Podcasts about Critical Role

While dealing with the Dark Dagger Gang smugglers, Clash discovers a very effective weak point on most humans. Lovelace, on the other hand, searches the library of a nearby university for esoteric writings. Follow us on Twitter! http://twitter.com/ambiguouspod Like our Facebook page! https://www.facebook.com/AmbiguousPod Subscribe to our Youtube channel! http://bit.ly/moralambiguityYT Listen to "When Is it My Turn?" http://bit.ly/whenisitmyturn BACKGROUND MUSIC/AMBIANCE CREDITS Shadowsense: http://shadowsense.bandcamp.com/ Critical Role: https://open.spotify.com/album/4bnkEga6KDahzV5eMkVwxm?si=3CnKZq6GTcubxCqVtyvpsg Kevin MacLeod: https://incompetech.filmmusic.io/ Tabletop Audio: http://tabletopaudio.com/ Sword Coast Soundscapes: http://swordcoastsoundscapes.bandcamp.com/ (License: http://creativecommons.org/licenses/by/4.0/) --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

As the Goldeneyed Griot continues his tale, Mooti and Ongenagama face painful losses, difficult decisions, and a tragic showdown. Get the tissues ready for this one, folks, because it's a DOOZY! Featuring our incredible guest star:Luyanda Unati Lewis-Nyawo (they/them) as Ongenagama (she/her, The Strong Lionblood, Oath of the Ancients Paladin/Beast Barbarian) Starring: Shamini Bundell (she/her) as Reth (they/she, Eland's Blessing Swala, Squared Circle Pugilist)Liv Kennedy (she/her) as Juji Osei (she/her, Bloom Emere, Circle of Stars Druid 4/Twilight Cleric 2)Jonathan Charles (he/him) as Aboade (he/him, Copper Ironmaster, Battle Smith Artificer)Jasper William Cartwright (he/him) as Mooti Qobaa (he/him, Half Moon Daa'ima)and Jeremy Cobb (he/him) as your Very Neighborhood Dungeon Master! Post-production by Seth Leue and Daniel Ramos Join us for D&D in a Castle!D&D in a Castle Round 1 (March 6-10) - Jeremy & Jasper DMinghttps://shop.dndinacastle.com/collections/round-1-march-6-10-2023  You can now buy merchandise here! as featured on Critical Role! Support us on Patreon at patreon.com/tbhalflings for your Shirefolk Shoutout and Bonus Episodes. Connect with us on Twitter, Instagram, and Facebook @3blackhalflings, on our Discord, or email secondbreakfast@tbhalflings.com See omnystudio.com/listener for privacy information.See omnystudio.com/listener for privacy information.

When the Away Team reunites in Brigarune City to travel to Greyhaven for Grom's upcoming Punch Bowl match, Selene discovers something unsettling in a hill giant's possession. Efimia wrestles with the thought of Thorn being in such a powerful position, Zag pretends to be a god, Grom justifies Ascended Corp.'s assassination attempts, and Selene has an out-of-body experience through the eyes of one of Lathander's Celestial Blade elites.Support our show by going to https://patreon.com/knocked and subscribe for as little as $2 a month for hours and hours of bonus content!

Rolling In The Netherdeep Ep 18Mother's DayNorth is reunited with his mother. Wilvan and Orgoth celebrate the day's events and Lapuhs goes on a far reaching side quest.Watch us live on Wednesdays 4:30 Eastern/1:30 Pacific on Twitch!Thanks to Wizards of the Coast, DnD Beyond, and Critical Role for helping us build worlds of adventure!Ron Murphy – DM, @ron88keysRBDMWilvan Grandmane – Ross Griffin, @griffRMLaphus Prismawing - Jaiden, @foxtrotfalloutOrgoth Skullcrusher - Bill Roper, @billroperNorth Star Maedrick - Jaime, @suburbancrypticFollow us on Twitter at @SeveredSonsDnD!Join our Discord! Join our Patreon!Give us a review on Apple Podcasts, Podchaser, Spotify,  GoodPods or on our Twitter page and we'll read it on the air.  Keep on rolling! Support the show

In this episode, some of our heroes try to get some money for the troubles they endured in the Posemphney Forest. Will they succeed in getting what's owed to them? Or will they end up on a wild goose chase?Visit www.fateofisen.com to learn more.Fate of Isen is one of the Feedspot top D&D podcasts in the world! Check out Feedspot here.If you like the show, please feel free to follow us on social media (@fateofisen) or support us on Patreon!Intro, outro, and recap music by freesound user, Tyops, and ambient sound by TabletopAudio.com ★ Support this podcast on Patreon ★

The great forest is dying and with it the barbarian Ulvson clan. The decline began with the emergence of the hideous boar faces and their mysterious leader, the Light Eater. To save his people, Torv sets out to destroy the bringer of the Black Night.

What drives fear into the hearts of the Cool Story Guys? In this episode, we discuss the tangible and existential dreads that haunt our everyday existence. Other topics include Jeff's general inability to listen to good advice, the impending emergence of the Shrimp Summoner, and an introduction to the physically, emotionally, and temporally separated "Distant Ethan."

     In this episode Saul and Jolene discuss shopping in RPGs.  This topic was put forth by a Facebook post asking Saul to read a blog about shopping.  Saul mentioned it to Jolene who didn't think there would be much opinion on the subject, but even Saul was surprised by how adament people's opinion on the subject was.       From the players and GMs that absoulutely hated shopping in a RPG session to some that made it a feature of starting of their campaign.        Saul and Jolene discuss their experiences with shopping and how their kids really liked shopping when the party got to town.  This episode mentions living in the middle of nowwhere, Little House on the Praire, Critical Role and many other subjects seemingly not associated with shopping.       Web Art by Jim Foster      Episode Art by Michael Shean-Jones     Music by Captive Portal, song They Went Shopping    Available from Freemusicarchive.com    Attribution-ShareAlike: http://creativecommons.org/licenses/by-sa/4.0/  

I had the distinct pleasure of recording my first video interview with Sumalee Montano!   We talk about her new movie, The Deal. From coming up with the movie concept, producing, and acting in it. We also talk about her experience with Critical Role, and being a part of so many different fandoms.   From Star Wars to Mass Effect, Voltron, Transformers, Justice League, Dragon Age, and so many more. Just scroll her IMDB credits... you'll find a massive list of shows she's been in as a face actor or voice actor!   She's been a part of so many that I had to ask... which fandom that she hasn't been in, would she like to be - and I think her answer may surprise you. You can find Sumalee at: https://twitter.com/sumaleedotcom https://www.sumalee.com/ https://www.instagram.com/sumaleedotcom/ You can find The Deal on: https://therokuchannel.roku.com/details/cdd0ef1e2e2157ff95c3bc0fb8d40197/the-deal You can find this episode in video format at: https://www.youtube.com/watch?v=o1UfYGZZ6sk

Join us on Patreon: https://www.patreon.com/blankcoverpodcast Blank Cover Podcast Series 3 Episode 56 Let's talk GAMES! BCVs Jenny and Benjy discuss SO MANY VIDEO GAMES! Bayonetta, Ragnarok, Mario, Teenage Mutant Ninja Turtles and... video game crushes. Enjoy! See more from us: https://linktr.ee/blankcover Get in touch with us: via twitter @PodcastCover email blankcoverpodcast@gmail.com Intro music by HumanoideVFX Outro music by Longzijun Our thanks to Pixabay

