Podcasts about Elegans

Let's get ready to RUMMMMMMMBBBLLLEEE!! In this corner, we have a normal human who is definitely not a psychopath, and in the opposite corner we have… a fly. Just like, a fly. Also Julian is here and has an amazing story about melting gold with acid rain!QUESTIONSJulian: "Could we produce enough air pollution to make the sky rain aqua regia? At what point would it begin to dissolve gold?" from MateoTrace: "What is the smallest creature that can be knocked out with a punch?" from SeanDo you have an absurd question? Maybe it's silly idea you had, a shower thought about the nature of reality, or a ridiculous musing about your favorite food? If you want an answer, no matter the question, tell us!HOW TO ASK A QUESTION

In this episode of Genetics in Your World, Early Career Scientist Multimedia Subcommittee member Tammy Lee has a conversation with Dr. Jordan Brown, a recent alumnus from the University of Chicago, about factors involved in gene silencing mediated by small RNAs. Read Dr. Brown's paper titled, “Sensitized piRNA reporter identifies multiple RNA processing factors involved in piRNA-mediated gene silencing,” published in the August 2023 issue of GENETICS: ​​https://doi.org/10.1093/genetics/iyad095. Music: Loopster Kevin MacLeod (incompetech.com). Licensed under Creative Commons: By Attribution 3.0 License, http://creativecommons.org/licenses/by/3.0/ Hosted on Acast. See acast.com/privacy for more information.

Hi Friends, We have shifted our focus to 'Rising Mountain' this symbolises a transcendental awareness, where heaven meets earth and so much more. The Macrocosm - Microcosm is life itself. Rising Mountain is within the biophysical nature that is all of life, our podcasts within our new tag name are about igniting the art of inner enquiry, recognising frequencies that emit infinite sound vibrations. We will be sharing more video content with narrations by nature, & audio podcasts as we hike into different areas within our nature world, connecting to the different ecosystems, we also connect to a deeper understanding of the metaphysical within the physicality of life that knows no separation. Our team is expanding, illuminating and constantly shifting as we grow and dive deeper into a communicative nature and how we are particles that are constantly oscillating. We are a constant in an eternal flow, in this podcast we invite you to reflect if that resonates with you, connect within the ether - space and allow your being to shine. Namaste Rising mountain team.

Euthanasia Coaster är ett konceptuellt konstprojekt i form av en berg- och dalbana som är designad för att döda sina passagerare.Vem har kommit på denna udda idé? Och varför?Wikipedia säger sitt om Euthanasia Coaster. Hosted on Acast. See acast.com/privacy for more information.

BUFFALO, NY- June 11, 2024 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “CCR4-NOT complex in stress resistance and longevity in C. elegans.” The ability to mount an adaptive response to environmental stress is crucial in organismal survival and overall fitness. In the context of aging, many genes that mediate resistance to stressors are also important in longevity, and aging has been shown to cause a decline in stress resistance. In their new editorial, researchers Cheng-Wei Wu and Hadi Tabarraei from the University of Saskatchewan wrote that recently, during a screening for genes that are required for the transcriptional response to heavy metal and oxidative stress in C. elegans, they found that depletion of subunits within the evolutionarily conserved CCR4-NOT protein complex compromises stress resistance and decreases lifespan. “The CCR4-NOT (Carbon Catabolite Repression 4 – Negative On TATA-less) is a multi-protein complex tasked with regulating RNA metabolism across multiple steps including mRNA decay, transcription initiation and elongation, mRNA quality control and export, and mRNA translatability (reviewed in [3]).” Studies in yeast have shown that CCR4-NOT is required for transcriptional elongation of stress responsive genes and that loss of function mutants of this protein complex have increased sensitivity to replication stress caused by DNA damaging agents [4, 5]. An expansive role for the CCR4-NOT complex in stress-induced transcriptional programming was demonstrated in C. elegans via whole-transcriptome sequencing analysis [2]. “Together, while the CCR4-NOT complex has been extensively studied for the past 3 decades, new studies in the model organism C. elegans have revealed an important new role for this protein complex in regulating normal aging as well as a requirement for many well-characterized and evolutionarily conserved pro-longevity pathways including reduced insulin signaling, mitochondrial suppression, enhanced stress response, and dietary restriction.” DOI - https://doi.org/10.18632/aging.205918 Corresponding author - Cheng-Wei Wu - michael.wu@usask.ca Video short - https://www.youtube.com/watch?v=UFi7Dq5JXJ4 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205918 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, oxidative stress, C. elegans, CCR4-NOT About Aging-US Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer's disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.). Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Hoe werk die mens se brein? Kom ons begin klein... baie klein en kyk na die mees primitiefste diertjie wat nie net gereeld in die ruimte kuier nie, maar die bestudering van dit het gelei het tot 'n Suid Afrikaanse Nobel prys - C.Elegans. Wikipedia: https://en.wikipedia.org/wiki/Caenorhabditis_elegans OpenWorm: https://openworm.org/ Hoe 'stroom' in neurone werk: https://www.youtube.com/watch?v=HUuUUJktL6E

Elegans och stepp är två ord som hänger samman med danslegendaren Fred Astaire. Vad var det som gjorde honom unik? Per Feltzin går till arkiven. Lyssna på alla avsnitt i Sveriges Radio Play. Fred Astaire levde 1899-1987 och var aktiv i över 75 år, medverkade i dussintalet musikaler på scenen, 31 musikalfilmer främst på 1930-talet plus många andra filmer som skådespelare.I ett utdrag ur Klassikern om Fred Astaire gjort av P2:s Per Feltzin, hör vi bland andra dansaren Karl Dyall.

