Podcasts about episode thirty

Hello and welcome to Episode Thirty-One 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 English Language Transcript can be found below But as always we start with Reader's Advisory! The Reader's Advisory for Episode Thirty is The Yield by Tara June Winch. If you like The Yield you should also check out: On Earth We're Briefly Gorgeous by Ocean Vuong, The Meursault Investigation by Kamel Daoud, and The Round House by Louise Erdrich. My personal favorite Goodreads list The Yield is on is Modern Mrs Darcy Podcast Lists. Happy Reading Everyone Today’s Library Tidbit is about familiar spirits. It’s fall Halloween was just a few days ago and seemingly spooky things have been on everyone’s mind. So on today’s tidbit I’m going to dive into what familiar spirits are, their history in different cultures, and why you should never appropriate a different cultures terminology and understanding of them. This last little bit is the reason why I will be using the term familiar and familiar spirit throughout this tidbit as I am mostly European and it is the pan-European term for this concept. I am not going to be going into the practice of witchcraft or be discussing if familiar spirits are real or their morality. A familiar spirit is an entity, animal, plant, or other natural thing, that you form a special bond with. This connection is not a light bond but rather a bond that you feel connects you to something on a spiritual or soul level. This idea is something that exists in cultures and time periods across the world. These familiar spirits exist to guide a person, either teaching them specific magics or guiding them through person life dilemmas and through personal growth. A non-religious familiar might be a centering touchstone that someone finds comfort in because it reminds them of attributes that they share. European traditions mostly use the term familiar or familiar spirit. Native and Indigenous groups have multiple different words but English speakers typically use the word totem to describe all of them. It is important to remember that different tribes will have their own word for this concept. Totem poles are specific to the Pacific Northwest area of the continent of North America, from Alaska to Washington and British Columbia. Spirit Animal is another term used by Native tribes to describe tutelary guides. Totems are one type of spirit animal but used specifically by the Northwest Pacific tribes. However, most of the information about totems that I have just said also applies to spirits animals. In other words, spirit animal is a Native term and should be respected as a Native term. In Norse culture there exists the fylgjur plural, fylgja singular. Across Mesoamerica exists the belief in the nagual and the tonalli or tonal. Some sources will say that they nagual is related to a spirit guide, however, they are more therianthropy. In other words Naguals are shape shifting witches. Tonals, on the other hand, are familiars that are assigned at birth. Tonals are attached to the Aztec horoscope calendar and are guardian spirits. Other words for familiar in other cultures that either have very broad definitions or have characteristics that don’t fit into my tidbit today are spirit, spirit guide, doppelganger, personal demon, spirit companion, ayami and syven. Familiar spirits are deeply personal and often important both religiously and culturally for different people groups. Because of this it is insulting to use language from a culture you are not a part of casually. Unfortunately, due to colonization, most people are too comfortable using words and concepts for themselves that are not part of their cultural heritage. I would encourage everyone to research into their own ancestry and pick a term that is part of their cultural heritage.

Hello and welcome to Episode Thirty 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 English Language Transcript can be found below But as always we start with Reader's Advisory! The Reader's Advisory for Episode Thirty is The Dragons, The Giant, The Women by Wayétu Moore. If you like The Dragons, The Giant, The Women you should also check out: Black Sunday by Tola Rotimi Abraham, The Best We Could Do by Thi Bui, and A Drop of Midnight by Jason Diakité. My personal favorite Goodreads list The Dragons, The Giant, The Women is on is Profiles in Silhouette. Happy Reading Everyone Today’s Library Tidbit is all about the movement of hurricanes. Hey remember in August when we had two storms in the Gulf at the same time? Why did Marcos and Laura hit roughly the same location when they formed in completely different geographic places? Hurricanes move along patterns created by global winds. Wind in general happens because of the uneven heating of the earth’s surface by the sun. Hot air rises and cold air sinks. Through convection this causes the atmosphere to move creating wind. Wind moves from the equator to the poles as it heats and then flows back to the equator as it cools. Now here is where things get a little confusing. Because the planet rotates the air at the equator moves faster than the air at the poles. This means that, in the Northern Hemisphere, as air moves from the equator towards the poles it ends up slightly to the right of the location it began at. This is called the Coriolis Effect. This is why hurricanes rotate. Storms rotate counter-clockwise in the Northern Hemisphere and clockwise in the Southern Hemisphere because of this effect. The Coriolis Effect also causes global winds to move in a large rotation. The interaction of the equatorial winds and the polar winds causes cells to form. The cell nearest to the equator, from about zero to 30 degree latitude is called the Hadley cell. This is the cell where hurricanes form and where the Gulf Stream begins. This cell also creates the trade winds. As the air at the equator heats and rises to the tropopause, which is the boundary between the troposphere and the stratosphere. As it hits this place air is no longer buoyant and the air rising below it pushes it northward and southward toward the poles. As it moves towards the poles it cools and sinks again. As it gets closer to the surface a frictional return flow pulls the air back towards the equator to rise again. The Coriolis Effect explains why air moving towards the north pole moves easterly and why the air coming back down from the north pole to the equator moves westerly. This circulation is what causes the North Atlantic Gyre, which is bordered on the west by the north moving Gulf Stream and on the east by the Canary Current which moves south. At the heart of the current is the Sargasso Sea, which, fun fact is where fresh water eels from both North America and Europe mate, but not to each other. Hurricanes form the same way that the winds that form the Hadley cell. Hot air along the equator rises causing an area of low pressure beneath it. Air from around flows into the new low pressure area. This air warms and also rises. This convection cycle causes the spin characteristic of a tropic storm or hurricane. The more the storm is fed by the hot air flowing the stronger the storm grows and the faster it rotates. The rotation causes an eye to form. The eye of the storm is an area of low pressure. Air that is being displaced by air moving up beneath it actually starts to flow back down through the eye. Hurricanes move predominately westward off the coast of Africa because the trade winds along the equator move consistently westward. As the storms move, however, the Coriolis Effect takes into effect and the storms begin to move more and more northward and...