Welcome to the magical world of Oz! This whimsical one-shot is presented in partnership with Andrews McMeel Publishing to celebrate the launch of their new Dungeons & Dragons book "OZ: A Fantasy Role-Playing Setting". Get your copy here: https://bit.ly/secondstarozMarkeia McCarty, Luis Carazo, Desirée Strother, and Andrew Strother, are led on a magical adventure through the land of Oz by Dungeon Master Joe Nuzzo. Our players' goal? To recover a stolen artifact and return it to Glinda, the Good Litch of the South, before the thief uses it to strip magic from Oz FOREVER!Character art and poster design by Andrew Kolb | https://www.kolbisneat.com/Stream design and opening credits by MTD Jake | https://twitter.com/mtd_jakeCast:Markei McCarty | https://twitter.com/markeiamccartyLuis Carazo | https://twitter.com/LuiscarazoDesirée Strother | https://twitter.com/desmazingAndrew Strother | https://twitter.com/rollpersuasionJoe Nuzzo | https://twitter.com/LeverPullFollow Andrews McMeel | https://twitter.com/AMUTTRPGSFollow Second Star Productions | https://twitter.com/secondstarshowBuy a copy of Oz | https://bit.ly/secondstaroz

The group ventures down into the Forgeheart to seek out a way to end the blight over Kaglemgrad!  JOIN OUR DISCORDCheck out the CAUSES WE SUPPORT to get involved and donate!Help support the show by visiting our Patreon and find even more content at our Website!Tracklist and Creative Commons Attribution Can Be Viewed HEREIntro/Outro Music “Jotunheim” Courtesy of Serpent Sound StudiosInterlude Music “Bit Quest” Courtesy of incompetechSound Effects Courtesy of SyrinscapeAdditional Music Courtesy of:Larian Studios: Creators of the Divinity Series WEBSITEThe Game Kitchen: Creators of Blasphemous WEBSITE / BANDCAMPCD Projekt Red: Creators of the Witcher series WEBSITE / USE POLICYOwlcat Games: Creators of Pathfinder: Kingmaker and Wrath of the Righteous WEBSITE

Top 3 Takeaways From This Value-Packed Conversation: Automation can help a customer find information and receive a genuine brand experience even in periods where you're offline. They may be doing late-night searches and discover your website, and having certain functions set up to run automatically will allow them to get the answers they seek without actual human assistance Despite the convenience automation can provide, you don't want to lean too far towards automating everything and removing the human experience. This can create disconnection between your brand and your customer, leaving them feeling unappreciated and undervalued when they want to take the next step towards patronizing you If you want to utilize automation in your business operations, be sure your brand can support it and it doesn't come at the expense of losing customers because of it   ______________________ Click here for complete show notes  It's time to take your brand from unknown to undeniable. Discover how to reach expert status and attract new clients, expand your network, and much more. Click here to learn more Get your copy of PodMatch Guest Mastery! MUSIC CREDIT: "Victory" courtesy of purple-planet.com

Picking up several months after the events in Cognouza, The Mighty Nein have all started new chapters in their lives. However, when some discover that there are still old chapters yet to be closed, our unsung heroes must reunite for more stories untold… Due to the improv nature of Critical Role and other RPG content on our channels, some themes and situations that occur in-game may be difficult for some to handle. If certain episodes or scenes become uncomfortable, we strongly suggest taking a break or skipping that particular episode. Your health and well-being is important to us and Psycom has a great list of international mental health resources, in case it's useful: http://bit.ly/PsycomResources Twitch subscribers gain instant access to VODs of our shows like Critical Role, Exandria Unlimited, and 4-Sided Dive. But don't worry: Twitch broadcasts will be uploaded to YouTube about 36 hours after airing live, with audio-only podcast versions of select shows on Spotify, Apple Podcasts & Google Podcasts following a week after the initial air date. Twitch subscribers also gain access to our official custom emote set and subscriber badges and the ability to post links in Twitch chat! Character Art and Thumbnail by Ariana Orner: https://twitter.com/ornerine Mighty Nein Opening Title animated by Kamille Areopagita and Kevin Areopagita “Your Turn To Roll (Critical Role Theme)” Written by Sam Riegel and Jason Charles Miller Original Music by Omar Fadel and Hexany Audio "Welcome to Wildemount” Art reel theme by Colm McGuinness Additional Music by Universal Production Music, Epidemic Sounds, and 5 Alarm

Efimia and Zag make contact with Zag's brother Thorn, the newly bestowed God of the Ten. Thorn comes up with a plan to break Efimia's pact with Orcus by using the ancient elven tradition of pranking him. Meanwhile, Grom and Selene are told who paid Gutrug and Vladrick off to try and kill Grom, and they get some time-pressing news about Grom's next Punch Bowl fight in the process.Get 10% off your entire order: metallicdicegames.com/ref/2518/Coupon Code: knockedVisit www.Patreon.com/knocked to support our Patreon and sign up as a patron for as little as $2 a month.

Having gained an audience with the Great Golden-Eyed Griot, it's time for the Debs to receive whatever wisdom he can impart. But why does the mere mention of the Spider Queen fill him with such dread? There's only one way to get to the bottom of this: it's time for a story! Featuring our incredible guest stars:Luyanda Unati Lewis-Nyawo (they/them) as Ongenagama (she/her, The Strong Lionblood, Oath of the Ancients Paladin/Beast Barbarian)Krystina Arielle (she/her) as Noma (she/her, Lionblood, Queen of Ejozini and Wielder of the Fro) Starring: Shamini Bundell (she/her) as Reth (they/she, Eland's Blessing Swala, Squared Circle Pugilist)Liv Kennedy (she/her) as Juji Osei (she/her, Bloom Emere, Circle of Stars Druid 4/Twilight Cleric 2)Jonathan Charles (he/him) as Aboade (he/him, Copper Ironmaster, Battle Smith Artificer)Jasper William Cartwright (he/him) as Mooti Qobaa (he/him, Half Moon Daa'ima)and Jeremy Cobb (he/him) as your Very Neighborhood Dungeon Master! Post-production by Seth Leue and Daniel Ramos Join us for D&D in a Castle!D&D in a Castle Round 1 (March 6-10) - Jeremy & Jasper DMinghttps://shop.dndinacastle.com/collections/round-1-march-6-10-2023  You can now buy merchandise here! as featured on Critical Role! Support us on Patreon at patreon.com/tbhalflings for your Shirefolk Shoutout and Bonus Episodes. Connect with us on Twitter, Instagram, and Facebook @3blackhalflings, on our Discord, or email secondbreakfast@tbhalflings.com See omnystudio.com/listener for privacy information.See omnystudio.com/listener for privacy information.

What a delightful surprise this podcast has been for us! Something we just threw together because we thought the name was funny, but in eighteen episodes we have learned so much about ADHD, D&D, and ourselves! And we want to dream up what other kinds of trouble we can get into. We're taking a very short break and will be back in the new year with Season Two, so please stay tuned. Topics include favorite moments of this year, and Alison's dive into Worldbuilding! While we're on "hiatus", we'll be working on our "D&D Spells" TikTok channel here, and asking some of our ADHD&D heroes if they would like to join us for some gabbin'. But in the meantime, please come and hang out in our Discord channel, which is filled with all manner of folx, including neurodiverse brains, professional TTRPG players, comic book, music, movie, and TV show aficionados, theater geeks and more. Just like you!! Dang, you're cool.And if you like this stuff and want to toss a few coins (to your Witchers), you can support us via our Patreon site. It's cheap and it buffs us with Bless so that we can keep making these podcasts!We recorded and edited this podcast using an incredible tool called Descript. It allows us to record audio and video, sure, but then edit that audio/video using the text transcription it produces. We're big into making podcasts accessible, so this is a no-brainer for us. We're not sponsored by them, but the link you just clicked is an affiliate one.