How does the brain actually work? And is there anything we can do when it doesn't? To find out, Dr. Charles Liu and co-host Allen Liu welcome Dr. Nicki Driscoll, CTO and Co-Founder of NeuroBionics. As always, though, we start off with the day's joyfully cool cosmic thing, the recently announced discovery of Super-Earth TOI-715 b that is within its star's habitable zone. It's roughly 1.5x the diameter of Earth and orbits an M-4 Red Dwarf star in a zone where liquid water could exist and be stable on the surface of the planet. And where there's liquid water, there is the possibility for life. Charles and Nicki quickly move from the search for intelligent to the actual activities inside the brain itself that give rise to consciousness. As Nicki points out, as incredible as it is that our brains can ponder what's out there, it's equally incredible how little we know about what's inside them... especially when things go wrong in the brain. Dr. Driscoll explains stochastic processes and brain complexity, with over a billion neurons, each behaving like its own little computer with thousands of connections with other neurons called synapses. You'll hear about white matter and gray matter, and what they have in common with the interstate highway system. Nicki points out how humans frequently create systems that mirror efficient systems found in nature. Chuck points out that when we map the large scale structure of the universe, including the cosmic background radiation and dark matter, it looks like a brain! Then it's time for a question for Nicki from the audience. Madison H. asks, “What is the most interesting thing about the brain that impacts the way humans think?” Nicki settles on the fact that the brain uses multiple mechanisms for signaling, from electrical signals in the neurons to chemical signaling via neurotransmitters and chemicals in the brain, and how they can vary due to minute differences. Nicki explains the field of neurotechnology, where her company NeuroBionics creates devices that allow us to interact with the brain, recording and even stimulating activity in the brain. She describes the two different areas of neurotechnology. The first, the domain of Elon Musk's company Neuralink, is recording neural activity with brain computer interfaces that use electrodes to record brain activity and then try to decode that activity to try to help people with paralysis or who are unable to communicate. The second area, which involves stimulating the brain, is called neuromodulation and is very useful for therapy for people with epilepsy and Parkinson's syndrome. NeuroBionics has developed a technique for neuromodulation that doesn't require invasive surgery by feeding very thin fiber devices into the brain through catheters in blood vessels using the same process that neurosurgeons already use in treating strokes. Our next question comes from Elene, who asks Nicki, “Since you have your PhD, do you think it was worth it or gratifying going through that many years of schooling?” Nicki answers with a resounding yes, for herself, but explains that it depends on your career goals. Elene also asks, “Do you think AI will ever reach a point where it will start dangerously affecting our day to day life such as job opportunities?” Charles and Nicki agree that AI is a useful tool, especially for scientists, but that the ability to generate misinformation and deep fakes is already troubling and that, like nuclear power, we should be able to maximize the positive use while minimizing the worst excesses. The subject turns to AI and brain science in games and science fiction, and Nicki describes the first book in a series she's reading, called “Children of Time.” In it, a character uploads their consciousness into a computer, and act which is still most decidedly in the realm of fiction. You'll hear about the still incomplete efforts to map the 212 neurons in the brains of C. Elegans, a simple primitive worm with a simple brain structure that scientists use to study the activity of individual neurons and small quantities of synapses. Before we run out of time, Chuck asks Nicki whether he should freeze his brain when he dies and whether supercomputers could  be used to recreate who he is – but to find out the surprising answer to that question (or perhaps not so surprising after all), you'll need to watch or listen to the episode. If you'd like to know more about Dr. Driscoll, follow NeuroBionics on LinkedIn or visit neurobionics.io. We hope you enjoy this episode of The LIUniverse, and, if you do, please support us on Patreon. Credits for Images Used in this Episode: – Illustration of Super-Earth TOI-715 b – NASA/JPL-Caltech, Public Domain – Map of “white matter” in the brain – Xavier Gigandet et. al. CC BY 2.5 – A growing slime mold – Christian Grenier, Public Domain – A large-scale simulation of the universe – Andrew Pontzen and Fabio Governato, CC BY 2.0 – C. Elegans worms – ZEISS Microscopy, CC BY 2.0t

Today's guest has argued that the present dominant way of doing systems neuroscience in mammals (large-scale electric or optical recordings of neural activity combined with data analysis) will be inadequate for understanding how their brain works. Instead, he proposes to focus on the simple roundworm C.elegans with only 302 neurons and try to reverse engineer it by means of optical stimulation and recordings, and modern machine-learning techniques.   

In this episode, we dive deep into the fascinating world of fasting with Dr. Chris Rhodes, the co-founder and CEO of Mimio Health. Dr. Rhodes shares insights into the transformative power of fasting and sheds light on the research behind calorie restriction, offering listeners a glimpse into the potential keys to a healthier and longer live. We also explore the concept of fasting mimicking, the breakdown of mTOR vs AMPK, and the powerful ingredients that make Mimio a unique and effective tool in the pursuit of health optimization.Dr. Chris Rhodes is the co-founder and CEO of Mimio Health. He has a PhD in nutrition and has always been fascinated by how we eat affects our health and longevity. Inspired by the power of fasting to enhance lifespan, he spent years researching the human body's response to a 36 hour fast and how it could unlock our built-in longevity bio-programs.Mimio is a biomimetic supplement, derived from bioidentical molecules to the most powerful metabolites produced by our own bodies during a prolonged 36-hour fast, clinically shown to support a wide range of health benefits including enhanced energy, mood, memory and cognition, metabolism, balance to dietary inflammation, and healthy aging.SHOW NOTES:0:53 Welcome to the show!1:44 Dr. Chris Rhodes' Bio2:45 Welcome him to the podcast!3:28 About Mimio4:03 Dr. Chris' background4:54 Fasting for Longevity & Healthspan6:4 Research on Caloric Restriction10:16 Why is mimicking fasting helpful?11:28 His experience with fasting14:44 Longevity & Social Connection14:39 mTOR vs AMPK17:00 Rapamycin: Mechanism of Action18:58 Hormetic Stress & AMP-Kinase20:45 Mimio's Ingredient Sourcing23:59 C.Elegans for Life Extension25:10 *Filter Optix*27:48 The Biomimetic Approach28:28 Mimio Key Ingredients30:47 Nicotinamide & NAD33:45 Dosing structure of Mimio36:30 *Magnesium Breakthrough*38:18 What is Spermidine?43:18 OEA (Oleic Acid)45:29 Optimal duration for fasting47:55 PEA Fatty Acids52:18 Biological Age Testing54:29 Best practices for Mimio57:01 His final piece of advice59:55 Thanks for tuning in!RESOURCES:Website: www.MimioHealth.com - Save 20% with code BHBABES20IG: @mimiohealthIG: @thatnutritiondrFilter Optix Blue-Blocking Glasses: filterpoptix.com/biohackerbabes - code: BIOHACKERBABES to save 15% offMagnesium Breakthrough: Bioptimizers.com/biohackerbabes - code: biohackerbabes10Support this podcast at — https://redcircle.com/biohacker-babes-podcast/donationsAdvertising Inquiries: https://redcircle.com/brands

  For the first time ever, parents going through IVF can use whole genome sequencing to screen their embryos for hundreds of conditions. Harness the power of genetics to keep your family safe, with Orchid. Check them out at orchidhealth.com. Today Razib talks to geneticist Erich Schwarz, a Research Professor in the Department of Molecular Biology and Genetics at Cornell University  since 2012. Schwarz has a molecular biology degree from Harvard and a Ph.D. from Caltech. After working with the fruit fly Drosophila melanogaster in graduate school, he switched to the nematode Caenorhabditis elegans, and has continued studying nematodes ever since. After helping to found the C. elegans genome database WormBase (wormbase.org) in the early 2000s, he began sequencing and characterizing the genomes of several nematode worms other than C. elegans, either because they are biologically informative or because they are worldwide parasites. His current work includes using the genome of Ancylostoma ceylanicum to help devise an anti-hookworm vaccine. Schwarz explains why C. elegans, often called “the worm,” has been so useful in developmental and molecular genetics, and its role in the career of the late Nobel laureate Sydney Brenner. With a simple anatomical structure, every single one of the 1,000 cells of  C. elegans has been mapped and detailed. Despite its small size, this organism has spawned a research community of thousands, documented in Andrew Brown's In the Beginning Was the Worm: Finding the Secrets of Life in a Tiny Hermaphrodite. In the age of hundreds of thousands of human genomes, Schwarz explains the decades-long period in the late 20th century when biological research was dominated by “model organisms,” simple and easy-to-experiment-on animals, plants and bacteria that could eloquently and plainly elucidate universal and essential mechanisms of function and structure.  Razib and Schwarz also discuss the future of model organisms in a genomic future, when high-throughput data analysis can supercharge decades-long experimental projects. Ultimately, the future is not likely to see model organisms set aside, but rather to witness them merged into the broader research community in human and medical genomics which has been driving technological changes in sppedspeed and volume of data collection.

