Podcasts about episode thirty four

Episode Thirty-Four features Amalia Mesa-Bains. She is an educator, artist and cultural critic. Her works, primarily interpretations of traditional Chicano altars, resonate both in contemporary formal terms and in their ties to her Chicano community and history. As an author of scholarly articles and a nationally known lecturer on Chicano art, she has enhanced understanding of multi-culturalism and reflected major cultural and demographic shifts in the United States. Throughout her cross-disciplinary career, she has worked to define a Chicano and Latino aesthetic in the U.S. and in Latin America. She has pioneered the documentation and interpretation of long Chicano traditions in Mexican-American art, both through her cultural activism and through her own altar-installations. As an artist her works have been exhibited in both national and international venues and her publications include “Homegrown-Engaged Cultural Criticism, a collaboration with bell hooks reissued by Routledge Press 2017. She is a recipient of a distinguished MacArthur Fellowship. Currently she is Professor Emerita at the Visual and Public Art Department at California State University at Monterey Bay. https://en.wikipedia.org/wiki/Amalia_Mesa-Bains  https://www.artnews.com/artnews/news/icons-amalia-mesa-bains-9988/  https://www.amazon.com/Homegrown-Cultural-Criticism-bell-hooks/dp/089608759X https://www.youtube.com/watch?v=wKAyFLgKJ14

A group of youngling Jedi face insurmountable odds as they go up against their greatest fears, the turncoat pirate Hondo Ohnaka, and an epic Marzplosion?! We discuss episodes 6-9 of Season Five of The Clone Wars and we ask pertinent questions like; where are the juggalos in the outer rim? Lightsabers, how do they work? And, do Jedi use the force to… nevermind. Just tune in because all your sabers are belong to us. 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 Four 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

Welcome to Episode Thirty-Four 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 Eight 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-Four features guest Django Phillips back again with host Captain Death for a really fun Two Part special about creepy games. If you've heard of Bloody Mary or Ouiji Boards, then you'll realize how kid friendly they are compared to this shit. PLEASE DON'T DO ANY OF THESE BUT ENJOY OUR HYPOTHETICAL ACTIONS:1 Man Hide-and-Go-Seek(11:16)The Midnight Game(21:44)100 Ghost Stories(30:54)This is a Test(35:17)Fortune Game(39:04)Kokuri San(42:42)The Shoebox Telephone(46:00)The Elevator Game(54:49)Listen 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

Episode Thirty-Four of Idea Pod. In this episode, we talk about stormbraining… or reverse brainstorming. Thanksgiving Edition. Read More The post #34 Thanking Gives- A Reverse Brainstorming Technique appeared first on Bandwidth Marketing.

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 Four is a live episode recorded at the Wharf Chambers in Leeds. Kiri and Rachel are chatting about the Vampire of Sacramento, Richard Trenton Chase. Paul McCartney also gets a mention, Kiri struggles with a hangover and we find out where you shouldn't put a test tube.

