Podcasts about episode twenty five

Episode Twenty Five of the Punk Rock Classrooms Podcast! "Being True to Yourself" Season two of punk rock classrooms is underway and the boys are focusing that punk rock ethos they honed in season one onto specific topics this go around. The punk scene let Mike and Josh be who they are and be true to themselves. Over the years they have found that when they aren't being true to who they are, they aren't as successful with connecting to others and doing what is right. On this episode they discuss why it's important to hold onto your convictions, your passions, and your values in all that you do. So take a look in the mirror and make sure you recognize you is looking back at you. Twitter twitter.com/punkclassrooms twitter.com/mikerearnshaw twitter.com/JoshRBuckley Intro music - "True Till Death" by Chain of Strength Outro music - "I'm a Poseur" by X-Ray Spex Check out our PRC Playlist here for all of the rad tunes we use: bit.ly/PRCPlaylist

Episode Twenty-Five features Jasmine Wahi, the Holly Block Social Justice Curator at the Bronx Museum, an Activist, TEDx Speaker, and a Founder and Co-Director of Project for Empty Space. Her practice predominantly focuses on issues of femme empowerment, complicating binary structures within social discourses, and exploring multipositional cultural identities through the lens of intersectional feminism. In 2010, Ms. Wahi Co-Founded Project For Empty Space, a not-for-profit organization that creates multidisciplinary art exhibitions and programming that encourage social dialogue, education, and systemic change through the support of both artists and communities. Though she does not consider herself to be an artist, Ms. Wahi has organized numerous interventions and happenings as part of her social activist work. In 2018, she served as the Co-Chair “Rape, Radicality, and Representation” for the College Art Association's "Day of Panels" with The Feminist Art Project (TFAP). organizing a day of intersectional feminist based performances, films, and conversations. In 2019, she spoke at TEDxNJIT on the idea of Resilience. In 2020, she curated the two part exhibition Abortion Is Normal, which received wide critical acclaim, and will be touring cross country as part of a campaign to get out the vote. Ms. Wahi’s curatorial work has been featured in the New York Times, The Wall Street Journal, Art News, Art Forum, Hyperallergic, Bloomberg, VICE, and NOWTHIS, to name a few. http://www.jasminewahi.com/ https://www.artnews.com/art-news/news/jasmine-wahi-bronx-museum-of-the-arts-1202678209/ http://www.projectforemptyspace.org/team https://www.artforum.com/news/bronx-museum-hires-jasmine-wahi-as-holly-block-social-justice-curator-82212 https://en.wikipedia.org/wiki/Jasmine_Wahi http://gallerygurls.net/art-convos/2017/9/24/in-conversation-with-jasmine-wahi?rq=jasmine%20wahi https://hyperallergic.com/539075/an-art-exhibition-reminds-us-that-abortion-is-normal/

We’ve hit the quarter century episode mark and so far no one has perished, although there have been some close calls lately, including on this very show! The good news is we get more Savage Opress, some insane lightsaber fights with some unexpected matchups. There are also force gods and all powerful daggers! Yup, you’ll find all this and more as we discuss Episodes 14-17 of Season Three of The Clone Wars! We also have a good bit of news to discuss, some classic Ralph McQuarrie art discussion and we sweet talk the Sarlacc Pit! 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 Five 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

Episode Twenty Five! So excited. Lindsey and Ronnie talk about the origins of witch hats, and the damiana plant! Of course we send some love to our pussy of the week. So grab your rollies and a bevy, kick-it and enjoy. As always be kind witches!