In this installment of Genetics in Your World, we talk to Ting Gong of UC Davis. She discusses the surprising results she found when disrupting meiotic chromosome segregation in C. elegans. Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Struggling Scientists, we are honored to have Nobel Laureate, Martin Chalfie, as our special guest. Join us as professor Chalfie shares his remarkable journey in science, from the initial struggles in the lab to the groundbreaking discovery that would ultimately change the field of biology. Since he was kind enough to talk with us for over an hour this episode will be split into two parts. In episode 70 we ask him questions about his scientific career, how he almost decided he was not cut out to be a scientist, and of course his discovery about using GFP as a marker. In episode 71 we will talk about the impact winning a Nobel prize has on your life and how he missed the announcement of his own Nobel Prize!Discover the story behind his pivotal work with the green fluorescent protein (GFP) as a genetic tag in cells and C. Elegans. With candid insights into the challenges he faced, the collaborative efforts that led to success, and the impact of his findings, this episode promises to inspire and captivate scientists and science enthusiasts alike.If you have any questions, comments, suggestions, or papers we really need to read, you can reach out to us via our website: https://thestrugglingscientists.com/Would you like to know more about becoming a guest on our podcast or sponsoring us? Then please check out the information on our website!Find your next funding opportunity now with https://thestrugglingscientists.com/Astound and use the code StrugglingScientist for 25% discount Check out the amazing writing assistant Jenni at https://thestrugglingscientists.com/Jenni and use the code SCIENCE20 for 20% discount

This is the 17th Annual Review episode of Brain Science, celebrating the first episode which aired on December 15, 2006. We review the highlights of 2023, which included both new guests and the return of several favorites. Episodes Released in 2023: BS 204 (Encore) and BS 205 featured molecular biologist Guy Caldwell, PhD from the University of Alabama. Caldwell uses the tiny roundworm C. Elegans to search for potential treatments of Parkinson's Disease. BS 206: Paco Calvo, PhD, author of Planta Sapiens: The New Science of Intelligence. BS 207 (Encore): Luiz Pessoa, author of The Cognitive-Emotional Brain: From Interactions to Integration. BS 208 Sander Van der Linden, author of Foolproof: Why Misinformation Infects Our Minds and How to Build Immunity. BS 209 Luiz Pessoa returned to talk about his new  The Entangled Brain: How Perception, Cognition, and Emotion Are Woven Together. BS 210 Basics of Neurotransmitters: a detailed introduction to neurotransmitters and the importance of receptor proteins. BS 211 Seth Grant returned for a record 6th time. We reviewed his career and discussed recent discoveries about how synaptic proteins change as we age. Grant is my favorite guest because he makes complex ideas accessible to listeners of all backgrounds. BS 212 (Encore) Thomas Metzinger, PhD, author of The Ego Tunnel: The Science of the Mind and the Myth of the Self. BS 213 Kevin J Mitchell, PhD returned to talk about his new book Free Agents: How Evolution Gave Us Free Will. Please visit http://brainsciencepodcast.com for the FREE episode transcript. Announcements: This is the last scheduled episode of Brain Science, but all episodes will continue to be available. Free content includes all review episodes, encore episodes and all episodes since December 2016. The entire back catalogue of Brain Science is available to Premium MyLibysn subscribers. This includes episode transcripts. Patreon supporters will continue to have access more recent transcripts and other content. The mobile called Brain Science Podcast remains free and MyLibsyn Premium subscribers can use it to access transcripts and other premium content. Please sign up for the the free Brain Science Newsletter Get updates about new content Get free gift "5 Things You Need to Know about YOUR Brain" Just text brainscience to 55444 to sign up. Connect on Social Media: Mastodon: https://neuromatch.social/@docartemis Twitter: @docartemis Facebook page: http://www.facebook.com/brainsciencepodcast Contact Dr. Campbell: Email: brainsciencepodcast@gmail.com

In this episode of The Struggling Scientists, we are honored to have Nobel Laureate, Martin Chalfie, as our special guest. Join us as professor Chalfie shares his remarkable journey in science, from the initial struggles in the lab to the groundbreaking discovery that would ultimately change the field of biology. Since he was kind enough to talk with us for over an hour this episode will be split into two parts. In episode 70 we ask him questions about his scientific career, how he almost decided he was not cut out to be a scientist, and of course his discovery about using GFP as a marker. In episode 71 we will talk about the impact winning a Nobel prize has on your life and how he missed the announcement of his own Nobel Prize!Discover the story behind his pivotal work with the green fluorescent protein (GFP) as a genetic tag in cells and C. Elegans. With candid insights into the challenges he faced, the collaborative efforts that led to success, and the impact of his findings, this episode promises to inspire and captivate scientists and science enthusiasts alike.If you have any questions, comments, suggestions, or papers we really need to read, you can reach out to us via our website: https://thestrugglingscientists.com/Would you like to know more about becoming a guest on our podcast or sponsoring us? Then please check out the information on our website!Find your next funding opportunity now with https://thestrugglingscientists.com/Astound and use the code StrugglingScientist for 25% discount Check out the amazing writing assistant Jenni at https://thestrugglingscientists.com/Jenni and use the code SCIENCE20 for 20% discount

BUFFALO, NY- November 22, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Antibiotics that target mitochondria extend lifespan in C. elegans.” Aging is a continuous degenerative process caused by a progressive decline of cell and tissue functions in an organism. It is induced by the accumulation of damage that affects normal cellular processes, ultimately leading to cell death. It has been speculated for many years that mitochondria play a key role in the aging process. In this new study, researchers Gloria Bonuccelli, Darren R. Brooks, Sally Shepherd, Federica Sotgia, and Michael P. Lisanti from the University of Salford aimed to characterize the implications of mitochondria in aging using Caenorhabditis elegans (C. elegans) as an organismal model. The C. elegans were treated with a panel of mitochondrial inhibitors and assessed for survival. “In our study, we assessed survival by evaluating worm lifespan, and we assessed aging markers by evaluating the pharyngeal muscle contraction, the accumulation of lipofuscin pigment and ATP levels.” Their results show that treatment of worms with either doxycycline, azithromycin (inhibitors of the small and the large mitochondrial ribosomes, respectively), or a combination of both, significantly extended median lifespan of C. elegans, enhanced their pharyngeal pumping rate, reduced their lipofuscin content and their energy consumption (ATP levels), as compared to control untreated worms, suggesting an aging-abrogating effect for these drugs. Similarly, DPI, an inhibitor of mitochondrial complex I and II, was capable of prolonging the median lifespan of treated worms. On the other hand, subjecting worms to vitamin C, a pro-oxidant, failed to extend C. elegans lifespan and upregulated its energy consumption, revealing an increase in ATP level. “Therefore, our longevity study reveals that mitochondrial inhibitors (i.e., mitochondria-targeting antibiotics) could abrogate aging and extend lifespan in C. elegans.” DOI - https://doi.org/10.18632/aging.205229 Corresponding authors - Michael P. Lisanti - m.p.lisanti@salford.ac.uk, and Federica Sotgia - f.sotgia@salford.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205229 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, C. elegans, lifespan, lipofuscin, antibiotics, mitochondria, metabolism, DPI About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Med Marcus Wilberg, Joachim Wernersson, Viktor Kjellander och Axel Insulander.

