Podcasts about Surfactant

Send us a textNeste episódio de "A Incubadora", Mariana e Marôla mergulham em uma série de discussões fascinantes e atuais sobre temas neonatais. As apresentadoras começam explorando um estudo que investiga como as tendências de contagem de monócitos podem ser utilizadas como uma ferramenta de diagnóstico para enterocolite necrosante, uma condição grave em recém-nascidos prematuros. Em seguida, o foco se volta para tratamentos inovadores na doença hemolítica do feto e do recém-nascido, além de novas abordagens com o uso de surfactante em bebês que desenvolvem displasia broncopulmonar.O episódio também traz uma análise detalhada de uma revisão sistemática sobre intervenções de melhoria da qualidade voltadas para a prevenção de hemorragia intraventricular em bebês prematuros, enfatizando os desafios de implementar estratégias eficazes, conhecidas como "neurobundles". Não perca essa conversa informativa e envolvente sobre os avanços e desafios da neonatologia!1. Blood Absolute Monocyte Count Trends in Preterm Infant with Suspected Necrotizing Enterocolitis, an Adjunct Tool for Diagnosis? Disponível em: https://www.researchsquare.com/article/rs-3722321/v12. Surfactant treatment at birth in a contemporary cohort of preterm infants with bronchopulmonary dysplasiaDisponível em: https://www.nature.com/articles/s41372-024-02061-83. Nipocalimab in Early-Onset Severe Hemolytic Disease of the Fetus and NewbornDisponível em: https://www.nejm.org/doi/pdf/10.1056/NEJMoa23144664. Quality Improvement Interventions to Prevent Intraventricular Hemorrhage: A Systematic ReviewDisponível em: https://publications.aap.org/pediatrics/article-abstract/154/2/e2023064431/197682/Quality-Improvement-Interventions-to-Prevent?redirectedFrom=fulltext Não esqueça: você pode ter acesso aos artigos do nosso Journal Club no nosso site: https://www.the-incubator.org/podcast-1 Lembrando que o Podcast está no Instagram, @incubadora.podcast, onde a gente posta as figuras e tabelas de alguns artigos. Se estiver gostando do nosso Podcast, por favor dedique um pouquinho do seu tempo para deixar sua avaliação no seu aplicativo favorito e compartilhe com seus colegas. Isso é importante para a gente poder continuar produzindo os episódios. O nosso objetivo é democratizar a informação. Se quiser entrar em contato, nos mandar sugestões, comentários, críticas e elogios, manda um e-mail pra gente: incubadora@the-incubator.org

Send us a textSurfactant treatment at birth in a contemporary cohort of preterm infants with bronchopulmonary dysplasia.Mueller C, Shepherd EG, Kielt MJ, Conroy S, Jensen EA, Bamat NA, Panitch H, Levin J, Guaman Cuevas M, Truog W, Abman SH, Nelin LD; BPD Collaborative.J Perinatol. 2024 Jul 17. doi: 10.1038/s41372-024-02061-8. Online ahead of print.PMID: 39020028As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

Enhancing plant health is key to boosting yields and profitability, and we've got the tips to help you do just that! Here we discuss the significant benefits of using Nonionic surfactants to improve spray coverage and absorption, along with the game-changing impact of adding sugar to your tank. Backed by research from the USDA and the University of Nebraska at Lincoln, these methods can lead to increased pest tolerance and higher yields. We will also stress the importance of diligent field scouting to catch aphids early and protect your crop yield. This is an episode packed with practical advice and insights to help you thrive in the ever-evolving agricultural landscape so tune in NOW!

Jonathan and Peter Reynolds, Consultant Neonatologist and Paediatrician based at Ashford and St. Peter's Hospital, Chertsey, UK, discuss the importance of building relationships with the families of premature babies and emerging trends and advances in neonatal care.  Please use the following timestamps to navigate the episode: (00:00)-Introduction (02:45)-Peter's journey from GP to paediatrics (05:22)-mOm incubator trial (09:28)-The DOLFIN study (15:01)-Feeding premature babies (17:05)-Surfactant delivery and guideline development (21:30)-Nasal High Flow (26:30)-Making the delivery room ‘parent friendly' (31:20)-IGF-1 supplements for neonates (34:34)-Inspiration Healthcare (40:49)-Emerging trends in neonatal care (48:09)-Peter's 3 wishes for healthcare  

This week on Journal Club we wrap up 2023 several interesting articles. From the POPART trial's insights into noninvasive surfactant delivery to the controversial use of saline boluses in preterm infants, this episode promises to give you things to think about during the holiday season. As we bid farewell to 2023, join us for a journey through the latest advancements that have challenged and enlightened us. We scrutinize the outcomes of administering oropharyngeal surfactant and examine the physiological effects of normal saline boluses on the tiniest patients. Each segment unveils critical takeaways, urging a reevaluation of established practices and spotlighting the synergy of interdisciplinary collaboration for enhancing neonatal health care.Looking ahead, we're excited to share a glimpse of the upcoming podcast series that will further our mission of education and support for both practitioners and families. From "At the Bench" with its focus on the nitty-gritty of basic science research to the NICU Family Podcast aimed at deciphering medical jargon for parents, we're expanding our network to bring diverse perspectives under one roof. Stay tuned as we recharge during our brief hiatus, and prepare to return with more episodes that promise to inspire, challenge, and evolve the world of neonatology. As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

In this episode, Ben and Daphna review the latest papers in neonatology trying to make sure you don't miss important papers published in 2023! They review a study comparing umbilical cord milking and delayed cord clamping in preterm infants. They also discuss two meta-analyses on cord clamping strategies and their effects on mortality and morbidity. Additionally, they review a study on late surfactant administration in preterm neonates and a study on the risk of hematological malignancies from CT radiation exposure in young individuals. In this episode, the hosts discuss various topics related to neonatal resuscitation and the role of medical education podcasts in pediatrics. They highlight the importance of evidence-based practices in neonatal care and provide key takeaways from recent updates on neonatal resuscitation. The hosts also explore the growing popularity of podcasts as a valuable educational resource and discuss the potential impact of podcasts on medical education. In this episode we also have the please of bringing to you Dr. Karen Puopolo and Dr. Dustin Flanery, from the EBNEO team, who share their commentary on a recently published paper on GBS vaccination. Ben and Daphna conclude the episode with an announcement of new content coming in 2024. As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

You know I love my ventilator... see the photo for how I reacted when we got the new Mindray Veta 5 in-house! But when using a ventilator in anesthesia, what do those modes even mean? Volume control, Pressure control, PEEP...it can get a bit confusing, so we have Glynis here to make sense of it all. Today we talk to Glynis Wileman. She has a PhD - AG Med, while she did not stay in that field, she has worked clinically for 13 years in STARS - specializing in Infant transport/ ECMO, and ventilation / Surfactant studies under Dr. Neil Finer, at RAH. Then onto Siemens/Draeger for Product development in Anesthesia / Ventilation platforms. She is a wealth of information when it comes to anesthesia and ventilation.

Many premature infants with respiratory distress are now supported with continuous positive airway pressure, or CPAP, rather than intubation and ventilation, and those with CPAP can receive surfactant via a minimally invasive approach. JAMA Associate Editor Tracy Lieu, MD, speaks with author Peter Dargaville, MD, from the Menzies Institute for Medical Research in Tasmania, Australia, about Two-Year Outcomes After Minimally Invasive Surfactant Therapy in Preterm Infants: Follow-Up of the OPTIMIST-A Randomized Clinical Trial. Related Content: Two-Year Outcomes After Minimally Invasive Surfactant Therapy in Preterm Infants

Join Michelle and Darla while they discuss pulmonary surfactant. Support the show

Join Michelle and Darla while they discuss pulmonary surfactant. Support the show

Join Michelle and Darla while they discuss pulmonary surfactant. Support the show

Join Michelle and Darla while they discuss pulmonary surfactant. Support the show

As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below.Enjoy!_____________________________________________________________________________________Show notes and articles can be found on our website: http://www.the-incubator.org/135/

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.23.533959v1?rss=1 Authors: King, S. D., Cai, D., Fraunfelder, M. M., Chen, S.-Y. Abstract: BACKGROUND: Atherosclerosis is a progressive inflammatory disease where macrophage foam cells play a central role in the pathogenesis. Surfactant protein A (SPA) is a lipid-associating protein involved with regulating macrophage function in various inflammatory diseases. However, the role of SPA in atherosclerosis and macrophage foam cell formation has not been investigated. METHODS: Primary resident peritoneal macrophages were extracted from wild-type (WT) and SPA deficient (SPA-/-) mice to determine the functional effects of SPA in macrophage foam cell formation. SPA expression was assessed in healthy vessels and atherosclerotic aortic tissue from the human coronary artery and WT or apolipoprotein e-deficient (ApoE-/-) mice brachiocephalic arteries fed high fat diets (HFD) for 4 weeks. Hypercholesteremic WT and SPA-/- mice fed a HFD for 6 weeks were investigated for atherosclerotic lesions in vivo. RESULTS: In vitro experiments revealed that global SPA deficiency reduced intracellular cholesterol accumulation and macrophage foam cell formation. Mechanistically, SPA-/- dramatically decreased CD36 cellular and mRNA expression. SPA expression was increased in atherosclerotic lesions in humans and ApoE-/- mice. In vivo SPA deficiency attenuated atherosclerosis and reduced the number of lesion-associated macrophage foam cells. CONCLUSIONS: Our results elucidate that SPA is a novel factor for atherosclerosis development. SPA enhances macrophage foam cell formation and atherosclerosis through increasing scavenger receptor cluster of differentiation antigen 36 (CD36) expression. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Driving on snowy or icy roads can be pretty dangerous.  That is why roads are salted or coated with sand to provide traction in icy weather.  But excessive use of these substances is bad for the environment and sometimes a storm will blow in before the roads can be coated. In a paper published in […]

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.12.523571v1?rss=1 Authors: Iezza, D., Predella, C., NI, K., Murray, J. W., Liu, H.-Y., Saqi, A., Glasser, S. W., Dorrello, N. V. Abstract: Childhood interstitial lung disease (chILD) secondary to pulmonary surfactant deficiency is a devastating chronic lung disease in children. Clinical presentation includes mild to severe respiratory failure and fibrosis. There is no specific treatment, except lung transplantation, which is hampered by a severe shortage of donor organs, especially for young patients. Repair of lungs with chILD represents a longstanding therapeutic challenge but cellular therapy is a promising strategy. As surfactant is produced by alveolar type II epithelial (ATII) cells, engraftment with normal or gene-corrected ATII cells might provide an avenue to cure. Here we used a chILD disease-like model, Sftpc-/- mice, to provide proof-of-principle for this approach. Sftpc-/- mice developed chronic interstitial lung disease with age and were hypersensitive to bleomycin. We could engraft wild-type ATII cells after low dose bleomycin conditioning. Transplanted ATII cells produced mature SPC and attenuated bleomycin-induced lung injury up to four months post-transplant. This study demonstrates that partial replacement of mutant ATII cells can promote lung repair in a mouse model of chILD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Infants in the NICU are patients that require specialized care with unique clinical considerations. Specific recommendations must be considered for all systems of NICU patients and the skin is not any different. Infants who are being cared for in the NICU, especially those that were born premature have an increased risk for skin trauma. On this episode, we review some of the skin care guidelines and recommendations available for clinical practice of NICU patients. As NICU clinicians, is is important to not only be aware of the anatomical variations of a term and preterm infant's skin, but to also know how that guides their clinical care and treatment plan. Many of the topics we cover on this episode have been standards of care for years, but there are also new recommendations for practice and products available based on recent research findings. NICU clinicians will hear a great review as well as up-to-date clinical recommendations for skin care of our specialized population in the NICU. The episode will also be beneficial for parents to hear the clinical practice guidelines and recommendations for term and preterm infants as well as some of the variations that may exist between different institutions. Our NICU Roadmap: A Comprehensive NICU Journal: https://empoweringnicuparents.com/nicujournal/NeoTech Products: https://www.neotechproducts.com/Solly Baby: http://shrsl.com/2py8hNICU Mama Hats: https://empoweringnicuparents.com/hats/NICU Milestone Cards: https://empoweringnicuparents.com/nicuproducts/Empowering NICU Parents Show Notes: https://empoweringnicuparents.com/episode36Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group: https://www.facebook.com/groups/empoweringnicuparentsPinterest Page: https://pin.it/36MJjmH

See the fungicide decision making video referenced by Jay, curated by Brian Buck and Josh Shofner: https://www.youtube.com/watch?v=379blvfOvl4 

In this episode, host Wolfgang Holtkamp meets Ann-Kathrin Briem, who is Environmental Engineer and Life Cycle Assessment Expert at the University of Stuttgart and the Fraunhofer Institute for Building Physics. They talk about sustainability assessment in the area of "mass personalisation" and also "function-optimised biosurfactants", a sustainable alternative to chemically synthesised surfactants. She also gives us an insight into her stay abroad in Canada and her work with students.

“If you're importing raw materials, don't run your inventories low. Make sure you're keeping some measure of inventory on hand and a buffer to guard against delays.” Listen as the Smart Acids learn more from International Trade Director Larry ‘Globetrotter' Ogden (02:08) about Omicron in China and its impacts on the interconnected global supply chain for the chemical and ingredients market and beyond. Eric ‘The Hit Man' Emery, product marketing manager, Phosphates, makes a special appearance (10:10) to review market breakdown across demand, supply and related costs—what end-use applications are impacted and how. Finally, David ‘The Forty-Year Old Retiree' Boraks, senior product marketing manager, Surfactants, (14:00) sheds light on this market, applications served, why the market is growing and the rising importance of paying attention to your supply chain.Smart Acids™ is the source for product insights and current market moves related to chemical and specialty ingredient distribution—breaking it all down one boron at a time. Join hosts Andy Erickson and Chris Ernst for straightforward and honest chat that speaks to the why behind pricing and supply, delivered in a smart, fun and entertaining way.About the hosts: Andy Erickson, director of product marketing, Essential Chemicals, and Chris Ernst, senior director of product marketing, Solvents, converse with guests from chemistry and specialty ingredient backgrounds who are keyed in to manufacturing and markets across industries.

In this podcast Mark Cave will be explaining what a surfactant is how it works and how your cleaning business will benefit from using surfactants in your softwashing activities. If you have any comments after this podcast please do not hesitate to contact us at SoftWash UK as we'd love to hear your feedback. Clever Wash Surfactanthttps://www.softwashing.uk/products/clever-wash-surfactant#softwashing#softwash#roofcleaning#guttercleaning#patiocleaning#externalcleaning#windowcleaning#rendercleaning#mossremoval#pressurewashing#jetwashing

ATS 2022 starts May 13. Register today: conference.thoracic.orgPodcast CreditsWriter: Ryan Thomas, MDProducer: Ryan Thomas, MDReviewers: Christina Barreda, MDElizabeth Fiorino, MDReferences: Andreeva AV Regulation of surfactant secretion in alveolar type II cells 2007 AmJPhyLung Banfi C, Agostoni P. Surfactant protein B: From biochemistry to its potential role as diagnostic and prognostic marker in heart failure. Int J Cardiol. 2016 Oct 15;221:456-62 Chroneos ZC, et al. Pulmonary surfactant: an immunological perspective. Cell Physiology and Biochemistry 2010; 25: 13-26. Cole FS, Nogee LM, Hamvas A. Defects in surfactant synthesis: clinical implications. Pediatr Clin N Am 2006; 53: 911-927. Guillot-Alveolar epithelial cells Master regulators of lung homeostasis 2013 IntJBiochemCellBio Frerking I, et al. Pulmonary surfactant: functions, abnormalities, and therapeutic options. Intensive Care Med 2001; 27: 1699-1717. Herzog EL Knowns and Unknowns of the Alveolus PROCATS57778 Mason RJ. Biology of alveolar type II cells-2006-Respirology Murray and Nadel's Textbook of Respiratory Medicine 5th ed. Accessed via MDConsult. Nathan N Surfactant protein A: A key player in lung homeostasis IntJBioCellBio 2016 Nkadi PO, et al. An overview of pulmonary surfactant in the neonate: genetics, metabolism, and the role of surfactant in health and disease. Mol Genet Metab 2009; 97: 95-101. Whitsett JA, Wert SE, Weaver TE. Alveolar surfactant homeostasis and the pathogenesis of pulmonary disease. Annual Review of Medicine 2010; 61: 105-119. Wert SE, Whitsett JA, Nogee LM. Genetic disorders of surfactant dysfunction. Pediatr Dev Pathol. 2009; 12(4): 253-274.