Hello and welcome to Episode Twenty Five of Page Turn: the Largo Public Library Podcast. 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 44:00 and ends 48:03 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 Five is Dear Committee Members by Julie Schumacher. If you like Dear Committee Members you should also check out: The Amazing Adventures of Kavalier & Clay by Michael Chabon, The Storied Life of A. J. Fikry by Gabrielle Zevin, and Ella Minnow Pea by Mark Dunn. My personal favorite Goodreads list Dear Committee Members is on is Interesting, Well Written Books That Are Not By Dead Old White Men. Today’s Library Tidbit is an interview with Holocaust survivor Marie Silverman. You can find more information about the Holocaust by visiting The Florida Holocaust Museum. You can find more of Marie Silverman's testimony here. 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 about a nonfiction book that we have in the Spanish collection entitled Stranger: The Challenge of a Latino Immigrant in the Trump Era by Jorge Ramos. Synopsis: Jorge Ramos, an Emmy award-winning journalist, Univision’s longtime anchorman and widely considered the “voice of the voiceless” within the Latino community, was forcefully removed from an Iowa press conference in 2015 by then-candidate Donald Trump after trying to ask about his plans on immigration. In this personal manifesto, Ramos sets out to examine what it means to be a Latino immigrant, or just an immigrant, in present-day America. Using current research and statistics, with a journalist’s nose for a story, and interweaving his own personal experience, Ramos shows us the changing face of America while also trying to find an explanation for why he, and millions of others, still feel like strangers in this country. Opinion: If you are not a Univision viewer, you may not be familiar with Jorge Ramos. He is a news anchor and reporter. Ramos became famous in the Anglo-Saxon public for having been expelled from an important press conference during the Iowa Caucus season for asking candidate Donald J. Trump too many specific questions about the central element of his campaign: the wall. Ramos was born and raised in Mexico City, but moved to the United States to receive additional journalistic training and looking for the opportunity to be freer in his journalistic practice. He was lucky in television journalism, but he has succeeded and has done quite well. He has also become a US citizen. In the book, Ramos addresses the story of the press conference immediately. It is not as dramatic as it looked on television, because the future president allowed him to return to the press conference and made a private interview with Ramos later. This moment set a couple of precedents, however. Trump and the press have had a difficult relationship, to put it mildly. Another precedent was also established. As Ramos cooled his heels outside the press conference, a Trump supporter, wearing a red "Make America Great Again" hat, told Ramos: "Get out of my country!" Ramos informed him that he was a US citizen, just to be told: "Whatever!" For the first time in years, Ramos felt that he was really a stranger in his adopted country, hence the title of the book. Ramos builds on this latest incident for a while, discussing how the President's behavior and comments have encouraged many to act, feeling a change in the political climate. He also talks about civil rights inequalities for Hispanics, his own mostly positive experiences and how the current political climate is disorienting for a man who has lived more than half of his life in ...

Episode Twenty Five 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 the girls take on two stories of twists and turns! Jena tells us the tale of Danny Filippidis, a Canadian man who vanished on a ski trip in Lake Placid, NY only to resurface in California six days later. Kennedy recounts the story of Elena Vavilova and Andrey Bezrukov, Russian spies who posed as Canadians, making a life and a home, unbeknownst to everyone including their children. ⠀

It’s here! The One Year Anniversary episode of Not for the Dinner Table! We’re joined by friends and family for a Weird Fact Extravaganza. We can’t quite believe that NFTDT is a year old. We been on a fantastic journey over the last year and we’re celebrating in style. We have a brand new jingle to celebrate created by the amazing Chris Scott @ScottyJax from the amazing Ask Karen Podcast We’re also joined by some fantastic podcasts. A massive thank you to: Kitsie and Clayton from Oddity Files The Podcat @OddityFIles Charlie Conlan from the Knowing My Nightmares Podcast @KMNPodcast Stacey from the Rough Giraffe @RoughGiraffePod Bailie and Vanessa from the Boos and Spirits Podcast @BoosandSpirits Katie and Olivia from What’s Her Name @WhatsHerNamePC The Illusive Host Verity Clayton from Scary Stories Podcast @PodcastScary Kathy from the Friends in your Ears Podcast @FriendsInEars We also have two special Listeners Leftovers from two awesome podcasts. A huge thank you to: Em from the Verbal Diorama podcast @VerbalDiorama Mike Brown from the Pleasing Terrors Podcast @pleasingterrors It’s Episode Twenty-Five of Not for the Dinner Table!! And we’re talking all about Body Snatchers. Not the movie though. If you want to send in your story email notforthedinnertable@gmail.com you can send us your weird sightings, spooky encounters or general strangeness. And remember everyone is welcome at our dinner table, except… Follow us on Twitter @NFTDT Follow us on Instagram @notforthe_dinnertable Follow us on Facebook @ Not for the Dinner Table You can listen to our podcast on the Apple Podcast App, Soundcloud, Stitcher, and Spotify or wherever you find podcasts. If you like the show, please leave a review wherever you have listened to this podcast. Welcome along to our dinner table where we have conversations that aren't suitable for the regular dinner table. We discuss ghosts, crypts, aliens and everything in between. We are not experts in our topics and this is not a deep dive podcast (all the time), but we are two people that enjoy discussing the stranger things in our world.