Weird little mouths! Hairy skin tubes! Demon nematodes! Antarctic explorer and Nematologist Dr. Holly Bik charms us into loving deep sea (benthopelagic) worms in a way you never thought possible. We also cover tiny worm brains, the smell of Antarctic mud, first-generation Ph.Ds, the research workhorse C. Elegans, deep sea mining machines, moisturizers, submersibles and more with a worm lady who has literally traveled to the ends of the Earth to ask: what's in that mud? We love her. Visit Dr. Holly Bik's website and lab and follow her on Twitter and TikTokA donation went to EarthjusticeMore episode sources and linksSmologies (short, classroom-safe) episodesOther episodes you may enjoy: SPOOKTOBER episodes, Maritime Archaeology (SHIPWRECKS), Medusology (JELLYFISH), Toxinology (JELLYFISH VENOM), Vampirology (VAMPIRES), Oceanology (OCEANS), Planariology (VERY COOL WORMS, I PROMISE)Sponsors of OlogiesTranscripts and bleeped episodesBecome a patron of Ologies for as little as a buck a monthOlogiesMerch.com has hats, shirts, stickers, totes!Follow @Ologies on Twitter and InstagramFollow @AlieWard on Twitter and InstagramEditing by Mercedes Maitland of Maitland Audio Productions and Jarrett Sleeper of MindJam MediaTranscripts by Emily White of The WordaryWebsite by Kelly R. DwyerTheme song by Nick Thorburn

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.04.552031v1?rss=1 Authors: Lang, C. F., Anneken, A., Munro, E. Abstract: The PAR polarity network is a paradigmatic example of how systems of mutually antagonism interactions among peripheral membrane binding proteins allow them to form and maintain complementary polar domains in response to a transient polarizing cue. The oligomeric scaffolding protein PAR-3 has emerged as a keystone member of the PAR network in many different contexts. In early C. elegans embryos, PAR-3 is required for all other PAR asymmetries, and it can form stable unipolar asymmetries when its known inhibitors are absent and all other members of the PAR network are cytoplasmic or spatially uniform on the membrane. But how PAR-3 forms stable unipolar asymmetries absent mutual antagonism is unknown. Here we combine single particle analysis with quantitative modeling and experimental manipulations to determine how the dynamics of PAR-3 membrane binding, oligomerization and dissociation allow PAR-3 to maintain stable asymmetries in the one cell C. elegans embryo. We find that two forms of positive feedback contribute to sustaining PAR-3 asymmetries: First, a sharp size-dependent decrease in oligomer dissociation rates makes the effective dissociation rate of PAR-3 decrease sharply with its membrane density. Second, membrane-bound PAR-3 promotes additional binding of PAR-3 to the membrane through a mechanism that requires the presence of anterior polarity proteins CDC-42, PAR-6 and PKC-3. Through a combination of modeling and quantitative measurements, we show that these two feedback loops are sufficient to dynamically stabilize asymmetries of the magnitude observed in polarized C. elegans zygotes. These results establish a dynamic basis for stabilizing monopolar PAR-3 asymmetries; they underscore a crucial role for the oligomerization and add to the growing body of evidence that point to a central role for oligomerization of peripheral membrane proteins in the establishment and maintenance of cell polarity. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 13, entitled, “Predicting lifespan-extending chemical compounds for C. elegans with machine learning and biologically interpretable features.” Recently, there has been a growing interest in the development of pharmacological interventions targeting aging, as well as in the use of machine learning for analyzing aging-related data. In this new study, researchers Caio Ribeiro, Christopher K. Farmer, João Pedro de Magalhães, and Alex A. Freitas from the University of Kent and University of Birmingham use machine learning methods to analyze data from DrugAge, a database of chemical compounds (including drugs) modulating lifespan in model organisms. “To this end, we created four types of datasets for predicting whether or not a compound extends the lifespan of C. elegans (the most frequent model organism in DrugAge), using four different types of predictive biological features, based on: compound-protein interactions, interactions between compounds and proteins encoded by aging-related genes, and two types of terms annotated for proteins targeted by the compounds, namely Gene Ontology (GO) terms and physiology terms from the WormBase's Phenotype Ontology.” To analyze these datasets, the researchers used a combination of feature selection methods in a data pre-processing phase and the well-established random forest algorithm for learning predictive models from the selected features. In addition, they interpreted the most important features in the two best models in light of the biology of aging. One noteworthy feature was the GO term “Glutathione metabolic process”, which plays an important role in cellular redox homeostasis and detoxification. The team also predicted the most promising novel compounds for extending lifespan from a list of previously unlabelled compounds. These include nitroprusside, which is used as an antihypertensive medication. “Overall, our work opens avenues for future work in employing machine learning to predict novel life-extending compounds.” Read the full paper: DOI: https://doi.org/10.18632/aging.204866 Corresponding Authors: Caio Ribeiro - C.E.Ribeiro@kent.ac.uk, and Alex A. Freitas - A.A.Freitas@kent.ac.uk Keywords: lifespan-extension compounds, longevity drugs, machine learning, feature selection Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.https://doi.org/10.18632/aging.204866 About Aging-US: Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.21.549990v1?rss=1 Authors: Fujii, K., Kondo, T., Kimura, A. Abstract: The centrosome is a major microtubule-organizing center in animal cells. The intracellular positioning of the centrosomes is important for proper cellular function. One of the features of centrosome positioning is the spacing between centrosomes. The spacing activity is mediated by microtubules extending from the centrosomes; however, the underlying mechanisms are not fully understood. To characterize the spacing activity in the Caenorhabditis elegans embryo, a genetic setup was developed to produce enucleated embryos. The centrosome duplicated multiple times in the enucleated embryo, which enabled us to characterize the chromosome-independent spacing activity between sister and non-sister centrosome pairs. We knocked down genes in the enucleated embryo and found that the timely spacing was dependent on cytoplasmic dynein. Based on these results, we propose a stoichiometric model of cortical and cytoplasmic pulling forces for the spacing between centrosomes. We also found a dynein-independent but non-muscle myosin II-dependent movement of the centrosomes in a later cell cycle phase. The dynein-dependent spacing mechanisms for positioning the centrosomes revealed in this study is likely functioning in the cell with nucleus and chromosomes, including the processes of centrosome separation and spindle elongation. 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/2023.07.15.549072v1?rss=1 Authors: Boor, S. A., Meisel, J. D., Kim, D. H. Abstract: Animal internal state is modulated by nutrient intake, resulting in behavioral responses to changing food conditions. DAF-7 is a neuroendocrine TGF-beta ligand that regulates diverse food-related behaviors of Caenorhabditis elegans, including foraging behavior. Here, we show that in C. elegans, interoceptive cues from the ingestion of bacterial food inhibit the expression of DAF-7, a neuroendocrine TGF-beta ligand, from the ASJ pair of sensory neurons, whereas food deprivation in the presence of external chemosensory cues from bacteria promotes the expression of DAF-7 from the ASJ neurons. We show that SCD-2, the C. elegans ortholog of mammalian Anaplastic Lymphoma Kinase (ALK), which has been implicated in the central control of metabolism of mammals, functions in the AIA interneurons to regulate foraging behavior and cell-non-autonomously control the expression of DAF-7 from the ASJ neurons. Our data establish an SCD-2-dependent neuroendocrine DAF-7 gene expression feedback loop that couples the ingestion of bacterial food to foraging behavior. 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/2023.07.10.548405v1?rss=1 Authors: Schwartz, A. Z., Abdu, Y., Nance, J. Abstract: Rapid and conditional protein depletion is the gold standard genetic tool for deciphering the molecular basis of developmental processes. Previously, we showed that by conditionally expressing the E3 ligase substrate adaptor ZIF-1 in Caenorhabditis elegans somatic cells, proteins tagged with the first CCCH Zn finger (ZF1) domain from the germline regulator PIE-1 degrade rapidly, resulting in loss-of-function phenotypes. The described role of ZIF-1 is to clear PIE-1 and several other CCCH Zn finger proteins from early somatic cells, helping to enrich them in germline precursor cells. Here, we show that proteins tagged with the PIE-1 ZF1 domain are subsequently cleared from primordial germ cells in embryos and from undifferentiated germ cells in larvae and adults by ZIF-1. We harness germline ZIF-1 activity to degrade a ZF1-tagged heterologous protein from PGCs and show that its depletion produces phenotypes equivalent to those of a null mutation. Our findings reveal that ZIF-1 switches roles from degrading CCCH Zn finger proteins in somatic cells to clearing them from undifferentiated germ cells, and that ZIF-1 activity can be harnessed as a new genetic tool to study the early germ line. 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/2023.07.05.547674v1?rss=1 Authors: Demirbas, B., Filina, O., Louisse, T., Goos, Y., Sanchez-Romero, M. A., Olmedo, M., van Zon, J. Abstract: FOXO transcription factors are highly conserved effectors of insulin and insulin-like growth factor signaling, that are crucial for mounting responses to a broad range of stresses. Key signaling step is the stress-induced translocation of FOXO proteins to the nucleus, where they induce expression of stress response genes. Insulin signaling and FOXO proteins often control responses that impact the entire organism, such as growth or starvation-induced developmental arrest, but how body-wide coordination is achieved is poorly understood. Here, we leverage the small size of the nematode C. elegans, to quantify translocation dynamics of DAF-16, the sole C. elegans FOXO transcription factor, with single-cell resolution, yet in a body-wide manner. Surprisingly, when we exposed individual animals to constant levels of stress that cause larval developmental arrest, DAF-16/FOXO translocated between the nucleus and cytoplasm in stochastic pulses. Even though the occurrence of translocation pulses was random, they nevertheless exhibited striking synchronization between cells throughout the body. DAF-16/FOXO pulse dynamics were strongly linked to body-wide growth, with isolated translocation pulses causing transient reduction of growth and full growth arrest observed only when pulses were of sufficiently high frequency or duration. Finally, we observed translocation pulses of FOXO3A in mammalian cells under nutrient stress. The link between DAF-16/FOXO pulses and growth provides a rationale for their synchrony, as uniform proportions are only maintained when growth and, hence, pulse dynamics are tightly coordinated between all cells. Long-range synchronization of FOXO translocation dynamics might therefore be integral also to growth control in more complex animals. 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/2023.07.04.547705v1?rss=1 Authors: Labarre, A., Schramm, E., Pilliod, J., Boyer, S., Lapointe, M., Maios, C., Leclerc, N., Parker, A. Abstract: In several neurodegenerative diseases including Alzheimer's disease (AD), tau, a microtubule-associated protein (MAP) enriched in the axon, becomes hyperphosphorylated, detaches from microtubules, redistributes to the somato-dendritic compartment and self-aggregates. The mechanisms leading to neuronal dysfunction and death by tau pathology remain to be fully elucidated. C. elegans has been successfully used by several groups including ours to identify mechanisms involved in neurodegeneration. We generated three strains, one overexpressing wild-type human tau (WT Tau), one a tau mutant mimicking hyperphosphorylation (hyperP Tau) and one preventing phosphorylation (hypoP Tau) in GABA motor neurons. A significant reduction of body size and egg laying was noted in these tau strains. Starting at day 1, we found that the worms overexpressing hyperP Tau were smaller than the N2 control strain and the worms either overexpressing WT Tau or hypoP Tau. Starting at day 5, the worms overexpressing WT Tau were smaller than control and the worms overexpressing hypoP Tau. Egg laying was reduced in both hyperP Tau and WT Tau worms. Survival was only decreased in WT Tau worms. Motility deficits were also observed. For age-dependent paralysis, a difference was noted between control and hyperP Tau. Swimming activity and speed were increased in hypoP Tau and decreased in hyperP Tau strains. Axonal integrity was altered in all tau strains. In the case of synaptic activity, at day 1, it was increased in the hypoP Tau strain and decreased in the hyperP Tau one. Collectively, our data revealed that overexpression of tau exerted neuronal and peripheral defects indicating that tau dysfunction could affect cell cell communication. 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/2023.06.28.546823v1?rss=1 Authors: Chauve, L., McLysaght, A., McGarry, A., Butler, L. Abstract: Gene duplications play a major evolutionary role by providing raw material for functional innovation. Whole Genome Duplication (WGD), or polyploidization, is a particular case of duplication encompassing the entire genome and has been implicated in evolutionary diversification. In plants, WGD is recognized as a major evolutionary force, and is linked to speciation and the ability to resist periods of stress and of environmental upheaval. In animals, examples of current polyploid species are rarer, but multiple ancient events are known, including the charismatic two rounds (2R) of WGD that occurred during early vertebrate evolution. The conditions favouring the success of polyploid lineages are unclear. One debated hypothesis states that polyploidy is adaptive in the short-term, however this has never been studied in animals. In this study, we investigated the consequences of polyploidy on physiology and stress resistance in Caenorhabditis elegans, where tetraploidy can be artificially constructed. Our results reveal that although tetraploidy reduces fitness by decreasing fertility and lifespan in regular conditions, tetraploid animals exhibit increased resilience under specific stress conditions related to temperature changes. While neotetraploid animals exhibit similar pathogen resistance, their response to heat stress is altered. They exhibit modest improvement in thermotolerance and prolonged hsp (heat shock protein) mRNA induction upon heat shock (HS) accompanied by altered hsp-16.2 nuclear localization upon HS. Most notably, under severe cold stress, gravid neotetraploids animals massively escape cold-induced death, and generate more progeny than diploid animals. These results suggest a potential adaptive value of tetraploidy under cold stress and might help explain recent correlations found between the frequency of extant animal polyploids and regions experiencing recent glaciation and large temperature variation. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Lead Story: The conserved endocannabinoid anandamide modulates olfactory sensitivity to induce hedonic feeding in C. elegans  Current Biology Laboratory worm Caenorhabditis elegans apparently gets the ‘munchies' when exposed to cannabis. After soaking in an endocannabinoid bath, worms preferred to eat nutrient-rich, rather than nutrient-poor, bacteria. They fed for longer than worms not exposed to endocannabinoid or worms without working endocannabinoid receptors. This shared trait points to the deep evolutionary origin of cannabinoid receptors and behaviors influenced by the molecules. Read this issue of the ASAM Weekly Subscribe to the ASAM Weekly Visit ASAM