 [intro music]   Hello, and welcome to Episode Thirty-Four of Multiple Sclerosis Discovery, the podcast of the MS Discovery Forum. I’m your host, Dan Keller.   This week’s podcast features a follow-up interview from last week’s episode with Dr. Pierre-Antoine Gourraud. This week, we interview Dr. Jill Hollenbach about killer immunoglobulin-like receptors – or KIR – and their relationship with human leukocyte antigen and MS. But to begin, here’s a brief summary of some of the latest developments on the MS Discovery Forum at msdiscovery.org.   Take some time to check out our most recent data visualization on our website. Under the research resources tab, you can find a series of interactive data visualizations useful for MS researchers. Our most recent one organizes 142 ongoing clinical trials into an interactive bubble chart. We have another visualization on the natural history of MS symptoms. The interactive bar chart allows you to see the change of various symptom severity in MS over a 30-year period.   If you enjoy this podcast and find MSDF helpful, please consider supporting us with a donation. MSDF is run by a small team of full-time employees and a few regular contributors. We are devoted to bridging the gaps between scientific disciplines to speed the flow of information from the lab bench to the bedside. Our ultimate goal is to facilitate the discovery of a cure. We believe one of the best ways to do that is to bring independent, research-focused news to a professional audience on a platform that fosters discussion and discourse. Help keep us going by visiting our website and clicking on the green “Support MSDF” button next to the “Research Resources” tab on the top right of our screen.   [transition music]   Now to the interview. Dr. Jill Hollenbach is an assistant professor in the department of neurology at the University of California, San Francisco. She met with science journalist Cynthia McKelvey, to talk about KIR in MS.   Interviewer – Cynthia McKelvey Why don’t we start by introducing what KIR is, how it’s different from the potassium channel and what its relationship is to HLA.   Interviewee – Jill Hollenbach Well, KIR is an acronym, it stands for killer immunoglobulin-like receptor. These are receptors on the surface on the surface of natural killer cells. They use generally, not in every case, but use HLA as their ligand and they have either an activating or inhibitory effect on natural killer cells.   MSDF You mentioned in your talk earlier today at UCSF that they are difficult to study. Why is that?   Dr. Hollenbach Just in terms of their genetic architecture. KIR occupy a complex on chromosome 19, it’s a multigene complex. And so on any individual haplotype that’s one chromosome, an individual can have between 4 and 14 KIR genes. These genes are really recently evolved, and so they’ve kind of arisen in humans as a result of repeated events of recombination and gene duplication. So what that means is that one KIR gene often at the nucleotide level looks an awful lot like another KIR gene. And so we’ve had a lot of issues. A lot of the methodologies that are available right now in terms of sequencing, part of this has to do with a lack of human genome reference alignments, but there has been a lot of difficulty in examining these genes because they look so much like one another.   MSDF How does that relate to why they haven’t really seen them on genome-wide association studies?   Dr. Hollenbach There’s a couple of reasons why we don’t see them on genome-wide association studies. One is that, as I mentioned, there haven’t been a lot of good reference alignments, so as a result we don’t actually see a lot of SNP markers on most of the common platforms that are used for genome-wide association studies. And then the markers that are there are often lost to quality control, because we have a lot of gene content variation, which is kind of like a copy number variant. And so if we only see a result for one chromosome, for example, for a given SNP, that is not going to pass general quality control thresholds. And, of course, you have to recognize that when you’re doing these GWAS studies, you’re looking at a hundred thousand, five hundred thousand, a million markers, two and a half million markers, so you’re not going one-by-one and saying, well this KIR-1, we expect to only see one copy or that sort of thing. So it just gets thrown out in the mix with things that don’t pass QC.   MSDF How does KIR relate to multiple sclerosis specifically?   Dr. Hollenbach Well, we’re trying to figure that out. So there’s been a small number of studies examining KIR in multiple sclerosis, and what seems clear is that variation in the KIR does play a role in susceptibility to multiple sclerosis. It may play a role in progression; we’re just not sure. There’s not been enough work done to say definitely what’s going on, but there’s enough evidence to say that something is going on. And some of the work that I talked about in my talk today, an analysis of KIR variation along with HLA in an African-American MS cohort, a very large study population, it seems clear that there is some association of KIR variation with susceptibility or protection for multiple sclerosis.   MSDF Why study the African-American cohort? What does that tell us about MS in general?   Dr. Hollenbach We want to study them because they’re different from one another; so an African-American population is going to look very different genetically with respect to KIR and HLA from a European-American population. So we want to know two things. We want to know is there something different going on with these genes with respect to disease in these different populations, OR at the same time we want to know is something the same going on? And so we can learn something both from these commonalities and differences, and both can be really important in genetics. So if there’s something that is important that’s specific in the African-American population, we want to know that, and we can only find out by looking at a number of different ethnic groups.   MSDF Let’s talk a little bit more about interaction between KIR and the HLA ligand, and how that plays in with Bw4. And if we can define all of those things, too, that would be great.   Dr. Hollenbach Okay. Well, so KIR molecules, as I mentioned before, need to see something, they need to have a ligand on their target cell. We have both inhibitory receptors and activating receptors. The job of the NK cell is to perform immune surveillance. So NK cells kind of wander around the body, and what they’re looking for are cells that don’t look healthy. So what does that look like and what is an unhealthy cell? It’s a cell that is virally infected, it’s a tumor cell. Those are the two main things that NK cells are looking for. And it’s a really important function because they’re part of what we refer to as the innate immune system; it’s the first line of defense against these kind of unhealthy events.   And so what does an unhealthy cell look like? Well, one of the things that happens in both viral infection and tumors is downregulation of MHC class I. That’s what the KIR are looking for. So when an NK cell encounters a healthy cell, it will see HLA class I, it immediately recognizes this is self, this is healthy cell at least in terms of what I’m able to see as an NK cell, and it will move on and it won’t cause any damage to the cell after making contact between the KIR and that ligand.   On the other hand, if the KIR doesn’t see this HLA ligand, the inhibitory KIR, an activating KIR – and we’re still not completely sure what the activating KIR ligands are – but the activating KIR is also bound to something on the surface of this cell. If the activating KIR is bound but the inhibitory KIR is not, what happens is the NK cell is going to lyse that cell which is presumably unhealthy in some ways – tumor or viral infected.   Now HLA class I – actually all HLA molecules – have another primary really important role which is antigen presentation to T cells. Class I molecules present antigen to the CD8-positive T cells, and so that’s how these T cells perform their role in terms of the active immune response. KIRs see a different part of the HLA molecule than the T cell receptors, and so they see kind of this piece of the HLA class I molecule that’s kind of on the side of where the T cell receptors sit. And the variation that they see on that HLA class I molecule can kind of be defined by these broad categories based on the particular amino acid residues. And it’s generally just from two to four amino acid residues that determine whether or not a given KIR can see a given HLA class I molecule.   So one of these epitopes, as we call them – and if they were originally defined on a serological basis because specific antibodies could recognize them – so one of these epitopes is referred to as Bw4; these are epitopes that we mainly see on HLA-B molecules – not all – so depending on the population, human population, may be from 40 to 60 or 70% of HLA-B molecules will have this Bw4 epitope. Some HLA-A molecules also bear the Bw4 epitope. So that’s what some KIR molecules, specifically KIR3DL1, is seeing is Bw4.   The results of the study that I talked about today and what we saw is in this African-American multiple sclerosis cohort, individuals that have both 3DL1 and HLA alleles with the Bw4 epitope appear to be protected from multiple sclerosis. And so we see higher frequencies of this combination in our control population relative to patients. So that suggests a protective effect of that combination, 3DL1 plus Bw4.   MSDF Where do you see the research going from here?   Dr. Hollenbach Right now the data that we’re looking at is strictly in terms of carrying frequencies for these particular genes. So these genes are actually highly variable at the allele level, so any given gene like KIR3DL1 has many, many variants that are already known, and likely many variants that we haven’t identified yet because the technology has not been there. The technology is just about now caught up to the point where we are able to examine at the sequence level the variation within these specific KIR genes, and so I think that that’s really the next step. And we’re actually taking steps to start examining this cohort and others in terms of this fine-grained variation in the KIR genes.   MSDF Very good. Thanks.   [transition music]   Thank you for listening to Episode Thirty-Four 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]

Nice to see you again:Episode Thirty FourElephants, dogs, cats, Klingons, hippos, Boris Johnson and quackery. What do these things have in common? Well, nothing, except that's what iszi and Simon were talking about this week.