discount/WAM?rfsn=8425577.918561&utm_source=refersion&utm_medium=affiliate&utm_campaign=8425577.918561 USE CODE WAM TO SAVE MONEY! GET YOUR FREEDOM KELLY KETTLE KIT HERE: https://patriotprepared.com/shop/freedom-kettle/ Use Code WAM and enjoy many solutions for the outdoors in the face of the impending reset! BUY GOLD HERE: https://firstnationalbullion.com/schedule-consult/ PayPal: ancientwonderstelevision@gmail.com FIND OUR CoinTree page here: https://cointr.ee/joshsigurdson JOIN US on SubscribeStar here: https://www.subscribestar.com/world-alternative-media For subscriber only content! Pledge here! Just a dollar a month can help us alive! https://www.patreon.com/user?u=2652072&ty=h&u=2652072 BITCOIN ADDRESS: 18d1WEnYYhBRgZVbeyLr6UfiJhrQygcgNU World Alternative Media 2025
Najdete-li zakrslá rajčata nebo jiné plodiny se žloutnoucími listy, častou příčinou je virus mozaiky okurek. Badatelé z Halle úspěšně vyzkoušeli nový způsob boje proti němu. Budoucí lék založili na rozbíjení molekul virové RNA.Všechny díly podcastu Laboratoř můžete pohodlně poslouchat v mobilní aplikaci mujRozhlas pro Android a iOS nebo na webu mujRozhlas.cz.
Episode 188: RSV Management and PreventionDr. Sandhu and future Dr. Mohamed summarize the management of RSV and describe how to prevent it with chemoprophylaxis and vaccines. Dr Arreaza adds some comments about RSV vaccines.Written by Abdolhakim Mohamed, MSIV, Ross University School of Medicine. Comments by Ranbir Sandhu, MD, and Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.What is RSV? -The Respiratory syncytial Virus (RSV) is an enveloped, negative-sense, single-stranded RNA virus of the Orthopneumovirus genus within the Pneumoviridae family. -RSV is a major cause of acute respiratory tract infections, particularly bronchiolitis and pneumonia, in infants and young children, and it also significantly affects older adults and immunocompromised individuals. -RSV infections cause an estimated 58,000–80,000 hospitalizations among children younger than 5 years and 60,000–160,000 hospitalizations among adults older than 65 years each year.-RSV is highly contagious and spreads through respiratory droplets and direct contact with contaminated surfaces. The virus typically causes seasonal epidemics, peaking in the winter months in temperate climates and during the rainy season in tropical regions. -Virtually all children are infected with RSV by the age of two, and reinfections can occur throughout life, often with milder symptoms.-Per the 2014 Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis, from the American Academy of Pediatrics, the most common etiology of bronchiolitis is RSV. -About 97% of children are infected with RSV in the first 2 years of life, about 40% will experience lower respiratory tract infection during the initial infection. Other viruses that cause bronchiolitis include human rhinovirus, human metapneumovirus, influenza, adenovirus, coronavirus, and parainfluenza viruses.When is RSV season?-Classically, the highest incidence of infection occurs between December and March in North America. Per CDC, there were typical prepandemic RSV season patterns, but the COVID-19 pandemic disrupted RSV seasonality during 2020–2022. -Before we dive into the seasonality patterns, for context, in order to describe RSV seasonality in the US, data was gathered and analyzed from polymerase chain reaction (PCR) test results reported to the National Respiratory and Enteric Virus Surveillance System (NREVSS) during July 2017–February 2023. -Seasonal RSV epidemics were defined as the weeks during which the percentage of PCR test results that were positive for RSV was ≥3%. Per 2017–2020 data, RSV epidemics in the United States typically follow seasonal patterns, that began in October, peaked in December or January, and ended in April. -However, during 2020–21, the typical winter RSV epidemic did not occur. The 2021–22 season began in May, peaked in July, and ended in January. -The 2022–23 season started (June) and peaked (November) later than the 2021–22 season, but earlier than prepandemic seasons. CDC notes that the timing of the 2022–23 season suggests that seasonal patterns are returning toward those observed in prepandemic years, however, warn that clinicians should be aware that off-season RSV circulation might continue.Treatment of RSVSome key points of the 2014 pediatric guidelines from the American Academy of Pediatrics.-AAP strongly do not recommend beta agonists or steroids for viral associated bronchiolitis because of no significant improved outcomes. “Clinicians should not administer albuterol (or salbutamol) to infants and children with a diagnosis of bronchiolitis (Evidence Quality: B; Recommendation Strength: Strong Recommendation).”-Epinephrine is not recommended for infants and children with a diagnosis of bronchiolitis (Evidence Quality: B; Recommendation Strength: Strong Recommendation).-Nebulized hypertonic saline should not be administered to infants with a diagnosis of bronchiolitis in the emergency department (Evidence Quality: B; Recommendation Strength: Moderate Recommendation), but hypertonic saline may be administered when they are hospitalized (Evidence Quality: B; Recommendation Strength: Weak Recommendation [based on randomized controlled trials with inconsistent findings]).-Chest physiotherapy should not be used in infants and children with a diagnosis of bronchiolitis (Evidence Quality: B; Recommendation Strength: Moderate Recommendation).-Antibiotics should not be administered in bronchiolitis unless there is a concomitant bacterial infection, or a strong suspicion of one (Evidence Quality: B; Recommendation Strength: Strong Recommendation).-Oxygen therapy may not be administered if the oxyhemoglobin saturation exceeds 90% in infants and children with a diagnosis of bronchiolitis (Evidence Quality: D; Recommendation Strength: Weak Recommendation [based on low level evidence and reasoning from first principles]).-Clinicians should administer nasogastric or intravenous fluids for infants with a diagnosis of bronchiolitis who cannot maintain hydration orally (Evidence Quality: X; Recommendation Strength: Strong Recommendation).How do we prevent RSV?Infant Immuno-prophylaxis:A clinical trial in 2022 demonstrated that a single injection of nirsevimab (Beyfortus®), administered before the RSV season, protected healthy late-preterm and term infants from RSV-associated lower respiratory tract that required medical treatment. Nirsevimab is a monoclonal antibody to the RSV fusion protein that has an extended half-life.Additionally, on August 3, 2023, the Advisory Committee on Immunization Practices (ACIP) recommended nirsevimab for all infants younger than 8 months who are born during or entering their first RSV season and for infants and children between 8-19 months who are at increased risk for severe RSV disease and are entering their second RSV season. On the basis of pre-COVID-19 pandemic patterns, nirsevimab could be administered in most of the continental United States from October through the end of March.Maternal Vaccination: The CDC recommends the administration of the RSVPreF vaccine to pregnant women between 32 0/7 and 36 6/7 weeks of gestation. This vaccination aims to reduce the risk of RSV-associated lower respiratory tract infection in infants during the first 6 months of life.At this time, if a pregnant woman has already received a maternal RSV vaccine during any previous pregnancy, CDC does not recommend another dose of RSV vaccine during subsequent pregnancies.Older individuals: -Each year in the U.S., it is estimated that between 60,000 and 160,000 older adults are hospitalized and between 6,000 and 10,000 die due to RSV infection-ABRYSVO's approval will help offer older adults protection in the RSV season.-On June 26, 2024, ACIP voted to give these recommendations: all adults older than 75 years and adults between 60–74 years who are at increased risk for severe RSV disease should receive a single dose of RSV vaccine (Abrysvo®).Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Hamid S, Winn A, Parikh R, et al. Seasonality of Respiratory Syncytial Virus — United States, 2017–2023. MMWR Morb Mortal Wkly Rep 2023;72:355–361. DOI: http://dx.doi.org/10.15585/mmwr.mm7214a1Hammitt LL, Dagan R, Yuan Y, Baca Cots M, Bosheva M, Madhi SA, Muller WJ, Zar HJ, Brooks D, Grenham A, Wählby Hamrén U, Mankad VS, Ren P, Takas T, Abram ME, Leach A, Griffin MP, Villafana T; MELODY Study Group. Nirsevimab for Prevention of RSV in Healthy Late-Preterm and Term Infants. N Engl J Med. 2022 Mar 3;386(9):837-846. doi: 10.1056/NEJMoa2110275. PMID: 35235726.Ralston SL, Lieberthal AS, Meissner HC, Alverson BK, Baley JE, Gadomski AM, Johnson DW, Light MJ, Maraqa NF, Mendonca EA, Phelan KJ, Zorc JJ, Stanko-Lopp D, Brown MA, Nathanson I, Rosenblum E, Sayles S 3rd, Hernandez-Cancio S; American Academy of Pediatrics. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014 Nov;134(5):e1474-502. doi: 10.1542/peds.2014-2742. Erratum in: Pediatrics. 2015 Oct;136(4):782. doi: 10.1542/peds.2015-2862. PMID: 25349312.CDC, per their published article Seasonality of Respiratory Syncytial Virus — United States for 2017–2023, in the United StatesWhat U.S. Obstetricians Need to Know About Respiratory Syncytial Virus.Debessai H, Jones JM, Meaney-Delman D, Rasmussen SA. Obstetrics and Gynecology. 2024;143(3):e54-e62. doi:10.1097/AOG.0000000000005492.Maternal Respiratory Syncytial Virus Vaccination and Receipt of Respiratory Syncytial Virus Antibody (Nirsevimab) by Infants Aged
Marama Labs, a rapidly growing scientific instrumentation innovator, announces the launch of its revolutionary new CloudSpec instrument for nanomedicine developers. CloudSpec's patented technology slashes development times for advanced nanoparticle drug formulations used in gene therapies, vaccines, and cancer treatments. Lipid Nanoparticle (LNP) therapies are a hugely valuable class of biopharmaceutical nanomedicines; their use in Covid vaccines demonstrated the power and speed-to-market that RNA-loaded LNPs enable. The LNP market is expected to grow 7x within the next 10 years, as new therapies are developed for some of the hardest-to-drug diseases in cancer, genetic disorders and even the common cold. CloudSpec accelerates LNP development by solving a critical bottleneck - quantifying the drug payload in seconds - while current methods take hours. Breaking the bottleneck in nanomedicine development LNPs are tiny insoluble particles embedded with RNA or DNA. They are difficult to analyse directly due to their small size and light-scattering properties. CloudSpec's Scatter-Free Absorption (SFA) technology enables fast and accurate results using a new approach based on easy-to-use UV analysis. CloudSpec eliminates the need to break up the particles for analysis and doesn't require hard-to-use fluorescent dyes. CloudSpec measurements take 15 seconds compared to 2 hours using existing methods. By measuring intact particles, CloudSpec provides results from sample to answer in just a few minutes. CloudSpec is expected to revolutionise how lipid nanoparticles are analysed and quantified. "We are thrilled to introduce the CloudSpec instrument to the market," said Brendan Darby, CEO of Marama Labs. "This innovative technology represents a significant advancement in the field of nanomedicine, and we are confident that it will transform research with lipid nanoparticles." "We worked with some of the leading names in RNA-LNP biopharma to develop CloudSpec for this market. It has received a hugely positive response from our users, who are desperate to get away from the current slow, labour-intensive and inaccurate fluorescence measurements. CloudSpec gets them over the drug assay bottleneck and will speed up delivery to market", said Darren Andrews, CCO of Marama Labs. CloudSpec's launch to market will be spearheaded by a webinar on 7 May 2025 from two of CloudSpec's users from our Early Access Programme - Dr. Emily Young of 4basebio (UK) and Dr. Johanna Simon of Merck KGaA (Germany). Registration for the webinar is available here https://beacon-intelligence.com/webinar/rna-dna-quantification-in-lnps/. For more information about CloudSpec and its capabilities, please visit our website at www.maramalabs.com.
