Podcasts about episode twenty six

Episode Twenty-Six features Mexican-French emerging artist Alexis de Chaunac. He was born in New York City and raised in Mexico City and Paris. As a child living in Mexico, he grew up surrounded by his mother’s family and his grandparent’s friends which included Mexican artists, intellectuals, historians, poets, diplomats, and writers. These brilliant minds had a profound impact on Alexis at an early age and as a result he draws from subjects such as literature, religion, art history and politics which overlap with his interests that include natural sciences, biology and botany. In April 2019, he exhibited at Sargent’s Daughters Gallery in New York. Alexis has also exhibited through group and solo shows in major museums in Mexico (Museo Carrillo Gil, Pinacoteca Diego Rivera) and at Zona MACO art fair in Mexico City. After receiving his BA from Sarah Lawrence College, Alexis is currently pursuing his MFA in the Painting and Drawing department at the School of the Art Institute of Chicago. Below are several links about Alexis de Chaunac’s work and those that influenced him as a child. Also included is the Jerry Saltz New York Magazine story stating that the exhibition “Vida Americana: Mexican Muralists Remake American Art, 1925–1945” at the Whitney Museum was one of the most relevant shows of the 21st century. Enjoy. https://www.alexisdechaunac.com/ http://columbiajournal.org/years-friendship-alexis-de-chaunac/ https://www.artsy.net/article/artsy-editorial-how-trilingual-painter-alexis-de-chaunac-wrestles-with https://www.whitewall.art/art/alexis-de-chaunac-a-dance-with-life-death https://www.vulture.com/2020/02/vida-americana-the-most-relevant-show-of-the-21st-century.html Influencers include https://en.wikipedia.org/wiki/Jos%C3%A9_Luis_Cuevas https://www.nytimes.com/1971/05/08/archives/cuevas-displays-his-mastery-of-line.html https://hammer.ucla.edu/radical-women/artists/ximena-cuevas https://www.imdb.com/name/nm7533624/ https://en.wikipedia.org/wiki/Octavio_Paz https://en.wikipedia.org/wiki/Homero_Aridjis

Hello and welcome to Episode Twenty Six of Page Turn: the Largo Public Library Podcast. After missing a month due to the SARS-CoV-2 pandemic we're back and so happy to be! I'm your host, Hannah! If you enjoy the podcast subscribe, tell a friend, or write us a review! The Spanish Language Book Review begins at 17:42 and ends 21:43 at The English Language Transcript can be found below But as always we start with Reader's Advisory! The Reader's Advisory for Episode Twenty Six is Speak No Evil by Uzodinma Iweala. If you like Speak No Evil you should also check out: Happiness, Like Water by Chinelo Okparanta, Every Kind of Wanting by Gina Frangello, and Where We Come From by Oscar Casares. My personal favorite Goodreads list Speak No Evil is on is Oooh Shiny! March 2018. Today’s Library Tidbit is all about tabletop gaming and Dungeons & Dragons. Tabletop game covers a very wide array of types of games, including chess, shogi, backgammon, mahjong, and go. However, Dungeons & Dragons specifically developed out of wargames. Wargames started as military training tools. The Prussian were the first known people to use tabletop wargaming and they did so for military training. Once the Prussian beat the French in the Franco-Prussian war wargaming became a more widely used training strategy and also spread to be a fun hobby. One of the more well known early wargames players was author H. G. Wells who created a rule book for a game called Little Wars that used toy soldiers, a large open area like a living room floor or a lawn, and spring loaded cannon to attack opponents with. Gary Gygax, a well known wargaming enthusiast, developed Dungeons & Dragons with Dave Arneson by adapting wargames by adding in fantasy elements. Some fantasy authors that influences Dungeons & Dragons include, but are very not limited to, J. R. R. Tolkien, Poul Anderson, Jack Vance, Fritz Leiber, and Lewis Carroll. Dungeons & Dragons is set up and the narrative run by a person called a Dungeon Master. This person is responsible for creating the dungeons (maps that the players go through), writing a narrative the players will be following, guiding the players using the narrative along the story path, playing the non-player characters and monsters, and oh yeah, keeping the rules. Players before starting the game role up a character sheet. A character sheet is where a player keeps track of their characters stats and inventory. Although D&D is famous for being played in person and on a shared “tabletop”, the game has a devoted online game scene in the modern day. Online D&D groups function the same as their offline counterparts with a Dungeon Master and a handful of players except instead of sharing a table, the group members meet over voice and video chat programs like Discord, Google Hangouts, Skype, or Zoom. If you're interested in playing Dungeons & Dragons online you can see if any friends have a group you could join, check out social media, and online discussion boards. Groups looking for new members or Dungeon Masters could post on D&D Beyond or the Looking For Group sub-reddit. You can also check out Facebook groups too! Several library workers here enjoy a variety of different types of tabletop gaming and we hope that if you’re interested that you look into trying out one using an online service. And now it's time for Book Traveler, with Victor: Intro: Welcome to a new episode of Book Traveler. My name is Victor and I am a librarian at the Largo Public Library. Today I am going to talk to you about a fiction book that we have in the Spanish collection entitled La Fruta del Borrachero by Ingrid Rojas Contreras. Synopsis: In this captivating debut, Ingrid Rojas uses by her own life to talk about the passage from childhood to adulthood of two powerful narrative voices. An exuberant story that, framed in one of the most convulsive times of Colombia, sheds light on the unexpected ties that can be born...

