Podcasts about Recombination

TWiV reviews new CBER chief at FDA, ending of Gates Foundation in 2045, gain of function executive order, origins of bat viruses ancestral to SARS-CoV and SARS-CoV-2, and single dose Sudan virus replicon vaccine protects guinea pigs from disease. Hosts: Vincent Racaniello, Alan Dove, and Rich Condit Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode Support science education at MicrobeTV Prasad replaces Marks at FDA (US News) Gates Foundation ends 2025 (Gates Foundation) Gain of function Executive Order (White House) DURC policy (HHS) Origins of bat viruses ancestral to SARS-CoV and SARS-CoV-2 (Cell) Sudan virus replicon vaccine (Nat Comm) Letters read on TWiV 1217 Timestamps by Jolene Ramsey. Thanks! Weekly Picks Rich – Andor Season 2 Alan – Sequencing Mendel's pea plant traits, and a good Science news article on the work Vincent – 2023 summer warmth unparalleled over the past 2,000 years Listener Pick Brian – Virology Capabilities Test (VCT): A Multimodal Virology Q&A Benchmark Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv Content in this podcast should not be construed as medical advice.

Check out our recap and breakdown of Season 4 Episode 11 of the Big Bang Theory! We found 4 IQ Points!00:00:00 - Intro00:09:14 - Recap Begins00:17:53 - Animal Facts! Starfish and Dolphins00:30:33 - The most apologetic candy00:54:02 - Why is Aquaman so hated?01:04:08 - Amazon Women! and Blonde Wonder Woman!Find us everywhere at: https://linktr.ee/theoreticalnonsense~~*CLICK THE LINK TO SEE OUR IQ POINT HISTORY TOO! *~~-------------------------------------------------Welcome to Theoretical Nonsense! If you're looking for a Big Bang Theory rewatch podcast blended with How Stuff Works, this is the podcast for you!  Hang out with Rob and Ryan where they watch each episode of The Big Bang Theory and break it down scene by scene, and fact by fact, and no spoilers! Ever wonder if the random information Sheldon says is true? We do the research and find out! Is curry a natural laxative, what's the story behind going postal, are fish night lights real? Watch the show with us every other week and join in on the discussion! Email us at theoreticalnonsensepod@gmail.com and we'll read your letter to us on the show! Even if it's bad! :) Music by Alex Grohl. Find official podcast on Apple and Spotify https://podcasts.apple.com/us/podcast/theoretical-nonsense-the-big-bang-theory-watch-a/id1623079414

Don't forget to share the good vibes by smashing that like button! Tracklist (Time – Title – Artist – Label): 00:00:00 – Lines – John Roberts – Dial 00:05:10 – Days Gone By – Carsten Jost – Dial 00:12:50 – Birth – Brendon Moeller – Echocord 00:18:51 – Wogen – Woo York – Digital Reflection 00:25:00 – Endless – Dadub – Stroboscopic Artefacts 00:29:26 – Stillpoint – Orphx – Hymen Records 00:37:46 – Nonexistent Reality – Cliche Morph – Granulart...Lire la suite Lire la suite

It's a bird! It's a plane! It's.... I forget the rest.We discuss Bob Newhart's passing, and comments from some of the Big Bang Theory castOur episode discussion includes a lot of love for Zack, Leonard and Penny, a fanvid tangent, and more!The "Story of Us" fanvid we talk about is on YouTube hereBrian Thomas Smith's post about the Zack Funko is hereDownload hereRunning time: 46:42, 28.2 MB

References Guerra, DJ. 2024. ImmunoBiochemistry lectures. Commun Biol. 2022; 5: 1292. ACS Chem. Biol. 2017, 12, 4, 958–968 Telemann, GP., 1750. Sonata in D major, TWV 44:1 https://youtu.be/xx8ooc-s7OQ?si=1vAKmdcLroNISa-P Vivaldi, A., 1708. - Gloria (RV 589) https://youtu.be/2eWjQOdYzMQ?si=hYSOqRuXkYUA8ATl --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

This is an accredited continuing education series of three (3) podcasts as downloadable audio files (MP3). These certified AMA/ABS/ANCC podcasts will clarify the rationale and best-practice approaches for HRRm testing to guide therapeutic strategies in metastatic prostate cancer. Clinical case scenarios are used to enhance the learning experience and provide practical considerations to achieve improved outcomes among patients.Launch Date: May 30, 2024Release Date: May 30, 2024Expiration Date: April 30, 2025FACULTY BIOAndrew Armstrong, MD, ScM, FACPProfessor of Medicine, Surgery, Pharmacology and Cancer BiologyDuke UniversityTanya Dorff, MDProfessor of MedicineCity of HopeThis podcast provides accredited continuing education credits. To qualify for credit, please read all accreditation information at the provided link below prior to listening to this episode.https://www.practicepointcme.com/CMEHome/talking-prostate-cancer-homologous-recombination-repair-gene-mutation-testing-in-metastatic-prostate-cancer-8

This is an accredited continuing education series of three (3) podcasts as downloadable audio files (MP3). These certified AMA/ABS/ANCC podcasts will clarify the rationale and best-practice approaches for HRRm testing to guide therapeutic strategies in metastatic prostate cancer. Clinical case scenarios are used to enhance the learning experience and provide practical considerations to achieve improved outcomes among patients.Launch Date: May 30, 2024Release Date: May 30, 2024Expiration Date: April 30, 2025FACULTY BIOAndrew Armstrong, MD, ScM, FACPProfessor of Medicine, Surgery, Pharmacology and Cancer BiologyDuke UniversityTanya Dorff, MDProfessor of MedicineCity of HopeThis podcast provides accredited continuing education credits. To qualify for credit, please read all accreditation information at the provided link below prior to listening to this episode.https://www.practicepointcme.com/CMEHome/talking-prostate-cancer-homologous-recombination-repair-gene-mutation-testing-in-metastatic-prostate-cancer-8