Dr. Monika Wolkers is a Group Leader at the Sanquin Blood Supply Foundation and an Associate Professor at the University of Amsterdam. Her research focuses on RNA-binding proteins and how they affect T cell function. She talks about γδ T cells in immunotherapy, targeting pediatric tumors, and how a sabbatical led her to study RNA-binding proteins.
Good morning from Pharma and Biotech daily: the podcast that gives you only what's important to hear in Pharma e Biotech world. Pharma industry tensions rise as Trump tariffs miss sector for now. FDA's interim CBER head appointed after key resignation. Xaira Therapeutics hires top AI academic. Novavax's COVID-19 shot review deadline missed by FDA. Trilink offers guide RNA for CRISPR workflow. Biotech sector sees investment surge. Beigene scraps candidate, Sarepta's gene therapy on hold in Europe. Biopharma professionals work long hours.In other news, there are safety concerns in Duchenne treatment. Democrats challenge Trump health cuts. And there are job opportunities in the biopharma industry.
Imagine your doctor could precisely predict your personal risk of disease, diagnose the cause of illness with pinpoint accuracy when it did occur, and develop an effective treatment plan with low side effects the first time, rather than through trial and error. That's the promise of personalized medicine. And it would be a revolution in healthcare. At the heart of this vision is the notion that our genetic differences have a big impact on how each of us responds to disease and treatment. To realize a future of personalized medicine then, we need to understand and investigate just how genetic variations, including mutations, contribute to illness and respond to doctors' attempts to address it. But how can scientists do that efficiently with a human genome that spans about three billion base pairs of DNA across tens of thousands of genes? That's where the work of PhD student Dawn Chen comes in. A student in Harvard's Department of Stem Cell and Regenerative Biology and the Systems, Synthetic, and Quantitative Biology Program, Chen was named a recipient of the 2025 Harold M. Weintraub Graduate Student Award for Outstanding Achievement and Exceptional Research in the Biological Sciences, presented by Seattle's Fred Hutch Cancer Center. With her colleagues in the lab of Harvard professor Fei Chen, Dawn Chen is developing an innovative gene-editing tool known as helicase-assisted continuous editing, or HACE. A breakthrough in genetic engineering, supported in part by funds from the National Institutes of Health, HACE makes edits to specific genes, allowing researchers to investigate how genetic variations contribute to disease. The technique could lead to the identification of specific mutations that influence the effectiveness of drugs and therapies for illnesses like cancer.
Dr. Vamsi Velcheti and Dr. Charu Aggarwal discuss the evolution of ctDNA as a critical tool in precision oncology and its implications for lung cancer management, including its potential role in the early-stage setting. TRANSCRIPT Dr. Vamsi Velcheti: Hello. I am Dr. Vamsi Velcheti, your guest host for the ASCO Daily News Podcast today. I am a professor of medicine and director of thoracic medical oncology at the Perlmutter Cancer Center at NYU Langone Health. The management of small cell lung cancer has rapidly evolved over the past few decades, and today, molecular testing and biomarker testing for lung cancer are absolutely critical in terms of designing treatment options for our patients with metastatic non-small cell lung cancer. Today, I'm delighted to be joined by Dr. Charu Aggarwal for a discussion on ctDNA (circulating tumor DNA) and the role of ctDNA in lung cancer management. Dr. Aggarwal is the Leslye Heisler Professor of Lung Cancer Excellence and section chief of thoracic and head and neck oncology at University of Pennsylvania Abramson Cancer Center. You'll find our full disclosures in the transcript of that episode. Dr. Agrawal, it's great to have you on the podcast today. Thank you for being here. Dr. Charu Aggarwal: Thank you for having me. Dr. Vamsi Velcheti: Let's start off with setting the stage for ctDNA technology. These technologies have rapidly evolved from experimental conceptual stage to essential clinical tools for day-to-day clinical practice. Could you briefly discuss how recent advancements in ctDNA technologies are shaping our approach to precision medicine, especially in lung cancer? Dr. Charu Aggarwal: Absolutely. And you know, I think we need to just level set a little bit. What exactly is circulating tumor DNA? This is a way to assess exactly that. Every tumor sheds little pieces of tumor-derived DNA into the bloodstream, and this occurs in a variety of solid tumors. But now we have the technology to be able to derive this DNA that's actually being shed from the tumor into the bloodstream, these minute fragments of DNA, take them out, amplify them and sequence them with a variety of different mechanisms. They can be DNA sequencing alone, they can be DNA and RNA sequencing, they can be whole transcriptome sequencing. The technology, as you rightly pointed out, Dr. Velcheti, has significantly improved from just being able to look at circulating tumor DNA to now being able to amplify it, sequence it, and use it to offer personalized therapy. I think lung cancer is definitely the poster child for such an approach as we have a lot of data that has shown clinical utility and validity of being able to use circulating tumor DNA next-generation gene sequencing to guide therapy. Dr. Vamsi Velcheti: There have been so many technological leaps. It's really impressive how far we've come to advance these sequencing platforms. Recent advances with AI and machine learning are also playing important roles in interpreting ctDNA data. How are these computational advances really enhancing clinical decision-making in day-to-day clinical practice? Dr. Charu Aggarwal: I think while we have firmly established the role of ctDNA in the management of patients with metastatic lung cancer, some of the approaches that you talked about are still experimental. So let me backtrack a little bit and set the stage for how we use ctDNA in clinical practice right now. I think most patients, when they come in with a new diagnosis of stage IV lung cancer, we want to test for biomarkers. And this should actually be the established standard. Now included in the NCCN guidelines and actually also international guidelines, is to consider using blood-based testing or plasma-based testing to look for biomarkers, not just tissue-based testing which had been our historical standard, but to use these plasma guided approaches to identify the seven to nine biomarkers that may be truly implicated in either first- or second-line therapy that are called as your immediately actionable mutations. What you're talking about is AI computational methods. I think there's a lot of excitement about how we can use genomic signatures that are derived from either tissue or ctDNA-based biomarker testing, combine it with radiomic features, combine it with histologic features, look at H & E patterns, use AI algorithmic learning to be able to actually predict recurrence scores, or can we actually come up with predictive signatures that may be extremely helpful? So, I think some of the techniques and technologies that you're talking about are incoming. They are provocative. I think they're very exciting, but very early. Dr. Vamsi Velcheti: I think it's really amazing how many advances we have with these platforms. You know, the challenge really is the significant gap in terms of uptake of molecular testing. Even today, in 2025, there are significant gaps in terms of all metastatic lung cancer patients being tested for all biomarkers. So, why do you think there's such a challenge in testing patients with lung cancer? In most academic practices, we try to achieve 100% testing for all our patients, but we know from recent studies that that's not the case across the country. What do you think the gaps are? Dr. Charu Aggarwal: Biomarker testing is so essential, like you pointed out, for us to be able to guide the right therapy for our patients. And we see this in our practice every day as you and I see patients with lung cancer, that a large proportion of our patients either don't get tested or they start therapy before their test results come back. So, I think this is a real problem. However, to add some optimism to this problem, I do think that we are making a move in the right direction. So, four or five years ago, there was a lot of data being presented at national meetings, including ones from the American Society of Clinical Oncology, where we saw that, nationally, the rates of biomarker testing were probably in the rate of 40 to 50%. However, now with the availability of both tissue and plasma, I do think that the rates of biomarker testing are increasing. And if you were to survey a sample or even perform retrospective data research, I believe that the number is closer to 70% of all patients with metastatic non-small cell lung cancer. And you know, you asked why is it not 100%? I think there are many reasons. I think the number one reason is tissue availability. Many times, the biopsies are small, or the tumor is very necrotic. So, either the tissue quantity itself is small, or the tissue quantity is insufficient to perform gene sequencing. And that's exactly where plasma comes in. When you don't have tissue availability, we have shown, as have others, that you can use plasma effectively to increase the proportion of patients who are not only tested but also receive the right therapy. I think there are also other barriers, including inertia. You know, I think this is both patient and physician inertia, where patients want to get started quickly, they don't want to wait. Physicians are very busy and sometimes want to be able to deliver treatment as soon as possible. We have seen there are some institutional barriers. Not every institution has in-house gene sequencing testing. So how do you really operationalize, send out these tests in a fast, efficient manner so that you get results back? Is it a pathologist who sends out the test? Is it the medical oncologist? Is it the pulmonologist or the interventionalist? I think there is this need to develop reflex testing mechanisms which some institutions do really well and some don't. And then finally, there are financial implications as well. How do we do this in a most cost-efficient fashion? So there are many barriers, but I'm happy to say that we are making a move in the right direction as we are understanding that it's important to do it, it's easy to do it maybe with a value add of plasma, and finally, as you said, you know, as these technologies become more available, they're actually getting more cost-effective. Dr. Vamsi Velcheti: Dr. Aggarwal, you've been at the cutting edge of these advanced platforms and testing. So, what do you do in UPenn? How do you handle all these barriers and what is your workflow for patients in University of Pennsylvania? Dr. Charu Aggarwal: One of the things that I mentioned to you was there may be institutional barriers when it comes to gene sequencing. So, we actually, several years ago now, instituted a very robust reflex testing paradigm where almost all of our patients, regardless of stage, with a non-squamous non-small cell lung cancer diagnosis, would automatically be reflexively sent to our molecular pathology lab where they would get gene sequencing both for the DNA as well as with an RNA fusion-based platform. And the reason we did this was because we wanted to expedite and reduce the turnaround time. We also wanted to ensure that we were not just doing DNA testing, which I think is really important for our listeners here. There are many fusions as well as certain skipping mutations like MET exon 14 that may be missed on DNA testing alone. So, it's really incredibly important to run both DNA and RNA samples. So, we do this routinely, and based on our research and others, what we also do routinely is that we send concurrent tissue and liquid biopsies or plasma MGS testing upon initial diagnosis. For example, if a patient comes in with a diagnosis of stage IV non-small cell lung cancer, their tissue might already be at my molecular pathology lab based on the reflex mechanism that I just described to you. But upon their initial meeting with me, we will send off plasma. And I will tell you this, that Penn is not just one institution, right? We have a large network of sites. And as part of my research, one of the things that we wanted to do was implement wide scale means to improve biomarker testing. And we have done this with the use of technology like you mentioned, Dr. Velcheti: How can we actually use AI? How can we leverage our electronic medical record to identify these patients? So, we have a nudge-based mechanism which actually