Listen to a blog summary of a trending research paper published in Volume 15, Issue 3 of Aging (Aging-US), entitled, "The lipidomes of C. elegans with mutations in asm-3/acid sphingomyelinase and hyl-2/ceramide synthase show distinct lipid profiles during aging." __________________________________________________ Lipids are a diverse group of biomolecules that are essential for life, including fats, oils, waxes, and steroids, and play crucial roles in cell membrane structure, energy storage and signaling. Lipidomics is the comprehensive analysis of lipids and their interactions in biological systems, with an aim to understand the role of lipids in cellular processes and their association with diseases. As we age, our cells undergo complex changes, including alterations in cellular lipid profiles. These changes are not only confined to humans; organisms such as the nematode Caenorhabditis elegans (C. elegans) are also subject to changes in lipid composition during aging. “For example, lipid classes including fatty acids (FA), triacylglycerols (TAG), sphingolipids (SL), and phospholipids (PL) have been identified as targets in lipid signatures related to aging [2, 3]. Furthermore, specific signatures are detected in the lipid profiles of those with age-related diseases, such as Alzheimer's Disease [4–9]. In addition, the abundance of many fatty acid subtypes differs between the youth, elderly, and centenarians [10, 11].” In a recent study, researchers Trisha A. Staab, Grace McIntyre, Lu Wang, Joycelyn Radeny, Lisa Bettcher, Melissa Guillen, Margaret P. Peck, Azia P. Kalil, Samantha P. Bromley, Daniel Raftery, and Jason P. Chan from Marian University, the University of Washington and Juniata College investigate the lipid profiles of C. elegans with mutations in the genes asm-3/acid sphingomyelinase and hyl-2/ceramide synthase during aging. On February 13, 2023, their research paper was published in Aging's Volume 15, Issue 3, entitled, “The lipidomes of C. elegans with mutations in asm-3/acid sphingomyelinase and hyl-2/ceramide synthase show distinct lipid profiles during aging.” Full blog - https://aging-us.org/2023/02/the-role-of-lipids-in-aging-insights-from-c-elegans/ DOI - https://doi.org/10.18632/aging.204515 Corresponding author - Jason P. Chan - jpchan@me.com Keywords - lipidomics, aging, sphingolipid metabolism, C. elegans, fatty acid metabolism About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

