Podcasts about myh

Today is a powerful conversation straight from my Trying to Conceive Accelerator group. This is a game-changer if you're on your fertility journey and might be unknowingly holding onto emotional or energetic blocks that could be impacting your ability to conceive. This episode is all about shifting your mindset, healing from the inside out, and creating space—mentally, emotionally & physically—for your future pregnancy! Chapters in this episode: 00:00 Navigating The Energetic Side of Fertility Challenges03:00 The Importance of Emotional and Energetic Health05:55 Understanding Trauma and Its Impact on Fertility09:12 Exploring Different Healing Modalities11:58 The Connection Between Mind and BodyWays to work with Corinne: Join the Mind Your Hormones Method, HERE! (Use code PODCAST for 10% off!!)Mentioned in this episode: Follow my go-to breathwork therapist Jordan Nolan on Instagram @jordanalexisnolan!& listen to a past MYH episode with Jordan here.Grab access to my FREE Trying to Conceive Masterclass, here! FREE TRAINING! How to build a hormone-healthy, blood-sugar-balancing meal! (this is pulled directly from the 1st module of the Mind Your Hormones Method!) Access this free training, HERE!Join the Mind Your Hormones Community to connect more with me & other members of this community!Come hang out with me on Instagram: @corinneangealicaOr on TikTok: @corinneangelicaFree Facebook group: Mind Your Hormones Podcast CommunityEmail Fam: Click here to get weekly emails from meMind Your Hormones Instagram: @mindyourhormones.podcast Disclaimer: always consult your doctor before taking any supplementation. This podcast is intended for educational purposes only, not to diagnose or treat any conditions. 

Under YH-forum i december 2024 hade vi eftersnack med de som pratade på scenen. I denna andra delen av två hör du eftersnacket med dels Kvalitetsgransning på MYH och dels Tillsyn på MYH. Dessa två eftersnack publicerades inte live under YH-forum men övriga eftersnack finns att se även med video på poddens Linkedin-sida: https://www.linkedin.com/showcase/yh-podden/ YH-forum arrangeras varje år av Yrkeshögskoleförbundet. Mer om verksamheten och YH-forum kan du läsa på deras hemsida: https://yhf.se/

Up to 70% off beginning Thurs, Nov 28!!! Mark your calendars for MYH Black Friday because it's kicking off Thurs, Nov 28, and ending Wed, Dec 4 at 11:59 pm NYC—no exceptions!! Plus, Monica's breaking down exactly what to expect next year as she becomes a MOTHER and a published AUTHOR all in one year!

I det här avsnittet pratar vi om LIA vilket är extra aktuellt nu när MYH under året genomför tematisk tillsyn på just lärande i arbete. Vi pratar om utmaningarna som finns med LIA, vilket ansvar som finns och vem som har det ansvaret samt om smarta knep i hur vi kan planera LIA-processen och säkerställa god kvalité kring LIA.

I det här avsnittet hälsar vi på i Västerås hos Myndigheten för Yrkeshögskolan (MYH) och för ett samtal med Magnus Wallerå som är ny Generaldiraktör (GD) för myndigheten sedan 1 november 2023. Ett spännande samtal om bland annat Yrkeshögskolans framtid och nuläge!

Vi summerar YH-forum 2023 som genomfördes 6-7 december. En snabb genomgång av allt viktigt som bland annat vad MYH informerade om och vad vi kan vänta oss av YH under 2024. Vill du kontakta oss så maila pelle@qlok.se

A little quickie “news broadcast” style episode to share more on what you can expect from MYH coming up over the next 6 months to a year! Monica's sharing the nitty gritty on upcoming program launches, juicy details about upcoming in-person events, PLUS how she's shifting the way she shows up on Instagram in the coming months going into wedding season (her DREAM!!) + preparing for motherhood in the next couple of years. ❤️ ***Skip to minute 10:36 if you want to skip the program updates and simply hear the shifts she's making on social media!*** +++++ As Mentioned In The Episode —  Join Monica's Email List: https://view.flodesk.com/pages/632a2bfbbf9a194f540c4ab0 Queen Alchemy: https://monicayateshealth.com/pages/queen-alchemy  **QA Round 12 registration closes on August 30, 2023 || Round 13 begins in February 2024** The Man: https://monicayateshealth.com/pages/the-man  Pop-Up LA One-Day Event: https://monicayateshealth.com/pages/la-event  2024 NYC Immersion: https://monicayateshealth.com/pages/immersion  Europe Immersion 2024 Waitlist: https://view.flodesk.com/pages/648c8b36910f3716796cca05 Monica's Book Waitlist (coming out March 2024): https://view.flodesk.com/pages/63bc867d329680c1aa644edf  Monica's YouTube Channel: https://www.youtube.com/@monicayateshealth/  +++++ Monica's Instagram: https://www.instagram.com/monicayateshealth  Full Podcast Directory: https://monicayateshealth.com/blogs/feminine-as-f-ck-podcast/podcast-directory  Business Journal Prompts Download (and other freebies): https://monicayateshealth.com/pages/freebies/  BTS Bubble: https://monicayateshealth.com/pages/monicas-bts-bubble  ***Remember to leave a written review on Apple Podcasts, screenshot it before you submit it, and email it to us at media@monicayateshealth.com to receive an exclusive meditation track as a 'thank you' from Monica. For 1:1 coaching inquiries, email us at support@monicayateshealth.com.