facilitates the pending of orders for biomarker testing for patients with new diagnosis of metastatic non-small cell lung cancer. And we are looking at our rates of biomarker testing but also rates of completion of biomarker testing before first-line therapy started. So many of our participating sites are clusters for our randomized control trial to increase molecular testing. And I'm really excited about the fact that we're able to implement it not just at our main satellite, downtown Penn Hospital, but also across our community. Dr. Vamsi Velcheti: I think that's great. Thank you so much for those insights, Dr. Aggarwal. I think it's so important because having the best technology is just not enough. I think implementation science is actually a real thing. And I think we need to all learn from each other, advance these things. So, I want to ask you about the new emerging paradigm in terms of using ctDNA. Of course, in the metastatic setting, we've been using ctDNA for molecular profiling for a while now. But the recent data around monitoring early-stage disease, especially post-operative monitoring, is an exciting area. There are a lot of opportunities there. Could you please talk us through the emerging data in lung cancer and how do we incorporate ctDNA-based monitoring MRD or should we even do that right now? Is the data ripe enough for us to kind of deploy this in a clinical setting? Dr. Charu Aggarwal: I think using ctDNA in the early-stage setting is our next frontier in lung cancer. I think naturally we have been able to successfully deploy this in the stage 4 setting. It made a meaningful difference in the lives of our patients, and we are a little bit behind the A ball in terms of how MRD is used in lung cancer. Because, you know, colorectal cancer has already done large-randomized trials based on ctDNA and MRD. It's routinely used in hematological malignancy. So, it makes sense that we should start to use it. However, when I say this, I say this with excitement, but also a little bit of gentle caution saying that we actually don't quite have the prospective randomized data just yet on how to deploy. Yes, intuitively we would say that if you detect ctDNA and MRD, that patient is at higher risk. So, we identify that, but we actually don't know what to do with the second part of that information once you identify a patient with high risk. Are there other techniques that we can then come in with or other drugs that we can come in with to modify that risk? And that's the thing that I think we don't have right now. The other thing that we don't have right now is the timing of the assay, when to use it. Is it to be tested in the pre-op setting? Is the post-op test the best timing, or is it monitoring and dynamics of ctDNA that are most important? And the third thing I will say in terms of precautionary cause is that we don't know which test just yet. There are actually a few commercially available tests out in the market right now. We know about them and I'm sure our community colleagues know about them. Some of them even have Medicare approval. However, many of these tests are currently tissue informed. We don't have tissue uninformed tests. And what does that mean? Tissue uninformed means that you actually take a piece of tumor tissue, you sequence that tumor and based on the gene profile of that tumor, you actually design a panel that can then be used to track the mutations in the blood-based pack. This requires, as the name implies, a tumor. So can this be used in the pre-op setting is a large question. Because coming back to the idea of tissue availability, you and I both know that when we get FNAS and we use it for PDL-1 testing and we use it for gene sequencing, there often isn't enough tissue left for us to then either do whole genome sequencing or even whole transcriptome sequencing, which may be required to build some of these assays. I think the future lies in this idea of tumor uninformed assays because if we could go to a blood only or a plasma only approach using novel signatures like proteomics or methylation, I think that's where the future is. But we're still a little bit early in the discovery stages of those, as well as to come are the validation stages so that we can be confident that these blood-only assays may actually give us an answer. So, with those three cautionary notes, I would say that optimism is still very high. I think ctDNA MRD is the right place to think about. We need to do this for our patients to better identify high-risk patients and to think about means to escalate treatment for them. Dr. Vamsi Velcheti: Yeah, I completely agree, and I think with all the changes and evolution of treatments in the management of early-stage lung cancer now with neoadjuvant and adjuvant, there's really a need for an escalation and de-escalation of therapies post-operatively. And I think it's a huge opportunity. I think we all could learn from our colorectal colleagues. I think they've done a really good job at actually doing prospective trials in this setting. I think we're kind of a little behind here. Dr. Charu Aggarwal: I think in the metastatic setting there are ongoing trials to look at this exact question. How do you choose an appropriate first-line therapy, a monitor ctDNA at the six-week trial? It's being evaluated in a trial called the “Shedders” trial, where if patients are still ctDNA positive at six weeks, then you can escalate treatment because they haven't “cleared” their ctDNA. There has been a lot of research that has shown that lack of ctDNA clearance in the metastatic setting may be a poor prognostic factor. We and others have shown that if you do clear your ctDNA or if you have a reduction in ctDNA load overall, that that is directly related to both an improved progression-free survival and overall survival. This has been shown with both tissue informed and uninformed assays. So I think it's very clear that yes, you can track it. I think the question is: Can you apply that data to the early-stage setting? And that's an open research question. A lot of groups are looking at that and I think it's completely reasonable, especially to determine duration of therapy, to determine optimal timing, optimal timing of scans even. And I think these are just such interesting questions that will be answered in the future. Dr. Vamsi Velcheti: And also like a kind of early detection of resistance patterns that might inform early initiation of combination strategies. And I think it's a lot of opportunities I think yet to be explored. A lot of exciting things to come and I'm sure we'll kind of see more and more data in the next few years. Dr. Aggarwal, thank you so much for sharing your fantastic insights today on the ASCO Daily News Podcast. It's been a pleasure to have you on the podcast today. Hope to see you at ASCO. Dr. Charu Aggarwal: Thank you so much. This was great and I remain so excited by all of the possibilities to improve outcomes for our patients. Dr. Vamsi Velcheti: Thank you to all the listeners for your time today. If you value the insights that you hear from the ASCO Daily News Podcast, please take a moment to rate, review and subscribe wherever you get your podcast. Thank you so much. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity or therapy should not be construed as an ASCO endorsement. Follow today's speakers: Dr. Vamsidhar Velcheti @VamsiVelcheti @vamsivelcheti.bsky.social Dr. Charu Aggarwal @CharuAggarwalMD Follow ASCO on social media: @ASCO on X (formerly Twitter) ASCO on Bluesky ASCO on Facebook ASCO on LinkedIn Disclosures: Dr. Vamsidhar Velcheti: Honoraria: Glavanize Therapeutics Consulting or Advisory Role: Bristol-Myers Squibb, Merck, AstraZeneca/MedImmune, GSK, Amgen, Taiho Oncology, Novocure, Takeda, Janssen Oncology, Picture Health, Regeneron Research Funding (Inst.): Genentech, Trovagene, Eisai, OncoPlex Diagnostics, Alkermes, NantOmics, Genoptix, Altor BioScience, Merck, Bristol-Myers Squibb, Atreca, Heat Biologics, Leap Therapeutics, RSIP Vision, GlaxoSmithKline Dr. Charu Aggarwal: Consulting or Advisory Role: AstraZeneca, Daiichi Sankyo/AstraZeneca, Regeneron/Sanofi, Pfizer, Boehringer Ingelheim, Takeda, Arcus Biosciences, Gilead Sciences, Novocure, Abbvie Speakers' Bureau: AstraZeneca (an immediate family member) Research Funding (Inst): Merck Sharp & Dohme, AstraZeneca/MedImmune, Daiichi Sankyo/AstraZeneca, Lilly@Loxo, Candel Therapeutics
This week on The Genetics Podcast, Patrick is joined by Salvador Rico, Chief Medical Officer at Encoded Therapeutics. They discuss Salvador's journey into drug development, his work on gene therapy for X-linked myotubular myopathy, and fundamental challenges and exciting advances in the genetics field.Show Notes: 0:00 Intro to The Genetics Podcast00:59 Welcome to Salvador and how he became involved in drug development11:01 Frustrations and rewards of the genetics field13:59 Salvador's study on gene therapy for patients with X-linked myotubular myopathy (XLMTM)19:46 Risk of liver issues in gene therapy trials and attempts to mitigate them24:22 Encoded Therapeutics‘ approach to drug discovery and what motivated Salvador to join the team27:22 Steps towards therapeutic targeting of gene regulatory elements 30:04 Advantages of different methods for drug delivery 32:31 DNA- versus RNA-based therapy 34:56 Insights from approaches in other fields, including psychiatry36:35 Considerations for using natural history studies40:32 Expectations and goals for Encoded Therapeutics' current and upcoming studies43:17 Closing remarksFind out moreEncoded Therapeutics (https://encoded.com/)Please consider rating and reviewing us on your chosen podcast listening platform! https://drive.google.com/file/d/1Bp2_wVNSzntTs_zuoizU8bX1dvao4jfj/view?usp=share_link
Die mRNA-Forschung hat die Impfstoffe gegen das Corona-Virus geliefert. Kann die RNA-Technologie irgendwann sogar den Krebs besiegen? Prof. Markus Landthaler arbeitet am Max Delbrück Center daran, die Wirkweise der RNA-bindenden Proteine zu entschlüsseln und nutzbar zu machen. Ein Porträt unseres Gesprächspartners Prof. Markus Landthaler findet ihr hier. >> Artikel zum Nachlesen: https://detektor.fm/wissen/forschungsquartett-mrna-forschung
Die mRNA-Forschung hat die Impfstoffe gegen das Corona-Virus geliefert. Kann die RNA-Technologie irgendwann sogar den Krebs besiegen? Prof. Markus Landthaler arbeitet am Max Delbrück Center daran, die Wirkweise der RNA-bindenden Proteine zu entschlüsseln und nutzbar zu machen. Ein Porträt unseres Gesprächspartners Prof. Markus Landthaler findet ihr hier. >> Artikel zum Nachlesen: https://detektor.fm/wissen/forschungsquartett-mrna-forschung
Good morning from Pharma and Biotech daily: the podcast that gives you only what's important to hear in Pharma e Biotech world.Sanofi and Alnylam have received FDA approval for the first RNAi treatment for hemophilia, with the drug, Qfitlia, indicated for both hemophilia A and B. This approval is significant as it can be given regardless of the presence of neutralizing antibodies against clotting factors VIII or IX. However, the sudden departure of FDA director Peter Marks has caused uncertainty in the biopharma industry. In other news, Vertex has cut a diabetes asset but analysts remain optimistic about their phase III option. Lilly's RNA silencer has shown promising results in lowering a key cardiovascular biomarker. Trilink is offering custom guide RNAs for CRISPR workflow to accelerate therapy discoveries. Despite market challenges, the cell and gene therapy sector has seen a 30% investment surge. Companies like Amgen, Aldeyra, and Argenx are among those with upcoming FDA actions. Arbutus has announced layoffs, while big pharmas are pushing boundaries in radiopharmaceuticals. Michelle Werner of AltoRNA is focused on making better drugs. Safety questions are looming in Duchenne as Dyne and Wave plan FDA filings. There are job opportunities available in data management and program leadership within the biopharma industry.Moving on to other news, several big pharmaceutical companies such as Novartis, Bayer, AstraZeneca, Bristol Myers Squibb, and Eli Lilly are competing in the radiopharmaceuticals market, which is projected to be worth over $13 billion by 2033. The FDA is expected to announce decisions on therapies for dry eye disease soon. Michelle Werner, CEO of AllTrna, is focused on developing trna-based treatments for various diseases.Safety concerns are emerging in the Duchenne muscular dystrophy space as companies like Dyne and Wave plan FDA filings. The EU rejected Lilly's Alzheimer's drug Kisunla, Biontech's bispecific showed promise in treating SCLC patients, and Wave's duchenne exon-skipper reversed muscle damage in a mid-stage trial. Job opportunities within the biopharma industry were also highlighted for those interested.Thank you for tuning in to Pharma and Biotech daily - keeping you updated on all the latest news in the world of pharmaceuticals and biotechnology.