As always, feel free to send us questions, comments or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through instagram or twitter, @nicupodcast. Or contact Ben and Daphna directly via their twitter profiles: @drnicu and @doctordaphnamd. enjoy!________________________________________________________________________________________Show notes and articles can be found on our website: http://www.nicupodcast.comThis podcast is proudly sponsored by Chiesi.

Editor's Summary by Preeti Malani, MD, Associate Editor of JAMA, the Journal of the American Medical Association, for the December 28, 2021 issue.

John Ingram's Knowledge Nuggets #8 — Surfactant. Presented by John Ingram, CCP.

SEGMENT 1: Surfactant Leaching Surfactant leaching is a somewhat common issue in newly painted bathrooms with high humidity. It can look TERRIBLE on your walls . . . but it's easy to take care of! SEGMENTS 2-4: Home Repair Services Home Repair Services is an organization in Kent County that we feel everyone needs to know about! We'll do our best as we spend three segments talking with Executive Director, Joel Ruiter.

Welcome Back Friends to your 40 Weeks of Pregnancy. This week your sweet little one is the size of a Zucchini and is starting to produce Surfactant (which helps his/her lungs). Please listen to learn more and let me know if you have any questions. Be sure to subscribe here to my Podcast and to check out my YouTube Channel as well for additional information about your Pregnancy, Childbirth, Breastfeeding, Postpartum, and Baby Care. Thank you for listening- Have a great day! --- Support this podcast: https://anchor.fm/BabyBumpLife/support

Greetings! It is yet another week of continuous productivity and new beginnings. The A Better Way to Farm team will never stop to provide you with tons of information and implementable strategies for growing your farm this season.   In this episode, Tyler meets Tyler, the grower who never lets limiting factors get in the way of a good harvest and greater yields. His quest led him to meet A Better Way to Farm and discover the Conklin strategies to learn better farming practices together with his father, uncle and cousin.   Be ready to listen and determine what's best for your farm! Let's take note of some practices which may apply to boost your farm's growth. Come on, tune in!

In this episode, Tyler meets Tyler, the grower who never lets limiting factors get in the way of a good harvest and greater yields. His quest led him to meet A Better Way to Farm and discover the Conklin strategies to learn better farming practices together with his father, uncle and cousin.

As always, feel free to send us questions, comments or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through instagram or twitter, @nicupodcast. Or contact Ben and Daphna directly via their twitter profiles: @drnicu and @doctordaphnamd. Papers discussed in today's episode are listed and timestamped below.enjoy!01:50 - Reviewing recordings of neonatal resuscitation with parents. https://fn.bmj.com/content/106/4/34610:55 - Associations between family presence and neonatal intubation outcomes: a report from the National Emergency Airway Registry for Neonates: NEAR4NEOS https://fn.bmj.com/content/106/4/39219:28 - A Retrospective Review Following the Addition of Clonidine to a Neonatal Abstinence Syndrome Treatment Algorithm. https://www.frontiersin.org/articles/10.3389/fped.2021.632836/full25:03 - Trial of aerosolised surfactant for preterm infants with respiratory distress syndrome. https://fn.bmj.com/content/early/2021/06/09/archdischild-2021-32164530:15 - Interface leakage during neonatal CPAP treatment: a randomised, cross-over trial. https://fn.bmj.com/content/early/2021/06/28/archdischild-2021-32157933:55 - Changes in Physicians' Perceptions and Practices on Neonatal Pain Management Over the Past 20 Years. A Survey Conducted at Two Time-Points. https://www.frontiersin.org/articles/10.3389/fped.2021.667806/full39:02 - The Experience of Housing Needs Among Families Caring for Children With Medical Complexity. https://pediatrics.aappublications.org/content/148/1/e202001893747:10 - Home Visiting for NICU Graduates: Impacts of Following Baby Back Home. https://pediatrics.aappublications.org/content/148/1/e202002939752:25 - An Infant Carrier Intervention and Breastfeeding Duration: A Randomized Controlled Trial. https://pediatrics.aappublications.org/content/148/1/e202004971756:37 - Severity of Bronchopulmonary Dysplasia Among Very Preterm Infants in the United States. https://pediatrics.aappublications.org/content/148/1/e202003000758:41 - Human milk feeding and cognitive outcome in preterm infants: the role of infection and NEC reduction. https://www.nature.com/articles/s41390-021-01367-z61:27 - Validity of Random Triglyceride Levels in Infants Receiving Parenteral Nutrition. https://www.frontiersin.org/articles/10.3389/fped.2021.601915/full62:40 - Degree of ventriculomegaly predicts school-aged functional outcomes in preterm infants with intraventricular hemorrhage. https://www.nature.com/articles/s41390-021-01631-2

DIY with 'The Resident Builder' Pete Wolfkamp Sunday 27th June 2021In this week's show, first caller Jim asks Pete for advice on behalf of his grandson on the best way and the process of landing an apprentice position in the building industry followed by caller Tina who is seeking advice about project managing her home reno to keep within the budget and save. What are the do's & dont's, health & safety, tradie talk etc... what's to be expected by taking on this role? Caller Murray is not happy after his bathroom reno is turning out to be flooded with disaster! Pete touches on Surfactant leaching, Sound rating requirements, Builders estimations, Hot water Cylinders, Boundary pegs, Bridge piping and more...Then My Mate the Tradie- guest 'Gordie' from JNL discusses 'The current supply vs demand for residential framing timber. Ruud Kleinpaste takes us out into the garden where we talk about Black silty mould on citrus, Transportation and relocation of plants, creepy crawlies and loads more garden questions... See omnystudio.com/listener for privacy information.

In this episode, we review non-invasive ventilation in the NICU, respiratory support without an endotracheal tube, but rather with a nasal cannula or face mask. If your baby currently has or had Respiratory Distress Syndrome, the chances are quite high that they are currently or were previously on at least one of the different modes of non-invasive ventilation, either nIMV or NIPPV, CPAP, HFNC, LFNC. This is a topic, I know so many of you will benefit from hearing. After listening, you will walk away with a much better understanding of the different options of non-invasive ventilation, why one method may be chosen over another, how they will be beneficial to your baby, and some of the potential complications. Tune in to gain a better understanding of the parameters set on each of the different modes of non-invasive ventilation including but not limited to rate, PIP, PEEP, i-time, L/min and FiO2. Grab your free graphics that correlate with the episode at: http://empoweringnicuparents.com/rds/https://empoweringnicuparents.com/nicuimage/Empowering NICU Parents Show Notes:https://empoweringnicuparents.com/episode11/Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group:https://www.facebook.com/groups/empoweringnicuparents

Do you have a baby in the NICU who is intubated and on a ventilator? Are you desperately trying to understand what the care team is talking about when they mention positive pressure with SIMV, PIP, and PEEP, or volume-targeted with tidal volume, or high frequency ventilation? In this podcast episode, we break down the different modes of invasive ventilation commonly used in the NICU. First, we review respiratory distress syndrome in newborns as well as some key concepts including surfactant deficiency, atelectasis, lung compliance, and functional residual capacity to help you understand why a particular mode of respiratory support may be chosen versus another. Next, you will hear a review of conventional ventilation modes including SIMV, assist control, and volume guarantee followed by a discussion of 2 different types of high frequency modes of ventilation. Tune in now to proudly walk away with a better understanding of not only the concepts and goals of effective ventilation and oxygenation in the NICU, but how those parameters are met with the different modes of ventilation used most often for NICU babies. NICU parents will gain core information and education to help empower you as a NICU parent, without any overwhelm or confusion.  Grab your free graphic that correlates with the episode at: http://empoweringnicuparents.com/rds/Empowering NICU Parents Show Notes:https://empoweringnicuparents.com/episode10/Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group:https://www.facebook.com/groups/empoweringnicuparents

*Warning: may contain Ben’s weakest analogy* All of us “covid nurses” know how to handle a good case of ARDS. But do we know why? Or the pathophysiology of ARDS? This week, you WILL learn. ***DEFINITELY WILL BE ON CCRN*** TOPICS: ARDS, Surfactant, PEEP, Vent Settings, P/F Ratios

In this episode, we take a deep dive into Respiratory Distress Syndrome or RDS in newborns. RDS is the dominant clinical problem preterm infants face. But, RDS it is not exclusive to just premature infants. Tune in to learn more about RDS, what causes it, what infants can be affected by it, the common symptoms infants present with, how it is diagnosed, as well as the common methods of prevention and treatment including antenatal steroids, respiratory support, specifically CPAP, and artificial surfactant administration. You will gain a better understanding of how a deficiency of surfactant affects a baby's air exchange, oxygenation, breathing difficulties, and starts a cascade of events if it is not addressed or treated. Grab your free graphic that correlates with the episode at: http://empoweringnicuparents.com/rds/Empowering NICU Parents Show Notes:https://empoweringnicuparents.com/episode8/Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group:https://www.facebook.com/groups/empoweringnicuparents

The Beyond Clean GoldMind is a free innovative digital dictionary resource for Sterile Processing terms, featuring diverse voices from around the globe who provide definitions to the most common terms in our industry. Releasing 365 days a year, GoldMind is your daily dose of Sterile Processing education and insight to invest in yourself, your future, and the safety of your patient. It is a perfect addition to new technician on-boarding, certification studies, and educational programming in your facility. Subscribe on iTunes: https://podcasts.apple.com/us/podcast/beyond-clean-goldmind/id1534449762 Subscribe on Spotify: https://open.spotify.com/show/2NRaV0f3cWed7ZmxyYFYQB?si=BWjLs0L_QyO2sP1WhjBAGQ For more creative Sterile Processing education & resources, visit us at http://www.beyondclean.net #GoldMind #BeyondClean #DigitalDictionary #WordOfTheDay #Education #SterileProcessing #Voices #Network #Listen #Learn #ChangeTheWorld

Welcome To The MedFlashGo Podcast. This Is Your Daily 4 Minutes Or Less Rapid Review for medical students. Topics are based on medical board examinations including USMLE, COMLEX, And Shelf Exams. We release a new episode every weekday! In this question of the day, Sean asks students to identify the relationship between surfactant production and gestational age. These questions are powered by MedFlashGo The First Voice-based interactive medical question bank currently available on Alexa. This tool allows medical students to study medical topics and be interactively tested without the use of a screen. You can study on your couch, in your car, and on the move without the use of a screen. To get access to the free audio-interactive question bank, click here or go to your Alexa application and search medflashgo In the skills section. To learn more details go to medflashgo.com and check out our frequently asked questions section. Please know that these questions were creatively designed by medical students and physicians for the purpose of education and do not replace health information given from your health professionals. We have tried our best to make sure the information is accurate please, so please let us know if you find any errors and we will be sure to correct them. --- Send in a voice message: https://anchor.fm/medflashgo/message

Neonatologist and researcher Dr. Sandra Leibel discusses her research into a particular gene therapy process involving a lung organoid model. She explains her research and surrounding issues, including the basics of lung research, and specifically the importance of the surfactant process in keeping lungs from collapsing; how mutations lead to the need for surfactant protein b deficiency treatment in babies; and  how her model showed positive treatment possibilities but what must happen before treatment is available clinically. Dr. Sandra Leibel is an assistant clinical professor in pediatrics at UC San Diego School of Medicine and a neonatologist specialist at Rady Children's Hospital in San Diego.  She's currently focused on the lab side of her work involving a gene therapy process. Dr. Leibel created a model using induced pluripotent stem cells, or embryonic stem cells, and differentiated them into three-dimensional lung organoids. She's using these models to test a possible surfactant protein b deficiency treatment.  She explains to listeners the basics of lung geography and mechanics and how of the 40 different lung cell types, she uses the epithelial cells in her model. She describes the surfactant production that happens in the distal portion of the lung, which is the furthest portion, yet serves the whole lung by reducing surface tension and keeping our lungs from collapsing.  These alveolar type 2 cells can undergo a mutation during embryonic development that damages the b protein of those cell; they cannot then produce effective surfactant. These babies are born needing to be on a breathing machine until they are able to get a lung transplant. However, she's found an exciting advancement in her research, namely that by introducing a virus vector that carried a healthy b gene, she measured signs of the model cells completely normalizing into surfactant-producing cells. In other words, she was able to cure the disease in a dish.  She explains the implications of this, the timing for clinical use, and other related issues. For more, google her name and see her page at UC San Diego: https://profiles.ucsd.edu/sandra.leibel