It’s Episode Twenty-Five of Not for the Dinner Table!! And we’re talking all about Body Snatchers. Not the movie though. We’ve got some NFTDT news all about pilots spotting UFO’s and Sophie’s trip to the Littledean Jail, which holds a huge collection of occult and true crime memorabilia and an array of oddities. Not to be confused with Grave Robbers, Body Snatchers were all together much more macabre and in NFTDT fashion we’re scratching the surface into this creepy practice. Sophie is exploring the strange custom of Ghost brides and ghost weddings in China. Whilst Dave is looking into one of the most famous “Resurrection Men” Grandison Harris and a few facts about the Mortesafe. To finish off we have a fantastic listener’s leftovers about an abandoned hospital and a murder that took place there. If you want to send in your story email notforthedinnertable@gmail.com you can send us your weird sightings, spooky encounters or general strangeness. And remember everyone is welcome at our dinner table, except… Follow us on Twitter @NFTDT Follow us on Instagram @notforthe_dinnertable Follow us on Facebook @ Not for the Dinner Table You can listen to our podcast on the Apple Podcast App, Soundcloud, Stitcher, Spotify and Podcoin or wherever you find podcasts. If you like the show, please leave a review wherever you have listened to this podcast. Welcome along to our dinner table where we have conversations that aren't suitable for the regular dinner table. We discuss ghosts, crypts, aliens and everything in between. We are not experts in our topics and this is not a deep dive podcast (all the time), but we are two people that enjoy discussing the stranger things in our world.

Welcome to Episode Twenty-Five 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 Nine 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.

Our guest this week is the architect Larry Malcic. Larry was born in St Louis in the American mid west. He later went on to study architecture at the University of Pennsylvania, being taught for a time by the hugely influential architect Louis Khan. After University it was in St Louis that Larry started his own … Continue reading "Larry Malcic – Episode Twenty-Five"

Episode Twenty-Five features first time FEMALE-READER Cannibal Siren, with host Captain Death, for our BIG QUARTER episode. We read some Stories to Tell Alone at Night and some TrollPastas, so sit back, relax, and grab yourself a cold one(cold hand of death, I mean): As a Child I Wanted to be a Mermaid(4:55)10 Years Ago I Taught a Creative Writing Course; Two Student's Stories still Haunt Me to this Day(13:55)Annora(32:30)Old News(43:47)Cackling(46:39)Treats of Insanity(53:28)The Pretty Cake Room(56:40)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-Five of IdeaPod. In this episode, we talk about BIG Ideas under 5 minutes… Yeah.. that’s it. Pretty Self Explanatory. We randomly pick a company name and come up with an idea under 5 minutes…or so. So listen to ... Read More The post #25 IdeaPod goes POP! appeared first on Bandwidth Marketing.

Episode Twenty Five of Hairy London

Episode Twenty Five covers current Mormon standings on sealings and unrighteous  dominion in marriage relationships. Turns out, we're not a huge fan of the latter.

Episode 25: Formatting Your Self-Published Book in Microsoft Word and Scrivener Welcome back to Episode TWENTY-FIVE of the Writing and Publishing Erotica Podcast. I am H. K. Kiting and I am Dean Chills and we’re your hosts for the show. This is the podcast where we talk about writing and publishing in general, and include ...read more

[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]          