En podcast om vår tids stora förändring och behovet av att ställa om   Med femtio procent fler platser på fem år har Yrkeshögskolan expanderat i raketfart under generaldirektör Thomas Perssons ledning. Och det är inte slut än – expandera mera är hans önskan, när digitalisering, automation och grön omställning förändrar arbetsmarknaden i grunden. I det här avsnittet av Digitala influencerpodden berättar Thomas Persson om en världsunik utbildningsmodell med stor träffsäkerhet, om bristyrken och snabba skiften. Dessutom förklarar han vad data och it-branschen kan ha att lära av byggsektorn när det kommer till att få in fler kvinnor.   Tidskoder och citat. 1.51 Detta gör MYH. 2.37 Därför har yrkeshögskolan ökat antalet utbildningsplatser så snabbt. 3.25 Så bibehåller man kvaliteten när man står inför en så kraftig utbyggnad.  4.54 Borde utbildningsväsendet titta mer på hur yrkeshögskolan gör? 6.00 Om det faktum att många som idag pluggar kommer att jobba med jobb som idag ännu inte finns. 6.54 Så många får jobb efter avslutad YH-utbildning. 7.27 Därför vill Thomas att MYH ska expandera ännu mer. 9.35 Här råder det kompetensbrist på arbetsmarknaden.  11.27 Så gör man för att snabbt anpassa utbildningarna efter behoven på arbetsmarknaden. 13.40 Här skulle ordinarie utbildningsväsende kunna ha något att lära av MYH. 15.26 Så ser det ut med avhopp från IT-utbildningarna på MYH. 17.11 Så har andra branscher jobbat, som liksom data och it haft svårt att få in kvinnor. 19.13. Så ser kännedomen om YH som möjlighet ut. 20.56 Thomas om omställningsstudiestödet som finns sedan 2022. 22.35 Thomas Perssons Fem snabba favoriter. 25.14 Så påverkas yrkeshögskolan av AI-utvecklingen. 27.02 Om försöken att stoppa studenter från att använda AI. 28.04 Thomas Persson rekommenderar en gäst till kommande poddar. 28.59 Så följer du Thomas och MYH:s fortsatta expansion. 29.54 Det här ska Thomas göra när han stigit av sitt uppdrag i höst.

MYH har beslutat vilka utbildningar som får starta 2023 och framåt! Som vanligt har vi direkt grävt oss in i beslutet och analyserat statistiken. Var i Sverige blev det flest nya utbildningar? Vilka utbildningsområden ökar och minskar? Vilken anordnare lyckades bäst? Och mycket mer!

Subscribe to the show: Apple Podcasts | Spotify | Google PodcastsToday's episode begins with a discussion of how border militarization and foreign intervention create a feedback loop of increasing violence and restrictions on freedom.We then take those lessons and apply them to the broader question of how we should approach politics and public policy, and the ways our thinking can get tripped up by over-investment in narrow paths to change.Myh guest is Nathan Goodman, a Postdoctoral Fellow in the Department of Economics at New York University. His research focuses on defense and peace economics, self-governance, institutions, and public choice.Support the show and get every episode two weeks early, as well as access to the Discord community. Sign up here: https://www.reimaginingliberty.com/subscribeProduced by Landry Ayres. Podcast art by Sergio R. M. Duarte.Music: Finding the Balance by Kevin MacLeod | Link | License This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.reimaginingliberty.com/subscribe

Today’s episode begins with a discussion of how border militarization and foreign intervention create a feedback loop of increasing violence and restrictions on freedom. We then take those lessons and apply them to the broader question of how we should approach politics and public policy, and the ways our thinking can get tripped up by over-investment in narrow paths to change. Myh guest is Nathan Goodman, a Postdoctoral Fellow in the Department of Economics at New York University. His research focuses on defense and peace economics, self-governance, institutions, and public choice. ReImagining Liberty is a project of The UnPopulist, and is produced by Landry Ayres. Podcast art by Sergio R. M. Duarte. Join the ReImagining Liberty Discord community and book club. Music: Finding the Balance by Kevin MacLeod | Link | License