Rolling In The Netherdeep Ep 17North and Lapuhs's Day OffThe eladrin rogue North Star Maedrick questions Question and deals with bureaucracy while the reborn necromancer Lapuhs Prismawing meets Irvan for a evening's skyship ride.NOTE: There was a malfunction with the audio at the beginning of the stream, but Ron has recorded a recap to cover the missing audio's events! Watch us live on Wednesdays 4:30 Eastern/1:30 Pacific on Twitch!Thanks to Wizards of the Coast, DnD Beyond, and Critical Role for helping us build worlds of adventure!Ron Murphy – DM, @ron88keysRBDMWilvan Grandmane – Ross Griffin, @griffRMLaphus Prismawing - Jaiden, @foxtrotfalloutOrgoth Skullcrusher - Bill Roper, @billroperNorth Star Maedrick - Jaime, @suburbancrypticFollow us on Twitter at @SeveredSonsDnD!Join our Discord! Join our Patreon!Give us a review on Apple Podcasts, Podchaser, Spotify,  GoodPods or on our Twitter page and we'll read it on the air.  Keep on rolling! Support the show

Live from IFPA's Global Show: Technology's Critical Role in Local Produce and Controlled Environment FarmingA very special live podcast from IFPA's 2022 Floral and Produce show! We are talking with Craig Hurlbert and Dave Vosburg of Local Bounti, John Purcell of Unfold, and Ali Daniali of HRVSTS.Join us as we discuss:Networking at a global level at the IFPA's Floral and Produce Show. Growing customer demand for locally grown produce Sustainability in the food system.The challenges and possibilities of controlled environment farming. Using Data to inform growing operations. Segment 1 - Craig Hurlbert (CEO) and Dave Vosburg (Chief Innovation Officer) of Local Bounti“Controlled environment food growing is very capital intensive, so this model will require management to have a strong understanding of running capital intensive operations.' - CraigLocal Bounti is an indoor farming company with an aggressive growth plan over the next five years to deliver delicious, great texture, flavorful products to their customers all across the United States, locally grown. The demand for locally grown produce is there, the logistics and infrastructure is evolving. People want convenience, less shelf time, flavor, and low price points. Salad kits are a good example of a winning product right now. Local Bounti is expanding to Texas and Oregon and looking into acquiring other facilities as well. Segment 2 - John Purcell (Chief Strategy Officer) of Unfold“Controlled environment [farming] is a confluence of amazing technologies; I like to describe it as Silicon Valley meets Salinas Valley.” — John According to John, this industry is a huge mashup of many sectors in tech, “a confluence of technologies.”People are drawn to this work because they want to use their skills on something that matters. The reason they get attracted to this is because of the work done producing food in a way better for the planet. It's new in some ways, but in some ways, it's not. There's a cross fertilization of ideas and technologies from outdoor crop growing and indoor crop growing happening all the time these days.John suggests we look at the technologies that are out there, and let's figure out how to apply them.Segment 3 - Ali Daniali (CEO/Founder) of HRVSTS“We've flipped the equation. For growers, it's actually a push versus pull type of equation, where the buyer is actually telling the grower what to grow” — AliHRVSTS grows and sells specialty produce to food service companies. Using data they can get specialty leafy greens from seed to customer in 7 weeks or less, depending on the crop. They use data to eliminate the inefficiencies in the system and also contract with small growers and help new farmers get online quickly. Guest ResourcesLocal Bounti - https://localbounti.com/Craig Hurlbert - https://www.linkedin.com/in/craighurlbert/David Vosburg - https://www.linkedin.com/in/bdavidvosburg/Unfold - https://unfold.ag/John Purcell on LinkedIn: https://www.linkedin.com/in/jppurcell/HRVSTS - https://hrvsts.com/Ali Daniali -

Janine and Neil join Kova, Stephanie and Spoiler Steve  to discuss Netflix's The Wonder, PrimeVideo's The People We Hate at the Wedding and She Said. 00:01:23 – Intro | Box Office & Christmas Movies 00:22:30 – The Wonder 01:04:22 – The People We Hate at the Wedding 01:49:14 – She Said 02:38:34 – The Banter Corner | Nachos, Hallmark movies, Tom Holland's Spider-Man Trilogy, You've Got Mail, True Blood, Run Sweetheart Run, Slumberland, Raymond and Ray, Spirited, The Menu, Tulsa King, Air Force One, New Girl, Key and Peele, Cabinet of Curiosity, I'm A Stalker, Critical Role, The Legend of Vox Machina, Great British Baking Show, The World Cup and Dead to Me Support us on Patreon HERE **NEW SHOWS ARE COMING TO OUR PATREON** Read Stephanie's review of Top Gun: Maverick HERE Listen to Stephanie on the StarkCast here Listen to Spoiler Steve on the StarkCast here Listen to Kova on the StarkCast here Listen to our twenty-first episode of The Blindspot reviewing The Crow here Listen to our twenty-fourth episode of Back to the Movies covering the Mannequin here Listen to the sixth episode of Back to the Shire covering the third act of Lord of the Rings: The Two Towers – Extended Edition here Send us emails and feedback to info@sceneitcast.com Check out our website sceneitcast.com Check out Michael H. Cannon's work at @artildawn

Felice Gersh, MD is an award winning physician with dual board certifications in OB-GYN and Integrative Medicine.  She is the founder and director of the Integrative Medical Group of Irvine, providing comprehensive health care for women by combining the best evidence-based therapies from conventional, naturopathic, and holistic medicine.  Dr. Felice is a prolific writer and lecturer who speaks globally on women's health and is the best selling author of the PCOS SOS series and Menopause:  50 Things You Need to Know.Dr. Gersh was an early entrepreneur, starting her own medical practice from scratch early on.  She added additional practitioners to best support her patients with services such as Chinese Medicine.After deciding to stop seeing patients full time, she went back to school to learn more ways to help her patients.  She did a fellowship in Integrative Medicine and has continued to be a leader in her field.Expanding beyond pharmaceuticals and surgery is essential!It wasn't until 2015 that the FDA required that women be included in studies.The female body evolved for optimal success.Women have very different immune systems than men.  We need to be able to keep a body alive.XX chromosomes help to program the immune system of females to be stronger.There are estrogen receptors on every cell in the body.Innate immune systemCreates a life saving inflammatory responseEstrogen is an immune modulatorWhen you are pregnant you make Estriol, which binds to beta receptors which quiets the immune system to sustain the foreign invader...the baby.The immune response is down regulated during pregnancy.Estradiol is an immune modulator, ramping up and down regulating the immune system.Estrogen is amazing!Micronutrients are essential and nutritional deficiencies can lead to issues with the ovaries.The menstrual cycle is a reflection of women's health.  If there are issues with the cycle, the underlying cause needs to be addressed.When we hit menopause, reproduction ends, but life does not.  We are one of few animals that survives after reproduction has ended.All of our hormones interact.  So when we go through menopause, that balance is shifted.Integrative vs. alternative...using the best of both worldsNot sex hormones but "life hormones"Hormones are neuro-protective - essential for brain functionMolecular mimicry - our cells look similar to infection or other protein which can lead to autoimmunityWomen have higher immune response - 80% of autoimmunityOsteoporosis - hormone deficiencyMetabolic homeostasisOne Step:1-define the problem (choices you control that you could do better with)Pick the one that you can actually do tomorrow - make a commitment- and keep it!If someone loses their thyroid, they never say...that's ok, you don't need it anyway.But when ovaries stop working, that is what women are told.