Ok, we typically don’t like to critique the casting choices with The Clone Wars, but hear us out-- there was a huge missed opportunity to cast Joe Pesci as Jedi Master Even Piell! What a miscarriage of justice! Well, you can hear us rant about this missed opportunity, big pig midgets, Captain Tarkin, Gungan pelts and we hit the jackpot when we learn all about Dok-Ondar’s Den of Antiquities! Turn up your headphones, dial back your sensibilities, and join the wretched hive of scum and villainy as we take the low road to resistance on Episode Twenty Six of Force Insensitive!Send Email/Voicemail: mailto:forceinsensitive@gmail.comStart your own podcast: https://www.buzzsprout.com/?referrer_id=386Use our Amazon link: http://amzn.to/2CTdZzKFB Group: https://www.facebook.com/groups/ForceInsensitive/Twitter: http://twitter.com/ForceNSensitiveFacebook: http://facebook.com/ForceInsensitiveInstagram: http://instagram.com/ForceInsensitive

Good Morning! Episode Twenty Six is available. Join Shavon and Sam as they discuss their top 4 dating deal breakers. Also, thank you for a great half year! Almost one and still going. *New Episodes Every Wednesday* Please remember: We aren't doctors or psychologists. We are just two women sharing our unsolicited opinions. Please note, chances are high, one or both of us could be completely wrong about a great many things said during our podcast, but that's what makes it interesting. Like, listen, and follow!

Episode Twenty Six of Ms. Demeanor & Ms. Conduct. A bi-weekly, light hearted look at all things mysterious in Canada. Tales of murder, mystery, conspiracy, cults & much more. Miss & Misters, this week Jena takes on the story of Edwin Alonzo Boyd and The Boyd Gang. Kennedy recounts the story of Evelyn and John Dick and the Torso Murders.⠀⠀⠀⠀

We are freaking back. Episode Twenty Six of the least informative but most entertaining NC State podcast in the entire world. THIS WEEK We have our annual co-host Taylor King contributing to the podcast, but instead of shunning him to the couch before his segment as we did last year, we bring him in for whole kitten caboodle. We ketchup on fruitful basketball recruiting, a scary basketball stretch oncoming, NCAA punishment talk, Yurt7 hair, Popeye's Chicken Sandwich review, and Mannie Fresh cucking Juvenile. Then it's time for a ketchup on our overrated and underwhelming football team with a couple of losses against Louisville at home and Georgia Tech on the road. Spoiler alert, no one is happy. We then dive in to the FIRE DAVE tweets and realize we have a very rabid fanbase that doesn't understand Twitter trolling. Second to last, we preview the Carolina game, with one of the most heated takes on how much they will actually beat us by in the end. FINALLY We have a Six Pack ranking late night trash foods and if you have listened this far, you realize you have ran into the best content.