Today's episode is jam packed with juicy info about skin care! How conventional skin care products negatively effect our hormones (& skin!) & why organic plant oils are superior for glowing skin, anti aging, acne prone, dry & oily skin! We get into specific ingredients that are beneficial to the skin, ones to look out for & different skin care routines you can try out with the co founder of Skin Essence Organics, David Brooke.Join the Mind Your Hormones Community and Connect with me & other members of this community!Free facebook group: Mind Your Hormones Podcast CommunityMind Your Hormones Instagram: @mindyourhormones.podcastCome connect with me on my personal Instagram: @corinneangealicaConnect with Skin Essence Organics:Instagram: @skinessenceorganicsOnline: www.skinessence.ca (code "Corinne" saves you 15%)2 opportunities for FREE Skin Essence Organics productsShare your take aways from this episode on Instagram stories and tag @corinneangealica and @skinessenceorganics for an opportunity to win 3 free Skin Essence Organics products of your choice. Winner will be chosen by the end of May 2022. Free e-cream product with you spend $50 or more at www.skinessence.ca and use code "MYH" at checkout. LIMITED TIME OFFER.PRODUCT LINKSMy favorite Magnesium Powder & Vitamin D Drops from Gut Personal. Code CORINNEWant professional grade supplements for 10% off? Head to my dashboard! (Click HERE for the CANADIAN dashboard).If you're obsessed with organic, non-toxic skin care and you want one that's AFFORDABLE & EFFECTIVE check out my fave Skin Essence Organics and use code CORINNE for 15% off! If you love or want to try CBD, my absolutely favorite brand is MySoul CBD- Code CORINNE15 saves you 15%[DISCLAIMER: Always check with your medical practitioner before taking any supplements]So grateful you're here! XO Corinne

In the last of this 4 part mini series with Rob from MYH podcast, Andy asks him what his plans are for the podcast and where he wants to take it.  No matter how small you think a problem is, if you're struggling right now please reach out to any of the organisations below. Help is out there! The Lighthouse Club, the UK Construction Industry charity UK: 0345 6051956 Ireland: 1800 939122 MIND 0300 1233393 Samaritans 116 123 Papyrus 0800 0684141 Calm 0800 585858 Anxiety UK 03444 775774 Young Minds Text YM to 85258

Beslutet från MYH kring vilka utbildningar som får starta 2022 och framåt är här! Vi har grävt i statistiken och pratar om tilldelningen. Vilka län fick mest utbildning? Vilken anordnare lyckades bäst? Vilka utbildningsområden är störst? Och mycket mer! Denna gång dessutom med Jessica Niord som gäst!

Oláá sobrinhos! Olha como estou mais frequente agora haha. No episódio de hoje, sigo reclamando dos meus trabalhos da faculdade (meu Deus, um plano de negócio, eu tenho que fazer um plano de negócio), me declaro pro grande amor da minha vida que é o meu irmãozinho Gui, que fez aniversário semana passada, reclamo do elenco burro que o Carelli colocou dentro daquela fazenda e faço o booker do exame chunin de Boruto. Tudo isso enquanto o vestido de crochê da Prada que eu emprestei pra melhor influenciadora desse mundo, Thammy seca no varal. Ouçam e espalhem a palavra do Talk to Myh. --- Support this podcast: https://anchor.fm/talktomyh/support

Edellisen kerran mystiikkaa kompensoidaan konkreettisella ja todistettavalla. Satanismi on pohjimiltaan äärimmäisen tiedepositiivinen uskonto. Mutta mikä erottaa tieteellisen lähestymisen teistiseen maailmankatsomukseen? Ja mihin tarvitaan filosofiaa ja uskontoa konkreettisen maailmankatsomuksen kylkiäisenä? Myhäilemässä Pii, Paju ja Henri. Discord (Perkeleen Temppelin serverillä): https://discord.gg/h8fn5Uj Moderni ateistinen Satanismi on ilmiönä varsin tuore, eikä uskonnosta ole pahemmin tietoa etenkään suomenkielisenä tarjolla. Siksi tämä podcast tuo tietoa modernin Satanismin ihmisoikeusmyönteisestä ja tiedepohjaisesta maailmankatsomuksesta.

Bem-vindos a mais um episódio dessa bagunça de podcast! Sumi (nada novo sob o sol) mas voltei pra falar sobre o babado dos instas de fofoca, Mark burro e porque não deve existir ring girl em lutas que não tem round. Mais uma vez dedicando esse episódio aos reais criadores de conteúdo injustiçados pela merda que se tornou o Instagram e a todos que tiveram a paciência pra explicar o óbvio na live do Wrestlemaníacos no domingo, vocês foram justos e pacientes como era Jesus, eu no lugar de vcs já tinha dado meu escândalo. Lembrem-se sempre do conselho da tia Myh: não vale a pena se estressar com gente estúpida. JABÁMIGOS STONES (Loja da Thammy): https://www.instagram.com/usestones/?hl=pt-br MODINHA NA LUTINHA: https://talktomyh.medium.com/modinha-na-lutinha-01-camp-notes-of-seth-rollins-a751ae7fe5b1 --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/talktomyh/support