Farzana Nayani (she/hers), is a recognized DEI specialist, international keynote speaker, and business coach. Of multiethnic Filipina-Pakistani background, Farzana is a passionate advocate for the multiracial community, and through her coaching practice, she supports individuals to move towards healing, transformation and achieving their full potential in a culturally sensitive and grounded way.  Nayani talks about:  Taking care of your employees and giving them a sense of well-being with ERGs Supporting marginalized groups who have faced tragedy and also have to carry on with work: How can we support them effectively as leaders and colleagues, or, if we are these professionals ourselves – how do we best address these issues? Will women and other marginalized groups suffer the highest consequences of “quiet quitting” and "labor hoarding"

「今、日本で女性として働くにはいい時代だ」。   Third Arrow Strategies及びJapan Board Diversity Network代表のTracy Gopalさんはこのように話します。 それはなぜなのか。 それは、世の中が進化しているからです。 もっとも、全ての会社が変わったというわけではありません。依然として難しい状況は続き、男女が平等に競争できる環境にはありません。 しかし、ひと昔前のように、毎晩会社の飲み会やクライアントとのディナーに出る必要もなく、近年は女性の観点に立ったKPIが導入されたり、企業が一定数以上の女性を雇用、昇進させることに注力したりと、女性にとっては好機の時代が訪れています。 そう、日本は今あなたを必要としているのです！ さらに嬉しいことに、よりステップアップしていきたいと願う女性たちには、これまでにないほど強力なサポーターが沢山いるのです。例えば、Tracy Gopalのようにダイバーシティを強力に推し進めることで時代の先端を行く女性や、自身がすでに企業のトップにまで登り詰め、より多くの女性に企業での躍進をエンカレッジしている女性経営者などなど。 今あなたがキャリアのどのステージにいたとしても、今回のSasuga! Podcast Episode 202にきっとインスピレーションを受けるでしょう。今回Tracyさんと次のことについて対談しました： Tracyさんが自身の強みであるスキルや才能を社会的貢献に活かせるように、いかに粘り強く探し続けたか 女性役員が、その優秀さを発揮し、多様性を促進し、現状打破することで、いかに社会を変えられるか 海外投資家が日本のコーポレート・ガバナンスを評価する際に、取締役会や会社全体の多様性をどのように見ているか Enjoy!