This is an accredited continuing education series of three (3) podcasts as downloadable audio files (MP3). These certified AMA/ABS/ANCC podcasts will clarify the rationale and best-practice approaches for HRRm testing to guide therapeutic strategies in metastatic prostate cancer. Clinical case scenarios are used to enhance the learning experience and provide practical considerations to achieve improved outcomes among patients.Launch Date: May 30, 2024Release Date: May 30, 2024Expiration Date: April 30, 2025FACULTY BIOAndrew Armstrong, MD, ScM, FACPProfessor of Medicine, Surgery, Pharmacology and Cancer BiologyDuke UniversityTanya Dorff, MDProfessor of MedicineCity of HopeThis podcast provides accredited continuing education credits. To qualify for credit, please read all accreditation information at the provided link below prior to listening to this episode.https://www.practicepointcme.com/CMEHome/talking-prostate-cancer-homologous-recombination-repair-gene-mutation-testing-in-metastatic-prostate-cancer-8

Language – be it spoken, written, or signed – is a fundamental part of how we interact with the world and each other. It's also an important developmental milestone for children as they grow. Dr. Vittorio Tantucci from Lancaster University works on linguistic development, focussing on children from China and other cultures. His research examines the reasons and impact of how autistic children struggle to imitate and creatively reformulate others' speech - an ability called resonance.Read the original article: https://doi.org/10.1515/ip-2023-4001 

Hugues de ThéCollège de France - Année 2023-2024Oncologie cellulaire et moléculaireColloque - Explorer la réponse thérapeutique in vivo : How Homologous Recombination (HR)-Deficient Tumors Survive Genomic InstabilityIntervenant(s)Raphaël CeccaldiInstitut Curie/INSERM

Embark on an interplanetary journey with SpaceTime Series 27 Episode 59, where we unravel the enigmatic atmosphere of Venus and its waterless environment. Discover the startling new study that suggests Venus lost its water reserves to space, leaving it with a mere fraction of Earth's water despite their similar origins. The episode dives into the complex chemical reactions in Venus's atmosphere that may have turned a once Earth-like planet into a scorching, inhospitable world.Next, we explore the innovative ideas NASA is considering for future lunar logistics, including a magnetic railroad system designed to transport materials across the Moon's surface. This system could revolutionize the way we build and sustain lunar bases, pushing the boundaries of off-world construction and resource utilization.The episode then shifts to the launch of a cutting-edge satellite from the International Space Station. This new eye in the sky aims to provide early warnings of volcanic eruptions by detecting trace gases, a game-changer for disaster preparedness and environmental monitoring.Join us as we delve into these cosmic developments and more, including the implications of AI biases and the latest in tech from Apple.Tune into SpaceTime with Stuart Gary for a deep dive into the latest astronomical insights and technological advancements.(00:00) This is spacetime series 27, episode 59, for broadcast on 15 May 2024(00:42) Study claims Venus loses twice as much water every day through dissociative recombination(06:16) NASA is looking at building a railway on the moon to transport freight(16:23) Ultra processed junk foods associated with higher risk of premature death, study finds(18:52) Apple has formally released its new Apple Air and Apple Pro iPads(24:15) Spacetime is available every Monday, Wednesday and Friday through Apple podcastsSupport the show and access ad-free episodes at https://www.spreaker.com/show/spacetime. Follow our cosmic conversations on Twitter @stuartgary, Instagram, YouTube, and Facebook. Join us as we unravel the mysteries of the universe, one episode at a time.This episode is proudly supported by NordPass. Secure your digital journey across the cosmos with a password manager you can trust. Find your stellar security solution at https://www.bitesz.com/nordpass.Listen to SpaceTime on your favorite podcast app and follow us on Twitter @stuartgary, Instagram, YouTube, and Facebook.Become a supporter of this podcast: https://www.spreaker.com/podcast/spacetime-with-stuart-gary--2458531/support.

On this week's episode, Sagi Eliyahu is joined by Jason Winmill, Chair of Buying Legal Council and Managing Partner of Argopoint, to discuss the transformative power of aligning legal operations with business strategies and the significance of innovation in legal procurement.Key Takeaways:(03:40) Aligning legal operations with business strategies.(06:17) Recombination as a fundamental concept in innovation.(10:16) Collaboration versus isolation in competitive business environments.(13:15) Initiating small collaborative projects between legal and procurement.(16:43) Overcoming change resistance in legal departments.(17:30) Cost management through alternative fee arrangements.(18:14) Long-term learning commitments in legal departments.(19:06) Adaptive changes in procurement due to global disruptions.(20:09) Potential impact of AI on legal departments.(22:17) Viewing businesses as adaptive organisms in ecosystems.(25:14) The importance of networking and information gathering.(26:12) The crucial role of delivering value for departmental survival.(27:08) The impact of consistent presence on professional success.Resources Mentioned:Jason Winmill - https://www.linkedin.com/in/jason-winmill/Buying Legal Council - https://www.buyinglegal.com/Argopoint LLC - https://www.argopoint.com/This episode is brought to you by Tonkean.Tonkean is the operating system for business operations and is the enterprise standard for process orchestration. It provides businesses with the building blocks to orchestrate any process, with no code or change management required. Contact us at tonkean.com to learn how you can build complex business processes. Fast.#Operations #BusinessOperations

In this episode, Colin C. Pritchard, MD, PhD, a pathologist, and Heather H. Cheng, MD, PhD, a medical oncologist, discuss optimal biomarker testing to guide treatment decisions in advanced prostate cancer, with topics including: Rationale for targeting PARP in prostate cancer with ARI combinationsStudy design nuances and findings from key randomized phase III clinical trials evaluating combination therapy with a PARP inhibitor and ARI, including PROpel, MAGNITUDE, and TALAPRO-2FDA approvals of combination therapy with a PARP inhibitor and ARI, including a comparison of populations based on mutations Optimal biomarker testing for gene mutations in homologous recombination and mismatch repair pathwaysTips for optimal coordination between pathology and medical oncologyPresenters: Heather H. Cheng, MD, PhDAssociate ProfessorDepartment of MedicineDivision of Hematology and OncologyAttending PhysicianDepartment of Genitourinary Medical OncologyFred Hutchinson Cancer CenterSeattle, WashingtonColin C. Pritchard, MD, PhDCo-DirectorGenetics and Solid Tumors LaboratoryUniversity of Washington Medical CenterProfessorDepartment of Laboratory Medicine and PathologyUniversity of WashingtonSeattle, WashingtonContent based on an online CME program supported by an independent educational grant from Pfizer, Inc.Link to full program: https://bit.ly/3PFagxb

Learn from experts in the field on optimizing PARP inhibitor outcomes in cancer therapy. The information presented during the podcast reflects solely the opinions of the presenter. The information and materials are not, and are not intended as, a comprehensive source of drug information on this topic. The contents of the podcast have not been reviewed by ASHP, and should neither be interpreted as the official policies of ASHP, nor an endorsement of any product(s), nor should they be considered as a substitute for the professional judgment of the pharmacist or physician.