For this episode, we discuss the roles and sensitivity of mitochondria with Dr. Richard Frye, MD, PhD. Dr. Frye received an MD and a PhD in Physiology and Biophysics from Georgetown University. He is board certified in Pediatrics, Neurology with special competence in Child Neurology, and as a Certified Principal Investigator. In addition, he has a Masters in Biomedical Sciences and Biostatistics from Drexel University. Dr. Frye has over 300 publications in leading journals and book chapters.Dr. Frye shares many figures during the conversation so the listener can follow along.Dr. Richard Frye https://drfryemdphd.comRossingnol Medical Center Facebook https://www.facebook.com/RossignolMedicalCenterNeurological Health Foundation https://neurologicalhealth.orgHealthy Child Guide https://neurologicalhealth.org/the-guide-5/Daylight Computer Company https://daylightcomputer.com?sca_ref=8231379.3e0N25Wg3wuse "autism" in the discount code for $25 coupon.This is the future of tech.Chroma Light Therapy https://getchroma.co/?ref=autismuse "autism" for a 10% discount,0:00 Dr. Richard Frye0:58 Daylight Computer Company5:17 Chroma Light Devices8:27 History of Leucovorin; low risk, high reward; Folate Receptor Alpha (FRa)10:25 Blood Brain Barrier; Folate; CSF (cerebral spinal fluid)14:04 DNA, RNA; MTHFR (Methylenetetrahydrofolate reductase)17:34 Cerebral Folate deficiency; BH4, Placenta & Womb23:35 Folate deficiency & Autism26:21 Clinical Studies & Data29:28 Folate & Mitochondria; Cerebral Folate Antibodies; White Matter Findings (!)34:45 Cerebral Folate deficiency & Ranges; Autistic Phenotypes: Language, Communication, & Behaviors40:45 Language & Communication; Self-Injurious Behaviors; Hyperactivity, Agitation; Treatment duration42:53 Folate Autoantibodies & Maternal Health & Markers45:30 Studies & Behavioral outcomes; inflammation & thyroid findings46:58 Neural development; Language connections, white matter tracts & distal connections48:53 Leucovorin for different severity/levels of Autism; Spinal Bifida51:08 Preparing for pregnancy53:50 Transgenerational aspects of Folate Autoantibodies Research; Prenatal Care & Awareness59:32 Guidance & SupportX: https://x.com/rps47586Hopp: https://www.hopp.bio/fromthespectrumYT: https://www.youtube.com/channel/UCGxEzLKXkjppo3nqmpXpzuAemail: info.fromthespectrum@gmail.com
RNA stands for ribonucleic acid, and since the development of Covid vaccines a class of it known as ‘messenger RNA' or mRNA for short has been much in the news. Anna Durbin, a vaccine expert at Johns Hopkins, explains a … What is RNA and how is it used in vaccines? Elizabeth Tracey reports Read More »
The technology that produced the vaccines against Covid relies on a type of RNA known as messenger RNA. Johns Hopkins vaccine expert Anna Durbin explains why utilizing this approach stimulates an effective immune response. Durbin: What we like about mRNA … Why are mRNA vaccines effective? Elizabeth Tracey reports Read More »
For this special episode of the Astonishing Healthcare podcast, Andrew Barnell, CEO of Geneoscopy, joins Justin Venneri in the studio for an insightful discussion about colorectal cancer (CRC) screening in observance of National CRC Awareness Month! Andrew explains how he and his "very talented" sister, Erica Barnell, MD, PhD, co-founded Geneoscopy to develop diagnostic tests using RNA biomarkers extracted from stool samples. Their newly FDA-approved test, ColoSense™, provides a non-invasive alternative to traditional colonoscopies.Barnell highlights the rising incidence of CRC in younger adults, which prompted guideline changes to lower the recommended screening age to 45. He stresses the urgent need for increased screening awareness and greater access to screening tools, noting that employers can help overcome barriers to screening through education and by encouraging engagement in wellness programs. Other topics covered include:Over 135,000 people are diagnosed with CRC every year, and despite CRC being one of the most preventable cancers with good long-term survival rates following treatment, 50,000 people die from it annually. Preventive screenings are increasingly covered with no patient out-of-pocket costs, but insurers' expenses are rising.Increasing early screening is crucial: 30-40% of eligible individuals remain unscreened, particularly in the 45-49 age group.Geneoscopy's decentralized clinical trial and overall use of technology to conduct its pivotal FDA approval study virtually, which increased patient diversity and efficiency.Regulatory challenges remain: FDA approval is just one step; Medicare coverage and guideline inclusion are key hurdles.Bringing targeted therapy approaches to autoimmune diseases like IBD to improve patient outcomes and reduce costs is Geneoscopy's next goal.Related ContentMultitarget Stool RNA Test for Colorectal Cancer Screening. Barnell EK, Wurtzler EM, La Rocca J, et al. JAMA. 2023;330(18):1760–1768. doi:10.1001/jama.2023.22231Pharmacogenomics (PGx) 101: What You Need to Know for Rx ProgramsReference Materials/Other Links (courtesy of Geneoscopy)Projected Impact and Cost-Effectiveness of Novel Molecular Blood-Based or Stool-Based Screening Tests for Colorectal Cancer. Ladabaum U, Mannalithara A, Schoen RE, Dominitz JA, Lieberman D. Ann Intern Med. 2024 Dec;177(12):1610-1620. doi: 10.7326/ANNALS-24-00910. Epub 2024 Oct 29. PMID: 39467291.Colorectal Cancer—Patient Version. National Cancer Institute (NCI)Productivity savings from colorectal cancer prevention and control strategies. Bradley CJ, Lansdorp-Vogelaar I, Yabroff KR, Dahman B, Mariotto A, Feuer EJ, Brown ML. Am J Prev Med. 2011 Aug;41(2):e5-e14. doi: 10.1016/j.amepre.2011.04.008. PMID: 21767717; PMCID: PMC3139918.Follow Geneoscopy on LinkedInFor more information about Capital Rx and this episode, please visit Capital Rx Insights.
Dr. Betsy Young, a physician-scientist from UCSF provides an overview of her funded work: Tumor cGAS-STING repression drives immune evasion in osteosarcoma and is therapeutically targetable via host STING activation. This work was funded by an MIB Agents 2024 OutSmarting Osteosarcoma YI Hope grant Because of Charlotte.Osteosarcoma (OS) has an immunosuppressive macrophage-rich, T-cell-depleted tumor microenvironment (TME). By performing bulk RNA seq of OS cell lines treated with STING agonist, the lab has defined an OS-specific STING activation signature, which demonstrated a significant protective effect on survival in OS patient samples. In immunocompetent OS models, systemic STING agonism shows curative anti-tumor effects, shifts the tumor microenvironment towards a pro-inflammatory phenotype, and induces immunologic memory. Importantly, host STING activation is sufficient to promote this anti-tumor immunity. The lab has demonstrated that STING activation has anti-tumor benefit in animal models and a protective effect in the human disease, nominating this innate immune sensing pathway as an important therapeutic target in OS.As a physician-scientist and a pediatric oncologist, Dr. Young's aim is to advance the field of pediatric oncology in her research career focused on the immunobiology of osteosarcoma. She completed her Pediatric Hematology/Oncology fellowship training at UCSF, receiving strong clinical training in high-risk pediatric solid tumors and early-phase clinical trials. Now, as a faculty member, she is investigating the pathogenesis of osteosarcoma metastasis in the Sweet-Cordero lab at UCSF, with a specific focus on immuno-oncology translational therapeutics.
In this episode, Dr. Robert Malone, highlights his scientific career, personal experiences, and controversial perspectives on COVID-19 and RNA technology. Dr. Malone has been a significant figure in the Freedom Movement, especially notable after appearing on the Joe Rogan Experience in 2021. He discusses his background, growing up in California, and how his upbringing in a tech and military-industrial complex environment influenced his career. Dr. Malone delves into his pioneering work in mRNA technology, the contentious patent disputes, and his journey through academia and biodefense sectors, which led to significant roles during pandemics like Zika and COVID-19. The conversation covers his interactions with CIA operatives, his contributions to early COVID-19 treatments, and his journey through intense public and media scrutiny after expressing dissenting views on COVID-19 vaccines. He explains the concept of fifth and sixth generation warfare and its implications. Dr. Malone also talks about his efforts in homesteading and community building as a form of resilience against modern socioeconomic pressures. Connect with Dr. Malone here: X Website Substack Malone Media Our Sponsors: Let's level up your nicotine routine with Lucy. Go to Lucy.co/KKP and use promo code (KKP) to get 20% off your first order. Lucy offers FREE SHIPPING and has a 30-day refund policy if you change your mind. With Happy Hippo, you're getting a product that's been sterilized of pathogens, tested for impurities and heavy metals, and sold with a guarantee. Go to happyhippo.com/kkp and use Code KKP for 15% off the entire store Organifi.com/kkp and grab a Sunrise to Sunset kit to be covered with Red, Green and Gold, with 20% off using code KKP Fast Growing Trees makes it easy to get your dream yard. Order online and get your plants delivered directly to your door in just a few days, without ever leaving home. Click here to order! Connect with Kyle: I'm back on Instagram, come say hey @kylekingsbu Twitter: @kingsbu Fit For Service Academy App: Fit For Service App Our Farm Initiative: @gardenersofeden.earth Odysee: odysee.com/@KyleKingsburypod Youtube: Kyle Kingbury Podcast Kyle's Website: www.kingsbu.com - Gardeners of Eden site If you enjoyed this podcast, please subscribe & leave a 5-star review with your thoughts!