Welcome to Episode Twenty-Six of Strange Pleasures Radio Lab. Your daily audio story podcast available through iTunes, Spotify and YouTube.Each day I will narrate a well known story in it's entirety. As a writer I will also include some narration of my own books that can be purchased through the Amazon Kindle Store, or through the Amazon Prime Kindle Unlimited subscription program.Today I will be narrating Part Ten the conclusion of The Lair Of The White Worm by Bram StokerYOUTUBE: https://www.youtube.com/channel/UC8MoqBN8-vdAsaoYBZX32OA?viewas=subscriber?subconfirmation=1HOME WEBSITE https://strange-pleasures-radiolab.pinecast.co/SPOTIFY https://open.spotify.com/show/6x2VOcohjOKeJ8ZIJpvi8rAMAZON AUTHOR PAGE https://www.amazon.co.uk/Robert-Knight/e/B07WH3QCML/ref=dpbylinecontpopebooks_1ITUNES https://podcasts.apple.com/gb/podcast/strange-pleasures-radiolab/id1476208251STRANGE PLEASURES VIDEO LAB: gaming channel with new content daily https://www.youtube.com/channel/UC0wqchZzHfwHTUdfnc5s6ggSupport Strange Pleasures Radiolab by donating to their Tip Jar: https://tips.pinecast.com/jar/strange-pleasures-radiolabFind out more at https://strange-pleasures-radiolab.pinecast.coThis podcast is powered by Pinecast.

Episode Twenty-Six features guest Disco Dracula back again, y'all, with host Captain Death, for another fun little episode where we talk about OUR WIVES. lol jk, we gonna die forever alone. I think we discussed Disney Channel Original Movies in the last episode, but WE TALK ABOUT THEM AGAIN, SO GET OVER IT. Then we read the chronicling of Madison the funny Unsettling Stories Girl. Good times. My Wife Didn't Want Me to Go into the Bedroom(14:43)My Wife(19:59)Madison's Stories(from Unsettling Stories)(32:17)CHECK THE YOUTUBE for EPs! SUBSCRIBE @https://www.youtube.com/channel/UCxoqIN-fkfdlmGEjWujypxwFeaturing wonderful ambient music from our fam in Sweden: CryoChamber, givin' us all the ooky-spooky tunage. Follow: @cryo-chamberThank you!"Are You Afraid of the Dark Theme Song," "Spooky Skeletons REMIX," and "You Reposted in the Wrong Neighborhood" are not my songs. Credit and All rights are reserved by the owners

Episode Twenty-Six of IdeaPod. In this episode, we teach you new brainstorm techniques. At the end of the podcast you should be able to utilize these techniques and start brainstorming away. Read More The post #26 Two Great Lists, One Killer Combo appeared first on Bandwidth Marketing.