Episode Thirty features Nicole Awai. She earned her Master’s Degree in Multimedia Art from the University of South Florida in 1996. She attended the Skowhegan School of Painting and Sculpture residency in 1997 and was artist in residence at the Studio Museum in Harlem in 2000. Awai was a featured artist in the 2005 Initial Public Offerings series at the Whitney Museum of American Art and was awarded the Joan Mitchell Foundation Painters and Sculptors Grant in 2011 and an Art Matters Grant in 2012. Her work has been included in seminal museum exhibitions including Greater New York: New Art in New York Now, at P.S. 1/ MOMA (2000), the Biennale of Ceramic in Contemporary Art, Italy (2003), Open House: Working in Brooklyn (2004), Infinite Island: Contemporary Caribbean Art (2007) both at the Brooklyn Museum; the 2008 Busan Biennale in Korea; The Pacific Standard Time: LA/LA II, A Getty Initiative exhibitions Circles and Circuits I: History and Art of the Chinese Caribbean at the California African American Museum and Circles and Circuits II: Contemporary Art of the Chinese Caribbean at the Chinese American Museum, along with Relational Undercurrents: Contemporary Art of the Caribbean Archipelago at the Museum of Latin American Art and the High Line Network exhibition New Monuments for New Cities. Her work has also been exhibited at the Queens Museum, Kemper Museum of Contemporary, Portland Museum of Art, Delaware Art Museum, Philip Frost Art Museum FIU, the Vilcek Foundation and the Biennale of the Caribbean in Aruba(2013). Other recent exhibitions include Splotch at Sperone Westwater, NY. Figuring the Floral, Wave Hill, NY; Summer Affairs at Barbara Davis Gallery, Houston, TX and Nicole Awai: Envisioning the Liquid Land at Lesley Heller Gallery, NY. Awai was a Critic at the Yale School of Art in the Department of Painting and Printmaking from 2009-2015 and is currently faculty in the Department of Art and Art History at the University of Texas at Austin. Awai is represented by Barbara Davis Gallery in Houston, TX.

Episode Thirty sees us recovering from the fish-related trauma of last week by shooting wildly into the wind with some short, barely there theories. Theory One: Is there a reason beyond putting together the leftover scraps of chocolate that goes into creating Cadbury's flakes?Theory Two: Do all cleaning experts from Kim and Aggie to Marie Kondo to the brave souls on Hoarders have the same basic idea?Theory Three: Is there a chance that Legolas is a shambolic drunk by elf standards and didn't realize what he was getting into when he signed up for the mission in Lord of the Rings?

Welcome to Episode Thirty of Strange Pleasures Radio Lab. Your daily audio story podcast available through iTunes, Spotify, Stitcher and YouTube.Please support the channel by subscribing, rating and reviewing on your preferred platform.Today I will be narrating Part Four of Frankenstein by Mary Shelley.YOUTUBE: https://www.youtube.com/channel/UC8MoqBN8-vdAsaoYBZX32OA?viewas=subscriber?subconfirmation=1HOME WEBSITE https://strange-pleasures-radiolab.pinecast.co/STITCHER https://www.stitcher.com/s?fid=465249&refid=stprSPOTIFY 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 THIRTY holy cow!!! Honestly, can't believe we made it this far, thanks so much for listening to us constantly bicker hahaha love u for that! Hope you stick with us for more more more :) xoxo Anyways, in this one we talk about our favourite thing to spend money on, our motivation for the podcast, and how every decision had to be made the way it was made or I wouldn't be in this exact moment right now... CRAZYNESS! Enjoy :)

Episode Thirty: upstaged. On this episode I’m talking about the current spice girls tour and how good it was but the open act was better (controversial) please follow me on Instagram, like me on Facebook and subscribe on YouTube. All music from the anchor podcast app. Thanks for listening Ta’Da

Episode Thirty three: Someone Knows with Lisa Scottoline: New York Times best selling author Scottonline, chats with Stacey and Evelyn about her newest domestic thriller! 

Episode Thirty-eight of the Graincast. This week we have Ray Larose, Cody Priebe, and Thomas Skrlj. We talk about re-editing photos, new film, what are presets and profiles, and all kinds of random things.

On today's episode we're kicking off the new year by talking about our stuff. As everyone makes New Year's resolutions, we're figuring out how to balance needs verses wants, and what we really want to fill our homes with. For show notes and episode extras, visit www.notterriblepodcast.com

Episode THIRTY! WHAT! This is a BIG one. CAPTAIN MARVEL. AVENGERS: ENDGAME. SUPER SMASH BROS ULTIMATE. THE GAME AWARDS. AHHHHHHHHHHHHHHHHHHHHHHHHHHHHHH!!!!!!!!!!! Be sure to follow us here and on Twitter and Instagram for more Good Content™. @whatthefuncast

The Underground’s feed is once again interrupted for the opinions and observations of Sandrel Creed – but ze is interrupted by yet another voice from zir own past. Also, “Bloodmoon Fury.” Please survive and flourish! •∂∆∑£ª¶¡ — Sandrel Creed: Zirself  — Grodan Rix: Itself  — Narrator: Maya Kralovna  — Episode Thirty-three-a,… Continue reading

Episode THIRTY!! You stopped listening? ...but we made you cocoa! This week we have regular features Quick Quotes Quiz, Tom's sort of game and Michael's Corner gets busy creating Tom's Riddle and the Quiz! Contact: Twitter - @aattapod, Facebook - /aattapod, email - aattapod@gmail.com