This month on Episode 42 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the October 28 and November 11th  issues of Circulation Research. This episode also features an interview with Dr Miguel Lopez-Ramirez and undergraduate student Bliss Nelson from University of California San Diego about their study, Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformations.   Article highlights:   Jia, et al. Prohibitin2 Maintains VSMC Contractile Phenotype   Rammah, et al. PPARg and Non-Canonical NOTCH Signaling in the OFT   Wang, et al. Histone Lactylation in Myocardial Infarction   Katsuki, et al. PCSK9 Promotes Vein Graft Lesion Development   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's Journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today, I'm going to be highlighting articles from our October 28th and our November 11th issues of Circ Res. I'm also going to have a chat with Dr Miguel Lopez-Ramirez and undergraduate student Bliss Nelson, about their study, Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformations. But, before I get into the interviews, here are a few article highlights.   Cindy St. Hilaire:        The first article is from our October 28th issue, and the title is, PHB2 Maintains the Contractile Phenotype of Smooth Muscle Cells by Counteracting PKM Splicing. The corresponding author is Wei Kong, and the first authors are Yiting Jia and Chengfeng Mao, and they are all from Peking University. Insults to blood vessels, whether in the form of atherosclerosis, physical injury, or inflammation, can trigger vascular smooth muscle cells to transition from a contractile state to a proliferative and migratory one. Accompanying this conversion is a switch in the cells' metabolism from the mitochondria to glycolysis. But what controls this switch? To investigate, this group compared the transcriptomes of contractile and proliferative smooth muscle cells.   Among the differentially expressed genes, more than 1800 were reciprocally up and down regulated. Of those, six were associated with glucose metabolism, including one called Prohibitin-2, or PHB2, which the team showed localized to the artery wall. In cultured smooth muscle cells, suppression of PHB2 reduced expression of several contractile genes. While in rat arteries, injury caused a decrease in production of PHB2 itself, and of contractile markers.   Furthermore, expression of PHB2 in proliferative smooth muscle cells could revert these cells to a contractile phenotype. Further experiments revealed PHB2 controlled the splicing of the metabolic enzyme to up-regulate the phenotypic switch. Regardless of mechanism, the results suggest that boosting PHB2 might be a way to reduce adverse smooth muscle cell overgrowth and conditions such as atherosclerosis and restenosis.   Cindy St. Hilaire:        The second article I'm going to highlight is also from our October 28th issue, and the first authors are Mayassa Rammah and Magali Theveniau-Ruissy. And the corresponding authors are Francesca Rochais and Robert Kelly. And they are all from Marseille University. Abnormal development of the heart's outflow track, which ultimately forms the bases of the aorta and the pulmonary artery, accounts for more than 30% of all human congenital heart defects. To gain a better understanding of outflow tract development, and thus the origins of such defects, this group investigated the role of transcription factors thought to be involved in specifying the superior outflow tract, or SOFT, which gives rise to the subaortic myocardium, and the inferior outflow tract, which gives rise to the subpulmonary myocardium. Transcription factor S1 is over-expressed in superior outflow tract cells and the transcription factors, TBX1 and PPAR gamma, are expressed in inferior outflow tract cells.   And now this group has shown that TBX1 drives PPAR gamma expression in the inferior outflow tract, while Hess-1 surpasses PPAR gamma expression in the superior outflow tract. Indeed, in mouse embryos lacking TBX1, PPAR gamma expression was absent in the outflow tract. While in mouse embryos lacking Hess-1, PPAR gamma expression was increased and PPAR gamma positive cells were more widespread in the outflow tract.   The team also identified that signaling kinase DLK is an upstream activator of Hess-1 and a suppressor of PPAR gamma. In further detailing the molecular interplay regulating outflow tract patterning, the work will shed light on congenital heart disease etiologies, and inform potential interventions for future therapies.   Cindy St. Hilaire:        The third article I want to highlight is from our November 11th issue of Circulation Research, and the title is Histone Lactylation Boosts Reparative Gene Activation Post Myocardial Infarction. The first author is Jinjin Wang and the corresponding author is Maomao Zhang, and they're from Harbin Medical University. Lactylation of histones is a recently discovered epigenetic modification that regulates gene expression in a variety of biological processes. In inflammation, for example, a significant increase in histone lactylation is responsible for switching on reparative genes and macrophages when pro-inflammatory processes give way to pro-resolvin ones.   The role of histone lactylation in inflammation resolution has been shown in a variety of pathologies, but has not been examined in myocardial infarction. Wang and colleagues have now done just that. They isolated monocytes from the bone marrow and the circulation of mice at various time points after induced myocardial infarctions, and examined the cells' gene expression patterns. Within a day of myocardial infarction, monocytes from both bone marrow and the blood had begun upregulating genes involved in inflammation resolution. And, concordant with this, histone lactylation was dramatically increased in the cells, specifically at genes involved in repair processes.   The team went on to show that injection of sodium lactate into mice boosted monocyte histone lactylation and improved heart function after myocardial infarction, findings that suggest further studies of lactylation's pro-resolving benefits are warranted. Cindy St. Hilaire:        The last article I want to highlight is titled, PCSK9 Promotes Macrophage Activation via LDL Receptor Independent Mechanisms. The first authors are Shunsuke Katsuki and Prabhash Kumar Jha, and the corresponding author is Masanori Aikawa, and they are from Brigham and Women's Hospital in Harvard. Statins are the go-to drug for lowering cholesterol in atherosclerosis patients. But the more recently approved PCSK9 inhibitors also lower cholesterol and can be used to augment or replace statins in patients where these drugs are insufficient.   PCSK9 is an enzyme that circulates in the blood and destroys the LDL receptor, thereby impeding the removal of bad cholesterol. The enzyme also appears to promote inflammation, thus potentially contributing to atherosclerosis in two ways. This group now confirms that PCSK9 does indeed promote pro-inflammatory macrophage activation and lesion development, and does so independent of its actions on the LDL receptor.   The team assessed PCSK9-induced lesions in animals with saphenous vein grafts, which are commonly used in bypass surgery but are prone to lesion regrowth. They found that LDL receptor lacking graft containing mice had greater graft macrophage accumulation and lesion development when PCSK9 activity was boosted than when it was not. The animal's macrophages also had higher levels of the pro-inflammatory factor expression. Together, this work shows that PCSK9 inhibitors provide a double punch against atherosclerosis and might be effective drugs for preventing the all too common failure of saphenous vein grafts.   Cindy St. Hilaire:        So, today with me I have Dr Miguel Lopez-Ramirez and undergraduate student Bliss Nelson from the University of California in San Diego, and we're going to talk about their study, Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformation Disease, and this article is in our November 11th  issue of Circulation Research. Thank you both so much for joining me today. Before we talk about the science, want to just maybe tell me a little bit about yourselves?   Bliss Nelson:                My name is Bliss Nelson. I'm a member of Miguel Lopez-Ramirez's lab here at UC San Diego at the School of Medicine. I'm an undergraduate student here at UC San Diego. I'm actually a transfer student. I went to a community college here in California and I got involved in research after I transferred.   Cindy St. Hilaire:        What's your major?   Bliss Nelson:                I'm a cognitive science major.   Cindy St. Hilaire:        Excellent. You might be the first undergrad on the podcast, which is exciting.   Bliss Nelson:                Wow. What an honor. Thank so much.   Cindy St. Hilaire:        And Miguel, how about you?   Miguel Lopez-Ramirez: Yes, thank you. Well, first thank you very much for the opportunity to present our work through this media. It's very exciting for us. My name is Miguel Alejandro Lopez-Ramirez, and I'm an assistant professor in the Department of Medicine and Pharmacology here at UCSD. Cindy St. Hilaire:        Wonderful. I loved your paper, because, well, first, I don't think I've talked about cerebral cavernous malformations. So what are CCMs, and why are they so bad?   Bliss Nelson:                Cerebral cavernous malformations, or CCMs for short, are common neurovascular lesions caused by a loss of function mutation in one of three genes. These genes are KRIT1, or CCM1, CCM2 and PDCD10, or CCM3, and generally regarded as an endothelial cell autonomous disease found in the central nervous system, so the brain and the spinal cord.   The relevance of CCMs is that it affects about one in every 200 children and adults, and this causes a lifelong risk of chronic and acute hemorrhaging. CCMs can be quiescent or dynamic lesions. If they are dynamic, they can enlarge, regress, or behave progressively, producing repetitive hemorrhaging and exacerbations of the disease.   Other side effects of the disease could be chronic bleedings, focal neurological deficits, headaches, epileptic seizures and, in some cases, death. There's no pharmacological treatment for CCMs. There's only one type of option some patients may have, which would be to have surgery to cut out the lesions. But of course this depends on where the lesion or lesions are in the central nervous system, if that's even an option. So sometimes there's no option these patients have, there's no treatment, which is what propels our lab to towards finding a pharmacological treatment or uncovering some of the mechanisms behind that.   Cindy St. Hilaire:        Do people who have CCM know that they have them or sometimes it not detected? And when it is detected, what are the symptoms?   Bliss Nelson:                Sometimes patients who have them may not show any symptoms either ever in their lifetime or until a certain point, so really the only way to find out if you were to have them is if you went to go get a brain scan, if you went to go see a doctor, or if you started having symptoms. But also, one of the issues with CCMs is that they're very hard to diagnose, and in the medical community there's a lack of knowledge for CCMs, so sometimes you may not get directed to the right specialist in time, or even ever, and be diagnosed.   Miguel Lopez-Ramirez: I will just add a little bit. It is fabulous, what you're doing. I think this is very, very good. But yes, that's why they're considered rare disease, because it's not obvious disease, so sometimes most of the patient, they go asymptomatic even when they have one lesions, but there's still no answers of why patients that are asymptomatics can become symptomatics. And there is a lot in neuro study, this study that we will start mentioning a little bit more in detail. We try to explain these transitions from silent or, quiescent, lesion, into a more active lesion that gives the disability to the patient.   Some of the symptoms, it can start even with headaches, or, in some cases, they have more neurological deficits that could be like weakness in the arms or loss of vision. In many cases also problems with the speech or balance. So it depends where the lesion is present, in the brain or in the spinal cord, the symptoms that the patient will experience. And some of the most, I will say, severe symptoms is the hemorrhagic stroke and the vascular thrombosis and seizure that the patients can present. Those would be the most significant symptoms that the patient will experience.   Cindy St. Hilaire:        What have been some limitations in the study of CCMs? What have been limitations in trying to figure out what's going on here?   Bliss Nelson:                The limitations to the disease is that, well, one, the propensity for lesions, or the disease, to come about, isn't known, so a lot of the labs that work on it, just going down to the basic building blocks of what's even happening in the disease is a major problem, because until that's well established, it's really hard to go over to the pharmacological side of treating the disease or helping patients with the disease, without knowing what's going on at the molecular level.   Cindy St. Hilaire:        You just mentioned molecular level. Maybe let's take a step back. What's actually going on at the cellular level in CCMs? What are the major cell types that are not happy, that shift and become unhappy cells? Which are the key players?   Bliss Nelson:                That's a great question and a great part of this paper. So when we're talking about the neuroinflammation in the disease, our paper, we're reporting the interactions between the endothelium, the astrocytes, leukocytes, microglia and neutrophils, and we've actually coined this term as the CaLM interaction.   Cindy St. Hilaire:        Great name, by the way.   Bliss Nelson:                Thank you. All props to Miguel. And if you look at our paper, in figure seven we actually have a great graphic that's showing this interaction in play, showing the different components happening and the different cell types involved in the CaLM interaction that's happening within or around the CCM lesions.   Cindy St. Hilaire:        What does a astrocyte normally do? I think our podcast listening base is definitely well versed in probably endothelial and smooth muscle cell and pericyte, but not many of us, not going to lie, including me, really know what a astrocyte does. So what does that cell do and why do we care about its interaction with the endothelium?   Miguel Lopez-Ramirez: Well, the astrocytes play a very important role. Actually, there are more astrocytes than any other cells in the central nervous system, so that can tell you how important they are. Obviously play a very important role maintaining the neurological synapses, maintaining also the hemostasis of the central nervous system by supporting not only the neurons during the neural communication, but also by supporting the blood vessels of the brain.   All this is telling us that also another important role is the inflammation, or the response to damage. So in this case, what also this study proposed, is that new signature for these reactive astrocytes during cerebral malformation disease. So understanding better how the vasculature with malformations can activate the astrocytes, and how the astrocytes can contribute back to these developing of malformations. It will teach us a lot of how new therapeutic targets can be implemented for the disease.   This is part of this work, and now we extend it to see how it can also contribute to the communication with immune cells as Bliss already mentioned.   Cindy St. Hilaire:        Is it a fair analogy to say that a astrocyte is more similar to a pericyte in the periphery? Is that accurate?   Miguel Lopez-Ramirez: No, actually there are pericytes in the central nervous system as well. They have different roles. The pericyte is still a neuron cell that give the shape, plays a role in the contractility and maintains the integrity of the vessels, while the astrocyte is more like part of the immune system, but also part of the supporting of growth factors or maintaining if something leaks out of the vasculature to be able to capture that.   Cindy St. Hilaire:        You used a handful of really interesting mouse models to conduct this study. Can you tell us a little bit about, I guess, the base model for CCM and then some of the unique tools that you used to study the cells specifically?   Bliss Nelson:                Yeah, of course. I do a lot of the animal work in the lab. I'd love to tell you about the mouse model. So to this study we use the animal model with CCM3 mutation. We use this one because it is the most aggressive form of CCM and it really gives us a wide range of options to study the disease super intricately. We use tamoxifen-regulated Cre recombinase under the control of brain endothelial specific promoter, driving the silencing of the gene CCM3, which we call the PDCD10 betco animal, as you can see in our manuscript. To this, the animal without the Cre system, that does not develop any lesions, that we use as a control, we call the PDCD10 plox. And these animals are injected with the tamoxifen postnatally day one, and then for brain collection to investigate, wcollected at different stages. So we do P15, which we call the acute stage, P50, which we term the progressive stage, and then P80, which is the chronocytes stage. And after enough brain collections, we use them for histology, gene expression, RNA analysis, flow cytometry, and different imaging to help us further look into CCMs.   Cindy St. Hilaire:        How similar is a murine CCM to a human CCM? Is there really good overlap or are there some differences?   Miguel Lopez-Ramirez: Yes. So, actually, that's a very good question, and that's part of the work that we are doing. This model definitely has advantages in which the lesions of the vascular formations are in an adult and juvenile animals, which represent an advantage for the field in which now we will be able to test pharmacological therapies in a more meaningful, way where we can test different doses, different, again, approaches. But definitely, I mean, I think I cannot say that it's only one perfect model for to mimic the human disease. It's the complementary of multiple models that give us certain advantages in another, so the integration of this knowledge is what will help us to understand better the disease.   Cindy St. Hilaire:        That's great. I now want to hear a little bit about your findings, because they're really cool. So you took two approaches to study this, and the first was looking at the astrocytes and how they become these, what you're calling reactive astrocytes, and then you look specifically at the brain endothelium. So could you maybe just summarize those two big findings for us?   Miguel Lopez-Ramirez: Yeah, so, basically by doing these studies we use trangenic animal in this case that they give us the visibility to obtain the transcripts in the astrocytes. And basically this is very important because we don't need to isolate the cells, we don't need to manipulate anything, we just took all the ribosomes that were basically capturing the mRNAs and we profile those RNAs that are specifically expressed in the astrocytes.   By doing this, we actually went into looking at in depth the transcripts that were altered in the animals that developed the disease, in this case the cerebral cavernous malformation disease, and what we look at is multiple genes that were changing. Many of them were already described in our previous work, which were associated with hypoxia and angiogenesis. But what we found in this work is that now there were a lot of genes associated with inflammation and coagulation actually, which were not identified before.   What we notice is that now these astrocytes, during the initial phase of the vascular malformation, may play a more important role in angiogenesis or the degradation of the vessels. Later during the stage of the malformation, they play a more important role in the thrombosis, in the inflammation, and recruitment of leukocyte   That was a great advantage in this work by using this approach and looking in detail, these astrocytes. Also, we identified there were very important signature in these astrocytes that we refer as a reactive astrocytes with neuroinflammatory properties. In the same animals, basically, not in the same animal, but in the same basically the experimental approach, we isolated brain vasculature. And by doing the same, we actually identified not only the astrocyte but also the endothelium was quite a different pattern that we were not seeing before. And this pattern was also associated with inflammation, hypoxia and coagulation pathways.   That lead us to go into more detail of what was relevant in this vascular malformations. And one additional part that in the paper this is novel and very impactful, is that we identify inflammasome as a one important component, and particularly in those lesions that are multi-cavernous.   Now we have two different approaches. One, we see this temporality in which the lesions forms different patterns in which the initial phase maybe is more aneugenic, but as they become more progressive in chronocytes, inflammation and hypoxy pathways are more relevant for the recruitment of the inflammatory cells and also the precipitation of immunothrombosis.   But also what we notice is that inflammasome in endothelial and in the leukocytes may play an important role in the multi-cavernous formation, and that's something that we are looking in more detail, if therapeutics or also interventions in these pathways could ameliorate the transition of phases between single lesions into a more aggressive lesions.   Cindy St. Hilaire:        That's kind of one of the follow up questions I was thinking about too is, from looking at the data that you have, obviously to get a CCM, there's a physical issue in the vessel, right? It's not formed properly. Does that form influence the activation of the astrocyte, and then the astrocytes, I guess, secrete inflammatory factors, target more inflammation in the vessel? Or is there something coming from the CCM initially that's then activating the astrocyte? It's kind of a chicken and the egg question, but do you have a sense of secondary to the malformation, what is the initial trigger?   Miguel Lopez-Ramirez: The malformations in our model, and this is important in our model, definitely start by producing changes in the brain endothelial. And as you mention it, these endothelium start secreting molecules that actually directly affect the neighboring cells.   One of the first neighboring cells that at least we have identified to be affected is the astrocytes, but clearly could be also pericytes or other cells that are in the neurovascular unit or form part of the neurovascular unit. But what we have seen now is that this interaction gets extended into more robust interactions that what you were referring as the CaLM interactions.   Definitely I think during the vascular malformations maybe is the discommunication that we identify already few of those very strong iteration that is part of the follow up manuscript that we have. But also it could be the blood brain barrier breakdown and other changes in the endothelium could also trigger the activation of the astrocytes and brain cells.   Cindy St. Hilaire:        What does your data suggest about potential future therapies of CCM? I know you have a really intriguing statement or data that showed targeting NF-kappa B isn't likely going to be a good therapeutic strategy. So maybe tell us just a little bit about that, but also, what does that imply, perhaps, of what a therapeutic strategy could be?   Bliss Nelson:                Originally we did think that the inhibition of NF-kappa B would cause an improvement potentially downstream of the CCMs. And unexpectedly, to our surprise, the partial or total loss of the brain endothelial NF-kappa B activity in the chronic model of the mice, it didn't prevent or cause any improvement in the lesion genesis or neuroinflammation, but instead it resulted in a trend to increase the number of lesions and immunothrombosis, suggesting that the inhibition of it is actually worsening the disease and shouldn't be used as a target for therapeutical approaches.   Miguel Lopez-Ramirez: Yes, particularly that's also part of the work that we have ongoing in which NF-kappa B may also play a role in preventing the further increase of inflammation. So that is something that it can also be very important. And this is very particular for certain cell types. It's very little known what the NF-kappa B actually is doing in the brain endothelial during malformations or inflammation per se. So now it's telling us that this is something that we have to consider for the future.   Also, our future therapeutics of what we propose are two main therapeutic targets. One is the harmful hypoxia pathway, which involves activation, again, of the population pathway inflammation, but also the inflammasomes. So these two venues are part of our ongoing work in trying to see if we have a way to target with a more safe and basically efficient way this inflammation.   However, knowing the mechanisms of how these neuroinflammation take place is what is the key for understanding the disease. And maybe even that inflammatory and inflammatory compounds may not be the direct therapeutic approach, but by understanding these mechanisms, we may come with  new approaches that will help for safe and effective therapies.   Cindy St. Hilaire:        What was the most challenging part of this study? I'm going to guess it has something to do with the mice, but in terms of collecting the data or figure out what's going on, what was the most challenging?   Bliss Nelson:                To this, I'd like to say that I think our team is very strong. We work very well together, so I think even the most challenging part of completing this paper wasn't so challenging because we have a really strong support system among ourselves, with Miguel as a great mentor. And then there's also two postdocs in the lab who are also first authors that contributed a lot to it.   Cindy St. Hilaire:        Great. Well, I just want to commend both of you on an amazing, beautiful story. I loved a lot of the imaging in it, really well done, very technically challenging, I think, pulling out these specific sets of cells and investigating what's happening in them. Really well done study. And Bliss, as an undergraduate student, quite an impressive amount of work. And I congratulate both you and your team on such a wonderful story.   Bliss Nelson:                Thank you very much.   Miguel Lopez-Ramirez: Thank you for Bliss and also Elios and Edo and Katrine, who all contributed      enormously to the completion of this project.   Cindy St. Hilaire:        It always takes a team.   Miguel Lopez-Ramirez: Yes.   Cindy St. Hilaire:        Great. Well, thank you so much, and I can't wait to see what's next for this story.   Cindy St. Hilaire:        That's it for the highlights from October 28th and November 11th issues of Circulation Research. Thank you so much for listening. Please check out the Circ Res Facebook page and follow us on Twitter and Instagram with the handle @circres and #discovercircres. Thank you to our guests, Dr Miguel Lopez-Ramirez and Bliss Nelson. This podcast is produced by Ashara Retniyaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Some of the copy text for our highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire, and this is Discover CircRes, you're on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, please visit ahagenerals.org.