I cannot WAIT for you to hear today's episode with Amanda Paliotti! She dives deep into the side effects she experienced from the pill, the fear she felt when deciding to transition off, how she did it & how she's doing now! Some of the health struggles she experienced were IBS, migraines, acne, anxiety & no period. Amanda explains how her doctor reacted when she told him she was stopping birth control. She goes into how she really struggled with anxiety & how difficult that journey was. How she transitioned off the pill using nutrition, lifestyle & supplementation, what she experienced once she stopped the pill (specifically really sore boobs!) & how she's never felt more like herself. Amanda is a personal development junkie, multi-passionate woman, and the host of Embracing the Climb podcast. She is obsessed with all things human behavior, exploring nature & plant-based nutrition. She is always actively looking for ways to better herself, her health, and her life which is why she decided to join the 12 week coaching program MIND Your Hormones 101 in Jan 2021 followed by HONOR Your Cycle in April 2021! Follow her on Instagram @manda.pali Check out her podcast Embracing the Climb Check out Episode 9 of Embracing the Climb where Amanda interviewed me on her podcast all about how I left my 9 year teaching career.   WAYS WE CAN CONNECT! For more information on the 12 Week Coaching Program MIND Your Hormones 101, click HERE & text me "MYH 101" Hop on my FREE text list where I send weekly texts about all this HEALTH, HORMONES & MINDSET! CLICK HERE to join! Come hangout with me on instagram @corinneangealica Checkout my website Want professional grade supplements for 10% off? Head to my dashboard! (Click HERE for the CANADIAN dashboard). Just Thrive Health brand is my fave probiotic. Use code CORINNE for 15% off! If you're obsessed with organic, non-toxic skin care and you want one that's AFFORDABLE & EFFECTIVE check out my fave Skin Essence Organics and use code CORINNE for 15% off! (Canadian website) I am SOOO happy you're here! Thank you for being part of this community! XO

Nesta nova edição do Mesa Quadrada, falamos sobre a segunda noite da WrestleMania 37. Podcast comandado por Anna DeMarco, com Guilherme da Silva e participações especiais de Felipe Fernandes, do Elas Que Lutem Podcast e Myh Santos, do podcast Talk to Myh. Edição: Lucas Costa.

Voltei, quer vocês queiram, que não. Esse é um esquenta pra estreia oficial da segunda temporada que começa a partir do dia 3. Falando de BBB e da Fazenda (com duras críticas a Rodrigo Carelli). Me segue no insta se quiser ficar com a carinha mais linda comprando meus ecopads de crochê no @ellesants. Juro que a partir daqui, o circo vai ficar mais organizado. Espero que gostem e se divirtam pq o objetivo é esse. Beijos da tia Myh. --- Support this podcast: https://anchor.fm/talktomyh/support

Beslutet från MYH kring vilka utbildningar som får starta 2021 och framåt är här! Vi har grävt i statistiken och pratar om tilldelningen. Vilka län fick mest utbildning? Vilken anordnare lyckades bäst? Vilka utbildningsområden är störst? Och mycket mer!

IAEEEEEE PESSOAL! Cês tão bem?! Cês tão bons?! Eu espero que estejam muito bons pq depois de muito tempo sem falar sem parar neste lugar, eu voltei trazendo um tema que faz parte da minha vida e creio que da vida de muitos vcs, estou falando da nossa amiga autossabotagem! Eu espero que vcs entendam tudo que eu falei nesses mais de 40 minutos (pq geralmente eu me enrolo bastante pra falar e vai que ninguém entende né kkk). É isso. Beijos da tia Myh! --- Support this podcast: https://anchor.fm/talktomyh/support

Ett avsnitt om alla ansökningar som inkommit till MYH om att bedriva YH-utbildningar med start 2021 och framåt. Vi analyserar ansökningarna, pratar om trender och såklart berör vi även pandemin som råder lite och digitalisering av YH-utbildningar.

Please consider supporting The Muslim Vibe on a monthly basis. Just £10 per month would go such a long way: www.themuslimvibe.com/support -- This week Salim speaks to Zohra Khaku, Director of the Muslim Youth Helpline. She talks about mental health and the growing struggles that youth are facing, especially now, and how MYH tries to play a role in tackling that. They discuss how the taboo around mental health has weakened over time, and how we can continue to normalise the talking about and getting help for it. Lastly, the conversation moves towards the topic of addiction, with Zohra mentioning how the number of behavioural addiction cases has grown past that or substance addiction over the years. Winding down, they note that ultimately, whilst we must acknowledge the progress we have made in destigmatising mental health, we've still got quite a ways to go. -- To learn more about the Muslim Youth Helpline, visit https://www.myh.org.uk/ Listen to our last podcast with Zohra: https://anchor.fm/themuslimvibe/episodes/Ep-7---Discussing-MuslimsLikeUS-with-Zohra-from-the-show-e3f4hp Enjoying the podcast? Subscribe and let us know by giving us 5 stars! ⭐⭐⭐⭐⭐ Join our Facebook group to continue the conversation! https://www.facebook.com/groups/tmvpodcast/?ref=share --- Send in a voice message: https://anchor.fm/themuslimvibe/message

Taki l00zacki odcineczek z Tomeczkiem i Myhą o nadchodzącym sezonie Ultraligi. Troche toxyczność było ( ͡° ͜ʖ ͡°)

Beslutet från MYH kring vilka utbildningar som får starta 2020 och framåt är här! Vi har grävt i statistiken och pratar om tilldelningen. Vilka län fick mest utbildning? Vilken anordnare lyckades bäst? Vilka utbildningsområdet är störst? Och mycket mer!