This month's episode is an encore presentation of an interview with Dr. Guy Caldwell from the University of Alabama. Dr. Caldwell explains how tools from molecular biology make it possible to use the famous C. Elegans roundworm to improve our understanding of neurodegenerative diseases like Parkinson's disease. Dr. Caldwell will return to Brain Science next month to give us an update on his work. Links and References: Visit the Wormshack at the University of Alabama Molecular neurodegeneration, 14(1), 29. https://doi.org/10.1186/s13024-019-0329-1 C. elegans Alpha-Synuclein Models of Parkinson's Disease. Brain sciences, 9(4), 73. https://doi.org/10.3390/brainsci9040073 See show notes for BSP 59 for additional references. Scroll up or click here for the free episode transcript.     Listener Support is greatly appreciated:   brainsciencepodcast.com/donations  Announcements: Please take a few minutes to complete this audience survey. Contact Dr. Campbell if you are interested a listener meet-up or sponsoring a talk by Dr. Campbell during her trip to Europe in April 2023. Please subscribe or follow Brain Science in your favorite audio app and please share it with others. Get free gift "5 Things You Need to Know about YOUR Brain when you sign up for the free Brain ScienceNewsletter to get show notes automatically every month. You can also text brainscience to 55444 to sign up. Check out the Brain Science podcast channel on YouTube Support Brain Science by buying Are You Sure? The Unconscious Origins of Certainty by Virginia "Ginger" Campbell, MD. (Autographed copies are available) Check out the free Brain Science Mobile app for iOS, Android, and Windows. (It's a great way to get both new episodes and premium content.) Learn more ways to support Brain Science at http://brainsciencepodcast.com/donations Connect on Social Media: Twitter: @docartemis Facebook page: http://www.facebook.com/brainsciencepodcast Contact Dr. Campbell: Email: brainsciencepodcast@gmail.com

A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 1, entitled, “The innate immune signaling component FBXC-58 mediates dietary restriction effects on healthy aging in Caenorhabditis elegans.” Dietary restriction (DR) is a highly effective and reproducible intervention that prolongs longevity in many organisms. The molecular mechanism of action of DR is tightly connected with the immune system; however, the detailed mechanisms and effective downstream factors of immunity that mediate the beneficial effects of DR on aging remain unknown. In this new study, researchers Jeong-Hoon Hahm, Farida S. Nirmala, Pyeong Geun Choi, Hyo-Deok Seo, Tae Youl Ha, Chang Hwa Jung, and Jiyun Ahn from the Korea Food Research Institute and the University of Science and Technology (in Daejeon, South Korea) investigated the immune signaling that mediates DR effects. The team used Caenorhabditis elegans (C. elegans) to understand the underlying molecular mechanisms of aging and immunity. “We found that the F-box gene, fbxc-58, a regulator of the innate immune response, is a novel mediator of DR effects on extending the health span of C. elegans.” Fbxc-58 is upregulated by DR and is necessary for DR-induced lifespan extension and physical health improvement in C. elegans. Furthermore, through DR, fbxc-58 prevents disintegration of the mitochondrial network in body wall muscle during aging. The researchers found that fbxc-58 is a downstream target of the ZIP-2 and PHA-4 transcription factors, the well-known DR mediator, and fbxc-58 extends longevity in DR through an S6 kinase-dependent pathway. Thus, the team proposed that fbxc-58 may provide a new mechanistic understanding of the effects of DR on healthy aging and elucidate the signaling mechanisms that link immunity and DR effects with aging. “Thus, we propose that investigating the molecular mechanism of action of F-box proteins, including fbxc-58, in DR will shed light on means to prevent sarcopenia and offer a potentially practical means of encouraging healthy aging via DR.” DOI: https://doi.org/10.18632/aging.204477 Corresponding Authors: Jeong-Hoon Hahm - hahmjh@kfri.re.kr, Jiyun Ahn - jyan@kfri.re.kr Keywords: dietary restriction, aging, innate immunity, F-box protein, Caenorhabditis elegans Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204477 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://youtube.com/Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ For media inquiries, please contact: media@impactjournals.com

Recently, Pope Francis used his Christmas speech to warn of an 'elegant demon' lurking in the shadows of the Church, one that 'does not make a loud entrance' but instead arrives with 'flowers in his hand'. Taken figuratively he is speaking of Roman Curia and the need of officials to be cautious of temptation. Taken literally there are plenty of actual demons which may fit the criteria of ‘elegant', such as Asmodeus, Lucifer, and Volac. For as 2 Corinthians warns, for "Satan himself masquerades as an angel of light." Thus, devil in all his forms appears as a savior and helper but also as a false prophet and anti-christ. This should make us all wonder about the things we keep close to us, the things we bring into our homes, and our definitions of monsters, or good and evil. Apparently, nothing is safe anymore from demonic influence. Santa Clause has been turned into a villain and online stories even talk about the seemingly harmless Elf on the Shelf being possessed by a spirit. We can't seem to escape this evil. It comes to us in holiday decorations, movies, tv, video games, comics, and children's toys. Even in sports, Aaron Rodgers, quarterback of the Green Bay Packers. says he is still haunted in 2022 by the Hat Man who appears to him holding dead rabbits. Interestingly, the rabbit seeks only pleasure and avoids conflict, the very essence of the 2022 word of the year, goblin mode. The new year 2023 is also the year of the rabbit.

Dr. Lorraine Kalia's research looks at testing different compounds in C. Elegans and how it can lead to a better understanding of Parkinson's disease and new therapeutic targets. The best part: some of these compounds are already approved for use in humans. Through Dr. Kalia's research we may be able to repurpose these compounds for the neurodegenerative condition.