HEY YALL ~~~ SOTB is back for EPISODE THIRTY and it is a GOOD ONE, folks. This week we r talkin **mass incarceration** with some of the most exciting guests in this show's H I S T O R Y . Buckle up bc we're talking abt the cooptation of incarcerated folks' labor, the ties between environmental degradation and ICE and the prison industrial complex, and the ways that a capitalist bail industry keeps innocent people behind bars for months or even years at a time. SO PUT THOSE HEADPHONES IN UR EARHOLES AND LETS GET TO IT !!!! About our guests: Bypolar is a longtime activist who currently works with the Northwest Community Bail Fund in Seattle. They are in the midst of a legal battle over an unjust prosecution. If u are looking for a CONCRETE WAY to fight the effects of mass incarceration, help them out by calling Seattle prosecutor Pete Holmes at 206-684-8200 and asking him to drop all charges against Matthew Erickson (Bypolar's legal name) and to end the persecution against Seattle's black activist community. Read more at https://stoplegallynching.wordpress.com/ and check out NCBF here: https://www.nwcombailfund.org/ May also works with the Northwest Community Bail Fund and has recently led seminars on the intersection of climate and criminal justice with Bypolar. You can learn more about their work on climate justice at https://fighttoxicprisons.wordpress.com/ and check out the Queer Ecojustice Project as well! (That's at http://queerecoproject.wixsite.com/qollective.) May is also passionate about a new project called Bloc the Juvi, an artist collective organizing against construction of a juvenile detention center in Seattle. Find them on facebook here: https://www.facebook.com/BloctheJuvi/. Nellie is a teacher in El Paso, Texas. She is also a member of the Detained Migrant Solidarity Committee there! Read more about them here: https://dmscelpaso.wixsite.com/dmscelpaso Shaina is a law student at NYU, who has worked with the Orleans Defenders, a public defense law group in Louisiana, and the Petey Greene Program, which seeks to expand educational opportunities for incarcerated folks. Find out more about the Orleans Defenders here: http://www.opdla.org/ and the Petey Greene Program project here: http://www.peteygreene.org/ ps---if u wish this convo would NEVER END ur in luck because this is a TWO WEEK SPECIAL! U MAY HAVE NOTICED THAT BC WE END AT A WEIRD MOMENT LMAO ITS ALL GOOD YALL U JUST HAVE 2 WAIT 7 MORE BEAUTIFUL DAYS FOR THE REST pps May provided us with a list of EVEN MORE RESOURCES for u to check out & educate urself. thanks May!!!!! here they are: Northwest Detention Center Resistance http://www.nwdcresistance.org/ Prisoner Hunger Strike Solidarity https://prisonerhungerstrikesolidarity.wordpress.com/ Incarcerated Workers Organizing Committee https://incarceratedworkers.org/campaigns/operation-push-florida-prison-strike Prison Ecology Project https://nationinside.org/campaign/prison-ecology/ Prison Legal News https://www.prisonlegalnews.org/ Prison Radio http://www.prisonradio.org/about Books to Prisoners http://www.bookstoprisoners.net/ theme music as always by Brandon Payton-Carrillo

Episode Thirty features guest Terry the Tickler back again with host Captain Death. Today they're tackling a big hitter. And by big hitter, I mean, big shitter. Jeff the Killer, the memer who has haunted nightmares for ages; the picture being the only creepy thing about this internet phenomenon, there's nothing scary about the story. Then we read a long and deliberately awful troll pasta. ENJOY: Jeff the Killer(11:54)A Meeting with Al Qaeda (45:06)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," "You Reposted in the Wrong Neighborhood," and "Blue(Da Ba Dee)" are not my songs. Credit and All rights are reserved by the owners. Fair Use in effect for parody and criticism of intellectual property

Episode Thirty of the IdeaPod. In this episode, using the idea crash brainstorm technique, Rob and Michelle come up with Halloween costumes ideas from random objects. Read More The post #30 We Want Your Brainzzz….storming! appeared first on Bandwidth Marketing.

Episode Thirty of Hairy London

Join comedians Rachel Fairburn and Kiri Pritchard - McLean as they explore a shared passion, serial killers. Each episode the pair will talk all things murder and macabre and have a right laugh doing it. Episode Thirty one and they're talking about the ABC Killer, Moses Sithole. Naturally Rachel and Kiri go off piste and this episode includes a dubious accent, plenty of knicker chat and Rachel makes it clear how she feels about bums.

Join comedians Rachel Fairburn and Kiri Pritchard - McLean as they explore a shared passion, serial killers. Each episode the pair will talk all things murder and macabre and have a right laugh doing it. Episode Thirty part three and now we've got to know this horrible pair, it's time we talked about their crimes, there's plenty to talk about too. Not to mention the other bits Rachel and Kiri get distracted with; alternatives to perfume, dirty underwear and Rachel loses her rag in the final minute of the podcast.

Join comedians Rachel Fairburn and Kiri Pritchard - McLean as they explore a shared passion, serial killers. Each episode the pair will talk all things murder and macabre and have a right laugh doing it. Episode Thirty part two and we're meeting the other half of this horrible pair,"Dozy Rosie" herself, Rosemary West. Kiri and Rachel also get massively distracted talking about their top five.

Join comedians Rachel Fairburn and Kiri Pritchard - McLean as they explore a shared passion, serial killers. Each episode the pair will talk all things murder and macabre and have a right laugh doing it. Episode Thirty and it's a big one, Fred and Rose, the Gloucester House of Horrors. This is part 1 and we're getting to know Fred West. Just don't get too close because he doesn't brush his teeth and eats onions like apples.

Episode Thirty-six. A murder engine versus a Swearengen as Stephanie Edd, author of The Clear Case and The Halyard Hitch, drops the hammer again. Hawkeye arrives with future Tarantino cast "The Almost Eighteen"... Seth opines on the nature of bullies, and how they never know when to shut the fuck up... In the voting queue, a well-intentioned Charlie nonetheless defines "White Privilege"... Joanie promises herself to Jane, a rare moment of sweetness in this otherwise upsetting de facto series finale... That Twin Peaks actor Matt has teased the hooples about all podcast long finally appears (or does he?)... Al sacrifices an innocent to spare the camp from garbage human George Hearst, who unjustly fucks over our heroes at every conceivable turn. ... Also, Chris has stern words of criticism for Seth Bullock's successor, yet entertains us with the tale of a pitiful rain-soaked sad sack. (Gentlemen, don't forget to vote against the opium ordinance!) | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded August 7 & 13, 2016. Released August 22, 2016. [Warning: Explicit Language.]