All right, welcome KBMD Health and Gut Check Project bring you COVID Files, episode number one. It's a little bit different setting right now. I am not sitting in front of or next to Ken Brown my partner. What's up, Ken?What's going on Eric? Yeah, you sound a little bit different, but that's all part of it. We are practicing some social distancing.We definitely are. Brown does have a nice brick wall behind him. And I've kind of got one back over here. So if you happen to be looking on YouTube, you can see we've got a wild lamp. Yeah, just in case just in case somebody accuses us of lying. There's two brick walls.Yeah, there's there's definitely two two brick walls. So Brown is...Ken you're sittin' what about 60 miles from me? And but we both been having to stay up to date with the facilities that we served the anesthesia you and gastroenterology you could call it a hospital that's actually handled a patient.We had our first death two days ago from COVID 19. So this is a real thing. I was working in the hospital. This is something that I felt like, it's time although I'm not a virologist, you're not a virologist. Neither one of us are epidemiologists, we do have an obligation as healthcare workers to try and describe everything that we've been reading to get it out to people. So this is something that we cannot ignore meaning as a opportunity and a platform to give some information. Hopefully, we can give something that anybody watching this will at least clarify a few things. That's my goal here is to discuss some of the definitions get into what we're going to look at, should we panic, should we not panic? where's this going? All the things that I asked? Because I spent a lot of time looking at literature, we've got graduate students working for us, we've got nurses working for us, that look up a lot of things. So that's what I want to do in this show today is try and discuss all of it out there. Because the more informed you are, the more that you will be part of the solution. That's the important thing, and realistic, and a healthy amount of fear is appropriate. But not freaking out is the key here.I agree 100%. And something else I've been home just like you have and in between taking care of work and then keeping up with work. And then obviously, having a great amount of family time while being in a social quarantine, you end up consuming a lot of different information. So what I don't want our show today to be is just the personal emotional things only really we want to do exactly what Brown said. And that is move into information that you can use. Top to bottom, we want to explain things from the top level down so that we can we want to get everybody into understanding. There's unfortunately because it's a new novel virus. There's lots of misinformation in terms of what does it do? How is it affecting us and rather than take a guess I think that what Ken has for you here today is lots of up to date information, we're going to try to put it into a, a mode that you can use, accept and improve and protect yourself.Because I think what ends up happening is a lot of people, especially people that are trying to quarantine themselves, or they're staying at home, they do binge social media mediaing Is that right? Where they just kind of get on social media and just binge all of it? And it seems like if you look at that, there's going to be two camps of people. You've got the oh, what's the big deal? Nothing's going on. And I see these videos in Florida where people are playing tug of war on the beach, and there's hundreds of people and I'm just like, ph my goodness. And then it's the no, we're in a zombie apocalypse and they, you know, take all the toilet paper and hand sanitizer from the stores. So the only thing I've learned from that is that apparently zombies really hate toilet paper is the best I can tell about that. They can't stand it.They can't stand it. So the zombie apocalypse if that's the case, throw toilet paper at them. Unlike Walking Dead where you have to like smash them in the brain apparently toilet paper is the biggest defense that you can have against zombie apocalypse. Yeah, we don't this is not this is not an avenue the COVID File Episode One is not an avenue to drive people to go and make a bunch of unnecessary purchases or to go in and hoard things that your neighbor needs. So this is let's stay factual. And honestly, Brian, I'm going to kick it off to you and let you kind of lay out the template now outline on how we're going to address the different things andYeah so you know, normally, I mean, one of the things that I really like to do on Gut Check Project because, you know, joke around and make light of things but I'm having a really hard time making light of this particular thing. So I am neither in the camp that this is oh, what's the big deal and I'm not in the zombie apocalypse, but I do really think that we all need to take this particular thing extremely serious, and we need to get into it. One of the things that I've noticed is a lot of people have trouble with the different terms that are being used in the news. I mean, they get on press conferences, and they just throw these terms out. How is this changing the world? I mean, there are single moms that are waitresses that their restaurant it has been closed. And this is there's a lot of things going on like that. And I've actually, I knew that we were onto something when I've been trying to get an infectious disease doctor to come on the Gut Check project that physically come on for it really kind of ramped up here in the US, and a few of them were like, nah, I'm good. I think I'm gonna lay low and try and separate myself. And, you know, they basically said, you're on your own on this and I'm like, okay, so this is, I'm gonna have to learn about this myself. And I just want to share the information that I have uncovered about my concerns. And so my concerns are what are all these different terms after we get that, you know, how do you actually present? What's going on with the numbers? What are these numbers real? How infective is this? And then I want to get into some good news about what's going on. And that's where a lot of the research is happening. So we can talk about all these things. Because when I asked my nurses, hey, these different terms, what do these mean to you? Most people don't really get it because CNN, and Fox and these different news stations, they interchange all these names. And so let's start with that. Let's learn the four virus related terms so that everybody's on the same page, because when you read medical literature, they refer to it as one way when you listen to the news, they refer to it, and then they lump everything into COVID19. So let's just start with this. So the definitions, SARS, CoV2, so when people when scientists talk about this, they always talk about as the SARS CoV2, you'll hear infectious disease doctors refer to it as that. It is a type of Corona virus. In the beginning when everybody kept saying this is a Corona virus virus you Google it and I remember I've had friends and stuff go, what's the big deal? It causes a cold like symptom. Well, the thing is, that's a family of viruses, the Corona the reason why when they first came out, they said this was a novel Corona virus, which was not the word that they should have used. That is the word that infectious disease doctors would say they should have said we have a scary Corona virus here. That would have been catching people's attention a little bit more but novel Corona virus meant that it was a different type of coronavirus. So in that family this Corona virus is the SARS CoV2 two because it is a SARS meaning as severe acute respiratory Syndrome type Corona virus like SARS CoV nothing in 2003. That's how come these names are so confusing. So it's SARS CoV2 is this virus, which the closest thing we can relate it to, is SARS Cov, which was in 2003. So that's the virus. The current virus is not called COVID 19. COVID 19 is the infectious disease caused by this virus. So SARS CoV2 is the actual virus, and it owns it basically owes its name to its genetic similarity to the original virus, the SARS CoV. So that is short for severe acute Respiratory Syndrome Corona virus 2. So that's the definition that's the actual virus. Corona virus. Corona viruses are this big family. SARS CoV is the 2003 one SARS CoV2 is the novel Corona virus that we're dealing with. So that's the guy that we're actually dealing with. COVID19 is the disease that you get from this. Currently there are seven Corona viruses that can cause human disease. With the three most severe being the SARS MERS, which is the Mediterranean one and then COVID19.And just for clarification, the D itself does mean disease. So it is CO for Corona VI for virus and then D for disease and then 19, I believe is assigned because it was first discovered at the end of 2019.That's exactly right. So this is exactly what like what we're saying when we first discovered human immunodeficiency virus, and then you would develop Acquired Immunodeficiency Syndrome AIDS. So it's very similar to that where you can there's the virus, it causes this disease, and so CoV...so COVID19 is the infectious disease caused by the SARS CoV2 virus. What's alarming is that as a much higher fatality rate than the flu, so a lot of people were saying I don't really understand more people died of the flu, more people died of the flu because the flu is more ubiquitous. If this thing takes off, then you're gonna have a much higher mortality rate. What the people don't really well, now everybody starting to understand and...so I mean, by the way, everything changes daily. I've listened to a lot of experts. And they're like, as of March 19, this is what we know, because they're freely admitting that as of March 22, we may have something new information on this. So what we do know is that it's the incubation period is quite long, which is why it spreads so easily because you may not have any symptoms. And then you're out there looking and feeling healthy and not taking any precautions, and then you get in contact with somebody, and we're going to talk about that a little bit later. Same reason why we're doing the social isolation, we both feel great. We're not doing it because we have a fever or we have a cough or anything bad's going on. We're doing it because we understand that you can already be infected and keep spreading it. So we're gonna sit there and do this. So I'm gonna now I'm going to quiz you because you've been doing a lot of reading. So how does the typical presentation happen when somebody is exposed to the SARS CoV2 virus?Typical presentation, and I guess you're asking me if somebody happens to have been infected, and now they're complaining of symptoms, is that what you're talking...?Correct. What is what are the typical symptoms people should be looking out for?The first thing, or most common, I believe is just a mild fever, followed by a little bit of discomfort and malaise. If they then later in developing something along the lines of a shortness of breath is going to be a key player, which hopefully at that point, the person has then decided that they need to seek help, but unfortunately, the way that I've been reading the timeline, oftentimes people are just simply not going until the progression grows. And if I understand correctly, and feel free to correct me if I'm wrong, but what we're looking at by the time that symptoms generally set up is about a five day play out from the first time that somebody experiences a fever, and unfortunately waiting until the fifth day before seeking to find out if the cause of the fever happens to be related to this particular Coronavirus may be too late for those who are somewhat compromised, because the development of shortness of breath is the early stage of and we'll get into it, but the inflammation and bring it down to the lung tissue. And that begins a small little snowball that turns into a big avalanche of different things that we'll get into here in a moment. But it's interesting and I don't want to walk backwards here but you said what is the presentation the unfortunate part is the once someone becomes infected and then becomes contagious to the world around them before they show symptoms, that that five day stretch could take off after the second day they've been exposed, or can wait all the way until it looks like the 14th day. And unfortunately for the human race, we may be those particular people may be infectious or contagious to the world around them for up to 14 days without ever knowing it, spreading the virus.Absolutely. So we're gonna get into that because then we're going to talk about the epidemiology and why this is a little bit frightening if we all don't do our part, right. So the bottom line is you're exactly right sore throat, malaise, fever. In 80% of the infected people we believe right now, that symptoms include this kind of mild situation, we're going to call that mild so a lot of people think they had a small cold or they had the slight flu or whatever. 20% of the people, you're going to end up with a 20% of the people, you're going to end up with a more serious respiratory infection, which is pneumonia. Now approximately 2 to 3% of those people will will die. And if you end up with a severe pneumonia, and a severe inflammatory reaction, then what will happen is that if you end up getting bad enough to go on a ventilator, we're seeing that 86% of those people die. So the people that do get sick get really sick. So, yesterday, I was actually preparing this and this is one of the things so when I sit there and watch these videos in Florida of people saying, man, it's not a big deal and I say Florida because somebody sent me a video of people in spring break in Florida. I'm not trying to bash Florida in any way. So I get on a website where I can sit there and kind of track these things sort of real time. Yesterday, March 19 the Corona virus cases were 236,728...236. Today, 266,000. 30,000 people have been diagnosed since yesterday.It's a logrith...it's a logarithmic growth.Oh, yeah. And we're gonna get into that why because I think that's where the real it's not that the science the science of the of the virus and everything is super. If you're a virologist, it's interesting and everything, but when you and this is an epidemiologist's, nightmare slash, the thing that they went to school for. So a lot of them are geeking out, they're doing all these modeling and all these other things that are going out there. So there was 9,828 deaths yesterday. Today, we're up to 11,186. As far as the US yesterday, we had 11,348 cases today, 16,000, 5000 cases 16,491. The death toll went from 171 to 224. So the US here's the good news is that up until just about a week ago, the US fatality rate was around 3%. Because and this is kind of what's going to happen when we diagnose more people. Now it's down to 1.5% what that means is rescreening more people, people that normally wouldn't even go get screened are going to do this. So but you contrast that to Italy, that over the past three days, the death percentage was around 6%. And then just yesterday, it was 8%. You were gonna say something?No, no, that's I was just pointing out I mean, it's unfortunately their, their rate versus versus diagnosis is actually moving in the wrong direction over the last 48 hours.Yes, it is. And so Italy is and the the really scary part is, is I sent a graph to all our team members that we were outpacing Italy with our cases, at the at the day to day rate, and I get that we have a higher population and all these other things people can argue that but it'sBut I will say in the balance and it is hard. Just as you and I wanted to always present things in balance. The hard part is we have a limitation of testing capacity just as much as we do carrying capacity. And the hard part is is where are we going to get to the point of growth in number equals the sample, and by the sample the number of people in the United States, so it isn't nearly as alarming to me and probably not to you either Ken to watch the number of diagnoses skyrocket it probably on the on the on the front end? It's just that we're testing more people. It's just where is our ratio and our rate going to fall for morbidity and unfortunately, also mortality? Because I don't know. But testing is going to be imperative for to grow.We're going to talk about that because some new data has come out about the testing. As I said, day to day Remember, this is a world wide issue. So every single day scientists from China scientists from South Korea from France from Spain from Italy, Everybody's collaborating, and everybody's pulling their data. And we're learning more and more and more on a daily basis, but we're going to talk about the testing. What we do know is that the doctors in Italy described that most patients displayed this bilateral interstitial pneumonia. So unlike getting a pneumonia, where you have it, so typically what happens is if you have pneumonia, it's an infection, it will, in fact, a portion of the lobe of your lung or a whole lobe, but basically you have the rest of your lungs to compensate. Here, it's both sides, and it's in everything. And when that happens is bilateral interstitial pneumonia, meaning that it's on well, I'm not going to get into the pathology of it, but basically, the cells get infected, they die and then we lose the ability to produce surfactant. Surfactant is the lubrication that allows your cells, your alveoli to exchange oxygen, and this is a little bit more in your wheelhouse with your anaesthesia. Why don't you comment on that?Yeah, no, it's, it's it's exactly what I had some experience managing for several years early on. And oftentimes people that fall into this category long before Coronavirus lent itself to, to this epidemic here there was a situation or a diagnosis called ARDS or acute respiratory distress syndrome. And typically, the way to best describe it is it's almost like a localized immune autoimmune disease for your lungs. It happens because as the cells begin to break down and we all have these little bitty finger like cilia on our lungs, right, or to help with gas exchange and to hold a surfactant to break down the fluids, so that we can exchange it. The surfactant is breaking you down what happens is is that are immune cells which should.Eric, just really quick backup to right before you said Sir fact that you froze on me and I missed what you said, what were you saying but right right before the surfactant thing,Sorry about that it's surfactant level, it should be breaking down the fluid to allow for better gas exchange. And what's happening is our immune system in this particular state of ARDS is breaking down cells faster than they can be carried away. And when that happens, we have fluid buildup, it dilutes the surfactant and I don't want to talk over anyone's head. But essentially, our immune system begins to attack both bad cells and good cells, allowing for too much degradation or breakdown of our lungs and the tissue that we exchange the gas with. And then things begin to build up. And essentially you begin to drown from the inside we think of drowning or, you know, bringing in water and being being submerged not being able to breathe this being an awful existence. But imagine the fluid building up from in your lungs, you you're not consuming the fluid. It's here it's inside. So, pneumonia itself is kind of like that. But just as Ken said, if we catch it early enough, it's it's isolated. That happens in one lobe or one area of the lung with ARDS, which is what this could turn into, it happens all over the lungs all over the body. And what we do with an ARDS patient, is we tried to ventilate them by putting a tube in, we secure the airway, and what we tried to do is more or less force gas exchange by using what we call positive pressure ventilation, by blowing air through the tube, and so that we can force it into the lungs and then it can be exchanged. And then what ends up happening with those same patients is, is we normally would think of laying in bed on our backs and our head slightly raised. The lungs themselves can become damaged if the fluid is allowed to just basically sit there for a while. And the only way to keep the air movement in there is to rotate the bed. So oftentimes you'll see an ARDS patient who is intubated. And there'll be on their back side that they face down. And they have to continually be rotated to preserve the integrity of the lungs and actually to facilitate to facilitate good gas exchange. And I'll stop there with the management of the ARDS patient because you and I both know somebody else who does even the next level, which is the ECMO and we can get into that.Yeah, we well...so here's the problem with all that is that we know that from the account from the Italian doctors and our Chinese physicians, even young patients were developing this interstitial pneumonia and they were developing very dramatic, shocking pulmonary situations with this bilateral interstitial pneumonia. Now, the mortality of the critically ill patient of a SARS CoV2 pneumonia is extremely high. If you end up on a ventilator, it's 86%. Now, Eric, what you're talking about is the highest level of care. We're going to get into why almost nobody is getting these very isolated, very unique beds that can actually do this. And we know...I'm glad you said that. And well, what do I want to I want to just restate what you just said, what I just described is if you happen to be the most serious, that would be the optimal situation that you would be fortunate enough to end up in.That would be there's two, maybe two beds like that in a hospital in a large hospital. And when somebody is at that point, you call up for that bed, and you walk in and you watch this incredible science going on where it's the physiology and the pathophysiology at this battle. But we're we're going to get into this and that is the real issue is that getting the appropriate care to everybody. Remember that a lot of these Chinese doctors that first well the whistleblower that first discovered it other doctors. 40 year old doctors were dying from this. So this is and there were doctors in a hospital dying. So this is this is actually very that's what kind of perked my interest several weeks ago where I went. And I admittedly was the person that was like, why are we all getting all worked up about this because I know and I was trying to defuse the situation and be like, this looks like A Boy That Cried Wolf by the media. It's not a big deal, quit running out buying, you know, all this other stuff. And then I started reading about stuff going on in China and I'm like, holy cow, wait a minute, doctors and nurses are dying. So this is a big deal. So one of the things that I really started looking into, I'm like, okay, the only comparison we have to this is the SARS of 2003. Now, the reason why we didn't have to really deal with that, except pretty much stayed in the we're gonna call it the eastern side of the world. So a lot of these countries like South Korea, that have been so prepared for SARS CoV2 is because they...this is round two for them. They they saw it coming. They had testing kits, they did quarantine immediately. And they really put this thing on lockdown because they've already been through this, because the thing about SARS 2003 is that the mortality rate was really high. It was like 20% it was brutal. But we have now shown that this SARS CoV2 scientists believe is 1000 times more infective than the SARS 2003. And this is due to a lot of different reasons but due to the high mutation rate of the spike proteins, everybody's seen the example of the little spiky ball protein that the the media loves to play. This virus is showing a pattern of much higher infectiousness so a study released in released by some scientists in Germany on March 8, in 2020 found that this particular coronavirus could be found in the throat well before symptoms...well before symptoms. So what they're seeing is that there could be a huge increase in viral load in the back of the throat, way before any symptoms show up. So upon taking throat swabs from these patients, then they tried to show that all the results from day one to five tested positive for COVID19. But the high viral load from these early throat swabs indicated potential viral replication in the upper respiratory tract earlier. This means that you can have active viral replication in the throat during the five, first five days, and it will continue just like you explained for 14 days, which is why if people are going around, I feel fine. And I'm, you know, by the time we're asking if you have a fever, we're learning this is why it's there. Now, everybody's like what makes it so inffective. This gets a little bit hairy. And Eric, you and I have talked about this because we've tried to figure it out. I was just on PubMed looking at some different studies and one of the studies was discussing specifically the ACE-2 receptor. And people may be talking about this, but it appears that this particular virus binds to at least the H2 receptor, and possibly a Furan receptor. And the names of them are irrelevant. But the thing that's interesting is that both of these are kind of ubiquitous in the body, but they're heavily concentrated in the lung, and in the GI tract. So now we're seeing that you can get this both through your upper respiratory system and your gastrointestinal tract. One of the things a study just came out, Dr. Idim and I were talking about this this morning, because I just saw it this morning. This is how fast it changes. You get on the news and you're like, oh my gosh, it appears that 20% of people with COVID19 will actually gastrointestinal symptoms before they actually show the upper respiratory type symptoms. So this is what I mean. And it was no joke in the beginning when we were talking, protecting your gut is super important. So this is why a gastroenterologist is talking about COVID19, I at least have a role to protect your gut to make sure that that line of defense is taken care of. So what will happen is, is that this virus super tricky, will bind to this H2 receptor, and then it kind of knocks on the cell door and then the cell lets it in. And then the virus comes in, and basically hijacks a cell and lets the cell become the manufacturing plant for its own mRNA or its own RNA. And by having that happen, then it can develop more viruses. This is actually how the virus works. And so people argue, is it a living organism is not a living organism. I think most people have always felt that they're not living. But the fact that they can do these things they just need. It's the classic, or the most perfect example of a parasite. They hijack a cell, they get the cell to do what it wants. And that's how these viruses work.They're just kind of brainless. I mean, they you said it best, the mRNA the RNA is what is taken and replicated. And not to get too scientific. But I've always learned that viruses, although we don't say that they are completely unliving. They're not really living organisms. They're just, they're just RNA in a strand, they're not even DNA. They're just programmed to go in and disrupt a cell and basically hijack the replication capacity of a cell and make it to what it wants to become, which unfortunately, is usually to the demise of the cell itself.Yeah. And so in the most simplistic way, imagine the cell attaching to a lung to a lung cell and it does this then that lung cell gets taken over and it starts producing the virus. Well eventually that cell dies. And then that's where the cell dies. And it can no longer produce the surfactant can no longer do the other stuff that we're talking about. And then enough of that happens, and then you have this demise of the lung tissue and you cannot aerate. Well, something else happens. If it gets into other tissues, or if it does this, or if you have a healthy immune system, we now know that young people can actually have something called a cytokine storm. So what happens is your body overreacts to that, like your body goes, this is nuts. We've got this viral invasion, we have to get rid of it. And this may be one of the reasons why younger people are having this massive thing. So the only comparison to that is the Spanish Flu of 1918 of the reasons why it was so deadly, is because it actually created the cytokine storm in the most of the people that are infected. So what that means is that people with the healthiest immune systems died-that was 18 to 25 year olds, that's what made that particular flu so devastating.Yeah, I even saw a bar graph, it specifically addressed that almost every pandemic almost on the ends. If you're an infant or very, very old, it's almost where the highest mortality rate is. And for Spanish flu, it's kind of interesting. The ends are spiked. And then it goes down in the middle, it comes right back up into a spike, where we generally have our healthiest population and it was for precisely the same reason you described, it's, it elicits a cytokine storm, which is just people who happen to be in shape and the immune system doesn't know what to do. So it unleashes everything. It's almost like just self destruction.Okay, so that's our basic science class and I'm sure we're gonna get some calls from some neurologists to be like yeah, you missed you almost had it right. But whatever, but this is not we're not getting deep into the science. What we really my my other thing is why do we need to is this a time for some serious caution. And this is the part that I'm gonna get into that is a little bit scary. I'm not the first one to be talking about this. I have been looking at this for quite a while. But now I overheard Governor Cuomo talking about this people, the politicians are discussing all of this, and it's not the death rate. It's the need of the hospital system that is the scary part.Yeah, definitely and needs to the hospital system. And we can get into it. We can get into the specific numbers here just in North Texas. And just to use it as comparison, I think around 80% of our