Although molecular testing offers promising opportunities for diagnosis and targeted treatment of cancers, prostate cancer has lagged behind other types of cancer. Recently, homologous recombination repair testing in prostate cancer has provided a means to achieving targeted treatments for patients as well as opening new avenues of collaboration between pathologists and oncologists.On this episode of Inside the Lab, hosts Ms. Kelly Swails, MLS(ASCP), and Dr. Ali Brown, MD, FASCP are joined by Heather Cheng, a medical oncologist and associate professor of hematology and oncology at the University of Washington and Fred Hutchinson Cancer Center, and Colin Pritchard, molecular pathologist and professor of laboratory science and director of the Genetics and Solid Tumors Laboratory at the University of Washington Medical Center.Our panelists discuss the current treatment landscape for prostate cancer and how HRR testing can improve patient outcomes in this context.Topics Covered  An introduction to metastatic prostate cancer testing, and what types of tests are standard of care, and the rationale for targeting prostate cancer using PARPKey findings from recent phase III randomized clinical trialsStandards for optimal testing in prostate cancer, particularly concerning sample sources and the choice between next-generation sequencing (NGS) and polymerase chain reaction (PCR) methodscommon pitfalls or challenges in the arena of accurately reporting and interpreting findings from HRR testsPractical tips for optimal coordination among a multidisciplinary, cross-departmental team of healthcare providers and laboratory professionals when utilizing HRR testing in prostate cancer management.Connect with ASCPASCPASCP on FacebookASCP on InstagramASCP on Twitter Connect with Dr. ChengDr. Cheng on LinkedIn Connect with Dr. PritchardDr. Pritchard Connect with Ms. Swails & Dr. BrownMs. Swails on TwitterDr. Brown on Twitter ResourcesASCP Membership 2024Proposed FDA Regulation of Laboratory Developed TestsPublic Comment on the FDA's Proposed RuleInside the Lab in the ASCP Store 

Omnifest, the beloved Science Museum tradition, is back! Catch five stunning experiences on the Omnitheater's giant screen Feb. 24 through April 7, 2024.This movie festival is like no other, featuring larger-than-life treks through unknown corners of the cosmos and playdates with nature's cutest creatures.During Omnifest, you'll learn how science meets technology to protect the planet from asteroid strikes, discover what it takes to bring species back from the brink of extinction, cuddle up to some of  the world's cutest panda cubs, dive deep into the awe-inspiring images of NASA's James Webb Space Telescope, and so much more. Back-to-back showings every day mean you can choose one, two, or even all five in one day!Keep track of your adventures with this year's Omnifest Passport. Collect stamps for each movie and redeem it for a prize at our Explore Store! Download the passport below or pick up a copy at our Member Help desk.Aside from a daily free movie and discounts, members get early and extra Omnifest with a week-long sneak preview (Feb. 19-24) featuring:activities in the Omni Queuea screening of Ancient Caves with a book signing by special guest, longtime director of the Science Museum's Omnitheater and producer of 15 films for the giant screen, Mike Dayfree tickets to Recombination snacks and drinks in the member lounge, and more!Join today at smm.org/member.Keep track of your adventures with this year's Omnifest Passport. Collect stamps for each movie and redeem it for a prize at our Explore Store! Download the passport below or pick up a copy at our Member Help desk.OMNIFEST PASSPORT

BUFFALO, NY- January 8, 2024 – A new #review paper was #published in Oncotarget's Volume 14 on December 22, 2023, entitled, “Transformation-associated recombination (TAR) cloning and its applications for gene function; genome architecture and evolution; biotechnology and biomedicine.” Transformation-associated recombination (TAR) cloning represents a unique tool to selectively and efficiently recover a given chromosomal segment up to several hundred kb in length from complex genomes (such as animals and plants) and simple genomes (such as bacteria and viruses). The technique exploits a high level of homologous recombination in the yeast Sacharomyces cerevisiae. “TAR cloning has become a valuable procedure for the selective and efficient isolation and manipulation of large DNA molecules. [...] The ability to isolate individual gene alleles will help to clarify whether a particular allele is associated with predisposition to different diseases, including cancer.” In this new review, researchers Natalay Kouprina and Vladimir Larionov from the National Cancer Institute's Developmental Therapeutics Branch summarized multiple applications of the pioneering TAR cloning technique, developed previously for complex genomes, for functional, evolutionary, and structural studies, and extended the modified TAR versions to isolate biosynthetic gene clusters (BGCs) from microbes, which are the major source of pharmacological agents and industrial compounds, and to engineer synthetic viruses with novel properties to design a new generation of vaccines. TAR cloning was adapted as a reliable method for the assembly of synthetic microbe genomes for fundamental research. “In this review, we also discuss how the TAR cloning in combination with HAC (human artificial chromosome)- and CRISPR-based technologies may contribute to the future.” DOI - https://doi.org/10.18632/oncotarget.28546 Correspondence to - Natalay Kouprina - kouprinn@mail.nih.gov Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28546 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, transformation-associated recombination, TAR, microbes, biomedicine, biotechnology About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget 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/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Is History driven by heroic individuals or by variation and selection? What determines the speed of innovation? Matt Ridley is a science writer, journalist, and businessman. His books include The Red Queen, The Origins of Virtue, Genome, Nature via Nurture, Francis Crick, The Rational Optimist, The Evolution of Everything, and How Innovation Works.Matt and Greg discuss the integral role freedom, idea exchange, and trade play in driving innovation. They delve deep into the concept of creative destruction and how it's essential for large corporations to reinvent themselves to stay competitive or be allowed to cease to exist suddenly. Matt talks about the debate surrounding the origin of COVID-19, its implications for virology, and the spread of false information in our interconnected world. The discussion examines the controversial lab leak hypothesis and the impact of China's rise on global innovation.*unSILOed Podcast is produced by University FM.*Episode Quotes:Why is it that evolutionary thinking is like the gift that keeps on giving?02:25: The message of my book, "The Evolution of Everything," is that we don't want to let this insight remain confined to biology. It's just as useful as a way of understanding human society in lots of different aspects. Not just economics, but social change as well. Because really, the simple idea that if there's variation, if there's trial and error, if there's experimentation going on, then some ideas are going to survive at the expense of others. And that's going to lead to progressive adaptation. That's going to lead to progressive improvement in some technology, in some social habits, whatever it might be.Innovation is more about rearranging the world14:20: Recombination of existing genes is the main way that innovation happens in evolutionary biology, much more common than de novo mutation, and that's true of us too. Most of the new products we produce in the world by innovation are actually just the same old materials combined in new and interesting ways. Innovation is more about rearranging the world than it is about coming up with completely new things.Crony capitalism extends corporate lifespans, stifling innovation27:41: Crony capitalism, corporate favoritism, is a tried-and-true and tested way to stay in the game. But it tends to come at the expense of innovation, and it tends to leave you more and more vulnerable to collapse when you do. Get to face real competition. It tends to leave the company vulnerable to disappearing. Everybody thinks they know innovation, but only few people can pin it down30:46: The main reason we're living lives of far greater comfort than we did 500 years ago is still somewhat mysterious. We can tell you things like it needs freedom, it needs trial and error, and things like that, but we can't switch it on and off, let alone tell you when and where it's going to happen. In that sense, it's a surprisingly slippery thing, innovation. Everybody talks about it. Everybody thinks they know about it, but surprisingly, few people can really pin it down. And as I say, you can't put it in a mathematical model, at least not in a very convincing way.Show Links:Recommended Resources:Intentional stanceGreat man theoryFrancis CrickInfinite Improbability DriveMemeGeoffrey WestLinear modelFrancisco MojicaCOVID-19 lab leak theoryZoonosisMichael ShellenbergerGuest Profile:Speaker's Profile on Chartwell SpeakersMatt Ridley's WebsiteMatt Ridley on LinedInMatt Ridley on XMatt Ridley on YouTubeMatt Ridley on TEDTalk Matt Ridley on Talks at GoogleHis Work:Viral: The Search for the Origin of COVID-19The Rational Optimist: How Prosperity EvolvesHow Innovation Works: And Why It Flourishes in FreedomThe Evolution of Everything: How New Ideas EmergeThe Red Queen: Sex and the Evolution of Human NatureGenome: The Autobiography of a Species in 23 ChaptersThe Origins of VirtueNature Via Nurture: Genes, Experience, and What Makes Us HumanFrancis Crick: Discoverer of the Genetic CodeClimate Change: The Facts 2017