Bells Hells reflect upon the latest and strangest moon developments as they near the Gloomed Jungles and prepare for a potential rendezvous with the Gorgynei lycans... Due to the improv nature of Critical Role and other RPG content on our channels, some themes and situations that occur in-game may be difficult for some to handle. If certain episodes or scenes become uncomfortable, we strongly suggest taking a break or skipping that particular episode.Your health and well-being is important to us and Psycom has a great list of international mental health resources, in case it's useful: http://bit.ly/PsycomResources Watch Critical Role Campaign 3 live Thursdays at 7pm PT on https://twitch.tv/criticalrole and https://youtube.com/criticalrole. To join our live and moderated community chat, watch the broadcast on our Twitch channel. "It's Thursday Night (Critical Role Theme Song)" by Peter Habib and Sam RiegelOriginal Music by Omar Fadel and Hexany Audio"Welcome to Marquet" Art Theme by Colm McGuinnessAdditional Music by Universal Production Music, Epidemic Sounds, and 5 AlarmCharacter Art by Hannah Friederichs Twitch subscribers gain instant access to VODs of our shows like Critical Role, Exandria Unlimited, and 4-Sided Dive. But don't worry: Twitch broadcasts will be uploaded to YouTube about 36 hours after airing live, with audio-only podcast versions of select shows on Spotify, Apple Podcasts & Google Podcasts following a week after the initial air date. Twitch subscribers also gain access to our official custom emote set and subscriber badges and the ability to post links in Twitch chat!