Episode Thirty-five. Longtime Deadwood fan Andrew is our guest for this pivotal penultimate episode. The murder of a beloved individual unites the camp against the grotesque George Hearst... Trixie is the loopiest of loopy cunts, and we couldn't love her more for it... Aunt Lou fires the opening salvo in restaurant wars... At the schoolhouse, Jane plays Duck-Duck-Goose with the children (or, if you are an insufferable Minnesotan, Duck-Duck-Gray Duck)... One hundred and fifty Chung Kuo cocksuckers are summoned to Deadwood to swell the ranks of our heroes. ... Also, Alirio speaks to the character and accomplishments of Seth Bullock, and asks his fellow citizens to reelect him Sheriff. | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded July 24, 2016. Released July 30, 2016. [Warning: Explicit Language.]

Episode Thirty-four. Does David Milch hate the Irish? Our guest Jonathon thinks so! As shots ring out in the thoroughfare, Al has his hero moment... Alma somersaults after eating Jewel's breakfast... If Hearst is "Socrates," then Hugo is willing to get down on his knees and be his "Alcibiades."... The hooples are confused by a cavalcade of tremendous brunettes... And, what is happening in Con's pants? It appears as though Con's erect penis has detached itself from his groin and is now moving independently down his pants. ... Also, Nuchtchas shares amusing local brevities, and a statement from Long Dog of the Black Hawk in which he claims all Indians hate the white men. | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded July 10, 2016. Released July 16, 2016. [Warning: Explicit Language.]

Episode Thirty-three. HoopleCast offers a proud prelude to the climax of the final season, and a chance for our guest Cory to show us his skills and hidden talents! The Earps exchange insults with Pinkerton agents... Joanie becomes unmoored due to a Norwegger's whimsical construction of the new schoolhouse... Hearst authors a response to the publication of Seth's letter... The entire camp marvels at Richardson's juggling prowess. ... Also, Christiana promises the Langrishe Theatre's production of The Road Agents of the Hills: A Romance of Deadwood will enlist a lively interest in our play-going community. | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded June 26, 2016. Released July 3, 2016. [Warning: Explicit Language.]

Episode Thirty-two. We welcome back to the podcast Will of Down Below: A Babylon 5 Introcast, The Sense8 Podcast, and (coming late 2016) SpartaCast. A scheme to keep General Fields in camp backfires on Steve... Brothers Wyatt and Morgan Earp arrive in Deadwood, because there aren't already enough fucking goddamn characters in this series... Chesteron--line? line?--is boosted over the metaphorical cliff... Langrishe embarks upon a campaign of feints designed to occupy the leviathan Hearst. ... Also, Stephanie Edd regales us with a report of last evening's very successful, albeit culturally insensitive, masquerade ball. | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded June 12, 2016. Released June 18, 2016. [Warning: Explicit Language.]

Episode Thirty-one. Skyping from the middle of a cornfield is our guest Randal of The Grawlix Podcast. Odell holds his fuckin' own as George Hearst's dinner companion... Gustave, the tailor, fashions the latest in colorful stump covers for Al... A stirring letter to the family of the slain Pasco Carwen moves the camp elders... Steve offers the General a fig leaf... The hooples attempt to pair Alma with one of Deadwood's eligible bachelors, and discuss the recent troubles at HBO. ... Also, Moira pleads: won't someone please think of the capitalists? | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded May 22, 2016. Released June 5, 2016. [Warning: Explicit Language.]

Episode Thirty. Laurel returns for the aftermath of the infamous bout that left our Dan a Neanderthal. Disgusted by her ladyship's bad habits, Trixie ponders employment elsewhere, but is quickly admonished by life coach Al Swearengen. (Loopy cunt!)... Aunt Lou's son Odell arrives in Deadwood, boasting of a gold discovery in Liberia... Steve, beset with guilt and grief, denounces all racist attitudes and works diligently at the livery--Kidding! He's still awful as fuck. ... Also, Robin reports that General Fields, recently assaulted by snowballs, is now under the county's protection for his involvement in the Gay-Forbes affair. | Send feedback to hooplecast@gmail.com. Find our recording schedule, show notes, discussion threads, and more at hooplecast.com. | Recorded May 15, 2016. Released May 20, 2016. [Warning: Explicit Language.]

Episode Thirty-seven!! …Jeremiah Isaac?? What’s a Jeremiah Isaac?!? Listen in to find out!! Performer, musician, and all around awesome guy Jeremiah is in the studio this week for Black History Month. He shares his experiences about living life overseas as a black man (we’re allowed to used the term ‘black’ to describe him – we … Continue reading #37 – Jeremiah Isaac →