[intro music]   Hello, and welcome to Episode Twenty-Five of Multiple Sclerosis Discovery, the podcast of the MS Discovery Forum. I’m your host, Dan Keller.   This week’s podcast features a special interview with actor and science advocate, Alan Alda, whom you may remember as Hawkeye Pierce in M*A*S*H. But to begin, here’s a brief summary of some of the latest developments on the MS Discovery Forum at msdiscovery.org.   Positive thinking may lead to positive clinical outcomes, according to a new meta-analysis. The investigators found that interventions such as cognitive behavioral therapy helped patients deal with physical symptoms like fatigue and pain. They suggested that psychological well-being should be assessed and treated along with physical disability in people with MS. The researchers also called for studies that examined the connection between the psychological and the physical more directly.   Moving from the macro to the micro, we recently published an article about axonal transport. Axons rely on motor proteins to carry cargo across long tracks of microtubules in order to survive. A disruption in this process is associated with neurodegeneration. Recently a team of researchers discovered that axonal transport is disrupted in mice with EAE. In this animal model of MS, even normal-appearing axons failed to transport organelles as quickly or as effectively as healthy axons. But the researchers were able to reverse the process, suggesting a potential new therapeutic target for drug development.   [transition music]   Now to the interview. Alan Alda is an actor known for his television roles in M*A*S*H and The West Wing. But he’s also a longtime advocate of science and scientific literacy and the founder of the Alan Alda Center for Communicating Science at Stony Brook University. He met with MSDF recently to talk about the art of good science communication.   [Interview]   Interviewer – Dan Keller What, at this point, would you say are the one or two biggest pieces of advice you could give to any technical person or a scientist trying to get his point across to the general public?   Interviewee – Alan Alda I think the most important thing to remember is that it’s not nearly so important to worry about what you have to say to the other person, as it is to think about how the other person is receiving what you have to say. We know this intellectually because everybody knows that you want to know your audience, everybody knows you want to start where the student is, you know, find out what they know and build on that, that kind of thing. We all know that.   But one of the things that I think that we’ve found at the Center for Communicating Science that I helped start is that you need to get in the habit of doing that; you need to really go through the experience of actually opening up to other people, getting their feedback, being able to read from the signals that they give you on their face and their body language – all the various signals you can get – whether or not they’re really paying attention and really following you. If you miss one of the crucial words I say at the beginning of a paragraph, the rest of the paragraph is dead; you’re spending most of your time trying to figure out what I’m talking about.   MSDF As an example, say, in Scientific American Frontiers, you elicited great storytelling; I mean, I assume part of that was picking the right speakers, but how do you coax it out of them in an understandable way? I mean can you essentially guide people without saying, “Hey, come on, bring it down, bring it down.”?   Mr. Alda I think Scientific American Frontiers worked as well as it did because in a way it was a rare thing – I hadn’t seen it done before and so maybe it has, but I hadn’t seen it – where you had a naïve person – ignorant, played by me – and I wasn’t acting. I made use of the natural fund of ignorance that I came in with. I didn’t aspire to an ignorance I didn’t possess, it was real; I really didn’t know what these people did in the laboratory, and I really did want to know what it was. And I wanted to understand it, so I badgered them until I understood it, and I didn’t pretend I understood it if I didn’t. That step where they actually had to come to terms with this person standing right next to them looking up in their faces where they had to actually make it clear to this one person, that changed them in some way, that brought out the human being in them. And they forgot about the camera, they forgot about the millions of people that they might have gone into lecture mode to explain this to. They were talking to one individual and that made a big difference, because they became much more human.   So, yeah, I think that we had people who were comfortable being in front of a camera, but regardless of how comfortable they were in making their language plain-spoken, they had to get even more so when they talked to me because I really, I just tugged at their coat until I understood it. And something happened between us, there was some kind of connection between us that was very watchable, very interesting. I think that helped draw other people in. After we did that, I really wondered if a scientist didn’t have this person dogging him or her to get the information out, but to get it out understandably, what would do it? How could they get accustomed to speaking as though they’re talking to another person who really wants to know? And that’s when it occurred to me that I bet we could teach them improvising and that would help them get more personal, and it has.     MSDF To envision one person.   Mr. Alda Well, when you improvise, at least the way we improvise with scientists, it’s not for the purpose of getting them to be comical, or to make things up on the spot, or to be clever. The whole thing is designed to get the scientists to be accustomed to observing the person they’re talking to, because you can’t play these improvising games unless you’re tuned into the other person in a very powerful way. Once they get used to that and when they turn and talk to an audience, they carry with them that same ability to talk to the people and not over their heads and not at them. They don’t spray information at them anymore, they actually engage the audience, and that’s a tremendous difference.   