audience that's watching and or listening happens to be in this area. So we'll get into some hard numbers on bed availability, ICU availability, what it is that we currently use without the issues of COVID19 and then where our resources get reallocated if we happen to experience which unfortunately, it looks like we most likely will a surge of patients. Yeah so, so this is not this is not my opinion. Like all things we let's let's talk about some of the science that's out there. So I was listening to Dr. Grewal out of, I think how you say his name out of New York City, and he did some quick calculations. This is actually on the on the Peter Attia, a podcast when he was there. And he was talking about how if they calculated the ICU beds in New York City, and at a growth rate that we're at right now, which we'll get into it, which is called the R-Not, I'll explain that in a second. In two weeks, all of the New York City ICU beds would be taken. Taking it further, a study came out of USA Today yesterday or the day before. It was an analysis that showed if the nation continues to grow at this rate in the effective mount, what R-Not is in epidemiologic terms, it's written as R-0 so you may see it as that or it's pronounced as R-Not that means that one person can infect three people. Right now our R-Not is being described somewhere between 2.8 to like four, let's just say it's three to be due to be a nice round number even at three, if we don't stop this and so whenever people talk about flattening the curve, what they're talking about is the R-Not because we have to change that. So a USA Today analysis show that if the nation continues with this R-Not that we have, there could be almost six seriously ill patients for every existing hospital bed-think about that. Six people needing that hospital bed. Then they got into the whole analysis of based on the data from the American Hospital Association, the World Health Organization is being fairly conservative. It assumes that all 790,000 beds would already be empty, but they're not. Most hospitals are already almost at capacity, with the other stuff that we deal with like heart attacks and strokes and diverticulitis and gallbladder disease and everything else that happens to humans. Car wrecks, trauma. You know, and so then I saw a really scary one, where somebody was saying that if this continues, then we could have essentially 17, including the beds are already counted already there. We could have 17 people waiting for a bed in the whole United States. Now, Germany just published the paper yesterday, this is how fast it changes, like I mean, you just get on and you're like, whoa, they said that they haven't R-Not of two. If it continues like this, that'll be over a million people and they will lose all their ICU beds in 100 days. So if we sit there and say, well, the mortality rate of this and it will continue to decrease as more people get diagnosed, but then if we utilize the health care system, then the mortality rates going to grow exponentially, because the usual stuff can't get in then. So that's two thirds that...I mean, we could literally have 70 people competing for an open bed. And this assumes that we continue with this are not the are not, is based on our social lifestyle. So the reason why we're doing this podcast this way is because we're trying to do our part to break this R-Not of 1:3. If we can get to 1:1 or something less than that, then what we're trying to do is buy a little time by slowing the curve. We need to buy a little time to allow the medical infrastructure to catch up, be prepared or whatever it needs to do, because we are doing a lot of cool things. So you wanna say anything about that?But just in terms of application, so as a young person and even even back when you and I were probably questioning the the seriousness of the new novel Coronavirus or COVID19, however you wish to phrase it about two and a half weeks ago before it really started to get our attention. So in that, in that element we somewhat dismissed it as flu. But the progression of somebody who's sick with flu does not require near the resources. And on top of that, they're, they're contagious stage is usually commensurate about the time they begin to show symptoms so that they know they kind of should remove themselves from public exposure. This is the opposite. And when you find someone who is young and healthy, who most likely will not have terrible symptoms or even know that they are necessarily infected, the younger that they are, here's how it can affect you. Or it can it can affect you not infect you but affect you. So Ken just laid it out why we have all these hospital beds and the different resources that will be made available to somebody if the R-Not continues at a factor of three. Here's some hard numbers with DFW for instance. So in the DFW Metroplex, we have roughly 7.5 million people give or take. And that's that's the rough range, right? In this area, though, and all accounting and not including surgical centers, but high level hospital beds, we have roughly 15,000 beds. Well, that sounds okay. But right now before Coronavirus or COVID diagnoses have been affected or played a part in that. Already, two thirds of those beds are being used. Yeah. So we have less than 5000 beds total. Now that does not include Intensive Care Unit beds. So as it begins to break down the numbers, what we're looking at is roughly 80% of the people that will present and being diagnosed with COVID will be what they call mild to moderate. Even some of those moderate cases. I think it's around 40% of moderate cases will require some hospitalization. Okay, well, that plays into some of the numbers. How long is it hospitalization, roughly two to four days, then you move into the severe that makes up roughly 14% of everybody else who gets diagnosed with COVID. 14% of those people require supplemental oxygen and check in. Their hospital stay typically is lasting almost seven days. Now, that's a week. So 14% of the 80% of seven and a half million we're really starting to press, press out against what we have for a resources. That's not even the worst of it. If you are critical, meaning you get diagnosed with respiratory or organ failure requiring a ventilator, we typically only count an ICU room is one that has the capacity to handle a mechanical ventilator. That's less than 2,000 of those beds. And I can't remember what the current census count is on our ICU beds that are taken right now but I think it's 60%.Did you see how long that if you have COVID19 And you're put on a ventilator, what the average length is?It's almost two and 2.8 weeks, isn't that correct?Yeah, it's somewhere between three to six weeks.So the sad part here is, is it doesn't necessarily if it were in a vacuum and one person were diagnosed with severe COVID, and we could take them and do everything that we were talking about with a typical ARDS patient, we would have the best chance at a great outcome for that particular person. But that's not what we're up against. Now we have, let's just use some some fake numbers, but we have 1,000 beds, but with 5000 people that need them. And as people begin to pile up, even if someone gets there on a Tuesday, and then you get diagnosed on a Wednesday, you're going to have to wait three weeks for that bed. That's where the resources become incredibly stressed. And now how it comes back to those same people who said, well, it won't affect me, I'm too young. If you're in a car wreck, or you happen to be in happen to have just a completely different issue where your gallbladder is is giving you fits or you end up with diverticulitis, or you suddenly have a rectal bleed, or you suddenly get knocked while you're playing sports or whatever. And you require the ICU bed or that high level of acuity, unfortunately, COVID19 now is affecting you or loved one because it's not going to be available.I love how you say that because when you when when people are saying, well, it's not you know, it's not going to bother me, you know that President Trump keeps talking about how he really needs the millennials to be part of this because they have higher or according to him, they're not taking it serious enough. But you're exactly right. If you've got, I mean, I have all my patients that have Crohn's and colitis that are like what happens if I get a flare? What do I do? Well, it's gonna, and you're exactly right, putting in those terms. You're going to be squeezed out. I mean, it would be it would be one of the most horrific tragedies to have somebody die of oh something let's just say. Let's just take it out a little ways here. You said diverticulitis. diverticulitis is an inflammation of a diverticulum, which normally is easily treated. But if it doesn't get treated quickly, then it can form into an abscess then it can perforate, and then you have peritonitis, which leads to septicemia, which leads to death. So something that is completely preventable gets pushed out two weeks to try and get evaluated. And then well, that's a that's now we're...so I hope the whole point is not to do the oh my gosh, it does sound like a zombie apocalypse. But everybody needs to take this as serious as we're making it sound because the numbers when you listen to experts, these epidemiologists talk, they do not sugarcoat and they get very, very real, like the numbers you're talking about. Those are easily, you know, extrapolated and you can look at it, it's not like it's not Eric Rieger's opinion. This is just what's out there.No it is what's out there and those are the resources and in fact, when we were doing an inventory of what could be made shift ICU beds just to kind of give a glimpse on what what's being discussed in terms of people who typically do elective procedures, I do elective procedures predominantly, one of the surgery centers that cover happens to have four ORs. Each one of those ORs has an anesthesia machine. A lot of people don't know that's an anesthesia machine really is just a big ventilator, that has the ability to entrain volatile agents to help keep people asleep. Well, those four ventilators now, we now have makeshift ICU beds that's becoming a part of the count, which has never been a part of the community count of ICU beds before. So some of these surgery centers will be makeshift, more than likely COVID patient care units are where we will be able to monitor these people and give us more capacity, but it still won't be enough if we're not all on board to help stop the spread.So that is a lot of heavy science. That is a lot of doom and gloom. Let's get into some good news. So because I'm yeah, I'm hopeful we are going to get through this. This is a worldwide problem. And you've got some of the smartest scientists in the world collaborating together for the first time. So here's just a few of the things and this as golly I don't remember when I was this is a few days ago so who knows what's all going on right now. But I just mentioned that the US death curve went from 3% down to 1.5%. So that's awesome. China has flattened their curve as of yesterday, I believe that they did not report any new cases. So today is March 20th. Um in the Peter Attia podcast that I listen to, they were discussing that it could be that the corona test could only be 68% positive. And they were really scared about how devastating that would be if there were false negatives going out. A study just got published out of China. So a lot of this data that we're getting is the Chinese scientists doing retrospective studies and the Italians and the in the Iranians that have are now being able to look at the data that they have, and they're giving it to the world. There's, nobody's saying, oh, well, this is our information. And so but a study just published out of China was reporting a false positive rate of close to 40%. So the good news is, if that is true, what that means is that we're at least telling many people that you're positive quarantine yourself for two weeks, and so you're giving them a stamp of you have to be isolated. We don't like false positives or false negatives, but if you're going to have a poor sensitivity test, make sure that it is a It is a false positive in this particular case. So that people self quarantine. I believe that there are multiple vaccine trials going on. I think that US had its first human participant, and I believe Israel has human participants. Everybody's saying, when's that gonna happen? Well, as you know, as well, as I do that, you know, these vaccines probably are not going to be available for a long time. So that isn't something to hold our breath. But there are a few other things that makes it somewhat helpful. It appears that there are the President has been, well, not just the president, most government leader or most countries are really encouraging the private sector to get involved. And I think at least in the US, there are about 35 companies and academic institutions that are racing to create a vaccine, racing to see if there's some sort of treatment. So we know that there are studies being done on animals where they're looking at antibodies. So there's a lot of really exciting stuff. Now, some of the things that are going on, very hopeful is that some countries are using a drug. I believe it's by Gilead that was initially made for Ebola called Remdesivir. And they're combining that with a very old drug called hydroxychloroquine, which is called Plaquenil. Plaquenil yeah.Yeah. And they're seeing some success which is awesome. In fact, University of Minnesota is doing the first trial where they're going to do prophylactic hydroxychloroquine, called plaquenil versus placebo, and people that have had passive exposure. So that's another exciting thing. So if we can get people on this earlier, we may be able to take COVID survivors COVID19 survivors and spin down their answers. antibodies and give antibodies to other people so that you can do that they're doing that right now with macaque monkeys. I saw that that was going on. But all of this, the reason why that that's hopeful is because we need to buy time. And the only way to buy time is to you have to have this social isolation. I don't want to use the word social isolation. And we're going to get into that as the next part of this. Because what you need is the social or you need the physical quarantining. We know that social isolation, now I'm going to use that in a negative way, can also lead to, we've done we've talked about this on the gut check project that loneliness can be as deadly as smoking. And that's why I want to make sure that we end this on kind of an up note, and we know that social isolation can actually lead to inflammation. So we went through the science of it. We talked about the epidemiology. We talked about some of the doom and gloom we talked about some of the new things coming. I want to now discuss the fact that you and I are self quarantined. And as much as we can as healthcare workers, we cannot be completely self quarantined. I've been working in the hospital all week, tried to get in I've got I mean, I've, I, I've made sure that I've got alcohol wipes on me so that I can wipe down my phone I make sure that I've got I'm not hoarding, I'm not hoarding. I'll go to the hospital and say, give me a few alcohol wipes and give me a some some bleach things. I'm working really hard to not put the phone to my face and trying to do Bluetooth thing so I can talk that's another really important thing. We know that the everybody's talking about social isolation, but your phone may be a vector because we know that the virus can live from 72 to 96 hours on steel and plastic. It appears to not survive very well on porous material, like cardboard. And they can live in the air for up to three hours. So, you think you wash your hands and everything and then you put your phone down on a on a metal table. And then you pick it up, put your hand on it, put it right to your face, that's just like shaking someone's hand and slapping your face. So keep that in mind. Our phones are a vector of vector being something that can carry this,You know what's kind of interesting is that self quarantine allows you to let your guard down if you are in your same environment all the time with your same immediate family etc. You really can get to the point where you've been around the same people so really self quarantine with your home is going to allow you to not to overthink that kind of stuff so that whenever you leave, you become vigilant in the period of time that you run out to the to the grocery stores. Don't feel like that, just simply being you that you have to completely change and I've got to rinse my hands every three minutes before I go this direction. No, limit your exposure to the outside world. And that's when you would be on the most heightened alert. And it was interesting. I was listening to a radio show yesterday. And my wife and I were laughing because he was talking about how whenever he had to run to the grocery store, he found himself having to go to the bathroom. And I thought this was very keen. We've always been taught how to use the bathroom to wash your hands. But he said, as I walked into the bathroom, I realized before I touch the button on my jeans, wash my hands smarter and do my own pants because I'm going home with these pants. And so it's that kind of level of breakdown. And he even admitted had he not been practicing his own quarantine And then on the high end alert, he just would have been doing the same routine that he had been doing all along. So. That's a that's a really good point. We're gonna...I want to get into this but I want to play this because my friend, my childhood friend Brian Abood, it's his birthday today. So we're going to do a virtual birthday party and celebrate his birthday. She sent this to me and it's a I think it's going around social media. But basically, let's, let's hope it plays well.Because of Corona virus, you are going to be quarantined, but you have a choice, you A. quarantine with your wife and child, or B eaten.She didn't allow me in so I thought it was kind of funny. So she was saying that that's pretty much.Pretty much all there is to it.And I'm sure he was implying that Brian said that but that makes sense. Wash your hands before you touch your your jeans. So alright, so we're gonna end on a happy note. So I was listening to some other podcasts and I was reading the Washington Post article. And the the main weapon to combat this disease is social distancing. But that doesn't mean that we have to have social isolation. This is where I want to engage with everybody that listens to this, so that we can come up with ideas to try and make it so that you're not socially isolated. Because, you know, we...on social media, we see all these negative things all the time. But the reality is the majority of people, most of us are compassionate people. There's something called a carnival of compassion when there is a tragic event. You see it people after a hurricane people come out for volunteers, they want to help their neighbor, they want to help people they don't know. Carnival compassion, generosity feeds, with, you know, feeding kids and things like that. Most of us really feel that and so, the paradox when there's a tragedy is that we ultimately want to help and we have this impulse to be near somebody and hug them and say, you know, I want to help you, but that is exactly what we cannot do. So this, the other thing is, is that when we are in this social isolation there are people that may have some long term stigma from this social isolation like psychological fallout, so to speak. So there, like I said, there's studies showing that you can have increased inflammation, we know increased inflammation, you can have increased brain inflammation, which can lead to anxiety and depression and things like that. So I think here on the Gut Check Project, we want to end with trying to figure out a way that we don't have to make quarantine lonely, if you know what I mean.I do, I do know that I've got I've got a couple ideas that I haven't even told you about already.Well, I want to hear him here. I'll just finish up on kind of the science that I was looking at. People are people that are most physically susceptible to COVID19 or to SARS CoV2 are the same people that are most susceptible to loneliness. And so it's that double edged sword. So I purposfully you know, I called my mom today she's 78. And I was like, are you quarantine are you doing that? And she'd said, it's all these other things. So, you know, this is the thing that we all have in common now we all have this in common with everybody around the world. Don't get into this idea of panic scrolling through social media and overwhelming yourself, we need to intentionally interact. So I told you that today, I'm going to have a virtual birthday party. So that's how I'm going to intentionally interact. So I'm going to make sure that we that me and my friends stay connected. It's his birthday. Let's do this. I've got a green screen that will I don't want to take down my brick wall. That thing's I just had that thing put up a few months ago. But I'm gonna do a green screen, maybe put a little club back there, you know, and we can pretend like we're doing bottle service in Vegas or something. But anyways, that's kind of that's kind of what I want to do. And I want to see if our community can help us figure out how we can intentionally interact. What was your idea?Two things. One, you and I are communicating through zoom. So zoom.us, they're not paying us a penny. But if you ever just want to connect with a neighbor or get a bunch of different people on, it's free. If you want to have a conversation, I think up to what, 10 minutes or 15 minutes.40 minutes on the free account.Yeah, so 40 minutes, you can just invite whoever you want. Limited limited number of invites is the only thing about that. So I think you just have a few here we've got our business account. So we can this is what I'm going to do when I host my birthday party with Brian here shortly that we're going to, you know, invite however many people you want. SoThe other thing is is and I just discovered it today. So I'm going to place a couple of orders through Amazon to get a couple of small things that I'm missing but I'm a musician and a want to link up with some other guys. It'd be fun to jam with and we can't go to each other's home but there's a service that also isn't paying us a penny. It's called jamkazam.com. If you're a musician, you can actually link up and it allows you to real time jam and play music with people as long as you all have a good hard wired connection so I can't wait to get the stuff that I need to plug into the computer and and do that. So find ways to make community happen and in fact did you happen to see in Italy there were some people that a week and a half ago they're in their village, they were standing out on the balconies keeping their more than six foot distance banging tambourines and seeing I mean, singingYeah, it brought a lot of hope, brought a lot of hope. Absolutely. Yeah. So we want to do so anybody that's that's listening to this, please hit us up. And certainly, any ideas if you're like, you know what we're going to host a, I want to host a virtual coffee shop thing or whatever, but book club, we can do whatever. You know, I went on a quick side note, I read, let's pr...Steven McWilliams gave me a book to read when Lucas and I were in Panama. We were Panama the country and I read a memoir book with not medical, not business, because that's the first time I've read something non medical or non business in a long time. And it was called Let's Pretend This Never Happened. And I was laughing out loud. And then him and I were talking, we were doing a business call on zoom. And he had read the book, and then suddenly him and I were joking about it. And I'm like, oh, book club, virtual book club. There's a great way to go with it.No, that's awesome. Earlier, I was listening to Panama, by Van Halen. And that's kind of all there is to that story.Well, you can do that on your jamkazam, you can rock out some Panama there. So it would be interesting to bring the casual. So a lot of times and you and I do this with the show, you know, we kind of stress the show a little bit. We want to make sure that everything is tight and fine tuned, but in human interaction. It's never like that the casualness of the interpersonal play. We could start doing this. As we get better at it. We can start doing this virtually just kind of sitting there and you know if I have dinner with somebody where you don't have to be talking the whole time and it just be like, you know like you would with your, with your significant other or whoever you're not always just sitting there telling the coolest story ever. You're just taking a moment taking a bite. Look, I'm going broccolis good. Yeah. What did you do here? Oh, I added.Now that's awesome. Well, this is the first installment of COVID19 file for Gut Check Project. There's going to be plenty more to come we'll, we'll keep updating we didn't want to get out too early from the gate feeling like that we we wanted to have enough information to navigate the waters. There's been a lot out there before. I feel like that Ken and myself don't comfortable passing anything along. So let us know many of y'all have been keeping in touch. Just got three emails today from people who enjoy the fact that they could order What they could order obviously keeping your social distancing, but order or not does not matter. Let's keep the conversation Well, if you have questions that you want to know specifically or if you have a story, let us know. If it affects you directly, let us know. How are you handling it? How are you managing? So rounding out like. Well, yeah, the only thing that I want to add that I didn't want to get into today because clearly there was a lot to cover. This is the first foundation, but like something else everybody wants to ask me, what supplements are you taking? And I'm oh, as always, let's do a little disclaimer. I am a physician but I am not your physician. And so any advice we give here is strictly just an opinion and you're not to take my advice as medical advice speak with your physician about this and whatever it is that the the the typical jargon that has to be said of this is a show this is for entertainment, but it's also for information. So whenever reach...I think very clearly your your research, my research, these are not really our opinions, these are based off of us digging through a lot of research, at least during this period on these kind of things. You and I do have very strong opinions about a lot of other things. But we're not gonna do that here. So what I would like to do is a show based on the science of what supplements have been shown to affect different viruses and things like that is it a one to one translation? Nobody knows it's too early, but there's some different things that I think we could be doing.Definitely. Now, that'll be a great show in and of itself. And we'll back up everything that we say, with external science. It won't just be coming from, from Brown or myself for sure.Yeah. So hey, Eric, I appreciate you taking the time to do a different format. We're on the zoom. I do. I do miss your empty chair right here. But fortunately, I have a large cutout of you that I did that I printed a big picture of your head sits right there.That's okay. Because you're in the periphery. You can't see anything around me but my son's right here and he's trying to be really funny. Over hereYou think you're funny.I do think I'm funny.A boxing nun.That's what happens that's what happens away from the camera.Well, you could go ahead and let him know that I don't find that funny at all because I grew up Catholic and I've had some nuns punch me.That's gonna do it for the first installment of COVID files. It won't be long till we get the next one out we'll keep touch through email. If you are not a member already of the KBMD community just head up to gutcheckproject.com like and share you can sign up to have emailed information out to you. As more stuff becomes available through the weekend and into next week. We will definitely keep you abreast of all this information. One other thing also is that we're doing I'm really ramping up my telemedicine practice. So if if you happen to live in the state of Texas right now, I think they're opening the borders but we we are doing a lot of telemedicine and so just to recap because kind of scary. The virus is real. We need to do our part, there's a lot of really good things on the horizon, we just need to buy some time on this. And the only way to do that is to do what we're doing, which is stay your distance away. It is a highly infective virus. But we're going to get through this, we're going to get through it as a country. And when we come out the other side, we're going to learn so much more on the science of everything. There's never been such a collaboration of all scientists worldwide. Just saying here, what do you got? This is what I got. I think we're going to come out so much better as a human race as we get through this.Yeah I certainly hope so. I really do. So installment two, there is no schedule we're having Paul push this out as soon as he can get his hands on it. So we'll just keep 'em coming.But the biggest thing is, please stay in touch with us. If you've got questions. We've got we've got access to a lot of great scientists, a lot of good literature and I want to hear, I want to see you know what I'd like to see, I'd like to see people sending us pictures or small videos of them doing social interaction during quarantine.Yeah, send us your ideas.Even if even if you just spend all day playing with the boxing nun.I didn't get I did not get Mac's permission to do that but right, well, that's gonna I think that's gonna do it for this particular chapter. We'll be back in the next one we'll go through the science of keeping yourself safe with supplementation, etc. And then we'll just do another update to see where we're at.Let's do it. Stay safe, everybody.