In this episode, our heroes continue their desperate fight for survival against the horrors of the Posemphney Forest. Will they make it back to Lakeside in one piece? Visit www.fateofisen.com to learn more.Fate of Isen is one of the Feedspot top D&D podcasts in the world! Check out Feedspot here.If you like the show, please feel free to follow us on social media (@fateofisen) or support us on Patreon!Intro, outro, and recap music by freesound user, Tyops, and ambient sound by TabletopAudio.com ★ Support this podcast on Patreon ★

The Vermillion Dream Having arrived in the Jewel of Hope, the party confronts Galsariad and Aloysia, demanding answers.Watch us live on Wednesdays 4:30 Eastern/1:30 Pacific on Twitch!Thanks to Wizards of the Coast, DnD Beyond, and Critical Role for helping us build worlds of adventure!Ron Murphy – DM, @ron88keysRBDMWilvan Grandmane – Ross Griffin, @griffRMLaphus Prismawing - Jaiden, @foxtrotfalloutOrgoth Skullcrusher - Bill Roper, @billroperNorth Star Maedrick - Jaime, @suburbancrypticFollow us on Twitter at @SeveredSonsDnD!Join our Discord! Join our Patreon!Give us a review on Apple Podcasts, Podchaser, Spotify,  GoodPods or on our Twitter page and we'll read it on the air.  Keep on rolling! Support the show

The Rebels Triad are in the eponymous Marsh Town, looking for information and clues regarding a coven of Hags.  Does danger and mystery lurk around every corner, or is this place more dreary than deadly?Cast:Arlo - John Sand (@rapsquatch)Gozer - Hannah Eagle (@layspotatobitch)Jotun - Brian Foster (@rextestarossa) DM - Connor McKibbin-Vaughan (@connorcanwrite) Theme by John Sand

CHEERS CRUSTACEANS! In this week's brand new episode, we discuss Critical Role, C3 Episode 40: Compulsions. We also discuss what it is about DnD and TTRPG's in general that we love, and the strengths and possible weaknesses of Matthew Mercer. We also learn that Joey is lucky to be alive...for many reasons.

The Away Team splits the party in the Underdark city of Brigarune. Efimia and Zag go to share the great news of the removal of Driders with Bo Dega, while Grom and Selene meet up with some of Grom's old Dwarven high school bullies who promise Grom a set of Mithral Armor.Get 10% off dice: metallicdicegames.com/ref/2518/Coupon Code: knockedVisit www.Patreon.com/knocked to support our Patreon and sign up as a patron for as little as $2 a month.

This episode is sponsored by Nord VPN. Get 4 months for free on a 2-year plan here: NordVPN.com/criticalrole  It's risk-free with Nord's 30-day money-back guarantee! Players Laura Bailey, Aimee Carrero, Christian Navarro, Liam O'Brien, and Lou Wilson, are led by game master and sponsorship legend… Sam Riegel on a journey through the information superhighway (aka the internet). PLUS we'll unveil a special guest that you won't want to miss! Character Art by Justyna Rerak: https://twitter.com/Justyna_Rerak  Overlay Art by Christian Brown: https://twitter.com/DeepOmega   Players/ Game MasterLaura Bailey: https://twitter.com/LauraBaileyVO  Aimee Carrero: https://twitter.com/aimeecarrero  Christian Navarro: https://www.instagram.com/christianleenavarro/  Liam O'Brien: https://twitter.com/VoiceOfOBrien  Lou Wilson: https://www.instagram.com/sweetlouzinho/  Sam Riegel: https://twitter.com/samriegel  Matthew Lillard: https://twitter.com/MatthewLillard

Desperate for supplies, Ja and Kaia venture beneath the vine-covered ruins and find that not everything among the countless scattered bones has died.