References Mol Cancer. 2023 Apr 10;22(1):69 Proc Natl Acad Sci U S A. 2019 Jun 18;116(25):12410-12415 Semin Immunol. 2010 Dec; 22(6): 311–312 --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message

Reference Authentic Biochemistry Lecture synthesis --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.27.538600v1?rss=1 Authors: Cullati, S. N., Zhang, E., Shan, Y., Guillen, R. X., Chen, J.-S., Navarrete-Perea, J., Elmore, Z. C., Ren, L., Gygi, S. P., Gould, K. L. Abstract: The CK1 family are conserved serine/threonine kinases with numerous substrates and cellular functions. The fission yeast CK1 orthologues Hhp1 and Hhp2 were first characterized as regulators of DNA repair, but the mechanism(s) by which CK1 activity promotes DNA repair had not been investigated. Here, we found that deleting Hhp1 and Hhp2 or inhibiting CK1 catalytic activities in yeast or in human cells activated the DNA damage checkpoint due to persistent double-strand breaks (DSBs). The primary pathways to repair DSBs, homologous recombination and non-homologous end joining, were both less efficient in cells lacking Hhp1 and Hhp2 activity. In order to understand how Hhp1 and Hhp2 promote DSB repair, we identified new substrates using quantitative phosphoproteomics. We confirmed that Arp8, a component of the INO80 chromatin remodeling complex, is a bona fide substrate of Hhp1 and Hhp2 that is important for DSB repair. Our data suggest that Hhp1 and Hhp2 facilitate DSB repair by phosphorylating multiple substrates, including Arp8. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Something for almost everyone in this programme. We talk to dancer Mischa van Leeuwen of Scapino Ballet about the show he is currently on tour with, DE SPRONG VAN NIJINSKY. We also pay a visit (@ 8mins40)to The Dome at the Meseon-Omniversum in The Hague to see the amazing RECOMBINATION -THE FULLDOME JOURNEY and talk to its creator Julius Horsthuis. And (@ 13mins30)we talk to two members of the Amsterdam-based English language theatre company Strike Me Pink about their new production CALAMUS.

Please be seated, try to keep up and don't drop your pencil. We've got a lot of material to cover. The science of genetic codes, vulnerable cell regions, jumping genes and lab designed viruses are successful. Recombination, transposition, metagenic properties, transposans and the transposase. How are the Ace2 receptors involved? Proven models from plants. Cauliflower and you. Where is the original corn? Gene regulations then and now. From apes you say? Where's the primate jumping gene? The basis for big pharma. Copy and paste within the human computer tower. Making porcine DNA the vector. Lactose intolerance and code problems. Carrying trace piggy DNA can be annoying. The great pig flu of 2009. The other, other white meat. HIV and human mutations. ALU elements prove insertions. Blood pressure related? The body is fixable. We've all been modified, but a reset is possible. The myth writers are done. There are no more scripts to follow. The future is now and we are good to go.  Learn more about your ad choices. Visit podcastchoices.com/adchoices

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.04.531117v1?rss=1 Authors: Milano, C. R., Ur, S. N., Gu, Y., Tromer, E. C., Zhang, J., Hochwagen, A., Corbett, K. D. Abstract: The meiotic chromosome axis coordinates chromosome organization and interhomolog recombination in meiotic prophase and is essential for fertility. In S. cerevisiae, the HORMAD protein Hop1 mediates enrichment of axis proteins at nucleosome-rich genomic islands through a central chromatin-binding region (CBR). Here, we use cryoelectron microscopy to show that the Hop1 CBR directly recognizes bent nucleosomal DNA through a composite interface in its PHD and winged helix-turn-helix domains. Targeted disruption of the Hop1 CBR-nucleosome interface causes loss of axis proteins from nucleosome-rich islands, reduces meiotic DNA double-strand breaks (DSBs), and leads to defects in chromosome synapsis. Synthetic effects with the disassemblase Pch2 suggest that nucleosome binding delays a conformational switch in Hop1 from a DSB-promoting, Pch2-inaccessible state to a DSB-inactive, Pch2-accessible state to regulate the extent of meiotic DSB formation. Phylogenetic analyses of meiotic HORMADs reveal an ancient origin of this domain, suggesting that these mechanisms are broadly conserved. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