The expansion of lungs for oxygen uptake is facilitated by lung surfactant. The groundbreaking discovery of this substance was made by Dr. John Clements. In this Discovery Talk, Clements details his scientific journey, touching on his early research, the resistance he encountered in the field, and the discovery of lung surfactant, which has saved millions of neonatal lives.

The expansion of lungs for oxygen uptake is facilitated by lung surfactant. The groundbreaking discovery of this substance was made by Dr. John Clements. In this Discovery Talk, Clements details his scientific journey, touching on his early research, the resistance he encountered in the field, and the discovery of lung surfactant, which has saved millions of neonatal lives.

What’s the safety and tolerability of the new enriched synthetic surfactant CHF5633? Associate Editor of ADC FN Jonathan Davis is joined by David Sweet (Royal Maternity Hospital, Belfast) to discuss a first-in-human clinical study of two human surfactant proteins in preterm babies with respiratory distress syndrome. Read the Archives of Disease in Childhood: Fetal & Neonatal's open access paper "A first-in-human clinical study of a new SP-B and SP-C enriched synthetic surfactant (CHF5633) in preterm babies with respiratory distress syndrome": http://fn.bmj.com/content/102/6/F497.

In this episode Dr. Smith speaks with Dr. Rick Chandra. They will discuss the article: Safety and tolerability of surfactant nasal irrigation. Read the article in International Forum of Allergy and Rhinology Listen and subscribe for free on Apple Podcasts, Google Play Music and Subscribe on Android

Grease is the word. Get rid of it with a dishwasher. Reduce surface tension and be happy.

Grease is the word. Get rid of it with a dishwasher. Reduce surface tension and be happy.

"Surfactant Replacement In Neonates" By Brian Walsh For OPENPediatrics by OPENPediatrics

Jasmina Aganovic is a cosmetics and consumer goods entrepreneur who received her degree in chemical and biological engineering from MIT, and she’s back on the podcast to talk about the progress AOBiome have made with their clinical trials. In this interview, we focus mostly on the potential treatment of acne and hypertension, but trials are also underway for allergies, eczema, wound healing, migraines and temperature regulation. Mother Dirt is the company focussed on commercialising the research of AOBiome, and I’ve been using their AO+ Mist spray product for over two years for the successful prevention of nappy (diaper) rash, saddle sores, and acne caused by bike helmets. I’ve also been using the spray in the place of a deodorant, and so far my wife hasn’t divorced me. Jasmina wanted to make it clear that although my N=1 experiences are exciting, nothing has been FDA approved. Head over to Mother Dirt and take advantage of the generous 25% discount on offer. Use the code NBT25. Sign up for our Highlights email and every week we’ll send you a short (but sweet) email containing the following: One piece of simple, actionable advice to improve your health and performance, including the reference(s) to back it up. One item we read or saw in the health and fitness world recently that we would like to give a different perspective on, and why. One awesome thing that we think you’ll enjoy! Here’s the outline of this interview with Jasmina Aganovic: [00:03:43] Environmental changes are leading to the loss of the ammonia oxidising (AO) bacteria. [00:05:14] Nitrogen cycle. [00:07:18] David Whitlock is the Inventor and co-founder of AOBiome. [00:07:34] Why horses roll in the dirt in March? [00:08:36] The link between the skin and the soil. [00:09:36] Developing a bioreactor. [00:10:28] Nappy rash. [00:11:05] Bicycle helmets. [00:13:11] The scientific process to validate the claims. [00:13:55] Phase II trials for acne. [00:14:26] A potential replacement for antiperspirant deodorant. [00:14:50] Prevention of saddle sores. [00:15:36] The war on P. acne. [00:16:49] It's all about balance. [00:17:23] C. diff overgrowths. [00:18:49] Mechanism of action: acid, base balance. [00:19:44] Nitrite and Nitric oxide. [00:20:55] Not nitrous oxide! Which mucks up methylation by oxidising cobalamin. [00:21:52] Hypertension. [00:24:05] Highlights sign-up. [00:25:09] Can nitric oxide made by the bacteria on the skin become systemic? [00:26:47] Why FDA approval. [00:29:37] Adverse events. [00:30:47] Drug: B244 on clinicaltrials.gov. [00:31:16] Romaine Bardet came 2nd in the Tour de France. [00:32:28] Increasing O2 deliverability. [00:33:46] Personal care product compatibility. [00:34:11] Surfactant sodium octyl sulfate (SOS) and sodium dodecyl sulfate (SDS) surfactants. [00:35:13] Castille and neem soap. [00:36:11] Nurses and hand sanitisers. [00:37:59] http://www.nourishbalancethrive.com/dirt/ use discount code NBT25. [00:38:35] Mother Dirt is the consumer-facing site, to learn about the clinical research go to AOBiome.