[intro music]   Dan Keller: Hello, and welcome to Episode Thirty-six of Multiple Sclerosis Discovery, the podcast of the MS Discovery Forum. I’m your host, Dan Keller.   This week’s podcast features an extended interview with Jenny Ting, an immunologist who studies the inflammasome, a multi-protein oligomer that’s part of the innate immune system. But to begin, we’d like to tell you something about why we started the MS Discovery Forum.   MSDF, located at www.msdiscovery.org, is an online portal providing news and information about research in MS. We offer a unique combination of news and background articles written by professional science journalists, viewpoints from thought leaders and subject matter experts, and technical resources that enable sharing and analysis of information and open discussion among MS stakeholders in academia, industry, and the clinic. Membership in MSDF is free, and all content on the site is provided on an open-access basis to the entire MS community.   MSDF stands apart for its comprehensive and independent coverage of MS research. Readers can depend on MSDF to report and verify, not merely re-run press releases. MSDF’s overarching goal is to accelerate progress toward clinically useful advances.   We launched MSDF in April 2012 with the aim of filling a knowledge gap in MS research. The plan was to promote collaboration among scientists who are separated by specialized skill sets, institutional boundaries, and geography. It’s well known that these individuals attend different meetings and read different journals. And while it’s common knowledge that scientific breakthroughs and medical advances most typically result from cross fertilization of ideas, in today’s world scientists still do not easily share ideas and collaborate on solutions. We wanted to change that, and to bring thoughts, knowledge and ideas out from the lab into the open to enlighten and inform all stakeholders in the effort to cure MS, including health care providers and people affected by MS.   To that end, we employ the highest standards for independent journalistic reporting, including the use of multiple viewpoints to give a full picture of a finding’s impact. We aim to make scientific findings accessible to everyone, from busy clinicians to cutting-edge researchers to people with MS and their loved ones. We avoid short-cuts, such as the use of jargon, that get in the way of comprehensibility. We highlight the potential clinical impact of the research we cover, even when we’re covering basic research that may be years from direct clinical relevance. And we seek innovative ways to communicate important information to our audience.   [transition music]   Now to the interview. Dr. Jenny Ting is Professor of Microbiology in the Institute for Global Health & Infectious Diseases at the University of North Carolina at Chapel Hill School of Medicine. In addition to MS, Dr. Ting’s research interests include the role of the immune system in infection, inflammation, and cancer. Science Journalist Carol Morton caught up with Dr. Ting at a recent Keystone meeting.   Carol Morton: I appreciate your taking time out to talk to MS Discovery Forum. So we’re at the Keystone meeting on Neuroinflammation in Taos, New Mexico, and you gave a very interesting talk today.   Jenny Ting: Thank you.   Morton: So can you tell us what you’re talking about when you’re talking about the inflammasome and the particular proteins that you’ve been looking at.   Ting: The groups of proteins that we work on are cytokines, and cytokines are made by immune cells. And they have a tremendous impact on inflammatory responses. As you know, in MS there is a big immune component, so these cytokines will influence it. And in most cases cytokines activate the immune system. One of the key cytokines that we’ve studied is called IL-1, interleukin-1 beta; this is the one, for example, that causes fever, inflammation, and so forth. So it’s called interleukin-1 because it was the first one discovered, and it turns out it’s probably one of the most important ones.   So because it’s a master cytokine, and once it goes it kicks off all the other cytokines, so there’s a cascade that goes on. So it could activate other cells to make other cytokines, so it’s like a vicious cycle. Obviously, this becomes a pretty important target to think about. The process that causes this cytokine to be produced is a very big molecule that’s comprised of different proteins. And these different proteins, they are, together, called the inflammasome for inflammation large complex because “some” means large complex. Inflam- is inflammation, as in inflammasome. It’s the name given by Jürg Tschopp.   And so this process where you have this big complex, and as a result you get the cytokine called interleukin-1 beta, what happens is that interleukin-1 beta has now been implicated in so many diseases including arthritis, very rare diseases that causes a lot of inflammatory responses. It’s involved in skin allergies. It’s involved in colitis, you name it, and it’s involved in smoke-induced chronic obstructive pulmonary disease, COPD, that we see advertised on TV. So all of these have this component of this molecule.   Morton: So anything that releases IL-1 beta, inside the cell there’s a cluster of proteins that have to come together to make it.   Ting: Right.   Morton: And then it gets secreted and does its job.   Ting: Yes. And as we learned today, and actually it’s been published, but may be new to some of the audience, is that this whole complex can also be excreted in some ways into the cell, you know, pushed outside of cells so it can go from perhaps one cell to the other. So we have previously found that this can be a complex that’s membrane bound, and that’s called an exosome. So it’s both just like a minicell that goes from one cell to the next and make the next cell inflammatory as well. The speaker today showed that, in addition to that, it can also go out as a complex, perhaps naked. It seems like they are not really membrane bound, so that’s a different form. So it could be different forms that goes out from one cell to the next causing inflammasomal activation in the next cell and therefore perpetuates this IL-1 process.   Obviously, in normal hosts there must be a way to turn off this process, otherwise we would be, you know, a little ball of pus sitting on a chair. So obviously these don’t go on forever. The problem with chronic inflammatory diseases is many of these things, they don’t go on probably all the time, but they do increase. So what we did is really look at mice lacking genes that can make these proteins. This complex is usually comprised of at least three components; you knock out one and you can’t make IL-1 anymore. Actually, I should say five components. So we did that, and what we found was that if you take this out, the models of MS suggests the well-known mouse model, EAE, and another model that we’ve been really pushing, although it was initially worked on in the late 1960s and early 70s, this model of neurotoxicant-induced demyelination. In both of those models this process of inflammasome/IL-1 turned out to be bad.   So if you remove this process, the disease is much more attenuated. So that’s one of the really interesting parts about what we had found is that potentially this could be a target. And the good thing is that there is certainly some companies that have successfully made anti-IL-1s. So there is an IL-1 receptor antagonist that inhibits this process. There is an antibody against IL-1 that will inhibit this process. So certainly there are therapies, if this is true, that this is part of the MS problem that this could be used as a therapy.   The other thing we have found, which I didn’t get a chance to talk about, is that we did look at the remyelination phase and found out that, for example, IL-18 is not very good for remyelination. Of course, remyelination is what everybody would like to have, is a reparative process. And so one possibility is, can we block the IL-18 pathway, and can we get better remyelination processes. So those are some of the thoughts that we have.   Morton: So have you examined a number of the ILs from 1 to 18 or…?   Ting: No, because 18 is the product. So this inflammasome actually has many different targets. One of them is IL-1 beta; that’s the key one. Another one is IL-18. So we went from there to look at what’s downstream of the inflammasome and found out that IL-18 actually has a role both in making MS disease models worse and in reducing the extent of remyelination. So it doesn’t look like it’s a great protein to have around. So the question is can we try to inhibit this molecule.   Morton: Just to make sure that I’m clear on that: the inflammasome is a cluster of proteins that come together in an immune cell, like a T-cell, or a…   Ting: Usually it’s a macrophage or a microglia or an astroglia.   Morton: A macrophage or a microglia. And then that makes the IL…   Ting: So what you have is – I don’t know if the audience might be familiar with the coagulation pathway where you have one protein that has to be cleaved into a smaller protein. Then this protein B goes and cleaves a second protein from a bigger form to a smaller form. And the smaller form, in every case, is the mature protein that has activity. The bigger protein is the inactive form that doesn’t do anything. So this exactly the same. Pro-IL-1 has to be cleaved into IL-1. Pro-IL-18 has to be cleaved into IL-18. And what that cleavage process is this inflammasome complex producing an enzyme that will cleave these proteins.   Morton: So the inflammasome is like Edward Scissorhands running around cutting proteins making them active.   Ting: Yes, that’s a great analysis. So it’s just exactly like that. The inflammasome produces this – like you said – Edward Scissorhand that then this guy can go and prune the roses and prune the bushes, and they’re different, and they have different functions.   