Episode Twenty Six of Hairy London

Episode Twenty Six

[intro music]   Host – Dan Keller Hello, happy new year, and welcome to Episode Twenty-Six of Multiple Sclerosis Discovery, the podcast of the MS Discovery Forum. I’m your host, Dan Keller.   This week’s podcast features an interview with Tim Kennedy about remyelination and neural development. But to begin, here is a brief summary of some of the latest developments on the MS Discovery Forum at msdiscovery.org.   According to a new clinical trial, azathioprine, or AZA, may be as effective as interferon beta. The generic immunosuppressant was effective in both reducing relapses and reducing new brain lesions in the multicenter trial. This may not be surprising since the drug has been used off-label to treat MS for several decades. If trials continue to go well, AZA may become the go-to alternative for patients who can’t afford brand name interferons.   A pair of Canadian studies recently showed that both neurodegeneration and inflammation may start in the early stages of pediatric multiple sclerosis. One team found epitope spreading in the blood of children shortly after the onset of MS, suggesting a potential new diagnostic tool. Though children comprise only 2 to 10 percent of the MS population, data gleaned from them may provide insights into the disease as a whole.   If you enjoyed our end-of-the-year interview with Alan Alda and find MSDF to be helpful, please consider supporting us with a donation. We share Mr. Alda’s philosophy that closing the gaps between scientific disciplines is key to improving scientific progress. To make a donation, visit msdiscovery.org and click on the green “Support MSDF” button next to “Research Resources”.   [transition music]   Now to the interview. Tim Kennedy is a researcher at the Montreal Neurological Institute. He met with MSDF to talk about the role of certain molecules and receptors necessary for oligodendrocyte development, maintenance, and function and their implications for remyelination.   Interviewer – Dan Keller Welcome, Dr. Kennedy. Let's talk about the life of oligodendrocytes. These are important for myelination and probably play a role in remyelination. What is the life of an oligodendrocyte? How does it start out? And what does it react to?   Interviewee – Tim Kennedy Many labs around the world have been studying the life history of an oligodendrocyte and also the lineage of the cells and how they differentiate during normal development. One of the reasons for doing this is that oligodendrocyte precursor cells are present in the mature nervous system and almost certainly contribute to remyelination in demyelinating diseases like MS. Oligodendrocyte precursors are born in the early embryonic CNS, and from the very restricted regions where they're born they then migrate away to populate all of the regions of the mature CNS where myelin occurs. In the lab here, we've been very interested in the molecular cues that direct and influence oligodendrocyte precursor migration. These include a family of proteins called netrins that we work on. And receptors for netrin like a protein called DCC. DCC stands for deleted in colorectal cancer. It was originally identified in cancer, and we now know that it has a critical role in the central nervous system in the migration, maturation, and maintenance of myelin by mature oligodendrocytes.   MSDF Some of these molecules take on different functions as the oligodendrocytes mature. How do they react, or what do these molecules do over time?   Dr. Kennedy When an oligodendrocyte precursor is born, it makes the netrin receptor DCC, but it doesn't make netrin. What the cell does is it responds to netrin in the environment, and through DCC reacts to it, and the netrin directs the cells to migrate. It tells them to initially migrate away from the position where they're born and sends them in the direction of axon tracks that require myelination. In mature myelinating oligodendrocytes, one of the huge surprises we had is that both of these proteins are made. Now, both netrin and DCC are required for normal neural development. If we examine a conventional knockout mouse that lacks either netrin-1 or DCC, those mice die within a few hours of being born, and there's a massive disorganization of the nervous system. So these are essential for normal neural development. When we look at the mature nervous system, we see that every single oligodendrocyte, every single mature myelination oligodendrocyte, makes readily detectable levels of netrin-1 and also the receptor for netrin-1, DCC. And a very simple statement of the question that we wanted to answer is what's the point of that? Why do these cells make these proteins that are essential for normal neural development but make them in the adult nervous system? In every adult human that we encounter, every single person, we're making netrin-1 and DCC in our brains right now. So what's the point? One of the functions that we've recently identified is that DCC produced by oligodendrocytes is required for the maintenance of myelin. Now what that means is that initially when we looked at the distribution of netrin-1 and DCC in relation to myelin we see that they're enriched at paranodal junctions. Paranodes are at the ends of internodes that are the regions of compact myelin that wrap and insulate an axon. The paranodes are a specialization that's made by the oligo that then connects it and ties it down to the surface of the axon. The paranodes