20e Congrès de pneumologie de Langue Française Fil rouge Pathologies interstitielles

Dr. Sheila Gephart. Photo courtesy of Dr. Sheila Gephart. Episode 8 features Dr. Sheila Gephart, neonatal nurse scientist and assistant professor at the University of Arizona College of Nursing. During this episode, Dr. Gephart provides a comprehensive overview of GutCheckNEC, a first-of-its-kind, 10-item risk assessment that she developed for the early detection of NEC in premature infants. She discusses: * Her transition from bedside nurse in the neonatal intensive care unit to her development of GutCheckNEC—what she calls a “real-time, early warning score for NEC,”* The 10 risk factors that make up GutCheckNEC, their associated symptoms, and how risk is communicated,* The development of NEC Zero, an intervention that has evolved out of the Unit NEC rate component of GutCheckNEC,* The strength of evidence for the use of probiotics in the prevention of NEC, and* The importance of shared decision making in the NICU. Copyright © 2015 The Morgan Leary Vaughan Fund, Inc. This episode was produced in part by the TeacherCast Educational Broadcasting Network. [powerpress] STEPHANIE VAUGHAN, HOST: Welcome to Episode 8 of Speaking of NEC—a free, audio podcast series about Necrotizing Enterocolitis. Produced by The Morgan Leary Vaughan Fund, and funded by The Petit Family Foundation, Speaking of NEC is a series of one-on-one conversations with relevant NEC experts—neonatologists, clinicians and researchers—that highlights current prevention, diagnosis, and treatment strategies for NEC, and the search for a cure. For more information about this podcast series or The Morgan Leary Vaughan Fund, visit our website at morgansfund.org. Hello, my name is Stephanie Vaughan. Welcome to the show. I’m the Co-founder and President of The Morgan Leary Vaughan Fund. Today, my guest will be Dr. Sheila Gephart, neonatal nurse scientist and assistant professor at the University of Arizona College of Nursing, who developed a first-of-its-kind, 10-item risk assessment for the early detection of NEC in premature infants called GutCheckNEC. During our conversation, she will discuss in varying degrees: Her transition from bedside nurse in the neonatal intensive care unit to her development of GutCheckNEC—what she calls a “real-time, early warning score for NEC,” The 10 risk factors that make up the acronym GutCheck and their associated symptoms How risk is communicated, The significance of the Unit NEC rate component in GutCheckNEC, and how that led her to develop the NEC Zero Intervention, The strength of evidence for the use of probiotics in the prevention of NEC, and The importance of shared decision making in the NICU. With that in mind, let me introduce my guest today. Hi, welcome to the show. This is my guest, Dr. Sheila Gephart. She is a neonatal nurse scientist from the University of Arizona College of Nursing. Hi, Sheila, how are you? DR. SHEILA GEPHART, GUEST: Good, thank you, Stephanie! STEPHANIE: Thank you! So, we have had more than one person mention you on our show in previous episodes, so I’m thrilled to have you join me today and would love to let you talk a little bit about your background and how you got involved with Necrotizing Enterocolitis. DR. GEPHART: Well, I am very thankful to be asked to be on the broadcast today, and I will tell you that I started my interest in Necrotizing Enterocolitis risk understanding when I was a bedside nurse. I have been a nurse since 1997, and I worked in the neonatal intensive care unit as a bedside nurse taking care of babies, and many of them were really convalescing. They were doing well, but then we had a subset of babies, or a clump of babies, that all developed this horrible disease within about three weeks. And now I know the clustering of NEC is very common, or not common, but it does happen. STEPHANIE: Right. DR. GEPHART: But then I didn’t really understand a whole lot about the disease, but I was very concerned because I realized that we had been concerned about these babies, as nurses, for hours to days before the actual diagnosis of NEC was made. So what happened at that point was I had the role of getting into the data for our NICU. I collected the data and reported the data for a large registry called the Vermont Oxford Network. And so I was focused on looking at the baby’s case and looking at the research and looking at the data, and I realized that there was a constellation of risk factors that kind of coalesced for these kids, that all of these things seemed to snowball with these babies who developed NEC, and we really had no context for talking to physicians to communicate why we were concerned. We were using terms like something’s not right with this baby, and from there, it really launched me into the next five years of understanding more about NEC risk. STEPHANIE: Okay. And can you talk to me a little bit about the protocol – I think it’s a protocol -- that you’ve developed called GutCheckNEC and how you got from starting to look at the data to compiling and understanding this set of risk factors? DR. GEPHART: Sure, I’m happy to talk about GutCheckNEC. So, being a bedside nurse, sometimes I would work in the middle of the night, and I needed a strategy for putting things together so I could remember them. And when I thought about NEC, I thought about well, we just need to check the gut. So GutCheck was kind of how it organized these risk factors, and I wrote GutCheck in a line straight down, and I remember one day I was at a delivery, and it was about three in the morning and it was taking a while for the baby to be born. And I was trying to understand all of the research that I had been reading about NEC risk and so what I did was I write GutCheck straight down on a napkin and horizontally for each letter I wrote the risk factor that was associated with that letter, and so that helped me organize what I was reading in the literature. But really it started out as just wanting to develop a risk assessment so nurses could really know what the risk factors were, physicians could know what the risk factors were, but then also put the symptoms in the context of what was going on with the baby. So that’s where I started, but then I went into a Ph.D. program, and in science you have to be very systematic. And so my literature review was the systematic beginning. But then what I did was I asked neonatal NEC experts how relevant they thought the different risk factors were to actually developing NEC. So I asked them to rate the relevance, and we went through three rounds of surveys to determine if we had the right list of risk factors, so that was very useful. We got rid of some, we kept most of them and added a few. And then, the next step was I got a very large dataset from a group of neonatal practices here in the US called The Pediatrics Medical Group, and I built, this is research speak, but I will tell you that I threw all of the risk factors into a statistical model to see what fell out as the most important, and the way statistical models work is that they keep the most important things that account for most of the explanation for what you’re looking at, and they get rid of everything that’s not quite so important. STEPHANIE: Okay. DR. GEPHART: So we went from like 33 risk factors down to essentially ten risk factors for GutCheckNEC. And then we tested it to see if it actually discriminated or told the difference between the kids that got NEC and the ones who didn’t, and it showed pretty good discrimination, or separation of groups, for the kids who had the most severe NEC compared to those who didn’t get NEC at all. STEPHANIE: Okay. DR. GEPHART: So that was the work we did, and now we’re taking this ten item tool and we’re trying to combine it with clinical science so that we can really have a real time early warning score for NEC. STEPHANIE: Great. Can you sort of go down the list just for parents that might be listening or family members if they’re seeing any of these risk factors? DR. GEPHART: Sure, I’d be happy to do that. The items that we kept in GutCheckNEC, like I said, there are two versions. There’s the one before the statistical modeling and then there is the one after, and the one that’s before is actually more comprehensive. And if you think about just writing GutCheck down linearly, you think for G, you’ve got growth restricted, so they’re born really small for gestational age, you’ve got gestational age. Those are the main ones that I always thought of with the G. And then with U, the one item that the experts recommended adding was the unit NEC rate, because infants who are in units with high NEC rates are more likely to get NEC, and so I didn’t understand that finding. I’ll talk about that in a minute, about the unit NEC rate. T, if you talk about T, transfusion. There is an association that we see in lots of studies with transfusion and NEC. We don’t see any evidence of causation, but the studies aren’t designed to show us that, so there is a temporal relationship or a time based relationship between transfusion and the most severe NEC. That said, there is a lot of babies who get transfusions and don’t get NEC. So that’s what makes it hard. STEPHANIE: Right. DR. GEPHART: What else goes with T? I’m going to stick to the final version, okay, as we think through the acronym. And then for C, signs of infection, so chorioamnionitis is when mom has a really bad uterine infection prior to the baby being born. Some preterm moms have this because—we don’t know exactly why they have this, but chorioamnionitis, particularly if it’s invasive, if it’s really severe, that is a risk factor. Also cardiac kids are going to be more at risk, so if you think of the C, kids who have had heart disease or heart malformations, particularly those that are low oxygenation kinds of defects… STEPHANIE: Right. DR. GEPHART: ..and there are some more for C but I don’t recall exactly what those were right now, but I’m just going to stick—oh, culture proven infection. That also goes with C. So if babies have had sepsis, particularly more than once, which sometimes these really early babies do get multiple bouts of infection, that is a risk factor. So that stayed in my model long term. Enteral feeding is definitely a risk factor that all babies are hopefully exposed to because we want them to be fed. That I understand a lot more now about the details of enteral feeding, and that particularly if the enteral feeding is formula, that is very important. We know formula is a high risk factor. There is a whole slew of argument about cow’s milk based fortifiers that go with that as well, so there is some argument about how extensive of a risk factor that is, but formula and enteral feedings certainly. And then the H, I skipped the H. That would be hypotension treated with medicines to bring that blood pressure up. So hypotension is low blood pressure. A lot of preemies have episodes of low blood pressure, but we know that the most sick are going to be hemodynamically unstable which means that their ability to regulate their blood pressure and keep their heart rate within a good level is not quite as solid as a kid who doesn’t have those light fluctuations, so that was a risk factor that did stay. Also race. Race stayed. The experts did not think that race was a risk factor, and they were pretty, if you remember the stages that we used to develop GutCheckNEC, we asked experts about how relevant they thought these risk factors were and they really didn’t think race was relevant. But it was so strong in the model, I couldn’t get rid of it. So if a baby is either black or Hispanic, that puts them at higher risk. Now, the reason for that we think, we don’t really know exactly why that stayed in the model, however, we know that black babies are very much less likely to get human milk… STEPHANIE: Okay. DR. GEPHART: ..than white babies, and that is something we can fix. So that’s really important. As I went through these risk factors that are in GutCheckNEC, I started to separate in my mind what’s modifiable, which is what of these can we do something about and what is non-modifiable? And what I saw really was quite a few of these things were modifiable that stayed in GutCheckNEC. You can do a query online for GutCheckNEC and it will pop up the actual, you’ll be able to find GutCheckNEC in the literature. It’s published so anybody can find it. But the thing that was so interesting to me, and I’m probably going to go off a little bit here, is that the NICU NEC rate consumed a huge amount of the variants in this tool which means that if we were to say that these items explained an infant’s risk for NEC. The NICU NEC rate explains three times as much as gestational age, three times as much as transfusion. So it was so important, and what we saw in the sample, we had 284 NICUs in the sample that we used to build GutCheckNEC and to verify it, of those 284 NICUs, we saw huge variance in NEC rates. So that was pretty concerning, and it wasn’t something that I went into the research expecting or looking for really even because I had read 70 papers about NEC risk, and invariably, they would start with Necrotizing Enterocolitis is a disease that we have very few answers for. We don’t really know why it occurs, but we know that premature babies are at risk and that is the most consistent risk factor across studies. So prematurity. STEPHANIE: Right. DR. GEPHART: Everybody blamed it on prematurity and low birth rate, and very few said anything about—oh, and we know, actually we have about six large studies from 20 years ago that show that unit NEC rate is consistently an issue. So that is something that I didn’t expect to find, but I found, and then I was able to go back into the literature and find other studies that verified it. STEPHANIE: Excellent. That’s a phenomenal amount of information, and I think that’s really great for parents going into the NICU to have in their minds. DR. GEPHART: And I think, I apologize to the parents for throwing out all these terms, but I know that you’re smart, and you can handle it. Okay, I’m just going to give you credit, because if you’re NICU parents, you’re super savvy, and you know how to find information. STEPHANIE: Right. DR. GEPHART: But one of the things we were really concerned about with NEC is how we communicate risk to parents and how parents are really the eyes and ears of understanding what’s going on with that baby just like the nurses are. STEPHANIE: Right. DR. GEPHART: And they are really better situated, honestly, to be able to identify the trends in their own kid, because that’s all they’re worried about. STEPHANIE: Right. DR. GEPHART: They’re not worried about the delivery down the hallway or all these other things, they are the expert. So one thing I’ve been working on trying to frame this message for parents as partners on the team looking for signs of any kind of complication and I think if they know to speak up. To keep track and to speak up if things don’t seem right, and I’ve heard many physicians actually say that it’s the parents indication of concern that will make them stop, and think slower, about what’s going on with that baby. So either the nurses concern or the parents concern, because often the physician, as excellent as they are, may not be right at that bedside… STEPHANIE: Right. DR. GEPHART: ..at that moment when something is changing. STEPHANIE: Right. Right And we did have an experience between Morgan’s surgeries where there was a concern in the NICU, and I can’t even remember who had mentioned it at rounds of attempting to give him—I don’t know if it was formula or breast milk—but giving him something that the surgeon had previously not agreed to—and it was a whole day of me trying to get in contact with the surgeon and making sure that nobody did anything until the surgeon had said yes or no. And he called me back from outside of the surgical room and said if anything like this happens, call me, I will call you back. So we definitely found that the doctors are very receptive, and especially when you raise an alarm, and to give people concrete things to look at for their babies I think is a wonderful tool. So thank you for sharing this. DR. GEPHART: Absolutely! And I can say that within the next few weeks, probably by the time this podcast is released, our website will be active, and on that website are parent materials that we’ve created that are designed to help them. Anyone can download these parent materials, they can use them in their NICU, and they are basically pamphlets to talk about things to watch for, what you can do to prevent NEC, and what the signs are, and a little bit about what happens afterwards. Because you know the first-hand experience of how different your life is… STEPHANIE: Right. DR. GEPHART: ..coordinating care for a child who’s had NEC. STEPHANIE: Right. DR. GEPHART: So the long term impacts of dealing with life after NEC, I know Laura Martin was on the broadcast… STEPHANIE: Yes. DR. GEPHART: ..recently… STEPHANIE: Yes. DR. GEPHART: ..and her story has been such an important part of my development as a nurse scientist. Think beyond just the NICU stay, to think about how NEC impacts these kids forever. STEPHANIE: Right, right, and we’ve been very lucky that Morgan has had (knock on wood) minimal residual effects. We see a little bit, but I mean, I looked at Laura’s story and they are doing a phenomenal job with him. He is a miracle. DR. GEPHART: Yeah, Joseph is pretty awesome. I haven’t had the chance to meet him in person yet, but Laura and I collaborated to write up his story, and that paper is going to be coming out in the next couple weeks in Journal of Perinatal and Neonatal Nursing, and it is a testament to his resilience. STEPHANIE: Right. Hers too and her husband’s and the family’s. DR. GEPHART: It’s pretty awesome. STEPHANIE: Definitely send me those links and we can certainly share that with everyone—direct links in the show episode notes. So I’ll ask you, now that GutCheckNEC is I’ll say standardized if that’s a correct term, is there anything that you’re looking towards in your research moving forward from GutCheckNEC? DR. GEPHART: Well, that’s a great question, and GutCheckNEC is a risk assessment, it’s a tool. It fits on one page. We’ve just gone through a process where we’ve added to it a structured communication protocol, so if a NICU wanted to use GutCheckNEC, we would have them complete a request form, and on one side is GutCheckNEC, and on the other side is the structured communication form, which also clues the nurses, the parents for which signs and symptoms to look for and how to communicate it. So that’s easy. So that’s where GutCheckNEC is going. We’re also trying to combine it with clinical science right now, so that’s the analysis I’m working on right now, and I’ve worked with a great collaborator, Sherry Fleiner from the Inner Health to do that work. But beyond that, one of the things with research, you do a project and then you have these findings and then there is something that just kind of nabs at you and it doesn’t fit like you expected it to. And for us, that was the unit NEC rate component of GutCheckNEC that carried so much weight in the score, and it demonstrated across the 284 NICUs how variable NEC rates can be. So what we did next is we asked the question, well, why are they different? Why are the NEC rates different? And what if we did something to try to standardize prevention care? So there are a couple of main things that prevent NEC. One is human milk—very, very important starting with colostrum for oral care. The other thing is standardized feeding protocols, stewarding antibiotics, and I can kind of get into more detail there, and then there is a lot of controversy about transfusions. STEPHANIE: Right. DR. GEPHART: So those components, those four things plus a strategy for early recognition, we’ve put those components into an intervention we call NEC Zero, and the name of it is designed to convey that we’re hoping to get NEC to zero rate. Now, this is an audacious goal. But why set goals if they’re not crazy? This is an audacious goal, but it was not my idea. There was an editor for Journal of Perinatology, his name is Jonathan Swanson, and he wrote a paper the year that I finished my dissertation, so I think that was in 2012, it might have been 2013, and the title of that paper was “Can We Get NEC to Zero”? And if you ask scientists this and clinicians this, you will hear a lot of concern that this is an audacious goal. Like of course, we’re not going to get NEC to zero, we don’t even know what causes it. However, we do know some things that consistently reduce the risk for NEC. So human milk is, like I said, those five components, but human milk is so primary. So now we’re trying to put those interventions together, make them implementable so that people in the NICU in Delaware could implement them with the same consistency and clarity that people in Texas could do. STEPHANIE: Right. DR. GEPHART: So that bundle of practices is NEC Zero. So the process for NEC Zero right now where we’re at in the project is that we’ve gone through kind of an expert process of refining the recommendations. So we’ve gone through that, we need to publish that, but we’ve got them. We had a really great expert group of almost 20 people, and four of those people were parents. Laura Martin was on that group. So we’ve got the recommendations, now we’re trying to break those recommendations into implementable steps, and we’re creating tool kit products to go with the NEC Zero intervention. So pieces of that are— GutCheckNEC is definitely a primary component of that. Frankly, GutCheckNEC has the least strong evidence of any of the components in the tool kit. But it’s something that is actionable, it’s something that we can use to monitor, and we know that monitoring and evaluation is a key component of implementation success for anything. So that’s where we’re at right now is we’re working on NEC Zero. STEPHANIE: Great, that sounds excellent. Do you have a projection of when people might see this? You said you’re looking to get it published, or the first stages of it getting published? DR. GEPHART: Right. We’re working on refining the recommendations really in terms of publishing any sort of a recommendation list or a guideline. They carry much more weight if you have the authority of a professional organization behind them. So our strategy right now is to try to link up with some professional organizations and see if we can get some endorsements for them. So if any of your listeners are prominent members of the American Academy of Pediatrics, the National Association of Neonatal Nursing, The Academy for Breastfeeding Medicine—any of those groups would be excellent proponents. So we have the recommendations, we have some parent products that will be available, like I said, within a few weeks once our website gets done, and the other pieces of it being available, I will say that we’re testing it right now. So with the testing, there are two things we’re doing. We have the recommendations, we’re asking experts to kind of assign relative importance to the different parts of the intervention, and that score, we’re creating a ten point score for the NEC Zero adherence score, and that’s almost done. And then we’re going to look at relationships between adoption of NEC Zero practices and NEC rates, because we really don’t have a great evidence body for understanding why NEC rates differ so much NICU to NICU. STEPHANIE: Right. DR. GEPHART: So this is kind of an effort to add to that body of evidence of understanding why are they different. We don’t know what we’ll find, that’s the beauty of research is you start with a hypothesis, you get your data, you test your hypothesis, and you see how it turns out. STEPHANIE: Excellent. This is great work, Sheila. I mean, it sounds like it’s really sort of simple, but I’m sure it’s not. DR. GEPHART: That’s right! It does kind of sound simple, doesn’t it? STEPHANIE: Or that it maybe should be simple. Hopefully it will be simple, but it sounds like parents in the NICU could really take this information and be able to be confident in their monitoring of their children and really confident in voicing any concerns that they see. DR. GEPHART: Right. STEPHANIE: So I think it’s great. DR. GEPHART: The challenge is that really statistically you’re not going to have a lot of kids get NEC. Even in a high rate NICU, you’re going to have a lot of babies who don’t get it, and a few babies who do. But the outcomes can be so devastating for those few babies. So the simple part is really important, and the other question is do the interventions of NEC Zero affect other outcomes? And really, the answer is yes, because interventions are things like human milk standardized feeding protocols, antibiotic stewardship—those things are good for any baby— STEPHANIE: Right. DR. GEPHART: Any baby! So the good thing is that any NICU clinician can implement those things with relative confidence. Now, the big wildcard here that people don’t agree to consistently is holding feeding during transfusion. So that piece is a little bit controversial, actually it’s a lot controversial right now, but that component—the health system I’m working with has already adopted a practice to do that, so that is part of our bundle, and we’re going to keep it that way, but as we get into the literature about transfusions and NEC, it is somewhat controversial, and the evidence is not really conclusive. STEPHANIE: Right. We actually had an episode with a Dr. Hussain from Connecticut Children’s Medical Center, and in his conversation about transfusion associated NEC, he had mentioned GutCheckNEC. So it does seem to sort of all circle around. DR. GEPHART: It does, and the thing with GutCheckNEC is that transfusions is a risk factor. So in our structured communications protocol, which is coupled with GutCheckNEC, understanding the context of if a baby has been transfused in the last 48 hours, that’s a trigger. STEPHANIE: Right. DR. GEPHART: So those two pieces put together do heighten our awareness of what a baby could be at risk for. STEPHANIE: This was a really great conversation, Sheila. I really appreciate you sharing all of this. A lot of this, even though I have done a lot of research myself is pretty new in this context to me. So I think it really sort of simplifies some really complicated information. So I appreciate you sharing this with us. DR. GEPHART: Well, it’s been my pleasure and honor to try to simplify things. I have to do that for my own brain. I will say that this is an audacious goal. STEPHANIE: Right. DR. GEPHART: People look at me cross eyed when I say NEC Zero. They think what are you talking about? Is that possible? But I will tell you that there are a handful of NICUs across the country who are getting to zero with their NEC rates, and they are models. STEPHANIE: Right. DR. GEPHART: The things they consistently do are they prioritize human milk feeding, it is critical, they use standardized feeding protocols, they start feedings early with trophic feedings, which is just small feedings, and they generally have a fairly specific approach to handling transfusions and feeding. So those things are very important. But the human milk is essential. STEPHANIE: Right. Right. So before we wrap up, is there anything else with regard to NEC or your research moving forward that you would like to share? DR. GEPHART: I appreciate that offer. I would like to just emphasize how we do have evidence. We have pretty good evidence about things that prevent NEC. Now, does that mean that we’re going to prevent every single case of NEC? I don’t know that yet. STEPHANIE: Right DR. GEPHART: But we have pretty good evidence, and one of the things that’s pretty controversial in our country right now is the use of probiotics. I don’t know if any of your experts have gotten into that realm yet, but- STEPHANIE: We’ve touched on it and they’ve sort of said the same thing you did that it is sort of a controversial topic because if I’m saying this correctly, the FDA regulations and the procedures around that, but I know in other countries that they have seen reduced rates of NEC with probiotics. DR. GEPHART: Right, right, and that is one thing that I would say is certainly controversial. There is one of the NICUs that I’m aware of that uses probiotics. They’ve been at zero for like six years. One of the issues we have, I’ve spent a lot of time lately understanding the strength of evidence for all of these components that prevent NEC, we don’t have randomized control trial evidence for most of them. But we have 24 randomized control trials that show a decreased risk for NEC with probiotics—thousands of babies—thousands, and even some people will say the preparations are different in these different studies, there is a recent study that actually pulled the results from just a certain type of probiotic and they still showed benefit. So the issue here we have in the United States is that probiotics are marketed as a food product. And so as a food product, their regulation is different with the FDA than as a medicine. STEPHANIE: Right. DR. GEPHART: However, I think parents should know this, frankly. STEPHANIE: Right. DR. GEPHART: I think this is one of those opportunities for shared decision making in the NICU where a physician, a nurse practitioner could bring up this issue with parents to say hey, look, we have this opportunity to give your baby probiotics and this is what is available, this is the evidence, this is the risk. See, this is shared decision making. STEPHANIE: Right. DR. GEPHART: You go and you have a test, your physician or nurse practitioner would say this is how you have to decide what’s important, but I think NICU parents are very, very smart people, and I think we’re at the point in the United States where it is time to open up the conversation about probiotics to make it a joint decision versus an “oh, we’re just not going to do it”. STEPHANIE: Right. DR. GEPHART: Because we have such strong evidence, it’s just that most of those studies were not done in the US. STEPHANIE: Right. DR. GEPHART: However, there are many things that have been developed in other countries that we can adopt. The other issue is a standard formulation, a safe, standard formulation. There was a case of sepsis a few years ago that was very concerning—that’s severe widespread infection in a premature baby. That is the risk. So that’s what the clinician would say to the parent. But it’s very, very small risk if you look at all of the benefits. STEPHANIE: Right. DR. GEPHART: So I’m not going to pretend we should be using probiotics, but I do think that parents need to start asking for them. They need to start asking why are we not using them… STEPHANIE: Right. DR. GEPHART: ..because we have such strong evidence. So we have actually stronger evidence for probiotics than we do for antenatal steroids or Surfactant. Those are common, important, consistently delivered interventions for NICU babies. But you have risks, and that’s the issue. STEPHANIE: Right. DR. GEPHART: So we’re at a place for decision making. STEPHANIE: Right. And actually ironically, or maybe not ironically, I know that my boys did get probiotics, and that was five years ago that they were born. DR. GEPHART: That is ironic. STEPHANIE: We had an anomaly with Morgan. Nobody can sort of figure out why he got NEC when he did, but we did do all of the sort of standard care practices, probably even advanced practices for five years ago, and we had one that got it and one that didn’t. So…but knowing now what I have learned is they were doing the very best practices at the hospital where my sons were born. So I think we were at the right place at the right time and had the best outcomes that we could hope for. DR. GEPHART: That’s awesome. That’s awesome. Did you feel like with Morgan that they were able to recognize it pretty fast and act? STEPHANIE: I really think they did. I think that is probably the key that saved his life because he developed NEC at four days old and had really only had two trophic feeds, and it was colostrum. DR. GEPHART: Okay. STEPHANIE: Actually after the conversation that I had with Dr. Hussein, I went back and looked and he did not have a blood transfusion within that timeframe, so he sort of, it’s my understanding he’s just sort of an anomaly, but that’s why we’re looking to the researchers to piece together all of these things. That’s sort of what drives me is he doesn’t easily fit into something that could have, should have, would have, maybe been different and that seems to be the riddle that’s NEC. DR. GEPHART: Sure. There’s an analogy for this it’s called, a wicked problem, I don’t know if you’ve heard of that term, but you were at my talk when we were in Connecticut,… STEPHANIE: Right. DR. GEPHART: ..and I talked about the wicked problem and how it’s like a forest fire, it’s not easily solved. There’s a lot of pieces to it,… STEPHANIE: Right. DR. GEPHART: …and I think NEC is really the neonatal wicked problem. STEPHANIE: Right. DR. GEPHART: So I’m so glad that Morgan got care so quickly and got such excellent care. And that’s the thing is that clinicians, physicians, dieticians, lactation consultants, nurses, nurse practitioners, they want to do the absolute best for your baby. STEPHANIE: Right. DR. GEPHART: Nobody has ill will. This is a team effort, but they’re human, and that’s the thing with wicked problems… STEPHANIE: Right. DR. GEPHART: ..is that you have humans operating in these complex systems, and trying to deal with things and what we know with solving wicked problems, like forest fires, it’s a combination of boots on the ground, and standard protocol. STEPHANIE: Right. DR. GEPHART: So it’s the strength and protection of both approaches that really is effective, maybe not taking away completely the wicked problem, but at least confronting it. STEPHANIE: Right. DR. GEPHART: So I’m so glad that Morgan got such great care. STEPHANIE: Thank you. We are too. We are too. And like I said, I think it goes to show that I’ve heard multifactorial used and all kinds of big words with regard to NEC, and just knowing that there are researchers out there like yourself who are trying to distill this information and simplify it for parents and practitioners as well that this is one of the ways that I think we will get to zero NEC. That’s our goal as well. So I really appreciate you talking to me today, and would love to talk to you again, and any of these links when the website is up, would love to share. So thank you! DR. GEPHART: Absolutely. It would be my honor to share those. It’s been fun to be with you. STEPHANIE: Thank you. You too. Direct links to more information about the GutCheckNEC can be found in this episode’s show notes. In closing, I’d like to share a few thoughts about today’s conversation with Dr. Gephart. Simply put, information is power. I believe that a risk assessment like GutCheckNEC can empower parents in the NICU by distilling complex medical information, and presenting it in a simplified, and actionable way. Morgan was diagnosed with NEC at four days old. My husband and I were still in shock, and hadn’t even begun to come to terms with our twin sons’ unexpected and traumatic birth, when Morgan was transferred to another hospital and underwent emergency surgery. In the days and weeks that followed, I diligently called two NICUs every morning after rounds for updates on our two babies. I took copious notes to share with my husband on weight gains, Oxygen levels, and whatever else each nurse made mention of during the phone calls. And during our daily visits, we spoke with each baby’s nurse personally about all of the day’s happenings. Since then, I’ve learned a lot more about prematurity and NEC. And if we were in the same situation today, I would have a lot more questions to ask about all areas of our babies care. In retrospect, I realize we didn’t know what questions to ask. We took our lead from the nurses, and we looked to them to tell us what we needed to know. GutCheckNEC presents parents the opportunity to learn what questions to ask about NEC. Objectively. And, proactively. And, it can help open up the dialogue between parents and caregivers in advance of potential crisis. Show your support for our smallest and most fragile babies, those who have the greatest risk for developing NEC. Show your support for continued research in NEC. And join our effort to raise awareness about, and funds for research in NEC by making a donation to Morgan’s Fund at morgansfund.org/donate. If you’ve had a personal experience with NEC and would like to share your story, or have a question or topic that you’d like to hear addressed on our show, e-mail us at feedback@morgansfund.org. We’d love to hear from you! Additional Information You can make a donation directly to Dr. Gephart’s research in NEC at the University of Arizona College of Nursing by visiting https://www2.uafoundation.org/NetCommunity/SSLPage.aspx?pid=341 You can become a donor to the College of Nursing by visiting http://www.nursing.arizona.edu/giving/leave-your-legacy Copyright © 2015 The Morgan Leary Vaughan Fund, Inc. The opinions expressed in Speaking of NEC: Necrotizing Enterocolitis (the Podcast series) and by The Morgan Leary Vaughan Fund are published for educational and informational purposes only, and are not intended as a diagnosis, treatment or as a substitute for professional medical advice, diagnosis and treatment. Please consult a local physician or other health care professional for your specific health care and/or medical needs or concerns. The Podcast series does not endorse or recommend any commercial products, medical treatments, pharmaceuticals, brand names, processes, or services, or the use of any trade, firm, or corporation name is for the information and education of the viewing public, and the mention of any of the above on the Site does not constitute an endorsement, recommendation, or favoring by The Morgan Leary Vaughan Fund.