This month on the Discover CircRes podcast, host Cindy St. Hilaire highlights three featured articles from recent issues of Circulation Research and talks with Steve Lim and James M. Murphy about their article on nuclear FAK regulation of smooth muscle cell proliferation. Article highlights: Li et al: Histone Turnover in Adult Heart Kurosawa et al: Celastramycin Ameliorates Pulmonary Hypertension Urban et al: NOS3 Gene Polymorphism and Coronary Heart Disease   Transcript Cindy S.:                               Hi, welcome to Discover CircRes, the monthly podcast of the American Heart Association's journal, Circulation Research. I'm your host Cindy St. Hilaire, and I'm an assistant professor of medicine and bioengineering at the University of Pittsburgh. My goal as host of this podcast is to share with you highlights from recent articles published in the July 5th and July 19th issues of the Circulation Research Journal. We'll also have an in-depth conversation with Drs. Steve Limb and James Murphy, from the University of South Alabama College of Medicine, who are the lead authors in one of the exciting discoveries presented in the July 5th issue. Cindy S.:                               The first article I want to share with you is titled, Replication-Independent Histone Turnover Underlines the Epigenetic Homeostasis in the Adult Heart. The co-first authors are Yumei Li, Shanshan Ai, Xianhong Yu, and the corresponding author is Aibin He. This research was conducted at the Institute of Molecular Medicine Beijing Key Laboratory of Cardiometabolic Molecular Medicine and the Peking-Tsinghua Center for Life Sciences. Both of which are part of the Peking University in Beijing, China. Cindy S.:                               In the nucleus of cells, DNA is packaged into a structure called chromatin. Chromatin can reside in an open state that is permissive to gene transcription, or closed state where transcription is inhibited. The core units of chromatin are called nucleosomes. A nucleosome consists of DNA that is wrapped around proteins called histones. It's the position of these nucleosomes that determines whether the chromatin allows for DNA transcription or not. There is a large body of research that is focused on understanding the epigenetic processes that promote or repress transcription. Most of this research focuses on the processes that read, write, and erase covalent histone modifications. But, histones are proteins, and proteins, as we all know, have finite half-lives. Cindy S.:                               Far less research has been conducted to understand the dynamics of histone assembly and disassembly on specific regions of DNA. In this study, the authors took a novel approach of using a GFP-tagged histone H2B protein to track in vivo the rate at which nucleosomes are replaced in cardiac chromatin, and to what extent this rate varies across the genome of those cells. This is particularly interesting, and a particularly good cell type to study, as cardiomyocytes rarely divide or proliferate in the adult heart. What they found was intriguing. Nucleosome recycling is not even across the epigenome of cardiac cells. Instead, gene promoters, enhancer, and other regulatory regions that are known to promote gene transcription all exhibited a higher histone turnover rate than regions of the epigenome that are not occupied by these permissive remarks. Cindy S.:                               Further, they found greater histone turnover at loci for cardiac specific transcription factors as compared to loci for pluripotency transcription factors. This implies preferential access to these regions. Digging further into the mechanism, they discovered that the repressive chromatin regulator, EED, promoted this histone turnover. The epigenetic signature is what helps to define the identity and function of a fully differentiated cell. This study suggests that loss of histone turnover may promote loss of the proper epigenetic signature of a fully differentiated cell. These exciting findings suggest replication independent histone turnover is a requirement in maintaining both epigenetic and functional homeostasis in the adult heart. From this, one may hypothesize that perhaps aberrations in histone turnover contribute to age related diseases in the cardiac tissue, as well as possibly other tissues. Cindy S.:                               The next article I'd like to highlight is titled, Identification of Celastramycin as a Novel Therapeutic Agent for Pulmonary Arterial Hypertension-High-throughput Screening of 5,562 Compounds. The first author is Ryo Kurosawa, and the corresponding author is Hiroaki Shimokawa, both from the department of cardiovascular medicine at Tohoku University Graduate School of Medicine in Sendai, Japan. This article is focusing on the disease pulmonary arterial hypertension. Cindy S.:                               Pulmonary arterial hypertension, or PAH, is a disease that stems from the increased proliferation of arterial smooth muscle cells in the lungs. This proliferation leads to a progressive occlusion of the pulmonary arteries. This occlusion also causes increased pressure in the right heart ventricle. That can lead to heart failure, and ultimately death. Basal dilatory drugs are currently used as therapy in PAH, as they help to open the blood vessels, which can alleviate some of the symptoms. However, these drugs do not target the underlying cause of the symptoms, which is the hyperproliferation of the smooth muscle cell. Cindy S.:                               To identify novel compounds that inhibit smooth muscle cell proliferation, Kurosawa and colleagues used a high-throughput approach. They isolated cells from patients with pulmonary arterial hypertension and used these cells in a high-throughput approach to test 5,562 novel molecules on their ability to inhibit the proliferation of these cells. This unbiased approach yielded several potential compounds that potentially reduced smooth muscle cell proliferation from these patients, and also had very minimal deleterious effects on healthy control smooth muscle cells. From there, the team tinkered with the structure of the drug Celastramycin to try to increase its efficacy, and with that tinkering they found in vitro, that their new molecule could reduce both the inflammatory signal that helps to drive the proliferation of the smooth muscle cells, as well as reactive oxygen species, which helps to drive the inflammatory signaling. Cindy