flank the node of Ranvier, which is the key point, the specialized region along an axon that regenerates the action potential. So if we think of the internode of compact myelin as the region where the oligodendrocyte insulates the axon and allows the action potential to jump from node to node, the paranodes are the specializations at the end that tie it down. Now, the paranode is where we see the netrin and DCC enriched. If we take away either netrin-1 or DCC from oligodendrocytes, what we see is that the paranodes begin to come apart. Now in a very recent publication, what we did was use a genetic trick called cre-lox recombination to selectively take DCC out of mature myelinating oligodendrocytes. In these mice, the mice develop perfectly normally, the nervous system develops normally, the myelin develops normally. But then, at two months of age, we induce the deletion of DCC only from oligodendrocytes. Now having taken DCC out of oligodendrocytes, what we see is that first the paranodal junctions start to come apart, and then as we let the mice age the compact myelin itself starts to become disorganized. Now, that's interesting because what we're able to document in these mice is a progressive disorganization of the myelin produced by the oligodendrocyte. The progression is interesting, obviously, because we believe that this has identified a new mechanism that maintains myelin, and we would then relate that to the progression of demyelinating disorders like multiple sclerosis. A consequence of having lost DCC is that the action potential conduction velocity in the nervous system is delayed, and when we look at the mice themselves – and look at their behavior, put them through behavioral tests – what we see is that they become uncoordinated and slower in their movements. So again, this would all be consistent with this disruption of the myelin along the axons in the central nervous system due to the loss of DCC. And it's an indication that DCC being made by oligodendrocytes is absolutely essential to maintain the appropriate organization of myelin.   MSDF That explains why myelin may become disorganized. Now, if there is a state in which it's already disorganized, which we look at someone with MS, is there any indication here how to remyelinate knowing what you now know about what's required for maintenance of myelin?   Dr. Kennedy Certainly. What's really exciting having found that DCC is essential to maintain myelin is that this is a new biochemical mechanism that is required to organize and maintain the structural paranodal junctions, and that that's critical for the integrity and the maintenance of compact myelin. Now, DCC is a transmembrane receptor, and every single component of the signal transduction pathway downstream of DCC is potentially a drug target that could be manipulated to enhance the maintenance of myelin. So this is a new biochemical mechanism that exists in oligodendrocytes that promotes myelin maintenance. And that has enormous potential for trying to encourage the persistence of myelin in demyelinating disease.   MSDF What about remyelination? I think you've said oligodendrocytes are born to myelinate. What's stopping them?   Dr. Kennedy If we go back to the oligodendrocyte precursor in early development, what our studies of the developing nervous demonstrated was that oligodendrocyte precursors are repelled by netrin-1. The normal function of netrin-1 in the early embryo is to drive oligodendrocyte precursors away from where they're born so that they can go out into the rest of the central nervous system, find axons that need to be myelinated and myelinate them. That indicates that in the early embryo netrin-1 is a repellent for these cells. Again, we recently reported that in human MS plaques netrin-1 is present in those plaques. Where that's likely coming from is from the wreckage of cells that have died in those plaques. So I had said that mature myelinating oligodendrocytes express netrin-1. When those cells die and when the myelin is lost, the debris from those cells remains behind and potentially even builds up in plaques. There are a number of inhibitors of oligodendrocyte precursor migration that we now know are present in human MS plaques. These include proteins like chondroitin sulfate proteoglycans, semaphorins, and now netrin. What that strongly suggests is that when oligodendrocyte precursors are migrating in the adult brain to sites of demyelination with the intention of remyelinating an axon that has been demyelinated these inhibitors will very likely prevent those cells from entering the plaque and doing what they were born to do, which is to remyelinate. A very exciting thing about MS research today is that we know that the brain contains stem cells that produce oligodendrocyte precursor cells that readily give birth to these cells. So all of us have oligodendrocyte precursor cells in our head. Those cells are born to myelinate. They will migrate towards plaques where demyelination has happened, and if they're allowed to enter the plaque find the axon that needs to be remyelinated. And if they can be encouraged to overcome whatever it is that is blocking them from remyelinating, potentially that aspect of MS remyelination could be encouraged to happen.   MSDF Do you have some ideas on how to overcome this blockage either clearing away the debris or making the oligodendrocytes insensitive to the inhibitors and the debris?   