Interview with Angela Kribs, MD, author of Nonintubated Surfactant Application vs Conventional Therapy in Extremely Preterm Infants: A Randomized Clinical Trial

Sharyl Attkisson of The Daily Signal published a shocking piece titled, "Full Disclosure: Did Government's Experiment on Preemies Hide Risks?" (June 03, 2014) The article outlines how the federal government's National Institute of Health (part of the Department of Health & Human Services) conducted a "study" called SUPPORT, which stands for "Surfactant, Positive Airway Pressure, and Pulse Oximetry Randomized Trial." The government-funded experiment ordered that 1,316 extremely premature infants be provided with different amounts of supplementary oxygen.  Half of the group received a 'higher' dose while the others received a 'lower' dose.   Many parents have come forward claiming that they were never told anything about oxygen levels being manipulated and only that the SUPPORT study was to offer 'support' to their delicate babies.  The study was published in the New England Journal of Medicine with the following conclusion: "A lower target range of oxygenation (85 to 89%), as compared with a higher range (91 to 95%), did not significantly decrease the composite outcome of severe retinopathy or death, but it resulted in an increase in mortality and a substantial decrease in severe retinopathy among survivors. The increase in mortality is a major concern, since a lower target range of oxygen saturation is increasingly being advocated to prevent retinopathy of prematurity. (ClinicalTrials.gov number, NCT00233324.)" So there you have it, the study confirmed that because certain babies were provided with less oxygen...they died. Is this the government that you want in charge of your healthcare system?