How can diversity drive innovation and inspire solutions? How can leaders unlock all of the innovation potential of their diverse teams? Frans Johansson is an entrepreneur, best-selling author, acclaimed international speaker, and leading thinker on the intersection of diversity and innovation. In this episode, we spoke with him about:How DEI unearths creativity and innovation in the workplaceWhy we're entering the great recombination eraSpecific actions leaders can take to cultivate innovationAt Metlife, we are committed to diversity, equity and inclusion and we believe making a difference in the lives of our customers, community, and the world around us is #AllTogetherPossible. Learn more and join us at MetLife.com.Subscribe to our podcast. Rate and leave us a review.Produced by Hueman Group Media.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.06.527258v1?rss=1 Authors: He, J., Guo, Y., Deng, R., Li, L., Huang, C., Chen, R., Wang, Y., Huang, J., Cheng, J., Chen, G.-Q., Zheng, J., Zhao, X., Yu, J. Abstract: Homologous recombination (HR) repair for DNA double-strand breaks (DSBs) is critical for maintaining genome stability and cell survival. Nuclear PTEN plays a key role in HR repair, but the underlying mechanism remains largely elusive. We find that SUMOylated PTEN promotes HR repair but represses non-homologous end joining (NHEJ) repair by directly dephosphorylating 53BP1. During DNA damage responses (DDR), p14ARF was phosphorylated and then interacted efficiently with PTEN, thus promoting PTEN SUMOylation as an atypical SUMO E3 ligase. Interestingly, SUMOylated PTEN was subsequently recruited to the chromatin at DNA-break sites. This was because that SUMO1 conjugated to PTEN was recognized and bound by the SUMO-interacting motif (SIM) of BRCA1, which has been located to the core of 53BP1 foci on the chromatin during S/G2 stage. Further, these chromatin-loaded PTEN directly and specifically dephosphorylated pT543 of 53BP1, resulting in the dissociation of 53BP1-complex, which facilitated DNA end resection and ongoing HR repair. The SUMOylation-deficient PTENK254R mice also showed decreased DNA damage repair in vivo. Blocking PTEN SUMOylation pathway with either an SUMOylation inhibitor or a p14ARF(2-13) peptide sensitized tumor cells to chemotherapy. Our study therefore provides the new mechanistic understanding of PTEN in HR repair and clinical intervention of chemo-resistant tumors. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Notes, links, and things to think about: Hinch et al. 2011. The landscape of recombination in African Americans. Nature 476:170–177, 2011. Eberle et al. 2017. A reference dataset of 5.4 million human variants validated by genetic inheritance from sequencing a three-generation 17-member pedigree. Genome Res 27(1):157–164. Altemose et al. 2017. A map of human PRDM9 binding provides evidence for novel behaviors of PRDM9 and other zinc-finger proteins in meiosis. Elife 6:e28383. Grey et al. 2018. PRDM9, a driver of the genetic map. PLoS Genet 14(8):e1007479. Stapley et al. 2017. Recombination: the good, the bad and the variable. Philos Trans R Soc Lond B Biol Sci 372(1736):20170279. Protacio et al. 2022 Adaptive control of the meiotic recombination landscape by DNA site-dependent hotspots with implications for evolution. Front Genet 13:947572. International HapMap Project 1000 Genomes Program CEPH panel (note: In the video/audio I said that the DNA is cultured in bacterial artificial chromosomes. This is probably incorrect as there is mention of lymphoblastoid cell lines in this link. It has been a long time since I read any of the documentation on this project! Biblical Genetics episodes mentioned: There is no Y chromosome clock Did we evolve from 10,000 people in Africa? Was Africa the cradle of humanity? Did Eve live in Southern Africa? Modern humans from Adam and Eve? You bet! Patriarchal Drive Images: A diagram of crossing over from Thomas Hunt Morgan, circa 1917. Two consecutive crossings leads to gene conversion (if they are close enough) HapMap data, Europeans, Chr 15 spanning the XXX gene. Each individual is represented by a pair of rows. Each column is a single letter in the genome, but the letters are separated by an average of ~1000 nucleotides, so this is not full sequence data. Same as above, but for West Africans. Two accidental three-generation families in the HapMap and 1,000 Genomes datasets. The dotted lines show where the two-parent-child trios connect. The three-generation, 17-member CEPH panel A recombination map of Chr1 for one child (child #5, if I remember correctly). Blue = letters that came from the paternal grandfather. Red = letters that came from the paternal grandmother. Green = a spacer region to represent the position of the centromere. The number of recombined blocks vs the length of each block among the 11 children in the CEPH panel. Note: I totally messed up the explanation (and my hand motions) when I was describing this. I had something else in mind, but after filming, when I went looking for the image I had in my head, I realized my mistake. Either way, it is still an interesting image. It cannot be known how many of the singletons are sequencing errors of 1-SNP gene conversions, but see the Eberle reference above and how they claim to resolve many of the apparent errors.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.22.524239v1?rss=1 Authors: Romero-Franco, A., Checa-Rodriguez, C., Castellano-Pozo, M., Miras, H., Wals, A., Huertas, P. Abstract: The maintenance of genomic stability is essential for cellular and organismal survival and fitness. Thus, when DNA gets damaged, is essential to repair it in the most accurate fashion. Among different DNA lesions, DNA double strand breaks are specially challenging. An exquisite regulatory network reacts to local and global cues to control the choice between different DNA double strand break repair mechanisms to maximize genomic integrity. Such regulation relies mostly at the level of DNA end resection, the initial steps of the homologous recombination repair pathway. On the other hand, most cellular and organismal activities follow a 24 h oscillation known as the circadian cycle. Such repetitive changes are controlled by an intrinsic, molecular clock built-in at the cellular level which core components are the heterodimers BMAL1-CLOCK and CRY-PER. These inherent rhythms control many different aspects of the cellular metabolism, including the fate of many different DNA transactions. Here we have explored the regulation of the choice between different DNA double strand break repair pathways along the circadian cycle. We observed that DNA end resection shows a circadian oscillation, with a peak at dawn followed by a progressive reduction until dusk. Such regulations depend on the cellular levels of the circadian clock core component CRY1. Consequently, repair by homologous recombination mirrors CRY1 expression levels. Such modulation is controlled through the circadian regulation of the anti-resection activity, but not the protein levels, of CCAR2, that limits CtIP-mediated resection preferentially at nightfall. Additionally, such regulation requires a crosstalk between the DNA damage-dependent phosphorylation of CRY1 by the kinase DNA-PK. Finally, such regulation has an impact in cancer progression and response to radiation therapy of specific tumors. One sentence summaryCCAR2-dependent inhibition of DNA end resection and homologous recombination is controlled by the intrinsic cellular circadian clock Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