This week your host Fred Williams and co-host Doug McBurney conclude Dr. Royal Truman's concerns with Professor Dave, and talk witnessing out in the world with Abbie Leash! *Welcome Back Dr. Truman: Royal Truman, PhD received his bachelor's degrees in chemistry and in computer science from SUNY Buffalo, an M.B.A from the University of Michigan, a Ph.D. in organic chemistry from Michigan State with post-graduate studies in bioinformatics at the universities of Heidelberg and Mannheim in Germany. Royal believes the God of Abraham created the universe recently, and that His Son Jesus Christ is the savior of the world. *Freshman Genetics: Concern #11, Dr. Truman points out that Professor Dave is incorrect when he says "every organism" has a genome with genes wrapped around histones, (by far, most organisms do not). *Expression of Ignorance: Concern #12, Professor Dave states that enzymes interact with promoters in the encoding region of the genome. (chemical reactions are not being catalyzed at promoter sites). *Mutant Claim: Concern #13, When Professor Dave claimed a mutation is a change in the genetic code, he incorrectly defined mutations. An insignificant proportion of mutations change the genetic code, and many mutations damage regulator functions instead of protein sequences. *But Who's Counting? Concern #14, Professor Dave's claims that "creationists lie about the proportion of the genome that is functional" and that "genes make up only 1-2% of the genome" are together a false accusation against creation scientists, and an erroneous reference to only the exons on mRNA. *What's Your Function? Concern #15, Dave's errant description of "coding DNA" overlooks that many categories of genes are not protein coding at all, so 1-2% is grossly wrong. Also, transfer RNA by definition is not coding DNA; and there is no such term as 'genes for ribosomes' in the definition of coding DNA. *Encode Project Anyone? Concern #16, The claim that "10% max" of the genome is functional ignores widely acknowledged regulatory and structural functions (already well understood before Professor Dave got his "science communicator" credentials on YouTube.) *Lies and Statistics: Concern #17, David James makes the absurd claim that creation science researchers do not allow for realignment after discrepancies are detected, which is a mathematically impossible explanation for the 84% value. This absurd claim is also directly contradicted by the papers published by the creation scientists. *Off the Leash! Listen to software engineer and creation speaker Abbie Leash discuss the battles of faith, creation and real science out there in the college-educated world.
This week your host Fred Williams and co-host Doug McBurney conclude Dr. Royal Truman's concerns with Professor Dave, and talk witnessing out in the world with Abbie Leash! *Welcome Back Dr. Truman: Royal Truman, PhD received his bachelor's degrees in chemistry and in computer science from SUNY Buffalo, an M.B.A from the University of Michigan, a Ph.D. in organic chemistry from Michigan State with post-graduate studies in bioinformatics at the universities of Heidelberg and Mannheim in Germany. Royal believes the God of Abraham created the universe recently, and that His Son Jesus Christ is the savior of the world. *Freshman Genetics: Concern #11, Dr. Truman points out that Professor Dave is incorrect when he says "every organism" has a genome with genes wrapped around histones, (by far, most organisms do not). *Expression of Ignorance: Concern #12, Professor Dave states that enzymes interact with promoters in the encoding region of the genome. (chemical reactions are not being catalyzed at promoter sites). *Mutant Claim: Concern #13, When Professor Dave claimed a mutation is a change in the genetic code, he incorrectly defined mutations. An insignificant proportion of mutations change the genetic code, and many mutations damage regulator functions instead of protein sequences. *But Who's Counting? Concern #14, Professor Dave's claims that "creationists lie about the proportion of the genome that is functional" and that "genes make up only 1-2% of the genome" are together a false accusation against creation scientists, and an erroneous reference to only the exons on mRNA. *What's Your Function? Concern #15, Dave's errant description of "coding DNA" overlooks that many categories of genes are not protein coding at all, so 1-2% is grossly wrong. Also, transfer RNA by definition is not coding DNA; and there is no such term as 'genes for ribosomes' in the definition of coding DNA. *Encode Project Anyone? Concern #16, The claim that "10% max" of the genome is functional ignores widely acknowledged regulatory and structural functions (already well understood before Professor Dave got his "science communicator" credentials on YouTube.) *Lies and Statistics: Concern #17, David James makes the absurd claim that creation science researchers do not allow for realignment after discrepancies are detected, which is a mathematically impossible explanation for the 84% value. This absurd claim is also directly contradicted by the papers published by the creation scientists. *Off the Leash! Listen to software engineer and creation speaker Abbie Leash discuss the battles of faith, creation and real science out there in the college-educated world.
Emerging cell and gene therapies represent areas of great promise for people with rare, genetic diseases, but the translation gap for these medicines can leave them stalled at the lab. Mass General Brigham in 2022 launched the Gene and Cell Therapy Institute, a research hub dedicated to advancing gene and cell therapies for various diseases to bridge the divide between academic labs and clinical development of therapies. The institute brings together more than 500 researchers and clinicians and boasts unique assets, such as its RNA Therapeutics Core, which enable it to produce cutting-edge circular RNA on-site. We spoke to Nathan Yozwiak, head of research at the Mass General Brigham Cell and Gene Therapy Institute, about the need it is seeking to address, how the institute operates, and what it might do to enable the development of bespoke therapies for ultra-rare diseases.
They told her she would never succeed, now her work has saved millions. In this episode, Ryan talks with Dr. Katalin Karikó, the scientist behind the mRNA technology that led to COVID-19 vaccines. She grew up in rural Communist Hungary, faced rejection after rejection, got demoted, and struggled financially but she never stopped chasing the science. Dr. Katalin Karikó opens up to Ryan about her experiences as an immigrant in the U.S., the grind of scientific discovery, enjoying the process rather than focusing solely on outcomes, misinformation in the scientific community, and the responsibility of scientists to communicate effectively with the public.Dr. Katalin Karikó is a Hungarian American biochemist who specializes in RNA-mediated mechanisms. She won the 2023 Nobel Prize in Physiology or Medicine with her colleague Dr. Drew Weissman for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19. Read the New York Times feature on Dr. Katalin Karikó hereFollow Dr. Katalin Karikó on Instagram @katalin_kariko Check Dr. Katalin Karikó's memoir Breaking Through: My Life in Science
BUFFALO, NY - March 18, 2025 – A new precision oncology paper was #published in Oncotarget, Volume 16, on March 12, 2025, titled “Worldwide Innovative Network (WIN) Consortium in Personalized Cancer Medicine: Bringing next-generation precision oncology to patients." Led by Oncotarget Editor-in-Chief Dr. Wafik S. El-Deiry and a global team of researchers, this special publication highlights the groundbreaking work of the Worldwide Innovative Network (WIN) Consortium, a global collaboration dedicated to transforming cancer care through personalized medicine. By leveraging artificial intelligence (AI), molecular profiling, and innovative clinical trials, WIN is helping clinicians tailor treatments to each patient's unique cancer profile—moving beyond the traditional one-size-fits-all approach. The WIN Consortium is a fast-moving, non-profit organization bringing together nearly 40 academic, industry, and research institutions, along with patient advocacy groups, across 18 countries and five continents. Founded in 2010 in France by Dr. John Mendelsohn (MD Anderson Cancer Center) and Dr. Thomas Tursz (Gustave Roussy), WIN has been led by different renowned experts. Currently under Dr. El-Deiry's leadership, WIN continues to break barriers in cancer research, ensuring cutting-edge treatments reach patients worldwide. “The WIN global consortium is ready to take up the challenge by bringing the best possible Precision Oncology trial to patients.” One of WIN's most significant contributions is the development of N-of-1 clinical trials, a revolutionary approach that personalizes cancer treatment based on a patient's specific tumor characteristics. Unlike traditional trials that test drugs on large groups, N-of-1 trials focus on finding the best therapy for an individual patient using AI-driven algorithms, genomic analysis, and real-world data. WIN's WINTHER trial was one of the first to use both DNA and RNA analysis to match patients with the most effective therapies, while the WINGPO trial builds on this approach by integrating AI and liquid biopsies to refine treatment selection. These innovations are helping clinicians make more precise treatment decisions and improving outcomes for cancer patients. While advancing research, the WIN Consortium is also addressing major challenges in precision oncology, including drug accessibility, regulatory barriers, and disparities in global healthcare. By working closely with governments, pharmaceutical companies, and advocacy organizations, WIN is aiming to ensure that life-saving treatments are accessible to all patients, regardless of location or financial status. WIN's mission is clear: to accelerate the future of precision oncology by delivering the latest scientific advancements into real-world cancer care. As the field continues to evolve, WIN remains at the forefront, developing next-generation trials and leveraging AI-driven insights to improve patient outcomes. Through global collaboration and groundbreaking research, the WIN Consortium is shaping a future where every cancer patient receives the most effective, personalized treatment possible. DOI - https://doi.org/10.18632/oncotarget.28703 Correspondence to - Wafik S. El-Deiry - wafik@brown.edu Video short - https://www.youtube.com/watch?v=XAdYfFoMvUM About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com. MEDIA@IMPACTJOURNALS.COM
Mitochondria are the energy powerhouses of our cells. They use oxygen to convert glucose to an energy-storing molecule called ATP, which plays a role in numerous functions involved in neurotransmission, muscle contraction, DNA and RNA synthesis, and more.With thyroid hormones playing a vital role in regulating energy production within the mitochondria, the relationship between thyroid health and mitochondrial function is critical to our well-being.Today I'm discussing the relationship between thyroid health and mitochondrial function and why balanced thyroid hormone levels are needed to maintain optimal mitochondrial function and overall health.In this episode, you'll learn about:- The effects of oxidative stress on the mitochondria- How thyroid hormones stimulate energy production and mitochondrial formation- The connection between autoimmune conditions and mitochondrial dysfunction- How thyroid medications can impact mitochondrial health- The potential effects of beta blockers on mitochondrial function- Common factors that contribute to mitochondrial damage- Selenium's role in thyroid health and its protective effects on mitochondriaAs always, I hope you find this episode valuable, and I look forward to catching you in the next episode!To learn more, visit the show notes at https://savemythyroid.com/podcast/how-does-the-thyroid-affect-the-mitochondria/. Do You Want Help Saving Your Thyroid? Access hundreds of free articles at www.NaturalEndocrineSolutions.com Visit Dr. Eric's YouTube channel at www.youtube.com/c/NaturalThyroidDoctor/ To work with Dr. Eric, visit https://savemythyroid.com/work-with-dr-eric/
In the early 2000s, news headlines were all reporting of the same terror: ricin laden letters. Once a person comes in contact with ricin and the poison is absorbed, cells lose the ability to perform translation. Without translation, the body is unable to synthesize proteins critical for life. In today's episode, we will explore the step by step process of translation along with the structural components involved (ribosomes and t-RNA).Translation YouTube Video Link: https://youtu.be/Vu6LBOQSqiE