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: AI Timelines via Cumulative Optimization Power: Less Long, More Short, published by jacob cannell on October 6, 2022 on LessWrong. TLDR: We can best predict the future by using simple models which best postdict the past (ala Bayes/Solomonoff). A simple model based on net training compute postdicts the relative performance of successful biological and artificial neural networks. Extrapolation of this model into the future leads to short AI timelines: ~75% chance of AGI by 2032. Cumulative Optimization Power[1]: a Simple Model of Intelligence A simple generalized scaling model predicts the emergence of capabilities in trained ANNs(Artificial Neural Nets) and BNNs(Biological Neural Nets): perf ~= P = CT For sufficiently flexible and efficient NN architectures and learning algorithms, the relative intelligence and capabilities of the best systems are simply proportional to net training compute or intra-lifetime cumulative optimization power P, where P = CT (compute ops/cycle training cycles), assuming efficient allocation of (equivalent uncompressed) model capacity bits N roughly proportional to data size bits D. Intelligence Rankings Imagine ordering some large list of successful BNNs(brains or brain modules) by intelligence (using some committee of experts), and from that deriving a relative intelligence score for each BNN. Obviously such a scoring will be noisy in its least significant bits: is a bottlenose dolphin more intelligent than an american crow? But the most significant bits are fairly clear: C. Elegans is less intelligent than Homo Sapiens. Now imagine performing the same tedious ranking process for various successful ANNs. Here the task is more challenging because ANNs tend to be far more specialized, but the general ordering is still clear: char-RNN is less intelligent than GPT-3. We could then naturally combine the two lists, and make more fine-grained comparisons by including specialized sub-modules of BNNs (vision, linguistic processing, etc). The initial theory is that P - intra-lifetime cumulative optimization power (net training compute) - is a very simple model which explains a large amount of the entropy/variance in a rank order intelligence measure: much more so than any other simple proposed candidates (at least that I'm aware of). Since P follow a predictable temporal trajectory due to Moore's Law style technological progress, we can then extrapolate the trends to predict the arrival of AGI. This simple initial theory has a few potential flaws/objections, which we will then address. Initial Exemplars I've semi-randomly chosen 15 exemplars for more detailed analysis: 8 BNNs, and 9 ANNs. Here are the 8 BNNs (6 whole brains and 2 sub-systems) in randomized order: Honey Bee Human Raven Human Linguistic Cortex Cat C. Elegans Lizard Owl Monkey Visual Cortex The ranking of the 6 full brains in intelligence is rather obvious and likely uncontroversial. Ranking all 8 BNNs in terms of P (net training compute) is still fairly obvious. Here are the 9 ANNs, also initially in randomized order: AlphaGo: First ANN to achieve human pro-level play in Go Deepspeech 2: ANN speech transcription system VPT: Diamond-level minecraft play Alexnet: Early CNN imagenet milestone, subhuman performance 6-L MNIST MLP: Early CNN milestone on MNIST, human level Chinchilla: A 'Foundation' Large Language Model GPT-3: A 'Foundation' Large Language Model DQN Atari: First strong ANN for Atari, human level on some games VIT L/14@336px: OpenAI CLIP 'Foundation' Large Vision Model Most of these systems are specialists in non-overlapping domains, such that direct performance comparison is mostly meaningless, but the ranking of the 3 vision systems should be rather obvious based on the descriptions. The DQN Atari and VPT agents are somewhat comparable to animal brains. How would you ran...

Britt is a postdoc in Erik Jorgensen's lab at the University of Utah after joining in October 2021. The lab studies the molecular basis of synaptic transmission, focusing on the mechanisms of synaptic vesicle fusion and synaptic vesicle regeneration, her research uses C. elegans. Britt earned her PhD in May 2020 from the University of Leeds which focussed on modeling single amino acid variants in the ryanodine receptor in C. elegans.

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: A concern about the “evolutionary anchor” of Ajeya Cotra's report on AI timelines., published by NunoSempere on August 16, 2022 on The Effective Altruism Forum. tl;dr: The report underestimates the amount of compute used by evolution because it only looks at what it would take to simulate neurons, rather than neurons in agents inside a complex environment. It's not clear to me what the magnitude of the error is, but it could range many, many orders of magnitude. This makes it a less forceful outside view. Background Within Effective Altruism, Ajeya Cotra's report on artificial general intelligence (AGI) timelines has been influential in justifying or convincing members and organizations to work on AGI safety. The report has a section on the "evolutionary anchor", i.e., an upper bound on how much compute it would take to reach artificial general intelligence. The section can be found in pages 24-28 of this Google doc. As a summary, in the report's own words: This hypothesis states that we should assume on priors that training computation requirements will resemble the amount of computation performed in all animal brains over the course of evolution from the earliest animals with neurons to modern humans, because we should expect our architectures and optimization algorithms to be about as efficient as natural selection. This anchor isn't all that important in the report's own terms: it only gets a 10% probability assigned to it in the final weighted average. But this bound is personally important to me because I do buy that if you literally reran evolution, or if you use as much computation as evolution, you would have a high chance of producing something as intelligent as humans, and so I think that it is particularly forceful as an "outside view". Explanation of my concern I don't buy the details of how the author arrives at the estimate of the compute used by evolution: The amount of computation done over evolutionary history can roughly be approximated by the following formula: (Length of time since earliest neurons emerged) (Total amount of computation occurring at a given point in time). My rough best guess for each of these factors is as follows: Length of evolutionary time: Virtually all animals have neurons of some form, which means that the earliest nervous systems in human evolutionary history likely emerged around the time that the Kingdom Animalia diverged from the rest of the Eukaryotes. According to timetree.org, an online resource for estimating when different taxa diverged from one another, this occurred around ~6e8 years ago. In seconds, this is ~1e16 seconds. Total amount of computation occurring at a given point in time: This blog post attempts to estimate how many individual creatures in various taxa are alive at any given point in time in the modern period. It implies that the total amount of brain computation occurring inside animals with very few neurons is roughly comparable to the amount of brain computation occurring inside the animals with the largest brains. For example, the population of nematodes (a phylum of small worms including C. Elegans) estimated to be ~1e20 to ~1e22 individuals. Assuming that each nematode performs ~10,000 FLOP/s,the number of FLOP contributed by the nematodes every second is ~1e21 1e4 = ~1e25; this doesn't count non-nematode animals with similar or fewer numbers of neurons. On the other hand, the number of FLOP/s contributed by humans is (~7e9 humans) (~1e15 FLOP/s / person) = ~7e24. The human population is vastly larger now than it was during most of our evolutionary history, whereas it is likely that the population of animals with tiny nervous systems has stayed similar. This suggests to me that the average ancestor across our entire evolutionary history was likely tiny and performed very few FLOP/s. I will as...

Richard Paige sits down with professors Erika Sorensen-Kamakian and Walter Novak and students Adam Berg '22 and Felix Valero-Davila '22, discussing gene editing round worms with the LOCKR protein, grant procedures, and co-laboratory collaboration (Episode 321).

El rover marciano descubre “vida” en Marte, Pedro descubre “vida” en código, y Javier descubre cómo escribir código en vida (aprendiendo JavaScript). Lo que no descubrimos es cómo extender la vida de una bombita de luz, y Javier roza la clandestinidad tratando de iluminar el misterio. Por último Pedro nos cuenta una nueva curiosidad sobre Japón.Notas del episodioUruguay es el mejor país (YouTube)Tiranos Temblad (YouTube)Foto de la “planta” marciana encontrada por el rover Curiosity (NASA)Foto del escarabajo y diente de spinosaurus de PedroOpenWormCharla TEDx sobre OpenWorm (YouTube)Video de OpenWorm controlando un robot (YouTube)Video de Veritasium sobre obsolencia programada de bombitas de luz (YouTube)Hiromi Go - Goldfinger 99 (YouTube)Ricky Martin - Livin' La Vida Loca (YouTube)Goldfinger - 99 Red Balloons (YouTube)Nena - 99 Luftballons (YouTube)

Flagship Interview Podcast:

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: We Haven't Uploaded Worms, published by jefftk on the LessWrong. In theory you can upload someone's mind onto a computer, allowing them to live forever as a digital form of consciousness, just like in the Johnny Depp film Transcendence. But it's not just science fiction. Sure, scientists aren't anywhere near close to achieving such feat with humans (and even if they could, the ethics would be pretty fraught), but now an international team of researchers have managed to do just that with the roundworm Caenorhabditis elegans. Science Alert Uploading an animal, even one as simple as c. elegans would be very impressive. Unfortunately, we're not there yet. What the people working on Open Worm have done instead is to build a working robot based on the c. elegans and show that it can do some things that the worm can do. The c. elegans nematode has only 302 neurons, and each nematode has the same fixed pattern. We've known this pattern, or connectome, since 1986. [1] In a simple model, each neuron has a threshold and will fire if the weighted sum of its inputs is greater than that threshold. Which means knowing the connections isn't enough: we also need to know the weights and thresholds. Unfortunately, we haven't figured out a way to read these values off of real worms. Suzuki et. al. (2005) [2] ran a genetic algorithm to learn values for these parameters that would give a somewhat realistic worm and showed various wormlike behaviors in software. The recent stories about the Open Worm project have been for them doing something similar in hardware. [3] To see why this isn't enough, consider that nematodes are capable of learning. Sasakura and Mori (2013) [5] provide a reasonable overview. For example, nematodes can learn that a certain temperature indicates food, and then seek out that temperature. They don't do this by growing new neurons or connections, they have to be updating their connection weights. All the existing worm simulations treat weights as fixed, which means they can't learn. They also don't read weights off of any individual worm, which means we can't talk about any specific worm as being uploaded. If this doesn't count as uploading a worm, however, what would? Consider an experiment where someone trains one group of worms to respond to stimulus one way and another group to respond the other way. Both groups are then scanned and simulated on the computer. If the simulated worms responded to simulated stimulus the same way their physical versions had, that would be good progress. Additionally you would want to demonstrate that similar learning was possible in the simulated environment. (In a 2011 post on what progress with nematodes might tell us about uploading humans I looked at some of this research before. Since then not much has changed with nematode simulation. Moore's law looks to be doing much worse in 2014 than it did in 2011, however, which makes the prospects for whole brain emulation substantially worse.) I also posted this on my blog. [1] The Structure of the Nervous System of the Nematode Caenorhabditis elegans, White et. al. (1986). [2] A Model of Motor Control of the Nematode C. Elegans With Neuronal Circuits, Suzuki et. al. (2005). [3] It looks like instead of learning weights Busbice just set them all to +1 (excitatory) and -1 (inhibitory). It's not clear to me how they knew which connections were which; my best guess is that they're using the "what happens to work" details from [2]. Their full writeup is [4]. [4] The Robotic Worm, Busbice (2014). [5] Behavioral Plasticity, Learning, and Memory in C. Elegans, Sasakura and Mori (2013). Thanks for listening. To help us out with The Nonlinear Library or to learn more, please visit nonlinear.org.

Join us for episode 62 of 17 minutes of Science as we talk with Dr. Jagan Srinivasan from Worcester Polytechnic Institute about his recently published paper using C. elegans to identify a sex-specific behavior.

For episode 58 of 17 minutes of Science we are joined by Dr. Oliver Blacque, an Associate Professor in cell biology and genetics at the University College Dublin. Dr. Blacque's research focuses primarily on cilia - understanding the molecular basis of their assembly, function, and links to human disease, specifically rare diseases. In his research, Dr. Blacque uses the C. elegans model and believes it is very well suited for his research. Tune in to episode 58 to learn more about cilia, how thy relate to human disease, and why C. elegans are such an ideal model for this type of research.

Chamaedorea elegans, the neanthe bella palm belongs to the Arecaceae family and is commonly known as parlor palm. It is ... Read more The post How to Care For Neanthe Bella Palm (Chamaedorea Elegans) appeared first on Plant Mom Care.

For episode 52 of 17 Minutes of Science we sat down with Dr. Valeria Vásquez from The University of Tennessee Health Science Center to talk about mechanosensitive channels - what are they, why are they important, and how is the Vasquez Lab utilizing C. elegans in their research. The Vásquez lab aims to understand the functional, structural, and molecular mechanism by which mechanosensitive channels respond to mechanical stimuli and help delineate a general framework for their roles in health and disease. The lab follows two main avenues: 1) in vitro biochemical and biophysical approaches to study protein-protein and protein-lipid interactions of bona fide mechanosensitive channel complexes, and 2) in vivo approaches to characterize mechanosensitive channels in C. elegans having novel physiological roles.

Hosts: Anna Brooks Allen and Audrey Best Guest: Dr. Guy Caldwell Dr. Caldwell studies neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease, and ALS by observing the model organism C. elegans in his lab called the Work Shack. He is a University Distinguished Research Professor at the University of Alabama.The researchers in the Caldwell lab investigate the molecular mechanisms of organismal regulation and metabolic response to protein stressors implicated in human neurological diseases including Parkinson's, Alzheimer's, and related disorders. The focus is on discovery of gene targets for therapeutic development and drug discovery, as well as environmental contributors to neurodegeneration using the nematode model system. For more information about The Caldwell Lab, check out his website: http://wormshack.ua.edu

For episode 44 of 17 Minutes of Science we are joined by Dr. Janis Weeks. Janis is a co-founder and chief global health officer at InVivo Biosystems in addition to being a Professor Emerita of Biology at the University of Oregon. Dr. Weeks is an expert in anthelmintic research, with experience and expertise in technology development for drug screening platforms, including anthelmintic (anti-nematode worm) drugs for human and animal health; nematode neurobiology and genetics; synaptic physiology; neural circuits for behavior; insect neurobiology; tropical infectious and parasitic diseases. Janis has taught neuroscience in Africa for 25 years, prompting her interest in neglected tropical diseases such as helminth infections. With funding from the Bill & Melinda Gates Foundation, she began working on parasitic nematodes to complement work in C. elegans. Her current research focuses on new technologies to advance research into anthelmintic drugs for animals & humans. Dr. Weeks joins us to talk about her recent paper which has been accepted pending minor revisions, Comparison of Electrophysiological and Motility Assays to Study Anthelmintic Effects in C. elegans.

For episode 40 of 17 Minutes of Science we are joined by Dr. Anne Hart, a neuroscience professor and Chair of Neuroscience at Brown University. Dr. Hart will be joining us to discuss her research using C. elegans which focuses on the molecular and cellular mechanisms underlying neurological disease, sensory signaling, sleep, and fatigue.

For episode 28 of 17 Minutes of Science, we are joined by Kyle Galford to discuss his recent publication, The FDA-approved drugs ticlopidine, sertaconazole, and dexlansoprazole can cause morphological changes in C. elegans. Kyle is a recent graduate of the University of Maryland (Spring 2019) where he worked with Dr. Antony Jose to conduct this research. Kyle now holds a sales position with Novogene. Kyle joins us to discuss the key findings of his research and why C. elegans were the ideal model for this study.

I had a wonderful conversation with Piyush Gupta, who is getting his PhD in Molecular Genetics, he's studying hibernation in C. Elegans, A type of microscopic worm, we talk about how his research could help with space travel and also touch on why science communication is important

Tune in weekly to our virtual series "Seventeen Minutes of Science" every Tuesday where we go live with a new guest each week to talk about how science and biotechnology is woven into their lives for (you guessed it) 17 minutes! This week's host is Sarah Cheesman, a Technical Solutions Scientist at InVivo Biosystems, who interviews Aaron Putzke, a professor at Whitworth University who uses both zebrafish and C. elegans in his lab. Take a listen to learn about more about how using multiple models, specifically zebrafish and C. elegans, has positively impacted Dr. Putzke's research and why he finds both models so interesting.