I've always said that the Name Game is nothing more than the peddler's playground, and they use crossbreeding to keep the Name Game alive. If the cross works, then they say it was a great cross. If the cross fails, then they say, cross them again, and again, and again. Thinking they are combining the traits of multiple bloodlines, to get the best of all worlds, all they are really doing is mongrelizing the breed, but yet we still attach useless names to them. The scary thing about this is that these peddlers are no longer hiding in the shadows. They are out where everyone can see them. In fact, they have YouTube channels and videos, and pretend to provide information, but their true aim is to sell birds. In this episode we are going show why crossbreeding is not the answer, and creating a true stain is always the best approach. This is a show you do not want to miss! We specialize in the breeding of gamefowl and chickens, and other breeding related topics. This includes the proper use of breeding programs. Also, it's our mission to provide our members a greater understanding of poultry genetics, poultry health care and disease prevention, and how to improve the production and performance ability of their fowl. If you are interested in creating a strain, or improving your established strain, you are going to enjoy this show.  We also want to encourage you to join us at “The Breeders Academy,” where we will not only help you increase your knowledge of breeding, advance your skills as a breeder, but improve the quality and performance of your fowl. If you would like to learn more, start by joining our Breeders Bulletins (newsletter): https://www.breedersacademy.com/free_bonus/ To Listen to the show, go to: https://www.breedersacademy.com #breedinggamefowl #breedingchickens #gamefowlbreeders #chickenbreeders #gamefowlbreeding #chickenbreeding, #gamefowlnation, #selectivebreeding, #evolution, #naturalselection #poultrygenetics #poultryhealth #backyardbreeders #breedersacademy #bredtoperfection #kennytroiano 

References Advances in Immunology. 2011 v.109.Pp125 Biomed J. 2014 Sep-Oct;37(5):269-83 Alcohol Clin Exp Res. 2011 Aug; 35(8): 1435–1444 Cell Reports 10, 2043–2054, March 31, 2015 Front. Immunol., 28 September 2015 | https://doi.org/10.3389/fimmu.2015.00493 Front. Immunol., 07 January 2021 Sec. T Cell Biology https://doi.org/10.3389/fimmu.2020.609891 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.19.512819v1?rss=1 Authors: Rodriguez-Real, G., Prados-Carvajal, R., Bayona-Feliu, A., Balestra, F. R., Huertas, P. Abstract: The centrosome is a cytoplasmic organelle with roles in microtubule organization which has also been proposed to act as a hub for cellular signaling. For example, it has been suggested that some centrosomal component are required for full activation of the DNA Damage Response, the cellular signaling network that is activated upon the appearance of chromosome breaks. However, if the centrosome and/or some of its components regulate specific DNA repair pathways is not known. Double strand breaks are mostly repaired by two alternative mechanisms, the homology-independent non-homologous end-joining and the homology-driven homologous recombination. Here, we show that centrosomes presence is required to fully activate recombination, specifically to completely license its initial step, the so-called DNA end resection. Additionally, loss of centrosome upregulates the non-homologous end-joining repair pathway. Furthermore, we identify a centriolar structure, the subdistal appendages, and a specific factor, CEP170, as the critical centrosomal component involved in the regulation of recombination and resection, albeit it does not control end-joining repair. Cells lacking centrosomes or depleted for CEP170 are, consequently, hyper-sensitive to DNA damaging agents. Moreover, low levels of CEP170 in multiple cancer types correlate with an increase of the mutation burden associated with specific mutational signatures and a better prognosis, suggesting this protein can act as a driver mutation but also could be targeted to improve current oncological treatments. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.17.512236v1?rss=1 Authors: Galea, G., Kuodyte, K., Khan, M. M., Thul, P. J., Neumann, B., Lundberg, E., Pepperkok, R. Abstract: Cells are constantly exposed to a multitude of DNA-damaging agents that can lead to mutation, dysregulation, and possibly cell death. To ensure genomic integrity, DNA Damage Response (DDR) mechanisms are set in motion to repair and mitigate any damage to the DNA structure. Although these pathways are well-studied in the context of nuclear function, relatively little is known of the regulatory function of cytoplasmic organelles. Here we show the first example of DDR regulation at the Golgi complex, coordinating Homologous Recombination (HR)-mediated DNA repair. We found that RAD51C, a regulatory HR protein, localises to the Golgi and nuclear compartments and in response to double-strand DNA breaks, the Golgi protein population of RAD51C redistributes to form nuclear foci. Furthermore, we found that the Golgi localisation of RAD51C is dependent on the Golgin Giantin. Depletion of Giantin induces the redistribution of the RAD51C Golgi pool to form nuclear foci, independent of DNA damage induction, and concurrent with a significant increase in genomic instability and inhibition of HR signalling regulators. This study presents evidence for a novel pathway where the Golgi is a central regulatory hub for HR DDR and potentially other repair pathways, a finding with important therapeutic implications. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Using the cosmological recombination radiation to probe early dark energy and fundamental constant variations by Luke Hart et al. on Monday 26 September The cosmological recombination radiation (CRR) is one of the guaranteed spectral distortion signals from the early Universe. The CRR photons from hydrogen and helium pre-date the last scattering process and as such allow probing physical phenomena in the pre-recombination era. Here we compute the modifications to the CRR caused by early dark energy models and varying fundamental constants. These new physics examples have seen increased recent activity in connection with the Hubble tension, motivating the exploratory study presented here. The associated CRR responses are spectrally-rich but the level of the signals is small. We forecast the possible sensitivity of future spectrometers to these effects. Our estimates demonstrate that the CRR directly depends to changes in the expansion history and recombination physics during the pre-recombination era. However, futuristic sensitivities are required for spectrometer-only constraints that are competitive with other cosmological probes. Nevertheless, measurements of the CRR can directly reach into phases that otherwise remain inaccessible, highlighting the potential these types of observations could have as a probe of the early Universe. A combination with ${it Planck}$ data further shows that a synergistic approach is very promising. arXiv: http://arxiv.org/abs/http://arxiv.org/abs/2209.12290v1