The American Studies Association has boycotted Israeli academic institutions since 2013. The Association for the Advancement of Anthropology has refrained from formal collaborations with Israeli academic institutions. And just this past summer, the American Association of University Professors opened the door to academic boycotts against Israel. Enter: two scientists at MIT who see firsthand the consequences of academic boycotts and the damage it can cause to scholarship and scientific progress. To ensure Israeli scholars and their American colleagues can collaborate freely, and foster research and innovation that benefits all of humanity, they formed The Kalaniyot Foundation (pronounced Ka-la-nee-yought), named after Israel's national flower. Hear from Drs. Or Hen and Ernest Fraenkel, co-founders of this initiative, on the impact of anti-Israel boycotts on academic collaboration with Israeli scholars, and what they're doing to rehabilitate the reputation of Israeli researchers in the eyes of the world. Listen – AJC Podcasts: The Forgotten Exodus: with Hen Mazzig, Einat Admony, and more. People of the Pod: U.S. Special Envoy Steve Witkoff on Gaza Reconstruction, Israeli Security, and the Future of Middle East Diplomacy Why Germany's Antisemitic Far-Right Party is Thriving Instead of Disappearing Follow People of the Pod on your favorite podcast app, and learn more at AJC.org/PeopleofthePod You can reach us at: peopleofthepod@ajc.org If you've appreciated this episode, please be sure to tell your friends, and rate and review us on Apple Podcasts or Spotify. __ Transcript of Conversation with Drs. Or Hen and Ernest Fraenkel: Manya Brachear Pashman: Since the Hamas terror attacks of October 7, 2023 many university campuses have been riven by anti-Israel protests, demonstrations, often unfortunately fueled by disinformation and rife with rhetoric that too often crosses the line into antisemitism. But even before October 7, Israeli scholarship had become a target of the boycott divestment sanctions movement. The American Studies Association has boycotted Israeli academic institutions since 2013. The Association for the Advancement of Anthropology has refrained from formal collaborations with Israeli academic institutions. Even study abroad programs that give students an opportunity to live and study in Israel have come under scrutiny. Enter: two scientists at MIT who see firsthand the consequences of academic boycotts and the damage it can cause to scholarship and scientific progress. To ensure Israeli scholars and their American colleagues can collaborate freely, foster research and innovation that benefits all of humanity, they formed The Kalaniyot Foundation, named after Israel's national flower. Dr. Or Hen and Ernest Fraenkel are with us now to discuss this initiative. Dr. Hen, Dr. Fraenkel, welcome to People of the Pod. Ernest Fraenkel: Thank you very much. Manya Brachear Pashman: So I want to work backward here a bit with a purpose. I want to start by sharing with our audience a little about your research. Dr Fraenkel, you work in health science, technology. What is the goal of your research and scholarship? Are there particular diseases you're trying to cure or treat? Ernest Fraenkel: We are interested in the diseases that are the hardest to treat, ones like Alzheimer's, ALS, Parkinson's, where we don't really know the root cause, and we believe that by gathering many different kinds of data about genes and molecules, about RNA and also about people's lived experience of these diseases, and using computational models, we can identify new targets for drugs and hopefully better therapies. Manya Brachear Pashman: Have you collaborated with Israeli scientists on this? Ernest Fraenkel: Yes, we collaborate with quite a few scientists all over the world, including top researchers in Israel. Manya Brachear Pashman: And Dr. Hen, you are a nuclear physicist, and you study the strongest force in nature, right? What is the goal of your research? Or Hen: So my research is very much on the fundamental curiosity driven science side of things, I am trying to understand how the fundamental building blocks of matter come about. We're building a new particle collider in the US called the electron hand collider. It's a $3 billion project funded by the Department of Energy, where we will try to understand why the proton and from that nucleus and all of us have mass. Trying to understand how we get the proton to a specific spin, which is the reason that we can go into an MRI machine and image ourselves. And I also try to understand things like, how do protons and neutrons interact with each other at extremely short distances, which tell us about exotic phenomena in the universe, like neutron stars. So trying to understand, really, the fundamental building blocks of matter and how they come about. Manya Brachear Pashman: Wow. And is there promising scholarship in this realm in Israel? Or Hen: Yes, there's quite a few groups working in this area. I did my own training in Israel. I am a graduate of the Hebrew University for undergrad and Tel Aviv University for grad school. And actually, ever since I came to MIT, I've still been collaborating with colleagues from Technion, Tel Aviv, Hebrew University, Weizmann, Ben Gurion. I've always had a strong collaboration with Israel, actually. Manya Brachear Pashman: So after October 7, or maybe even leading up to it, what were you seeing when it came to support of Israeli scholarship and collaboration in your institutions, in your fields, in academia in general? Ernest Fraenkel: I think before October 7, we were living in a bit of a bubble, because MIT is a special place which is very deeply immersed in science and technology. Where really, quite honestly, before October 7, I had no hint that there were biases against Israel, Israelis or Jews. I know that was not the experience in many other areas, especially in other fields. But things really turned 180 degrees on October 7, and what we've seen since then has been deeply disturbing. That some of the boycotts that have been bubbling for years in the humanities suddenly burst forth into the sciences and the engineering fields in ways that are both global and also very local. Seeing bias against individual researchers inside laboratories, as well as these kind of blanket attempts to boycott Israel. Manya Brachear Pashman: And Dr Hen, did you see the same? Or Hen: Yes, definitely. I work with a lot of international collaborations, actually, within collaborations, because there's structured bodies with bylaws and rules, It was very hard for anyone to object the presence of Israeli researchers. But what we have observed in many places is peer to peer collaborations dying down. We've seen a very significant social tax being applied to people who continue to collaborate with Israelis, and honestly, maybe in contrast a bit to what we know from academic boycotts in other areas, but are very much politically driven, within the STEM, within exact sciences, biosciences, etc, the social taxing is actually much stronger because we are people who usually instead, people keep a very clear separation between the politics and then, you know what they view from the work in the lab, which is very clear and data driven, and not a lot of room for opinions. It's very much exact. But on the other hand, the second that walking within Israel, and you know collaborating with Israel, is start costing other corporations, other people will now not work, then you get a problem. And that's what people really avoid and that's how an academic boycott within the STEM areas is progressing. It's a very deeply bound social tax that is just running in the air of the institutions. Manya Brachear Pashman: So what is the Kalaniyot Foundation doing to promote these collaborations? Can you give us some specific examples, or projects or partnerships? Or Hen: Yeah, so one of the things that we really believe in is that, at the end of the day, actually, what we see, also data shows, is, well, there is existing strong collaboration, that peer to peer, that person to person connection, is so strong that it's very hard to break that. You can go into my department and you can talk to people about Israel. And they know Or, and they know the person, right? And they might have a positive opinion about, you know, negative opinion about me. But whatever that opinion is, right, it's stronger than anything. They will try to protest and say, Okay, maybe there's a political issue. But you know, we know the researcher. We know the scientists. We know our colleagues. So the approach of Kalaniyot is to actually bring in more Israelis to campus, to bring in brilliant people who are excellent researchers that will come and enrich the academic environment, first and foremost, through this quality, and second, by the people that they are. Maybe Ernest, you want to continue with this? Ernest Fraenkel: So it's really this dual mission. We think that if we bring more top notch Israeli scholars to us campuses, it will normalize interaction with Israelis, humanize the Israeli, but there's a problem, right? Because if you just bring Israelis into campus environments that are hostile, they won't thrive. Many of them won't want to come, right? And so the other piece of it that's necessary is to build community, and that's something that we've been doing since October 7 of last year, trying to figure out how to do that, and what we found is face to face interaction is really critical. And so at MIT, we've been having weekly lunches of the Israelis, Jews, allies, everybody who felt isolated and left out of society by all the protests that were taking place. And the beautiful thing is that that started as a reaction, right, a sort of a safe place to retreat to, and it's actually become a wonderful, positive place. And still, now, you know, so far into this crisis, people are coming, and actually the numbers are even growing. And so on a typical week, we get more than 100 people in person. We, of course, feed them lunch, and it's just a wonderful place where you can make friendships, develop academic collaborations, and Israelis realize that there is a community here that appreciates them and welcomes them and it helps them thrive. Manya Brachear Pashman: Because, of course, food is a vital currency, both on college campuses as well in Jewish as in Jewish life. Food heals all. But I am curious, do you? In addition to building these thriving communities, are you also so that people are surrounded and comfortable but are you also trying to build bridges with people who perhaps do tend to throw the word Israeli around in a negative capacity, but you need to actually have some face to face contact. Or is that really not the purpose of Kalaniyot. Or Hen: I mean, it's a yes and a no. We certainly have done that, right. So if you think about how it all started very soon after October 7, basically after the first protest on campus at MIT. We went to talk to our president, three Jewish Israeli faculty, and we asked her. We said, Look, we hear from the students about what's happening in the dorms, what they're experiencing. It's really bad, and it's very hard to handle through the existing mechanisms. Please actually give us the budget. We'll get kosher food. I'm a Mizrahi, that's what I know how to do, feed people. Let's put everybody together, and let's make sure everybody feel welcome. And we also said, you know, we'll be your bridge. We'll help the students communicate with administration through our guidance, right? We'll be able to filter, to guide them, but also to pick up on the important things that you need to know. But then we said something else. We said, Look, this is going to become very tough, also for the students who are protesting out there right now. It was before Israel responded, but we knew exactly what happened in the kibbutzim, and we knew this is not going to be just another round with Gaza. This is going to be something different. So we actually suggested to the President that alongside starting our group, we will start a parallel group of peers who we might disagree with politically and have different perspectives on the Middle East, but we know that they are reasonable people that we can talk to, that we can collaborate with, that we can work with, despite or alongside disagreements. And so the idea was to start our lunch, to start a second lunch, and slowly, through the faculty leadership, bring the groups together. Some of it has worked. Some of it didn't work. We used to meet once a week as the faculty and say, students tell us that this and this is happening. Can you maybe walk with your students to tone that down, and they would tell us what's bothering them, etc. Getting the students to come together, that was a bigger lift, a challenging one. And there was another initiative that came about called the Third Space Lunch, that maybe Ernest can elaborate more on. Ernest Fraenkel: So just to add a little bit to that. So the faculty leads from the other group came to speak to our students. Were very respectful to them. The faculty listened quietly to the concerns of the Jewish students. And I think we did see an attempt by many of the faculty to bridge the gaps. Obviously, faculty are an extremely, you know, diverse group. We have extremists, we've got centrists, we've got moderates. And not everybody was trying to help, but many, many were, and I think that was very encouraging, and I've seen that continue throughout this. There are hidden allies. Probaby the average faculty member probably doesn't really want to know too much about Israel or Palestine. Doesn't want to have to understand the conflicts. They just want to go about their daily lives, teach what they love to teach, do the research they love to do, and they are natural allies in trying to bring order back to campus. And the more that we can engage them, the better off it is. Or Hen: But I think in terms of the formal program for Kalaniyot - Kalaniyot is really meant to bring in researchers and make sure that they have a supporting environment. And if people want to take that extra step of building bridges and building, that's all great, but it's not kind of a mandatory part of the program. Manya Brachear Pashman: I get it. You really just want to foster academic research and progress and innovation, right? Put political strife aside. You've named this foundation Kalaniyot after Israel's national flower. Can you describe for our listeners that flower and why you chose that name for this initiative? Ernest Fraenkel: The Kalaniyah looks a lot like a poppy. It's a red poppy, and during good times, there actually was an annual festival where Israelis would flock to the south in the area right around Gaza to see the bloom of this flower that would cover the otherwise fairly barren, quite honestly, countryside. And it was called the South Red, Darom Adom, and people would rush there to see it. And it was a symbol, which actually takes place right around the time we're recording. People have been sending us photos from from Israel the last few weeks of these flowers, the more they hear about the program. And it's a sign that the winter is going to end and spring is going to come, and everything will be renewed. And so it was the South in red, in a sense, that was all positive. And we think the same sort of thing is possible here, that while Israel is right now a touch point for conflict on campus, we want to see a time when Israel, this is something like, Oh, of course. You know, everybody wants to have some connection to Israel. That's where the best