S.:                               Moving forward to in vivo studies, the team found that their new treatment also reduced right ventricle systolic pressure and hypertrophy in three different rodent models of pulmonary arterial hypertension. This treatment improved exercise capacity in one of the models. Together, these exciting results indicate that Celastramycin could be developed as a potential therapy for pulmonary arterial hypertension. Cindy S.:                               The last paper we're going to talk about before switching to our interview with Drs. Steve Limb and James Murphy, is a paper titled, 15-Deoxy-Δ12,14-Prostaglandin J2 Reinforces the Anti-Inflammatory Capacity of Endothelial Cells With a Genetically Determined Nitric Oxide Deficit. The co-first authors are Ivelina Urban, Martin Turinsky, Sviatlana Gehrmann, and the corresponding author is Marcus Hecker, all from the department of cardiovascular physiology at Heidelberg University in Heidelberg, Germany. Cindy S.:                               Nitric oxide is a vasodilatory and anti-inflammatory molecule, and thus, beneficial to cardiovascular health. Homozygosity of a single nucleotide polymorphism, or SNP, is a gene nitric oxide synthase results in reduced ability of endothelial cells to produce nitric oxide, specifically in response to fluid share stress. Decreased bioavailability of nitric oxide in the vessel wall helps to promote atherosclerosis. The SNP that we're referring to in this paper is called T-786C, where TT homozygosity is considered the control, or healthy genotype, and CC homozygosity is the disease associated. CC homozygosity of this SNP is predictive of atherosclerotic related diseases, and consequently, individuals with CC homozygosity have an increased risk for coronary heart disease. Cindy S.:                               Now, despite this detrimental evidence, homozygous patients do not develop atherosclerosis at an accelerated rate. This suggests that there's a compensatory mechanism at play. To identify how CC homozygous cells compensate for reduced nitric oxide synthase activity, the authors utilized human umbilical vein endothelial cells, that are also called huvecs, that harbored either the TT or the CC version of this SNP. They also used these in combination with a monocytic cell line. Cindy S.:                               Urban and colleagues found that under fluid share stress conditions, human endothelial cells homozygous with for the CC variant, had increased production of an anti-inflammatory prostaglandin called 15d-PGJ2. Signaling, via this prostaglandin, helps to compensate in part for the reduced endo production. This prostaglandin suppressed monocyte activation by reducing expression of pro-inflammatory genes such as aisle 1 beta, and decreased monocyte transmigration through endothelial cells. The team also found that patients with coronary heart disease were more likely to have the CC homozygous variant than age match controls. Thus, not only did they identify a partial compensatory mechanism, the authors suggest that 15d-PGJ2 could be a useful biomarker for the diagnosis of coronary heart disease. Cindy S.:                               So that's it for the highlights of the July issues of Circulation Research. Thank you very much to Ruth Williams, who writes the In This Issue copy for the journal, as well as the editorial team at the journal and at the podcast. Cindy S.:                               Okay, so now we're going to talk to our team of first author and last author. Today's paper that we're talking about is Nuclear Focal Adhesion Kinase Controls Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia Through GATA4-Mediated Cyclin D1 Transcription. The first authors of this papers are Kyuho Jeong, Jung-Hyun Kim, and James M. Murphy, and the corresponding author is Steve Lim. Today, we're going to be speaking with James and Steve about this paper. So thank you, both of you, for joining us today. Steve Lim:                           Thanks for having us today. Cindy S.:                               Great. Congratulations on your beautiful paper. I was wondering if maybe we could just start by both of you introducing yourselves, telling us your current position, and maybe about how you came into this field. Steve Lim:                           Hi, Cindy. We appreciate the opportunity to discuss our paper. I'm Steve Lim, an associate professor in the department of biochemistry and molecular biology and medicine at the University of South Alabama. I received my PhD from University of Alabama at Birmingham. I did my post-doctoral training studying the law of FAK in cancer biology at UC San Diego Moores Cancer Center. In 2012 I started my own lab here at South Alabama, where I decided to focus on vascular biology using some pharmacy data I generated at the end of my post-doctoral study. James Murphy:                 I'm James Murphy, I'm a post-doctoral fellow in Dr. Lim's lab at the University of South Alabama. My path to science was a little different than most. I got an undergraduate and graduate degree in mathematics before I joined the PhD program here at South Alabama. Due to a family history of cardiovascular related deaths, I decided to join Dr. Lim's lab due to his interest in studying vascular disease to find new therapeutic targets. Cindy S.:                               Interesting, a math major. James Murphy:                 Yeah. Cindy S.:                               Has that been able to help with any of your basic science studies? James Murphy:                 I'm pretty good at doing concentrations. Cindy S.:                               You're the expert in lab math. James Murphy:                 Yeah. I think the logic skills and critical thinking skills that I picked up in math really help out here in science. Cindy S.:                               Oh, I bet, that's wonderful. You're the dream PhD student who can hit the ground running with M1V1 equals M2V2. Great. Well, thank you so much. I really liked this paper because I love the mechanosensing and how does a cell read what's outside, and how does that message get brought to the inside. Really, that's what you're finding in this paper, specifically looking at how FAK is mediating transcriptional regulation. Maybe you can start by just telling us, what was your overarching question when you started this study? Steve Lim:                           Sure. It is very well-known fact that promotes cell