Morton: And it’s the starting block for the activity of the IL-1 and IL-18.   Ting: Right, so the bushes are like – if the roses are the IL-1, you can decorate it; you can give it to somebody; you can make it into a bouquet. So that’s the kind of idea. And then if you have a bush, you know, you can potentially do other things with it. Or if he’s cutting some edible plants you can use that for cooking. So that’s the whole idea. Whatever you produce has different effects. And it turns out IL-18, in our hands, looked like it’s not a good molecule. We have previously found that a cytokine called TNF, which has different roles depending on what it binds. So if it binds to TNF receptor 1, then it’s not so good. If it binds to TNF receptor 2, it actually enhances remyelination, so again, something you want.   And there’s recent talks and there are small molecules where people tried to activate the TNF receptor 2 pathway, and they found that that really enhances the remyelination process. It’s kind of really neat; if you can dissect these pathways well enough, then you might be able to use drugs to target MS.   Morton: So what are the next questions that you’re asking? Where are you going from here?   Ting: So we have a number of directions. Certainly, like I say, I raised the concept of IL-18; so can we target that molecule? In our own lab we’re also looking at several other pathways. So we have found a pathway that’s really important for cell-cell interaction that’s important for MS activation. And the molecules are called plexins and semaphorins. And this is a pair of proteins that seems to activate the immune system especially during MS. So we’ve done that in disease models, and we actually produce a blocker of that pathway. And we have treated mice, and they look much better. We showed that when they’re going through relapse, we can actually prevent them from coming back with a relapse.   So, very similar to some other MS drugs that are on the market, we’d like to think about this as additional possibilities. So those are some of the things that we’re doing.   Morton: What cells are these on?   Ting: These are T-cells and dendritic cells so they’re…   Morton: They’re talking to each other.   Ting: Yes, exactly, they’re talking to each other. And in an MS situation they talk to each other, they activate T-cells, which destroys the myelin. So if you can block that interaction, many of the drugs that are used for MS actually are targeting exactly that interaction pathway. For example, Tysabri is one that’s not so much dendritic cells and T-cells, but it reduces T-cell migration through the vasculature into the blood brain barrier. So that’s one of them where they block T-cell activation. So we are trying to block T-cell activation as well, but at the face of these two cell types.   Morton: If the inflammasomes, if they were superheroes or characters in an Oscar-winning movie, what would their personalities be, do you think?   Ting: I think they would be very powerful because they impact a lot of disease processes, yet they have very strong roles so that, when they’re used properly, they can defend against all sorts of stuff. Whey they’re used improperly, they can really cause a lot harm. So if they’re a superhero, people always say Batman has a dark side, right, a really dark side and a really good side. Maybe that’s what they are.   Morton: That’s a good analogy.   Ting: They’re not like Superman because Superman seems like all good.   [transition music]   Keller: Thank you for listening to Episode Thirty-Six 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 Thirty 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 Dr. Seema Tiwari-Woodruff about estrogen in animal models of MS. But to begin, here’s a brief summary of some of the latest developments on the MS Discovery Forum at msdiscovery.org.   Last week, we reported on the results of another clinical trial for hematopoietic stem cell transplantation in relapsing-remitting MS. Compared to the “halt-MS” trial, which we reported on in January, this study used a less aggressive conditioning approach. Patients involved in the study demonstrated improvement in EDSS scores, and eighty percent of them were relapse-free at four years. The results raised important questions about how to prep MS patients for the transplant. Visit our “News and Future Directions” section to read the full story.   A recent study published in the Multiple Sclerosis Journal demonstrated a potential new way to monitor lesion repair using standard MRI techniques. Clinical trials usually look for new lesions in brain scans to monitor drug efficacy. Lead author, Daniel Reich, told MSDF it’s more important than ever to be able to visualize changes in tissue since drug development is shifting towards neuroprotection and repair.   We’re also pleased to announce that Daniel Reich is one of two new members of our Scientific Advisory Board. Dr. Reich is the director of the Translational Neuroradiology Unit in the National Institute of Neurological Disorders and Stroke, part of NIH. Our other new board member is Deborah Backus, an expert on rehabilitation who is Director of Multiple Sclerosis Research at the Shepherd Center in Atlanta, Georgia. Read their full bios in our “Who We Are” section under the “About Us” tab.   [transition music]   Now to the interview. Dr. Tiwari-Woodruff is an associate professor of biomedical sciences at the University of California, Riverside. She met with MSDF editor-in-chief, Bob Finn, to talk about her research on estrogen and multiple sclerosis.   Interviewer – Robert Finn Dr. Tiwari-Woodruff, welcome.   Interviewee – Seema Tiwari-Woodruff Thank you.   MSDF So what is the connection between estrogen and MS?   Dr. Tiwari-Woodruff It’s an interesting connection between estrogen and MS, because estrogen is actually a part of life in a way that our brains require it, our bodies require it at every moment of our life, I should say. Many years ago it was found that relapsing-remitting patients had less relapses when they were pregnant, and the causes of that was potentially estrogens – high levels of them – or progesterone or vitamin D. Many researchers went ahead and looked at those high levels of pregnancy estrogens called estriol and found that high levels of estriol were the reason why these women patients had lower levels of MS symptoms.   So eventually down the line, estrogens were parsed out of which estrogen was better. And it turns out that one type of estrogen, which is the estrogen of the alpha, is more immunomodulatory – it actually suppresses the immune response – and that is probably what makes MS symptoms better versus estrogens of the beta ligand was known not to have that much immunomodulatory effect; instead, it was actually directly neuroprotective. So estrogens of the alpha and beta both seem to have an effect on various cell types which are involved in multiple sclerosis.   MSDF So if estrogen seems to be protective in pregnant women with MS, why not just use estrogen, or an analog like estriol or estradiol, as a treatment?   Dr. Tiwari-Woodruff That’s a very good question. And, first, these therapies were thought that we were going to use those first, and a lot of clinical trials were going through with that. But what happens with high levels of estrogen is there are two things which are important to know. One is they have a feminizing effect, and the second one is they have a preponderance for causing uterine cancer or breast cancer. So you don’t want to stimulate those two types of cancer. So high levels of estrogen could be dangerous in that aspect. So that is why we don’t want to use that as potential therapy.   MSDF So you’ve done a lot of work with a specific estrogen receptor agonist called indazole chloride. First, tell me how you came upon this compound.   Dr. Tiwari-Woodruff So estrogens of the beta ligands are not just being looked at for multiple sclerosis, they were being looked at as a potential therapeutic for menopause – hot flashes included – rheumatoid arthritis, and other impairments like prostate cancer, etc. So there were quite a few chemists who were coming up with various different types of estrogen receptor beta ligands. So while I was doing my work with mouse models of MS in generic estrogen receptor beta ligand, which was the DPN – diarylpropionitrile – a study came out which was actually on indazole chloride which was developed by a chemist, John Katzenellenbogen; he’s done a lot of work on developing these molecules. And this particular compound showed that it decreased activation of astrocytes and microglia; this was published in Cell a few years back. And we met at a meeting, John Katzenellenbogen and myself – we were giving a talk at the same time in a meeting in Stockholm – and we decided to talk to each other. And he said, “Your research is very intriguing on estrogen receptor beta ligand, would you like to try this out?” And that’s how I got my hands on the indazole chloride. And we did some preliminary studies and showed good results. Then we decided to embark on a full-fledged study which was published in PNAS.   MSDF So you used indazole chloride in two different mouse models of MS, and you used it both prophylactically and in mice that are already showing symptoms. What did you find?   Dr. Tiwari-Woodruff So prophylactically when you use a compound, you are actually trying to see if you can inhibit the symptoms which are going to come up when you induce a disease, and that is all good. But when you are talking about patients who come to see the doctor, they’re always coming in with symptoms, so they already have the disease ongoing. So the second paradigm where you give the drug when the disease symptoms are already there is closer to what humans are going to be able to see. So the nice thing about indazole chloride was that, prophylactically, definitely it made the mice better, but therapeutically also; they were able to decrease the disease symptoms by nearly 50%.   