researchers are in every field. I often tell the story, when I was first on the faculty here, one of my first assignees as an undergraduate advisee was somebody from Hawaii, and he told me, asked him what he was going to do this summer, and he said he's going to Israel. So no, really, what's, what's your connection to Israel? He said, Oh, I don't have any I thought, maybe he's a strong Christian. I asked him about that. Said, no, no, I don't have any particular faith. I just heard it's startup nation, and I want to go and experience it. And I just think, how many students today is their first association with Israel, startup nation? Probably not that many anymore, but we can get back to that and realize that it's more than startups, right? It's basic science, it's the arts, it's culture. And so there's much that Israel has to offer the world, and we want to get back to the point where that's the first thing people think about Israel. Manya Brachear Pashman: So this initiative did start at MIT, but it appears to be sprouting, to use a pun, it appears to be sprouting on other campuses. Dartmouth is developing a chapter and Penn, right, the University of Pennsylvania. Are they being led by fellow scientists who have seen the consequence of this scholastic snub, for lack of a better word? Ernest Fraenkel: So at each university, and there are several others in the works that are still working their way through the administration at each university, and by the way, this is not a renegade effort. At each university, the faculty form a faculty board, we encourage them to find a diverse group. So it's not all the sciences on our board. And on those boards, there seem to be many members of humanities departments. Not all Jews, not all Israelis. And these diverse faculty boards are people who are allied with the goals, and we have bylaws. This is a program entirely about positivity. It's not attempting to suppress anybody else's speech. It's not attempting to make any political points. It's a purely academic program that will help restore the image of Israel as a place of academic excellence and help the United States maintain its academic edge through those collaborations. Or Hen: And I think you're hitting on a very unique point, right? And that is that this is entirely faculty led program. When you think about the role of faculty in universities, especially faculty from STEM fields, right, we don't lead a lot of things in the academic world that are not our research, right? Honestly, that's kind of, why am I here and not in Google, right? I would probably make a much bigger salary for Google these days. I'm here because I really care about my research, those open questions I really want to explore, and that's what I'm doing. So I'm teaching my class, and I'm focusing on my research. And me is everybody else around me, that's what we do. So there is a very high activation energy to get the faculty to do something that is not their research, their own research, but once you do that, faculty is a force of nature at the university. That's kind of what we're here to stay, right? We'll tenure, we're going to be at the retirement. We run the place eventually. So it's both to activate the people who can really make an impact from within in a very strong way. That's number one, who have these decades of connections, right? Well before the challenge, you know, I've had my 10 years of collaborations here at MIT, and this has a lifetime of more than 10 years of collaborations here, right? And many of us and people remember those connections, right? Remember how we teach together, how I lent them something from my lab, and stuff like that, right? We have these personal connections. So it is really the first and uniquely faculty led program that is very helping to come back, see faculty do that. There's a lot of power, and that's also why it's such an academically focused program, because that's what we know how to do. There's many other who can combat antisemitism and can give antisemitism training and title six and all that. And we don't do it, not because it's not important, just because we are not the people who bring in unique expertise in those areas, but when it comes to research collaboration, connections with Israel around those things, we are the ones who can really promote it from within in a way that's unpowered and parallel to anyone else. And that's the, I think the strongest point of Kalaniyot, the faculty leadership. Manya Brachear Pashman: In other words, you're not activists, you're not advocates. That's not what you set out to do. You are researchers, scientists who just want to do research in science. Or Hen: And when I see everybody around us do the best research and science possible, which means engaging with the brightest minds anywhere in the world, and that includes Israel. And we don't want to see that door shut down. There's no hiding it – Ernest and I are Zionists, we're not going to shy away from that. And we think that an academic boycott in the STEM is a risk to Israel. Israel doesn't have oil, right? What Israel has is the Jewish mind, and that mind is the thing that helps Israel, and that mind is the thing that helps the world. And we can go on and on about inventions and discoveries that came out of Israel and Israelis and Jews for the benefit of mankind. So both for the benefit of Israel and all of humanity, we don't want to see the Israeli Academy get isolated. It's going to be bad for all of us. Manya Brachear Pashman: Now I know that there is a program at Indiana University called Olamot, focusing on the humanities. Does this only apply to STEM fields, or do you also have partnerships and collaborations developing across multiple disciplines? Ernest Fraenkel: Yes, absolutely, this is a program that's open to all academic fields, and each university will craft a slightly different program, we're sure. At MIT, because we're STEM dominated, our Kalaniyot program is dominated by STEM, but it's not exclusively STEM here, either. We do have deep involvement with several of our board members in the humanities. Many of the people who come to our programming are in humanities. We're hoping that some of the scholars whom we will select in our first cohort of post doctoral and sabbatical visitors will be in the humanities, but that's going to be much a bigger component of it at other universities such as Dartmouth and Penn, where they have huge humanities programs. Manya Brachear Pashman: And are you getting mostly support, or are you getting any pushback from faculty members? Ernest Fraenkel: So this is really fascinating. Early on, when we first started formulating this program, we wrote a memo explaining, a letter, explaining why we were doing this for something called the faculty newsletter, which is usually a place where people write fairly anti-Israel things, and we kind of braced ourselves for the pushback. And nothing came back. There was no pushback. Because if you believe in academic values in the United States, unless you're a hardcore BDS person, there's really nothing objectionable here. Our goal is to bring brilliant scholars to campus and encourage them to be able to work broadly, without regard to nationality, religion, anything else, any other protective category. And so we were very pleased. And initially, you know, the administration was curious. They were interested. They wanted to review exactly what we're doing. The MIT administration went through everything we're doing, and they gave us the thumbs up, and they've now been helping us make connections and behind the scenes, I believe, I understand that, you know, some provosts and presidents occasionally talk about this when they meet and they, you know, tell each other it's not a bad thing to have at your University. Or Hen: I remember when we kind of got people to know the program, we met with a very high ranking individual at MIT. And that person said, Look, MIT stands on three legs: research, education, and entrepreneurship. Israel excels in all three. Of course, we want those connections. Of course we want those collaborations. And who in the right mind can say that this is anything political, right? Now I'm sure that some people will try at some point. But like Ernest said, we've worked very hard on the language and the messaging to make sure that the language and messaging reflects the way we really see it, as a very strong academic program. Manya Brachear Pashman: So, Dr. Hen, I do want to ask you a personal question. I have read that as a child, you navigated some pretty significant learning disabilities stemming from dysgraphia. You have difficulty translating your thoughts into written form, but the assessment to determine those disabilities also determined that you had a unique gift for abstract comprehension, the ability to conceptually pare down complex ideas to their fundamental core. So I wanted to ask you, in your opinion, what is at the fundamental core of these academic boycotts? Or Hen: Honestly, I do believe that the academic boycotts come from antisemitism. That's the core. I do believe that there are a lot of people who engage in that, not understanding that is what they're doing. I'd like to give people the benefit of the doubt. I think that a lot of people do see a difference between anti-Zionism, anti-Israel, antisemitism, right, which I personally do not share. And that's a different point of view, which is allowed. But I think at the end of the day, trying to isolate Israel, eventually is from a top level, and attempt to bring down the country, because that's the core. Core of Israel is its academics. That's really where it all starts. And if we don't have academia, if we're attacking the Israeli Academy, you're attacking Israel. And any person who takes the time to learn about the Israeli Academy, who listens to speeches by the head of Tel Aviv University about the judicial reform in Israel. Who listens to the head of the Israeli National Academy about how he sees democracy and what he sees about the war, situation, you would learn that the Israeli Academy is really the hallmark of independent academia that stands by itself, as an independent body that really promotes research and good for the world. And anyone who attacks that either doesn't know or doesn't care to know, and I'd like to hope that most people don't know, and once they'll know and appreciate the people, they will see different people. There is a core that doesn't want to know, and okay, we need to make sure that that call remains as small as possible. Manya Brachear Pashman: Dr. Fraenkel, do you agree? Ernest Fraenkel: I'm by nature, a centrist and not a political person, and I also have learned over time that it's very hard to understand other people's motivations. But I do think that one of the paths to it, to solving the problem, is to re-humanize Israel and Israelis in the minds of the people who are currently protesting. And I think we'll have good results if we do that. Manya Brachear Pashman: I'm curious, we've been talking a lot about Israeli research and innovation. Can you kind of share a piece of Israeli innovation that you've heard about recently, that maybe our audience has not and should know about? Ernest Fraenkel: I was just at a conference yesterday, and one of the best talks yesterday, this was at a conference on ALS, was given by a researcher from the Weitzman Institute, Eran Hornstein. And he spoke about an entirely new way to analyze what goes on inside cells in the course of disease. He calls it organellealomics, I think. It's kind of a mouthful, but it was completely innovative. No one has anything similar. It allows you to get a wonderful view of all the different processes that are going on in the cell at a very high level, in a way that is experimentally very accessible. And I think it's really going to transform a lot of how we research diseases, and may lead to some rapid advances in some of these tough cases. Or Hen: Yeah, I can add to that, you know, from the more industry side of things, right? We all have technology in our pockets, in our homes, in our offices, developed in Israel. The most advanced processors by Intel are built on architecture that was developed in Haifa. Apple has engineering centers in Israel. Facebook has engineering centers in Israel, Nvidia. All of us use Israeli technology day in and day out. We either know it or we don't. But there's not a single person in the western world that does not rely on Israeli technology sometime, someplace, some point in his day. Manya Brachear Pashman: And when you were at that conference, Dr. Fraenkel, or Dr. Hen, consider that, when you pull out your phone and consider the many ways in which we use Israeli technology, does that further validate, does it affirm that what you are doing is the right thing to do, and that this will only benefit humanity at large? Ernest Fraenkel: In biology, we often do these experiments where we delete a gene, we make it stop working, and we see what happens to the cell or to the animal that we're studying, right? And just do the thought experiment. What would happen to American science if it didn't have these strong collaborations with Israel? And be weaker in consumer electronics, and be weaker in AI, we would be weaker in all the underpinnings of all the technology that we're all walking around with every day. We'd be weaker in healthcare. Think about the contribution that Israel made to understanding what was going on during the COVID pandemic, right? It's just shocking how much we would lose from this small country not being there. And absolutely, when we think about that, it just drives us even more to try to get this program to spread across all the best universities in the United States, and hopefully we'll make inroads in Europe as well and really bring Israel back to the forefront in everybody's mind as a place where positive things are happening. Manya Brachear Pashman: Well, thank you both for joining us so much and for sharing about this program. Really do appreciate it. It's fascinating and refreshing to learn that academics are supporting academics. Ernest Fraenkel: Thank you very much. Real pleasure to speak with you.