proliferation and migration through interior receptors and gross factor receptor signaling. Both of which are key components in the smooth muscle cell hyperplasia. So naturally, we asked ourselves a simple question, "Is FAK activity important for smooth muscle cell proliferation, and leading into hyperplasia?" Cindy S.:                               So when you say FAK activity I think one thing that's interesting in your paper is, FAK really has kind of two different functions, and one is the kinase function. A kinase is when it can phosphorylate another protein, so it itself is an enzyme. But, then it has another function, so can you maybe tell us about those different functions of FAK? Steve Lim:                           Right. So FAK can function as a kinase, as well as a kind of independent scaffold, which can recruit different proteins. In the paper, we specifically described a kinase independent function as a nuclear function, nuclear FAK function. Cindy S.:                               Interesting. So what premise, or what gaps and knowledge were present before your study, that you were trying to address? Steve Lim:                           Actually, a study showed that the knocking off FAK in the smooth muscle cells prevented neointimal hyperplasia. As just you asked question, FAK has two different functions. Since FAK has both kind of dependent and independent [inaudible 00:14:48], this study lets the unanswered question, which of these two different functions of FAK plays a larger role in dealing with hyperplasia. We aimed to inhibit FAK activity to distinguish between FAK kind of dependent and independent roles in dealing with hyperplasia. Cindy S.:                               Interesting. How exactly were you able to do that? How could you take and dissect apart the two different functions of this protein? Steve Lim:                           We started off with a small pile of experiment to test if a small molecule FAK inhibitor could block neointimal hyperplasia, and we were very surprised at the degree to FAK inhibition actually prevented neointimal hyperplasia following vascular injury. Cindy S.:                               Yeah, and that's in figure one. I was looking at that, it's quite striking. Steve Lim:                           Actually, to distinguish these two different functions we generated new genetic FAK–Kinase-Dead mouse model in conjunction with a FAK inhibitor model, and that would allow us to study a lot of FAK activity in smooth muscle cells. Cindy S.:                               Great. James, could you tell us about the mouse model that you developed for this study, and the specific mutations that you created and what you were allowed to test with those models. James Murphy:                 So the FAK–Kinase-Dead knock-in model was actually generated during Dr. Lim's post-doctoral studies. Cindy S.:                               Is that the exciting data? James Murphy:                 The mutation is just a simple lysine to arginine mutation of amino acid 454. What they found was that, actually, homozygous kinase-dead embryos was lethal. So you need FAK activity to actually develop a full grown organism. We kind of had to cross a hetero wild-type kinase-dead mouse with a phlox FAK mouse, which eventually, if you cross with tissue-specific Cres, what you end up with is a phlox wild-type or a phlox kinase-dead mouse. Then, when you treat Tamoxifen in your Cre mouse, then you delete one copy of wild-type FAK and you're left with either a single copy of wild-type FAK, or a single copy of kinase-dead FAK. Cindy S.:                               Very nice. So for your study, you used, if I recall correctly, the myosin-11, Tamoxifen-inducible Cre model. Can you maybe talk about why you chose that model and why not the SM22 Cre or a non-inducible model? What was your strategy? James Murphy:                 As I mentioned, FAK activity is important for embryo genesis, so we thought we had to use an inducible model, so as to make sure we had an adult mouse at the time of the experiment. We originally actually had the SMA Cre model, however, some grant reviewers had told us that we should kind of shift to the more myosin-11 mouse to be more specific to the vascular. One downside to that, as we mentioned in the paper, is that that's actually only on the Y chromosome, so you can only use male mice. Cindy S.:                               Yes. But, at least it's in only the smooth muscle cells. Is that kind of the pros and cons of that model? James Murphy:                 Yes, and the MYH-11 Cre is kind of the most accepted model when you're doing smooth muscle studies. Cindy S.:                               Great. So can both of you go over some of the key findings of your paper? If we're going to say this in a tweet, what would we say? James Murphy:                 In a tweet. So I think, as we talked about, FAK can go to the nucleus. It's kind of constantly shuttling between the nucleus and the cytoplasm, at least what we've been able to observe in vitro. However, kind of a its localization in vivo still kind of was up in the air at the time. However, our immunostaining data actually rebuild that healthy uninjured arteries primarily showed FAK was in the nucleus. Suggesting that FAK was inactive, and maybe somehow suppressing smooth muscle cell proliferation by staying in the nucleus. But, after wire injury, FAK not only increased its activation, but also shifted to be primarily within the cytoplasm, and eventually we showed that that increase of GABA4 protein stability leading to proliferation. Cindy S.:                               Very interesting. That's great. So what was the hardest part of this whole study? James Murphy:                 Dr. Lim did the preliminary FAK inhibitor studies, but he had people when he started his own lab, he had to teach us how to do the wire injury. At first, learning gets kind of technical, you have to get used to using the microscope. Cindy S.:                               Could you describe the wire injury model for us? James Murphy:                 Yes. What you do is you anesthetize the mouse and you actually locate the femoral artery, and you want to kind of reveal the muscular branch. What you do is you add suture proximal and distal to the muscular branch of the femoral artery to stop blood flow. Then, you're going to cut a small incision in the muscular branch, and you insert a small wire through the branch up into the