Dr. Kennedy Both of those approaches would be very appropriate. So encouraging the nervous system to clear away the debris we would predict that that would encourage remyelination to happen. In addition, although I said there were multiple inhibitors present in MS plaques – and those inhibitors have different receptors – downstream of those receptors it's very likely that common signal transduction mechanisms are engaged. So targeting those common signal transduction mechanisms inside the migrating oligodendrocyte precursor cell could very potentially nullify all of the inhibitors at once. If it was possible to turn off the sensitivity to those inhibitors, then we would predict that the cells would enter the plaque more readily, and more of the cells would then be able to encounter the axons that require remyelination, and we would obviously predict that that would promote remyelination happening.   MSDF What are some of the big questions now to look at, solve?   Dr. Kennedy The oligodendrocyte is an absolutely fascinating cell type. It's a highly specialized cell type, critically clinically important. We still understand very little about these cells. The mechanisms that I've been talking about that regulate the maintenance of myelin, those have only very recently been discovered. And I think it's extremely exciting that this type of thing is being found in oligodendrocytes. But these are still very mysterious cell types. I think the more we understand about the cell biology of the oligo the more we'll be able to target pathways in the biochemistry of oligodendrocytes to try and promote things like myelin maintenance and the ability to remyelinate. Being able to do those things and essentially manipulate these cells in specific ways, we can then overcome specific clinical issues.   MSDF Does this go beyond MS? Are there other conditions that it applies to?   Dr. Kennedy I think there are two things built into that question. One is that there are many diseases for which the cause either isn't clear – and MS would be in that category – or there are also diseases that have many different causes, but they may manifest in similar ways. So by understanding oligodendrocytes and being able to encourage oligodendrocytes to remyelinate, that could have broad applicability for treating the symptoms of many different forms of demyelinating disease irrespective of the cause of those diseases. Beyond that, as we come to better understand how cells move in the nervous system, how they migrate, how they form attachments, how they connect to each other, and how they maintain those connections, those kinds of insights are going to have broad applicability for all sorts of neurodegenerative diseases where the basic problem in the neurodegenerative disease is that the networks that are the nervous system are coming apart. And if we can encourage those networks to just stay together or rebuild themselves, then I think that again has broad applicability to many types of neurodegenerative diseases in the myelinating field and outside of myelination, as well.   MSDF It sounds like it may even have applicability to not only neurodegeneration but in development where you may have miswiring such as potentially an autism or something like that.   Dr. Kennedy Yeah. An exciting thing is that a lot of the mechanisms that I'm thinking about and we're thinking about in the lab is that the insights that got us working on myelin, that brought us to work on myelin really came from neural development and better understanding neural development; the studies of neural development identified proteins and gene families that have very, very potent actions in the nervous system. When we then looked at expression, we saw that they were expressed in the mature CNS, and that brought forth a whole other group of questions related to the function of the normal adult nervous system and also the degeneration of the adult nervous system in neurodegenerative disease. The exciting thing about that is that as we understand the molecular biology of the central nervous system better that's going to be applicable to development, to normal function, to enhanced function, and also promoting function in degenerative conditions.   MSDF I appreciate it. Thank you.   Dr. Kennedy You're very welcome.   [transition music]   Thank you for listening to Episode Twenty-Five of Multiple Sclerosis Discovery. This podcast was produced by the MS Discovery Forum, MSDF, the premier source of independent news and information on MS research. MSDF’s executive editor is Robert Finn. Msdiscovery.org is part of the non-profit Accelerated Cure Project for Multiple Sclerosis. Robert McBurney is our President and CEO, and Hollie Schmidt is vice president of scientific operations.   Msdiscovery.org aims to focus attention on what is known and not yet known about the causes of MS and related conditions, their pathological mechanisms, and potential ways to intervene. By communicating this information in a way that builds bridges among different disciplines, we hope to open new routes toward significant clinical advances.   We’re interested in your opinions. Please join the discussion on one of our online forums or send comments, criticisms, and suggestions to editor@msdiscovery.org.   [outro music]          

We're six months old:Episode Twenty SixSimon examines the superficiality of Italian politics, while iszi realises it's just an excuse for him to stare at cleavage and bottoms. There's also talk of style, culture, travel and crayons.