MSDF What is the significance of the fact that it seems to work on two different mouse models of MS?   Dr. Tiwari-Woodruff So when you’re looking at a drug especially in a disease like multiple sclerosis which has two major components – one is inflammatory component and another one is a neurodegenerative component – if you can show that this drug is working in one way or both ways would be very useful for developing better drugs or better treatments. So what we did was when we treated the mice with indazole chloride, in one mouse model which is the experimental autoimmune encephalomyelitis which contains both the inflammatory and the neurodegenerative component, we saw a decrease in the disease symptoms. But we couldn’t tell if the indazole chloride was working in the inflammatory component or the neurodegeneration component, because it showed effect on both.   So we went to a second mouse model which is the toxic cuprizone diet model which doesn’t have a primary inflammatory component. The disease starts with oligodendrocytes, the cells which make the myelin. They die when you feed this diet to the mice, so they have massive demyelination in regions of the brain. When we gave the drug during the remyelination phase, we found that indazole chloride was able to remyelinate the axons better when the drug was present versus when it was absent. So this actually showed us that indazole chloride has two arms to it. One, it inhibits the inflammatory component and the second, it inhibits the neurodegenerative component independent of the inflammatory component.   MSDF Is it also sort of confirmatory? The EAE is not a perfect model of MS and neither is the cuprizone mouse model, but does it make you feel better that these two completely different models are showing similar effects?   Dr. Tiwari-Woodruff Absolutely, you really hit the point where… We are always looking for the best model for multiple sclerosis, but because the disease is so complex no one model can be said that it’s 100% mimicking multiple sclerosis. So for us to see that demyelination which occurs both in EAE and the cuprizone model was improved – we actually saw remyelination in both models – really gave us hope that this drug could be directly acting on oligodendrocytes which are forming the myelin, which is the cause of major mode of dysfunction in multiple sclerosis.   MSDF So does indazole chloride help these mice a little bit, or does it help them a lot?   Dr. Tiwari-Woodruff So that’s a very good question. Similar to what you might see in the patient population, in the mouse model of MS, especially in the EAE model, the disease is not consistent. So the lesions which appear in the brain of EAE animals are very diverse, unlike the cuprizone model where the demyelination is very consistent. So when you’re looking at these mice, especially in the EAE cohort, if the animal is really, really sick, you actually see the disease symptoms go down just a little bit. But if the animals were sick to the middle level, they actually showed a bigger difference, they showed better recovery. And we hypothesize that the axons which have been injured to the point of no return, if the axons have been demyelinated and injured, it doesn’t matter now when you give them therapeutic drugs, these are not going to improve. So there are certain number of axons in the brain which drop out and we don’t see recovery in those. But said that, overall we still saw a significant increase with indazole chloride treatment in both models.   MSDF Have you done histology?   Dr. Tiwari-Woodruff Yes. We’ve done histology, we’ve done electron microscopy. And we do one more thing my lab is very good at, we do electrophysiology. Because one of the things we always think is when you look at remyelination you can see myelin coming up, but is the myelin functional? If the axons can conduct faster or better, then you know that the myelin which has covered the axons is functional. So we do all three. And we also include behavioral testing. So one of the tests we included which a lot of people use is a Rota rod; it’s a motor test to show that the mice can stay on the Rota rod much longer after treatment with indazole versus just the vehicle.   MSDF Do you see any side effects?   Dr. Tiwari-Woodruff So that’s interesting. We did not see any side effects in these mice. Agreed, we treated them up to 60 days, we haven’t treated them longer than that, plus we were giving them at a 5 mg/kg/day concentration. So we didn’t see any kind of toxicity. But said that, we still need to do those studies in a thorough way before we can safely say that they had no side effects.   MSDF So what’s next in the development of indazole chloride as a potential MS treatment?   Dr. Tiwari-Woodruff So indazole chloride is a good target. And while these studies were going on last year, John Katzenellenbogen and myself, we were talking about how are we going to proceed with this because we were seeing really good results; this is even before I published the paper. And he said what would you like to do? And one of the things we said was is it possible to make better analogs of this compound which are going to be more specific, could be used in a lower concentration and may have a better therapeutic outcome?   So he came up with four analogs which he has sent to me, and we did some preliminary studies to see if they were toxic to cells in culture, because that’s the first thing you do. And they have no toxicity in cells, they actually have shown to behave well with proliferation – depreciation of the cell – and we haven’t seen more cell death or less cell death with them. So we are very excited about that. So coming next month, we are actually going to start treatment of EAE animals, and once that goes through the goal is to do toxicity studies on the two best compounds and see if we can find a company so we can have a backing on these drugs for potential human trials. It’s a couple years from now, at least – it could be even more – but we are actually moving in that direction.   MSDF Dr. David Baker in a commentary on his multiple sclerosis research blog seemed less than enthusiastic about indazole chloride. He suggested that many compounds seem to work similarly in mouse models. How do you respond to that criticism?   Dr. Tiwari-Woodruff So Dr. Baker has a very good point on saying that there could be many compounds which are good in EAE but they fizzle out and they don’t go up to clinical trial. I disagree on one point where it comes to indazole chloride, because we have precedence of estrogens showing good therapeutic indication in humans; there were clinical trials done in UCLA where they showed that there was improvement with estriol treatment. And estriol does target both ER-alpha and ER-beta – ER-beta a little more than ER-alpha – so I’m very confident that what we are seeing with estrogen receptor beta is not a fluke. And because it’s a steroid and a small molecule, it does not seem to have a lot of toxicity involved which could be somewhat which is brand new. So we’ll see. I hope Dr. Baker’s wrong and we do manage to get this drug to human patients and we see therapeutic efficacy in them.   MSDF Dr. Baker also said that a critical experiment had not yet been done. And let me quote from his blog post. He said, “The development of demyelination should be allowed to occur after this damage has abated, then punitive remyelinating drugs should be given.” How do you respond to that?   Dr. Tiwari-Woodruff Very good point made by Dr. Baker, but I have actually addressed those in the PNAS paper. We part off particularly this aspect of the disease. So the prophylactic treatment was before the disease started; that is what he’s mentioning in the blog. The second part is what is important where EAE disease was induced, and after peak disease had occurred we gave the drug, indazole chloride. At the peak disease, we actually see increased inflammation, but alongside with that we see demyelination and axon degeneration. So the damage has already started. The drug treatment after that is what caused the disease to get better. We saw increased conduction, we saw increased remyelination, and less axon damage.   Similar to that, we also did the experiment in cuprizone. The treatment paradigm was as such: We actually had nine week of demyelination ongoing in the cuprizone model, which is very chronic; it’s chronically ongoing where you have quite a bit of damage of the axons and you have acute demyelination. During the remyelination phases where we gave the drug either to one group and vehicle to the other group, what we saw was that the drug treatment, indazole chloride, actually increased remyelination and decreased axon damage. So I think Dr. Baker was trying to make a point on we haven’t done the right experiment, but I think we have done the right experiment. And further research with indazole chloride will let us know if this is a good drug or not.   MSDF Dr. Tiwari-Woodruff, is there anything you’d like to add?   Dr. Tiwari-Woodruff I would like to add one more thing. We have actually looked at indazole chloride in optic neuritis – EAE-induced optic neuritis – and we are going to be publishing a paper fairly soon showing that in optic neuritis we see less inflammation in the retina and increased remyelination in the optic nerve. So I’m very confident that it’s not just a phenomenology in one part of the brain which we picked last time – it was the corpus callosum – that we see increased remyelination and decreased damage caused by EAE with treatment of indazole chloride.   MSDF Well, thank you very much.   Dr. Tiwari-Woodruff Thank you.   [transition music]   Thank you for listening to Episode Thirty 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 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]