Baseline correction for FAST radio recombination lines: a modified penalized least squares smoothing technique by Bin Liu et al. on Tuesday 20 September A pilot project has been proceeded to map 1 deg$^2$ on the Galactic plane for radio recombination lines (RRLs) using the Five hundred meter Aperture Spherical Telescope (FAST). The motivation is to verify the techniques and reliabilities for a large-scale Galactic plane RRL survey with FAST aiming to investigate the ionized environment in the Galaxy. The data shows that the bandpass of the FAST 19 beam L-band is severely affected by radio frequency interferences (RFIs) and standing wave ripples, which can hardly be corrected by traditional low order polynomials. In this paper, we investigate a series of penalized least square (PLS) based baseline correction methods for radio astronomical spectra that usually contain weak signals with high level of noise. Three promising penalized least squares based methods, AsLS, arPLS, and asPLS are evaluated. Adopting their advantages, a modified method named rrlPLS is developed to optimize the baseline fitting to our RRL spectra. To check their effectiveness, the four methods are tested by simulations and further verified using observed data sets. It turns out that the rrlPLS method, with optimized parameter $lambda = 2 times 10^8$ , reveals the most sensitive and reliable emission features in the RRL map. By injecting artificial line profiles into the real data cube, a further evaluation of profile distortion is conducted for rrlPLS. Comparing to simulated signals, the processed lines with low signal-to-noise ratio are less affected, of which the uncertainties are mainly caused by the rms noise. The rrlPLS method will be applied for baseline correction in future data processing pipeline of FAST RRL survey. Configured with proper parameters, the rrlPLS technique verified in this work may also be used for other spectroscopy projects. arXiv: http://arxiv.org/abs/http://arxiv.org/abs/2209.09555v1

On Quantum and Classical Treatments of Radiative Recombination by Barabanov A. L. et al. on Thursday 15 September The quantum-mechanical solution to the problem of radiative recombination of an electron in a Coulomb field, obtained in the approximation of the smallness of the electron coupling with the radiation field, has been known for a long time. However, in astrophysics, the classical approach, which does not explicitly use this smallness, is sometimes used to describe similar processes in systems of magnetic monopoles or self-interacting dark matter particles. The importance of such problems is determined by the fact that recombination processes play a crucial role in the evolution of the large-scale structure of the Universe. Therefore, of particular interest is the fact that the classical and quantum expressions for the recombination cross section differ significantly in magnitude. It is shown that the applicability of quantum and classical approaches to radiative recombination is closely related to the radiated angular momentum and its quantization. For situations where the classical approach is not suitable, a semi-classical approach based on the angular momentum quantization is proposed, in some respects an alternative to the well-known semi-classical Kramers' approach. arXiv: http://arxiv.org/abs/http://arxiv.org/abs/2204.10860v2

Recombination of hot ionized nebulae: The old planetary nebula around V4334 Sgr Sakurai's star by Martin Reichel et al. on Thursday 08 September After becoming ionized, low-density astrophysical plasmas will begin a process of slow recombination. Models for this still have significant uncertainties. The recombination cannot normally be observed in isolation, because the ionization follows the evolutionary time scale of the ionizing source. Laboratory experiments are unable to reach the appropriate conditions because of the required very long time scales. The extended nebula around the very late helium flash (VLTP) star V4334 Sgr provides a unique laboratory for this kind of study. The sudden loss of the ionizing UV radiation after the VLTP event has allowed the nebula to recombine free from other influences. More than 290 long slit spectra taken with FORS1/2 at the ESO VLT between 2007 and 2022 are used to follow the time evolution of lines of H, He, N, S, O, Ar. Hydrogen and helium lines, representing most of the ionized mass, do not show significant changes. A small increase is seen in [N II] (+2.8 %/yr; significance 2.7 sigma), while we see a decrease in [O III] (-1.96 %/yr; 2.0 sigma). The [S II] lines show a change of +3.0 %/yr; 1.6 sigma). The lines of [S III] and of Ar III] show no significant change. For [S III], the measurement differs from the predicted decrease by 4.5 sigma. A possible explanation is that the fraction of [S IV] and higher is larger than expected. Such an effect could provide a potential solution for the sulfur anomaly in planetary nebulae. arXiv: http://arxiv.org/abs/http://arxiv.org/abs/2209.03634v1

References Dr Guerra's notes Oncotarget. 2016 Jan 26; 7(4): 4195–4209 FEBS J. 2017 Jun; 284(11): 1590–1605 Biochim Biophys Acta Mol Basis Dis. 2021 Oct 1;1867(10):166184. Biol. Cell (2007)99, 129–140 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

We've all heard about new Omicron subvariants with such names as BA.2, BA.4 and BA.5. The recent proliferation of variants begs the question: is Covid-19 mutating faster than ever before? Dr Sebastian Duchene explains. 

As an hypothetico-deduction, Dr. Guerra proposes that the Recombination Activating Gene-RAG System is a Potential Candidate in Age Associated Morbidity. In conjunction with a neutral sphingomyelinase and the subsequent synthesis of diacylglycerol thence promoting activation of a PKC-Zeta, T cell receptor translocation and activation are obtained. Prior RAG mediated recombination events in CNS-resident lymphocytes, associated microglia and neurons can lead to recombination event epigenomic ontologies that either promote or curtail a resident hyperimmune response leading to classical neurodegenerative diseases of the elderly. References: J. Biol. Chem. 1998;273:14550-14559 Frontiers in Immunology.2014. 5:100 Front Cell Dev Biol. 2019; 7: 226. --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Nels and Vincent review evidence for recombinant SARS-CoV-2 genomes arising in the B.1.1.7 lineage within the United Kingdom. Hosts: Nels Elde and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiEVO Links for this episode Recombination in B.1.1.7 lineage (Virological) CoVariants Letters read on TWiEVO 67 Time stamps by Jolene. Thanks! Science Picks Nels – Mars rover helicopter flight! Vincent – TWiN 17: Worms see the light with Michael Nitabach Music on TWiEVO is performed by Trampled by Turtles Send your evolution questions and comments to twievo@microbe.tv

