Podcasts about episode thirty six

Episode Thirty-Six features Francks Francois Deceus. He was born in Cap-Haitian, Haiti 1966. He currently resides and maintains a studio in Brooklyn, NY. Deceus received a B.A. in Sociology from Long Island University, NY in 1992 and studied Printmaking at Atlantis Arts Atelier, Gentily, France in 2007. His solo exhibitions include the Pounder-Kone Art Space, Los Angeles; Tilford Art Group, Los Angeles, CA. Group exhibitions include the Brooklyn Museum, NY; Museum of Contemporary African Diaspora Arts (MOCADA), Brooklyn, NY; The National Civil Rights Museum, Memphis TN; Hampton University, Hampton, VA; Aljira Center for Contemporary Art, Newark, NJ; Mana Contemporary, Jersey City, NJ; Prizm Art Fair Miami FL; Fridman Art Gallery, NY, NY; Gallery M, NY, NY. The works of Deceus have entered numerous public collections, including Xavier University, New Orleans, LA and the Schomburg Center, New York Public Library, NY. His work has been featured in publications such as Artillery Magazine, the International Revue of African-American Art, and The Village Voice. www.deceusart.com https://mocada.org/2020/04/28/digital-gallery-francks-deceus/ https://catalogue.swanngalleries.com/Lots/auction-lot/FRANCKS-DECEUS-(1966----)-Pilgrimage-14?saleno=2535&lotNo=181&refNo=767372 https://www.instyle.com/lifestyle/girls-in-the-window-recreated?utm_source=emailshare&utm_medium=email&utm_campaign=email-share-longform&utm_content=20200809

As we close in on Passionate Pioneer’s one year anniversary, I wanted to take a moment to share with you the lessons I’ve learned from our inspiring guests and how we all can integrate those lessons into our daily lives! In this episode, I’ll be sharing a recap and learnings from several previous episodes that exemplify the notion of determination, grit, perseverance, and passion. I look forward to hearing from you after you have tuned-in: what is your spark and passion to make our world a better place? Links Supporting this Episode: Episode Six with Amit Shah: (https://passionatepioneers.captivate.fm/episode/podcast-reversing-type-2-diabetes-in-100-million-people-by-20205-) Episode Nine with Matt Seefeld: (https://passionatepioneers.captivate.fm/episode/a-global-sober-tribe-builder-after-15-years-of-addiction) Episode Thirty-Six with Sonia Rhodes: (https://passionatepioneers.captivate.fm/episode/healing-healthcare-from-the-inside-out) Episode Eight with Carrie Kozlowski: (https://passionatepioneers.captivate.fm/episode/creating-personalized-healthcare-experiences) Mike Biselli LiknedIn page: (https://www.linkedin.com/in/mikebiselli/) Mike Biselli Twitter page: (https://twitter.com/mikebiselli) Subscribe to newsletter: (https://forms.gle/4XjvmqWxaaNe21PX6) Guest nomination form: (https://docs.google.com/forms/d/e/1FAIpQLScqk_H_a79gCRsBLynkGp7JbdtFRWynTvPVV9ntOdEpExjQIQ/viewform) Join our online community: (https://www.passionatepioneers.com/) Support this podcast

Holeeee motherflipping sith! We need to catch our collective breath after this set of episodes. So much happened and there was so much death! Duchess Satine, Savage Opress, Pre Vizsla and a rare appearance from Sexy Sidious himself! Wow… where do we even start? As we near the end of Season Five of The Clone Wars, we discuss the all important episodes 14-17. We’re scarred… and Rocky gets REALLY high taking so many hits for the fallen. So. Much. Murder. Turn up your headphones, dial back your sensibilities, and join the wretched hive of scum and villainy as we take the low road to resistance on Episode Thirty Six of Force Insensitive!Send Email/Voicemail: mailto:forceinsensitive@gmail.comStart your own podcast: https://www.buzzsprout.com/?referrer_id=386Use our Amazon link: http://amzn.to/2CTdZzKFB Group: https://www.facebook.com/groups/ForceInsensitive/Twitter: http://twitter.com/ForceNSensitiveFacebook: http://facebook.com/ForceInsensitiveInstagram: http://instagram.com/ForceInsensitive