Red Radio returns after a week's hiatus with an extended Episode Thirty!  First off, Erin Red has the pleasure of chatting with director and advocate James Costa about his groundbreaking new film, Lunch Hour, and his feelings on activism, veganism, and the future of health in the US. Next up, an enthusiastic journey through the whirlwind weekend that was The Seed: A Vegan Experience!  Erin Red shares every delicious detail and unapologetically brag about her brand new Vitamix!  Plus a very special Compassionate Clip of the Week - what a jam packed episode!!!  Please consider supporting Red Radio by visiting erinred.com and clicking the DONATE button, and subscribe to Red Radio on iTunes today!  If you love what you hear, leave a glowing review, or drop Erin Red a line at erinredradio@gmail.com.  You can also read her blog at erinred.tumblr.com, and find her on Facebook and Twitter @erinred. 

Episode Thirty-nine - A starlet and an ancient curse attack while the students explore individuality! Featuring "Getting What You Want" and "Blocks". --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-eight - Chaos advances and balance demands sacrifice! Featuring "The End of a Beginning" and "No". --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-seven - Join us as loss and memory are wrestled with and put to bed. Featuring "Bed 667" and "Memories in the Dark". --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-six - Join a scientist and doctor as they have first contact and final battles! Featuring "The Scientific Method" and "Time's Quartet, part 4 - End Game". --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-five - Love and lust collide as gods play games and humans fight! Featuring "Coffeshop of Love" and "Henpecked". --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-four - A simple man and a soldier take control of their lives...after they've died! Featuring "The Damned" and "Screen Door". --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-three - The real and fantastic collide as police investigate a murder on a horror movie set! --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-two - Lives are rocked in a moment as strangers collide in a subway and skyscraper! --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Episode Thirty-one - As mundane and fantastic events collide with their lives, two ordinary office workers deal with the remains! --Please leave us a rating on iTunes!-- Website: pendantaudio.com Twitter: @pendantweb Facebook: facebook.com/pendantaudio Tumblr: pendantaudio.tumblr.com YouTube: youtube.com/pendantproductions

Here we go with:Episode ThirtyThis week Simon takes a long hard look in The Mirror and only finds something worthless staring back at him. Meanwhile, iszi presents a guide to surviving Christmas. Literally.