同じ細胞から異なるタイミングでトランスクリプトームを複数計測できる技術Live-seqの原著論文を読みました。Show notes Genome-wide molecular recording using Live-seq BioRxiv 2021 … 今回紹介した論文。 NeuroRadio … 本格派の神経科学研究者系ポッドキャスト Rebuild Misreading Chat CSの論文読んで話をしよう サンキュータツオ 予備校のノリで学ぶ「大学の数学・物理」 (YouTube) PNE … 蛋白質核酸酵素 新着論文レビュー Manolis Kellis (YouTube) … Manolis KellisのYoutubeチャンネル。MITでの講義動画が盛りだくさん。 iBology Conversations in Genetics: Leland Hartwell (Cell Cycle Control in Yeast) Conversations in Genetics: Matthew Meselson (DNA Replication, Recombination and Repair) Conversations in Genetics: Sydney Brenner (Genetic Code, Worm Development) Conversations in Genetics: Elizabeth Blackburn (Telomeres, Cancer, Aging) Future of CRISPR (base & prime) and epigenome editing (Interview with Prof David R. Liu) Transcriptional recording by CRISPR spacer acquisition from RNA. Nature 2018 … Record-seqについての原著論文。 9. One-shot beautiful experiment … ゲノム編集を利用した情報の記録について話した回。 Editorial notes 雑談ばっかりにならないよう論文もどんどん読んでいきます (soh) 桜咲きました。いうて、研究者の方がやっているYouTubeもちらほらありますよね。(tadasu)

This episode covers viral recombination!

Dr. Haber begins his talk by explaining that broken chromosomes frequently arise during the process of DNA replication. In healthy cells, these double strand breaks (DSBs) are repaired by homologous recombination, an orderly process that preserves the genome.  If the homologous recombination machinery is impaired, DNA truncations, translocations, and deletions often occur, resulting in genome instability and cancer. All mechanisms of homologous recombination have one common principal; the broken ends of the DNA are repaired by base pairing with a sequence that is identical or nearly identical and acts as a template for repair enzymes.  Haber explains the general principles of homologous recombination and its critical role in maintaining genome stability.

Dr. Haber begins his talk by explaining that broken chromosomes frequently arise during the process of DNA replication. In healthy cells, these double strand breaks (DSBs) are repaired by homologous recombination, an orderly process that preserves the genome.  If the homologous recombination machinery is impaired, DNA truncations, translocations, and deletions often occur, resulting in genome instability and cancer. All mechanisms of homologous recombination have one common principal; the broken ends of the DNA are repaired by base pairing with a sequence that is identical or nearly identical and acts as a template for repair enzymes.  Haber explains the general principles of homologous recombination and its critical role in maintaining genome stability.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.04.367136v1?rss=1 Authors: Roy, U., Kwon, Y., Marie, L., Symington, L., Sung, P., Lisby, M., Greene, E. C. Abstract: Homologous recombination (HR) is essential for the maintenance of genome integrity. Rad51 paralogs fulfill a conserved, but undefined role in HR, and their mutations are associated with increased cancer risk in humans. Here, we use single-molecule imaging to reveal that the Saccharomyces cerevisiae Rad51 paralog complex Rad55-Rad57 promotes the assembly of Rad51 recombinase filaments through transient interactions, providing evidence that it acts as a classical molecular chaperone. Srs2 is an ATP-dependent anti-recombinase that downregulates HR by actively dismantling Rad51 filaments. Contrary to the current model, we find that Rad55-Rad57 does not physically block the movement of Srs2. Instead, Rad55-Rad57 promotes rapid re-assembly of Rad51 filaments after their disruption by Srs2. Our findings support a model in which Rad51 is in flux between free and ssDNA-bound states, the rate of which is dynamically controlled though the opposing actions of Rad55-Rad57 and Srs2. Copy rights belong to original authors. Visit the link for more info

SHR # 2594 :: Unique Safety Issues Associated With Virus-vectored Vaccines: Potential For Theoretical Consequences of Recombination with Wild Type Virus Strains - Keith Bell - The COVID-19 vaccine will be a virus-vector vaccine. In 2003 and 2013, the World Health Organization convened informal consultations on characterization and quality aspects of vaccines based on live virus vectors. In the resulting reports, one of several issues raised for future study was the potential for recombination of virus-vectored vaccines with wild type pathogenic virus strains. Our discussion today assesses this issue formulated by the Brighton Collaboration. Study Discussed On Today's Show https://www.sciencedirect.com/science/article/pii/S0264410X16302250?fbclid=IwAR1gsVw1VoikQyfbdHk4qfB8cSSeWbFi44WvSevNqni6ioHqPldb6hWXUxg

SHR # 2594 :: Unique Safety Issues Associated With Virus-vectored Vaccines: Potential For Theoretical Consequences of Recombination with Wild Type Virus Strains - Keith Bell - The COVID-19 vaccine will be a virus-vector vaccine. In 2003 and 2013, the World Health Organization convened informal consultations on characterization and quality aspects of vaccines based on live virus vectors. In the resulting reports, one of several issues raised for future study was the potential for recombination of virus-vectored vaccines with wild type pathogenic virus strains. Our discussion today assesses this issue formulated by the Brighton Collaboration. Study Discussed On Today's Show https://www.sciencedirect.com/science/article/pii/S0264410X16302250?fbclid=IwAR1gsVw1VoikQyfbdHk4qfB8cSSeWbFi44WvSevNqni6ioHqPldb6hWXUxg

Dr. Oliver Smithies is the Weatherspoon Eminent Distinguished Professor in the Department of Pathology and Laboratory Medicine at the University of North Caronlina at Chapel Hill School of Medicine. He received his PhD in Biochemistry at Oxford University and spent some time on the faculty at the University of Toronto, as well as the University of Wisconsin, Madison, before joining the faculty at UNC, Chapel Hill where he is today. Oliver is a distinguished scientist, and in 2007, he was a co-recipient of the Nobel Prize in Physiology or Medicine. Among many other accomplishments, he is the recipient of the Albert Lasker Award for Basic Medical Research, the Wolf Prize in Medicine, the Massry Prize, and the University of North Carolina's O. Max Gardner Award. Oliver is also a Member of the U.S. National Academy of Sciences, a Member of the U.S. Institute of Medicine, a Fellow of the American Academy of Arts and Sciences, a Fellow of the American Association for the Advancement of Science, and a Foreign Member of the Royal Society. Oliver is here with us today to tell us all about his journey through life and science.