MSDF Let me switch gears a little bit. I don’t know if you’ve ever noticed it, I’ve certainly noticed it, between different closely related scientific disciplines – I mean, I cover medicine mostly – and people in just very closely related things, there’s no cross-pollination. They’re surprised when they hear something that’s going on. Oh, you know, that could be applicable to me. And I think there’s even a lack of communication between the disciplines between scientists. They can certainly speak in the same jargon, but I don’t know if there’s a barrier or if they’re just so wrapped up in their own stuff.   Mr. Alda It seems to be a really serious problem that scientists need more and more to collaborate across disciplines, and the problem is that they often – I think I could say often – don’t understand one another much better than a layperson understands a scientist in a specialized field. So at a certain level, at a certain distance from one another’s work, they’re really in the position of an interested layperson rather than a collaborator, rather than a colleague. And we have to bridge that gap if we’re going to get the benefits of collaboration. And I’ve heard some horror stories of scientists getting together and not understanding one another. And on the other hand, I’ve heard these really heartbreakingly wonderful stories.   When we have a workshop with a range of scientists, scientists from several different fields, one of the wonderful things they say is this has been great, I got to understand, I got to hear about this guy’s work and I never knew anything about it before. They’re hearing an explanation of another person’s work in terms that they might say it to the lay public. It’s acceptable to the other scientists because we don’t ask them to dumb it down, we ask them NOT to dumb it down just to make it clear. So they’re getting a clear version of somebody else’s work that doesn’t include the jargon of that specialized field. It’s stripped of its jargon, it’s spoken in plain language. And the emotion, the passion that the scientist feels about it is allowed to come out because that’s part of the human story that science is. Science, rather than being passionless, is generated by passion. So it’s great that that comes out in this work.     MSDF In the training, obviously you can tell if there’s a difference between before and after. But have you ever been able to test the durability of this, that these people retaining these? Or do they lapse back? Or can you tell?   Mr. Alda It’s hard to get measurements on the success of this, but we’re beginning to get some early results because we’ve been working with teaching assistants. And teaching assistants are graduate students who are asked to give courses to undergraduates to see if the undergraduates want to go into science. And one of the problems has been that a lot of them drop out because they can’t get interested in the science partly because the teaching assistants don’t have any training in communication or in education; they know the material but they’re not really experienced at communicating. So we put them through a course of communication, and then we find some of the numbers we’re getting back are that the students are rating them as highly or higher than people who have been doing this for five years, and these are first-time teaching assistants.   Next thing we’ll check on is are their grades getting better and other things you can measure. But so far, the acceptance of the teachers is already better because there’s an attempt to personalize the experience. And so the students are accepting the teachers more, and by the same token, I assume they’re accepting the science more.   MSDF Have you ever thought of designing a curriculum that could be put into the science graduate programs, because these people are going to become scientists?   Mr. Alda What we’ve actually done is introduced a curriculum into Stony Brook University where I helped the Center for Communicating Science. And there are courses for credit taught to graduate students, and in addition there’s even at least one department that requires that the students take these communication courses. So it’s beginning to be seen as an essential element of the science education. And it’s a small beginning. But my feeling has always been isn’t communication essential to science itself, don’t we need to communicate science in order for it to take place or for the benefits of science to come to the surface? And not only that, that’s practical, but for the beauty of science to be enjoyed by the whole world, you definitely need communication. And that will help more science get done, and better science get done. More people entering science, if they understand how beautiful and engrossing it is – exciting. So it seems to me that since communication is such an important part of science, shouldn’t it be taught as part of a science education so that when you graduate as a capable scientist, you’re also a capable communicator?   MSDF Maybe you don’t even have an idea of this answer, but what got you into this passion for science?   Mr. Alda I’ve always been curious and that made me want to know more. I started reading Scientific American in my early 20s and since then I’ve read almost every article in almost every issue. And I love it, I just love it! I mean, I put the magazine down and I read other science magazines – I read Science & Nature and Science News, which I think does a very good job. Just the other day, I just slammed it down on the table and I said to my wife, “Arlene, you won’t believe this, listen to this.” You hear these wonderful stories of things you never imagined.   MSDF No, I agree. I mean, some people get turned off by it, some people get turned on by it.   Mr. Alda Well, it’s hard to believe anybody would get turned off by it unless they’re not hearing it the right way.   MSDF I think that a lot of people are turned off early because they weren’t encouraged or they were led to believe they couldn’t understand it.   Mr. Alda Yeah, it’s true.   MSDF I appreciate it. Thanks.   Mr. Alda Well, thank you very much.   [transition music]   Thank you for listening to Episode Twenty-Five of Multiple Sclerosis Discovery, our final episode for 2014. We’ll be taking a two-week hiatus for the holidays, but we’ll be back with new weekly episodes starting on January fifth.   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]  

Another dollop of supplementals:Episode Twenty FiveThis week Simon posits a theory about the decline of bees, while iszi does an awful lot of drugs. It's a heavyweight battle, with the Independent versus the Observer, and there can only be one winner.