Merry Christmas and Happy New Year everyone! This is EPISODE THIRTY-SIX of the "LOOK OUT, SIR! 40K PODCAST”, a Warhammer 40,000 podcast where we discuss the following topics: THE BIG FAT 40K QUIZ OF THE YEAR IS A THING WE’RE DOING AND IT’LL BE RELEASED ON CHRISTMAS DAY! Please check it out on YouTube (LINK TBD), though be aware it is also available in audio form on your chosen Podcast Provider. I couldn’t do links for all of those, mostly because I’m unsure where to find them. I’m sure you’ll work it out… 17:20 - WE DISCUSS OUR HOBBY HIGHLIGHTS AND OR BEST BITS FROM 2019. 2019 has been an interesting year for the 40k hobby. Dan, Joe and Phil have a chat about the various things they enjoyed and accomplished in 2019. Fingers crossed it’s not as smug or self-congratulating as it maybe could be. We did do a bit where we say how great we are for continuing to do this Podcast. Though the hope is that comes across as heart-warming and sincere. I guess we’ll let the various comment sections tell us what people think. 1:28:11 - WE DISCUSS THE FINER POINTS AND OR VIRTUES OF THE NEW CHAPTER APPROVED 2019 MATCHED PLAY MAELSTROM MISSIONS.Maelstrom has somewhat developed a reputation for being Eternal War’s poor cousin, the random nature of the card system leading to uncompetitive and frustrating games of 40k. So why is it that after the release of Chapter Approved 2019 we all agree that it’s not only better, but possibly the most interesting way to play 40k? Why not have a listen and see if you don’t end up agreeing with us. OUR SOCIAL MEDIA:If you would like to learn more about what we’re up to or are looking to reach out to any of us, please visit any of the below Social Media Links:Facebook: https://www.facebook.com/lookoutsir/ Instagram: https://www.instagram.com/lookoutsir40k/ • Dan’s Instagram: https://www.instagram.com/i.r.invested.in.unexpected/• Phil Instagram: https://www.instagram.com/beyondthetabletop/• Joe Instagram: https://www.instagram.com/subtlepainting/• Richard’s Instagram: https://www.instagram.com/viralninja/• Sean’s Instagram: https://www.instagram.com/maxpower_2112/• Tim’s Instagram: https://www.instagram.com/fickle_brush/ Thanks very much for taking the time to listen and by extension support our podcast. We hugely appreciate it and hope that you enjoy what we have to say on all the various 40k and or Games Workshop related things! Happy Christmas and or New Year all!

Welcome to Episode Thirty-Six of Strange Pleasures Radio Lab. Your daily audio story podcast available through iTunes, Spotify, Stitcher, Luminary and YouTube.Please support the channel by subscribing, rating and reviewing on your preferred platform.Today I will be narrating Part Ten 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=stprLUMINARY https://luminarypodcasts.com/listen/robert-knight/strange-pleasures-radiolab/7805fc0b-96a1-45d0-88d0-19244c9b3312SPOTIFY 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-Six! Is the AAF a football league or a petri dish? Who's tradeable? Who's untouchable? Who is a fake prospect created for humor purposes?

Episode Thirty-Six of the IdeaPod. In this episode, we show you how we solve our people problems through creative solutions with our section, “Pick Our Brains”. Read More The post #36 FMAO (Freezing my A** off) appeared first on Bandwidth Marketing.

Episode Thirty-Six features guest Disco Dracula back again with host Captain Death, reading more of their favorite stories related to SEX and GENITAL MUTILATION from Unsettling Stories(with Mr.SkellyBones on Spectator Mode cause he's too busy with his WEEB SHIT):Lost Episodes(9:04)Something Horrible is Happening to Me on Facebook(25:53)Assisted Suicide(34:22)Cracks in the Foundation(40:00)My Erection Lasted Longer than 4 Hours;I Didn't Call a Doctor(46:06)Far Too Much Sex(54:35)Our EPs are now on Youtube!https://www.youtube.com/channel/UCxoqIN-fkfdlmGEjWujypxwFeaturing wonderful ambient music from our fam in Sweden: CryoChamber, givin' us all the ooky-spooky tunage. Follow: @cryo-chamberThank you!"Are You Afraid of the Dark Theme Song," "Spooky Skeletons REMIX," and "You Reposted in the Wrong Neighborhood," are not my songs. Credit and All rights are reserved by the owners.I claim fair use copyright for use of parody//criticism

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 Six was chosen by you guys in a twitter poll so we're chatting about Beverley Allitt. She's a killer nurse with a shocking mullet and as well as chatting about her horrific crimes the pair find time to talk about Toys'R'Us, hospital schools and Coronation Street. Also, Kiri has a bone to pick with you lot...

[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]

Hello there.Episode Thirty SixThis week Simon takes great delight in iszi's reaction to the images rushing through her head. And they have nothing to do with Lost, pandas, Stalin or the new Google application for the Blackberry.