femoral artery towards the iliac branch. What this does is denude the endothelial layer and kind of causes an extension of the artery, damaging the smooth muscle layer. Once you remove it and suture off the muscular branch, then after a couple weeks you start to see hyperplasia. Cindy S.:                               Interesting. So what does this model clinically? James Murphy:                 This model kind of mimics angioplasty procedures that one may have if they have an occluded artery. There's multiple angioplasty procedures. There's a physical dislodging and opening of the artery. Then, there's some other methods such as using a stent to keep it open. Cindy S.:                               Great. Very interesting. What do you think would happen in maybe, I don't know, an LDLR knockout that was crossed with your FAK kinase deficient mutant? What do you think would happen in an athero model? James Murphy:                 We're actually- Cindy S.:                               Or is that the next paper? We don't have to talk about it if it's the next paper. James Murphy:                 We're actually currently testing that right now. Cindy S.:                               Oh, okay. James Murphy:                 So that's kind of our next step is to test this in atherosclerotic models to see what happens. Cindy S.:                               So, what might this mean for potential therapeutic target? How could we leverage this data to possibly translate it to the clinical setting, even if it's far off? What might we want to do moving forward? Steve Lim:                           Speaking of translational potential, currently most of the treatment options for narrow vessels rely on thrombolytic stents, that provides local delivery of anti-proliferative drugs. However, DES comes with several disadvantages, including location, work, size of these affected vessels. In fact, inhibitors are under cancer clinical development, have never been used in the vascular diseases. Our study, I think, at least to show the potential for using this type of FAK inhibitors in treating hyperplasia, which was not possible before. Cindy S.:                               That's interesting. So essentially, there's already potential, therapy's already available that would just have to be tested in this new ... in this new vascular realm, essentially. Steve Lim:                           Yeah. I was thinking about effication of these type of drugs. I think it could be, as you said, PAH could be one of the targets, because they're not really useful drugs available now. In the future, what we actually, we started already, but it's known, these moments of proliferation plays key role in the arthrosclerosis progression. Studies targeting neointimal hyperplasia and atherosclerosis, it's not existing. I think in the future probably, we would like to test whether in fact inhibition and the smooth muscle cells reduce its atherosclerity in animal models, and hopefully in humans. Cindy S.:                               Yeah, yeah, hopefully in humans, always. Yeah, and in those mouse models, there's always interesting studies where you can block things from the beginning. But, I think one of the beautiful things about the mouse model that you created, the fact that it's Tamoxifen inducible, you could essentially let that atherosclerotic plaque build up for a bit and then knock it out and see if it can reverse it. So the model you created is a really wonderful tool to use for a whole bunch of studies. So congratulations. Steve Lim:                           Thank you. Cindy S.:                               Yeah, I thought the most interesting aspect of this paper was really the fact that it could link this FAK protein, this integrin signal mediating protein to the transcription factor GABA4. So could you possibly tell us a little bit about that interaction, and exactly what GAB is doing in the smooth muscle cell? Steve Lim:                           I actually think that the identifying GABA4 factor actually was one of the difficulties, because normal cells do not express GABA4, that's what is known. I think it's because, based on our finding, the smooth muscle cells in vivo, you could package more predominantly localized in vivo, the nuclear FAK is predominant. So that nuclear FAK finds GABA4 and reduces ability through the process on degradation. But, actually, not changing ... Nuclear factor is not changed. GABA4 mRNA are the expression, so GABA4 is always expressed in smooth muscle cells. But, we never see in healthy, or very freshly isolated smooth muscle cells. We never see Gaba4. That was the most difficult part actually. Cindy S.:                               So the mRNA is always there, it's just never making it to a protein that accumulates in any measurable quantity. Steve Lim:                           So you become a protein, but FAK, nuclear FAK kills all GABA4 in the nucleus. Cindy S.:                               That's the proteasome mediated degradation? Steve Lim:                           Right. Then, GABA4 actually promotes cycling D1 transcription. So no GABA4, no cycling the new one, and smooth muscle cells do not cycle. Cindy S.:                               Interesting. So can you maybe close the loop and tell us essentially what's in figure nine, like this. Could you talk us through that? Steve Lim:                           It summarizes in figure nine, I think it would be best, we can put two different situations. In healthy R3, FAK is in the nucleus, and GABA4 is reduced, cycling D1 is not expressed, and smooth muscle cells become high acid. They don't proliferate. But, in injured, actually, FAK localization is it's the vaso injury promotes FAK localization, vaso injury shifts FAK nuclear localization to cytoplasm. Actually, FAK is activated. Now, GABA4, that increases cycling T1 expression. So that causes intimal hyperplasia. That could be a kind of summary. Cindy S.:                               No, that's perfect. Congratulations on a very nice paper. I thoroughly enjoyed reading it, and I enjoyed even more speaking with the two of you. So thank you very much. Steve Lim:                           Well, thank you so much. Cindy S.:                               Thank you for listening. I'm your host Cindy St. Hilaire, and this is Discover CircRes, your source for the most up to date and exciting discoveries in basic cardiovascular research.  

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