Do you struggle to lose weight and keep it off? It turns out, fat cells actually have a memory that can keep weight off after rapid weight loss!In this episode of Salad with a Side of Fries, Jenn Trepeck sits down with Professor Dr. Ferdinand von Meyenn, assistant professor at the Institute of Food, Nutrition, and Health at ETH Zurich, to explore his study with the intriguing finding that fat cells encode a memory which influences the ability to maintain weight loss and therefore impacts metabolic health. They delve into his groundbreaking research on bariatric patients and mice, uncovering how fat cells retain memory and can continue to impact the body long after weight loss. Dr. von Meyenn breaks down the role of epigenetics, why GLP-1 medications don't provide long-term effects, and the importance of proper nutrition and lifestyle when losing weight and keeping it off. They also discuss the hip-to-waist ratio versus BMI and why prevention is the most powerful tool for long-term well-being. The Salad With a Side of Fries podcast is hosted by Jenn Trepeck, discussing wellness and weight loss for real life, clearing up the myths, misinformation, bad science & marketing surrounding our nutrition knowledge and the food industry. Let's dive into wellness and weight loss for real life, including drinking, eating out, and skipping the grocery store. IN THIS EPISODE: (05:27) Ferdinand's research on fat cell memory and metabolic health(09:21) Research findings on bariatric patients and experiments on mice(17:28) Ferdinand defines epigenetics and GLP's don't give long-lasting effects(26:06) Losing weight too quickly and the set point concept(35:00) Weight loss is good, but proper nutrition is critical and discussion of adiponectin(38:27) Excess energy and body fat, the hip to waist ratio, and being overweight, and the long-term consequencesKEY TAKEAWAYS: Even after significant weight loss, an individuals' fat cells retain molecular changes (altered RNA and epigenetic markers) associated with their previous obese state. These long-lasting molecular markers in the fat cells predispose the body to regain weight as it responds more readily to an obesogenic environment.Weight loss significantly improves health, whether in humans or mice. However, fat cells have a form of memory, meaning that even after weight loss, some molecular changes persist. While these changes do not necessarily drive disease, they highlight the importance of sustained weight management strategies.Rapid weight loss, especially with methods like GLP-1 medications, can lead to muscle loss, negatively impacting metabolism and overall health. Since muscles play a key role in energy expenditure and physical stability (especially with aging), preserving muscle mass during weight loss is crucial for long-term success and well-being.QUOTES: (06:59) “Many times people get bariatric surgery, and despite that being a very significant intervention that restricts how much food you take in, people lose weight for a while, and yet some recover some of that body weight.” Ferdinand von Meyenn(13:46) “The cell predisposes these people to regain weight because their cells are signaling for the obesogenic environment that they became used to.” Jenn Trepeck(24:53) “I think this is connected to the set point idea that people have heard of how we go about ‘losing the weight'. That might play into this too.” Jenn Trepeck.(26:08) “If weight loss is too quick, it is also loss of protein mass, basically of muscle mass and that is really problematic.” Ferdinand von Meyenn(32:43) “If we build lean muscle mass over time, removing fat over time, giving the body time to adapt to this metabolically healthier environment, there's the possibility of easier maintenance.” Jenn TrepeckRESOURCES:Become A Member of Salad with a Side of FriesJenn's Free Menu PlanA Salad With a Side of FriesA Salad With A Side Of Fries MerchA Salad With a Side of Fries InstagramNutrition Nugget: Minnesota Starvation ExperimentGUEST RESOURCESLaboratory of Nutrition and Metabolic Epigenetics - WebsitevonMeyenn BlueSky - Social MediavonMeyenn Lab BlueSky - Social MediaMeyenn lab - XFerdinand - XFerdinand von Meyenn - LinkedInGUEST BIOGRAPHY: Ferdinand von Meyenn has been Assistant Professor of the Institute of Food Nutrition and Health at the ETH Zurich since January 2019.Ferdinand studied Biochemistry at the TU Müchnen, Germany, before moving to ETH Zürich for his PhD to study metabolism and type-2 diabetes. After graduating, he joined Prof Wolf Reik at the Babraham Institute in Cambridge, UK, investigating epigenetic mechanisms during development and ageing. In 2017 he joined King's College London as a Group leader and Research Fellow. Then, in 2019, he moved to ETH Zurich, where he was appointed Assistant Professor of Nutrition and Metabolic Epigenetics. His research focuses on the relationship between nutrition, metabolism and the epigenome, aiming to contribute to developing novel strategies to combat obesity and metabolic disease.
Chemist Jack Szostak wants to understand how the first life forms came into being on Earth. He and Steve discuss the danger of "mirror bacteria," the origin of biology in poisonous chemicals, and the possibility that life might exist on other planets too. SOURCES:Jack Szostak, Nobel laureate and professor of chemistry at The University of Chicago. RESOURCES:Is Earth Exceptional?: The Quest for Cosmic Life, by Mario Livio and Jack Szostak (2024)"Q&A: How ‘Mirror Bacteria' Could Take a Devastating Toll on Humanity," by Isabella Backman (Yale School of Medicine, 2024)."The virtual circular genome model for primordial RNA replication," by Jack Szostak, Lijun Zhou, and Dian Ding (RNA, 2021)."Protocells and RNA Self-Replication," by Gerald Joyce and Jack Szostak (Cold Spring Harbor Perspectives in Biology, 2018)."The Narrow Road to the Deep Past: In Search of the Chemistry of the Origin of Life," by Jack Szostak (Angewandte Chemie International Edition, 2017)."Jack Szostak on 'Life in the Lab' (And Autocatalytic Sets)" by Suzan Mazur (Huffington Post, 2014)."Jack W. Szostak Interview" (The Nobel Prize, 2009)."The Miller-Urey Experiment" (National Center for Science Education)."From Old Vials, New Hints on Origin of Life," by Kenny Chang (New York Times, 2008). EXTRAS:What Is It Like to Be an Addict?: Understanding Substance Abuse, by Owen Flanagan (2025)"UPDATE: What It's Like to Be Steve Levitt's Daughters," by People I (Mostly) Admire (2024)."We Can Play God Now," by Freakonomics Radio (2022).
TWiM describes Shigella infection is facilitated by interaction of human enteric α-defensin 5 with a colonic epithelial receptor, and an amino acid change in RNA polymerase that leads to resistance to β-lactams by preventing dysregulation of amino acid and nucleotide metabolism Hosts: Vincent Racaniello, Michael Schmidt, Petra Levin and Michele Swanson. Subscribe to TWiM (free) on Apple Podcasts, Spotify, Android, RSS, or by email. Become a patron of TWiM. Music used on TWiM is composed and performed by Ronald Jenkees and used with permission. Links for this episode National Black HIV/AIDS awareness day (CDC) Shigella infection and human enteric alpha-defensin 5 (Nature Microbio) RNA polymerase amino acid change and resistance to beta-lactams (Cell Rep) Take the TWiM Listener survey! Send your microbiology questions and comments (email or recorded audio) to twim@microbe.tv
The inner workings of our bodies, particularly what's happening inside our cells, can be kind of a black box—with countless tiny molecules constantly working and churning to keep us alive. A new technology that blends bioluminescence with cellular machinery may shine some light on the details of their comings and goings and interactions that can be hazy.Scientists had the bright idea to take that same enzyme that makes fireflies glow and tie it to RNA, the molecule that reads the genetic information in DNA. This developing technology has been used on mice, with the hope that these light-up molecules can help illuminate how viruses replicate or even how memories form in the brain.Flora Litchtman talks with Dr. Andrej Lupták, professor of pharmaceutical sciences at the University of California Irvine and Dr. Jennifer Prescher, professor of chemistry at the University of California Irvine, about their research on the topic.Transcripts for each segment will be available after the show airs on sciencefriday.com. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.
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