After forcing our protagonists to traverse through a vicious jungle, we discuss whether either of us has what it takes to survive in dire situations. Other topics include how it feels to write gross things, whether or not parents form strong bonds with their children, and all the nasty things Ethan thought about including in his chapter but decided against. 

A very special live podcast from IFPA's 2022 Floral and Produce show! We close out our season on nutrition with a panel of experts with Vonnie on the lasting impact technology has made and continues to grow on for the farming and fresh produce industries. Our panel includes Haven Baker, CBO at Pairwise, Jenny Du, Senior Vice President for Government Affairs at Apeel Sciences and Katie Seawell, Chief Commercial Office at Bowery Farming. Join us as we discuss: How technology can impact improving accessibility and lifespan of fresh produce Helping set up for the next wave of entrepreneurs in the health and food industry Improving access to produce to all communities How younger generations are creating higher demand for fresh produce

Critical Role, Campaign 3, Episode 40: Compulsions   Recap provided by: criticalrole.fandom.com

Welcome to Creative Block with Vee and Gene! In this episode, We're chatting with Carlos Luna! Carlos is a creative director and producer who's worked on Roll20, Critical Role, and Dimension20. Send in your drawing prompts and questions! Along the way, we talk about the hustle of having a band, finding solace in improv, the difference between marketing and advertising, and more! Watch this episode on YouTube to see us doodle while we chat ► https://youtu.be/TfQdSB9jG9I Become a Patron! ► https://www.patreon.com/crtvblock ■■■■■■■■■■■■■■■ CREATIVE BLOCK ► https://twitter.com/crtvblock GENE! ► https://twitter.com/genegoldstein VEE! ► https://twitter.com/violainebriat Editing by Clemence Briat ► https://twitter.com/clem_n_m Produced by Malik Gayle ► https://twitter.com/MalikGayle Theme song by Louie Zong ► https://twitter.com/everydaylouie --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/crtvblock/support

With our heroes in the midst of battle against the spellcaster Volomonari, they must gather together in order to bring this adventure near its close!JOIN OUR DISCORDCheck out the CAUSES WE SUPPORT to get involved and donate!Help support the show by visiting our Patreon and find even more content at our Website!Tracklist and Creative Commons Attribution Can Be Viewed HEREIntro/Outro Music “Jotunheim” Courtesy of Serpent Sound StudiosInterlude Music “Bit Quest” Courtesy of incompetechSound Effects Courtesy of SyrinscapeAdditional Music Courtesy of:Larian Studios: Creators of the Divinity Series WEBSITEThe Game Kitchen: Creators of Blasphemous WEBSITE / BANDCAMPCD Projekt Red: Creators of the Witcher series WEBSITE / USE POLICYOwlcat Games: Creators of Pathfinder: Kingmaker and Wrath of the Righteous WEBSITE

Jeremy: DM Lilth: Keres - "Human" Warlock Zaghrog: Hakim Ali - Human Wizard Navarran: Seeker - Warforged Ranger L: Prize - High Elf Cleric korvys: Kamron Esker - Human Rogue Thanks to all of our supporters at patreon.com/fsfilms for making this possible! Especially our $25+ Donors: Drevian Alexander Kat Waterflame L Samantha Bates Portions of the materials used may contain trademarks and/or copyrighted works of Critical Role. This material is not official, is provided for free, noncommercial entertainment purposes only, and is not endorsed by Critical Role.

Jeremy: DM Lilth: Keres - "Human" Warlock Zaghrog: Hakim Ali - Human Wizard Navarran: Seeker - Warforged Ranger L: Prize - High Elf Cleric korvys: Kamron Esker - Human Rogue ----- Thanks to all of our supporters at patreon.com/fsfilms for making this possible! Especially our $25+ Donors: Drevian Alexander Kat Waterflame L Samantha Bates Portions of the materials used may contain trademarks and/or copyrighted works of Critical Role. This material is not official, is provided for free, noncommercial entertainment purposes only, and is not endorsed by Critical Role.

Bells Hells must contend with the bureaucracy of being murder suspects before they can begin their turbulent travels to southern Marquet... Due to the improv nature of Critical Role and other RPG content on our channels, some themes and situations that occur in-game may be difficult for some to handle. If certain episodes or scenes become uncomfortable, we strongly suggest taking a break or skipping that particular episode.Your health and well-being is important to us and Psycom has a great list of international mental health resources, in case it's useful: http://bit.ly/PsycomResources Watch Critical Role Campaign 3 live Thursdays at 7pm PT on https://twitch.tv/criticalrole and https://youtube.com/criticalrole. To join our live and moderated community chat, watch the broadcast on our Twitch channel. "It's Thursday Night (Critical Role Theme Song)" by Peter Habib and Sam RiegelOriginal Music by Omar Fadel and Hexany Audio"Welcome to Marquet" Art Theme by Colm McGuinnessAdditional Music by Universal Production Music, Epidemic Sounds, and 5 AlarmCharacter Art by Hannah Friederichs Twitch subscribers gain instant access to VODs of our shows like Critical Role, Exandria Unlimited, and 4-Sided Dive. But don't worry: Twitch broadcasts will be uploaded to YouTube about 36 hours after airing live, with audio-only podcast versions of select shows on Spotify, Apple Podcasts & Google Podcasts following a week after the initial air date. Twitch subscribers also gain access to our official custom emote set and subscriber badges and the ability to post links in Twitch chat!

Big ol' spoilers today, you've been warned! We're finally talking about House of the Dragon—the good, the bad, and the icky! The Sib Nerds talk about casting, character arcs, epic moments, and things they're looking forward to seeing in Season 2. Did you watch House of the Dragon? What did you think? Josef is playing: - D&D - Cyberpunk 2077 - Resident Evil: Village (watching Hope) - Elden Ring Josef is reading: - Oathbringer by: Brandon Sanderson - Rhythm of War by: Brandon Sanderson - Hall of Smoke by: H.M. Long - Chainsaw Man by: Tatsuki Fujimoto Josef is watching: - Critical Role, campaign 3 (YouTube) - Ghost Files by: Watcher (YouTube) - Spy x Family (Crunchyroll) - My Hero Academia, season 6 (Crunchyroll) - Chainsaw Man (Crunchyroll) - Given (Crunchyroll) - Fate/Zero (Crunchyroll) - Andor (Disney+) Anna is reading: - The Tea Dragon Society by: Kay O'Neill - The Tea Dragon Festival by: Kay O'Neill - The Tea Dragon Tapestry by: Kay O'Neill - Critical Role: The Mighty Nein Origins—Caleb Widogast by: Jody Houser, Liam O'Brien et al. - Nettle and Bone by: T. Kingfisher - Howl's Moving Castle by: Diana Wynne Jones - Star Wars: The Princess and the Scoundrel by: Beth Revis - These Happy Golden Years by: Laura Ingalls Wilder Anna is watching: - Andor (Disney+) - Spy x Family (Crunchyroll) - My Hero Academia, season 6 (Crunchyroll) - Fate/Zero (Crunchyroll) - Critical Role, campaign 2, episode ??? (YouTube) - Critical Role, campaign 3 (YouTube) - Sister Wives (Discovery+) How many words has Anna written for NaNoWriMo: 0 (LOL) Don't forget, you can get bonus content by joining our Patreon! And voting rights for the new read along! Join us on our NEW read along through Red Seas Under Red Skies by: Scott Lynch! Find us on Twitter: @litround Find us on Facebook: https://www.facebook.com/LitRoundTable Find us on Patreon: https://www.patreon.com/thelitroundtable Art: Kris Easler: https://www.kriseasler.com/