Thu, 13 Feb 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/16630/ https://edoc.ub.uni-muenchen.de/16630/1/Thurm_Tobias.pdf Thurm, Tobias d

Background: Interstitial lung disease occurring in children is a condition characterized by high frequency of cases due to genetic aberrations of pulmonary surfactant homeostasis, that are also believed to be responsible of a fraction of familial pulmonary fibrosis. To our knowledge, ABCA3 gene was not previously reported as causative agent of fibrosis affecting both children and adults in the same kindred. Methods: We investigated a large kindred in which two members, a girl whose interstitial lung disease was first recognized at age of 13, and an adult, showed a diffuse pulmonary fibrosis with marked differences in terms of morphology and imaging. An additional, asymptomatic family member was detected by genetic analysis. Surfactant abnormalities were investigated at biochemical, and genetic level, as well as by cell transfection experiments. Results: Bronchoalveolar lavage fluid analysis of the patients revealed absence of surfactant protein C, whereas the gene sequence was normal. By contrast, sequence of the ABCA3 gene showed a novel homozygous G > A transition at nucleotide 2891, localized within exon 21, resulting in a glycine to aspartic acid change at codon 964. Interestingly, the lung specimens from the girl displayed a morphologic usual interstitial pneumonitis-like pattern, whereas the specimens from one of the two adult patients showed rather a non specific interstitial pneumonitis-like pattern. Conclusions: We have detected a large kindred with a novel ABCA3 mutation likely causing interstitial lung fibrosis affecting either young and adult family members. We suggest that ABCA3 gene should be considered in genetic testing in the occurrence of familial pulmonary fibrosis.

An interview with Andy Corr of Elevance on the sidelines of ICIS European Surfactant Conference in Brussels, earlier this year.

The July 2013 Episode of SurfAction reviews key events of the second quarter of 2013 in the surfactants market.

SurfAction reviews the proceedings of the 3rd ICIS World Surfactant Conference held in NYC May 16th and 17th, 2013

The state of oligomerization of surfactant associated protein-A (SP-A) monomers differs between individuals. This likely affects SP-A's functional properties and could thereby influence clinical status in patients with lung diseases. In this study we focus on SP-A structure in cystic fibrosis (CF) compared to both healthy subjects and disease controls. SP-A composition and function were assessed in both bronchoalveolar lavage (BAL) fluid and serum of 46 CF patients with mild disease, 25 patients with chronic bronchitis and 22 healthy subjects by gel chromatography and a functional agglutination assay. Relation of SP-A agglutination ability to disease severity of the subjects was explored. SP-A was present in seven major oligomeric forms with the majority of SP-A being structurally organized as complex oligomeric forms. More complex oligomeric forms were associated with better SP-A function with regard to its agglutination ability. These forms were more frequently observed in BAL than in serum, but there were no differences between disease groups. In CF patients, more complex forms of SP-A were associated with better lung function. Organizational structure of SP-A affects its functional activity and is linked to disease severity in CF.

Background: Surfactant protein C (SP-C) is important for the function of pulmonary surfactant. Heterozygous mutations in SFTPC, the gene encoding SP-C, cause sporadic and familial interstitial lung disease (ILD) in children and adults. Mutations mapping to the BRICHOS domain located within the SP-C proprotein result in perinuclear aggregation of the proprotein. In this study, we investigated the effects of the mutation A116D in the BRICHOS domain of SP-C on cellular homeostasis. We also evaluated the ability of drugs currently used in ILD therapy to counteract these effects. Methods: SP-C-A116D was expressed in MLE-12 alveolar epithelial cells. We assessed in vitro the consequences for cellular homeostasis, immune response and effects of azathioprine, hydroxychloroquine, methylprednisolone and cyclophosphamide. Results: Stable expression of SP-C-A116D in MLE-12 alveolar epithelial cells resulted in increased intracellular accumulation of proSP-C processing intermediates. SP-C-A116D expression further led to reduced cell viability and increased levels of the chaperones Hsp90, Hsp70, calreticulin and calnexin. Lipid analysis revealed decreased intracellular levels of phosphatidylcholine (PC) and increased lyso-PC levels. Treatment with methylprednisolone or hydroxychloroquine partially restored these lipid alterations. Furthermore, SP-C-A116D cells secreted soluble factors into the medium that modulated surface expression of CCR2 or CXCR1 receptors on CD4(+) lymphocytes and neutrophils, suggesting a direct paracrine effect of SP-C-A116D on neighboring cells in the alveolar space. Conclusions: We show that the A116D mutation leads to impaired processing of proSP-C in alveolar epithelial cells, alters cell viability and lipid composition, and also activates cells of the immune system. In addition, we show that some of the effects of the mutation on cellular homeostasis can be antagonized by application of pharmaceuticals commonly applied in ILD therapy. Our findings shed new light on the pathomechanisms underlying SP-C deficiency associated ILD and provide insight into the mechanisms by which drugs currently used in ILD therapy act.

Surfactant associated protein-A (SP-A) is the most abundant pulmonary surfactant protein and belongs to the family of innate host defence proteins termed collectins. The aim of the study was to elucidate the role of SP-A in human lung disease. This study was designed to analyze the relation between genetics, structure and function of SP-A in a CF, chronic bronchitis and asthma and healthy control population ex vivo. Beginning with the analysis of SP-A oligomeric forms, there were no correlations between serum and BAL SP-A distribution forms. The forms showed only a significantly different distribution comparing serum samples from bronchitis patients and controls. In serum and BAL of CF patients the forms containing the first peak were correlated with a better lung function (Fev1 (% pred.)age20). Also higher relative SP-A amount in the first peak is associated with a milder lung disease and a better course of lung disease. Additionally, SP-A self-agglutination is dependent on the amount of particular SP-A oligomers present in a sample, i.e. the relative strength of SP-A molecular forms in a sample. All SP-A structures self-agglutinate in serum better than in BAL in samples of the patients groups while in control samples BAL and serum SP-A showed the same abilities. There was also a difference between the self-agglutination ability of BAL samples from CF, Bro and control derived SP-A, but none in serum. SP-A from control BAL agglutinated better than from bronchitis BAL and this better than from CF BAL. These results are also supported by the fact that a better agglutination ability of SP-A was significantly associated with lung function. Therefore the degree of the presence of active oligomeric forms within a BAL or serum sample seems to be important for a better lung function outcome. The SP-A oligomerization is associated with one SFTPA1 rs1136451 and one SFTPA2 SNP rs17881665 which are coupled, while the mutated allele seems to cause a lack of complex oligomers. The wildtype alleles of the SP-A2 SNPs rs1965708 and rs1975006 were associated with CF compared to the bronchitis and control group. There was a significant association between the mean ∆ Fev1 (%pred.) / year and V50L a SNP in the SFTPA1 gene (p = 0.0038) while the mutated allele was associated with a worse course of lung disease. The SP-A BAL level was significantly associated with the SP-A1 SNP rs1136451 (p = 0.002) and the SP-A2 SNP rs17881665r (p = 0.002). The SP-A serum level was significantly associated with SP-A1 N9T (p = 0.028). In addition in the CF study population there was a significant association between the SP-A level in BAL and the Fev1 (% pred.) estimated for age 20 (p = 0.009). The higher the SP-A levels were in BAL the bigger were the values of the Fev1 (% pred.) estimated for age 20. There was no correlation between the SP-A BAL or serum level and any other clinical characteristic such as BMI, age, gender, IgG or IgE in serum. In conclusion, these results indicate a very important role for SP-A in human lung immunity. Future areas for clinical research include disease specific SP-A expression pattern and their functional consequences, the differential roles of SP-A1 and SP-A2 in human lung diseases, and therapeutic approaches to correct altered SP-A levels.

Defects of the NKX2-1 gene, encoding thyroid transcription factor-1, cause brain-thyroid-lung syndrome (MIM 610978), characterised by benign hereditary chorea, congenital hypothyroidism and respiratory disease. The case of a term infant with mild primary congenital hypothyroidism and neonatal persistent respiratory failure with fatal outcome at 10 months of age despite continuous ventilatory support is described. Congenital defects of genes known to disturb surfactant protein and lipid homeostasis (SFTPB, SFTPC, ABCA3) were excluded. Hypothyroidism prompted sequencing of NKX2-1, which revealed a heterozygous 29 bp deletion (c.278_306del29) disrupting the affected allele. Analysis of bronchoalveolar lavage fluid demonstrated an abnormally low amount of surfactant protein C (SP-C) in relation to SP-B, and low levels of surfactant phospholipids, indicating disturbance of SP and lipid homeostasis as a consequence of NKX2-1 haploinsufficiency. NKX2-1 haploinsufficiency may lead to lethal respiratory failure of the newborn due to disruption of pulmonary surfactant homeostasis. NKX2-1 gene analysis should be considered when investigating irreversible respiratory insufficiency of the newborn.

Fri, 10 Jun 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/13287/ https://edoc.ub.uni-muenchen.de/13287/1/Schiefelbein_Lars.pdf Schiefelbein, Lars ddc:540, ddc:500, Fakultät für Chemie und Pharmazie

Professor Jim McQuillan, Department of Chemistry, Division of Science. Inaugural Professorial Lecture, given on July 22, 2010.

Professor Jim McQuillan, Department of Chemistry, Division of Science. Inaugural Professorial Lecture, given on July 22, 2010.

Professor Jim McQuillan, Department of Chemistry, Division of Science. Inaugural Professorial Lecture, given on July 22, 2010.

Professor Jim McQuillan, Department of Chemistry, Division of Science. Inaugural Professorial Lecture, given on July 22, 2010.

Background: Monomers of the collectin surfactant associated protein-A (SP-A) are arranged in trimers and higher oligomers. The state of oligomerization differs between individuals and likely affects SP-A's functional properties. SP-A can form aggregates together with other SP-A molecules. Here we report and assess a test system for the aggregate forming properties of SP-A in serum and broncho-alveolar lavage samples. Methods: Anti-SP-A antibodies fixed to latex beads bound SP-A at its N-terminal end and allowed the interaction with other SP-A molecules in a given sample by their C-terminal carbohydrate recognition domain (CRD) to agglutinate the beads to aggregates, which were quantified by light microscopy. Results: SP-A aggregation was dependent on its concentration, the presence of calcium, and was dose-dependently inhibited by mannose. Unaffected by the presence of SP-D no aggregation was observed in absence of SP-A. The more complex the oligomeric structure of SP-A present in a particular sample, the better was its capability to induce aggregation at a given total concentration of SP-A. SP-A in serum agglutinated independently of the pulmonary disease; in contrast SP-A in lung lavage fluid was clearly inferior in patients with chronic bronchitis and particularly with cystic fibrosis compared to controls. Conclusions: The functional status of SP-A with respect to its aggregating properties in serum and lavage samples can be easily assessed. SP-A in lung lavage fluid in patients with severe neutrophilic bronchitis was inferior.

Background: Deleted in Malignant Brain Tumors 1 (DMBT1) is a secreted scavenger receptor cysteine-rich protein that binds various bacteria and is thought to participate in innate pulmonary host defense. We hypothesized that pulmonary DMBT1 could contribute to respiratory distress syndrome in neonates by modulating surfactant function. Methods: DMBT1 expression was studied by immunohistochemistry and mRNA in situ hybridization in post-mortem lungs of preterm and full-term neonates with pulmonary hyaline membranes. The effect of human recombinant DMBT1 on the function of bovine and porcine surfactant was measured by a capillary surfactometer. DMBT1-levels in tracheal aspirates of ventilated preterm and term infants were determined by ELISA. Results: Pulmonary DMBT1 was localized in hyaline membranes during respiratory distress syndrome. In vitro addition of human recombinant DMBT1 to the surfactants increased surface tension in a dose-dependent manner. The DMBT1- mediated effect was reverted by the addition of calcium depending on the surfactant preparation. Conclusion: Our data showed pulmonary DMBT1 expression in hyaline membranes during respiratory distress syndrome and demonstrated that DMBT1 increases lung surface tension in vitro. This raises the possibility that DMBT1 could antagonize surfactant supplementation in respiratory distress syndrome and could represent a candidate target molecule for therapeutic intervention in neonatal lung disease.

Thu, 27 Apr 2006 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/5414/ https://edoc.ub.uni-muenchen.de/5414/1/Schikor_Daniela.pdf Schikor, Daniela ddc:610, ddc:600,

Thu, 23 Mar 2006 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/5174/ https://edoc.ub.uni-muenchen.de/5174/1/Schumacher_Silja.pdf Schumacher, Silja

Background: Inspiratory activity is a prerequisite for successful application of patient triggered ventilation such as proportional assist ventilation (PAV). It has recently been reported that surfactant instillation increases the activity of slowly adapting pulmonary stretch receptors (PSRs) followed by a shorter inspiratory time (Sindelar et al, J Appl Physiol, 2005 [Epub ahead of print]). Changes in lung mechanics, as observed in preterm infants with respiratory distress syndrome and after surfactant treatment, might therefore influence the inspiratory activity when applying PAV early after surfactant treatment. Objective: To investigate the regulation of breathing and ventilatory response in surfactant-depleted young cats during PAV and during continuous positive airway pressure ( CPAP) early after surfactant instillation in relation to phrenic nerve activity (PNA) and the activity of PSRs. Methods: Seven anesthetized, endotracheally intubated young cats were exposed to periods of CPAP and PAV with the same end-expiratory pressure (0.2 - 0.5 kPa) before and after lung lavage and after surfactant instillation. PAV was set to compensate for 75% of the lung elastic recoil. Results: Tidal volume and respiratory rate were higher with lower PaCO2 and higher PaO2 during PAV than during CPAP both before and after surfactant instillation ( p < 0.05; both conditions). As an indicator of breathing effort, esophageal deflection pressure and PNA were lower during PAV than during CPAP in both conditions ( p < 0.02). Peak PSR activity was higher and occurred earlier during PAV than during CPAP ( p < 0.01), and correlated linearly with PNA duration in all conditions studied ( p < 0.001). The inspiratory time decreased as tidal volume increased when CPAP was changed to PAV, with the highest correlation observed after surfactant instillation ( r = - 0.769). No apneic periods could be observed. Conclusion: PSR activity and the control of breathing are maintained during PAV in surfactant-depleted cats early after surfactant instillation, with a higher ventilatory response and a lower breathing effort than during CPAP.

Background: Abnormalities of the intracellular metabolism of the hydrophobic surfactant proteins SP-B and SP-C and their precursors may be causally linked to chronic childhood diffuse lung diseases. The profile of these proteins in the alveolar space is unknown in such subjects. Methods: We analyzed bronchoalveolar lavage fluid by Western blotting for SP-B, SP- C and their proforms in children with pulmonary alveolar proteinosis ( PAP, n = 15), children with no SP- B ( n = 6), children with chronic respiratory distress of unknown cause ( cRD, n = 7), in comparison to children without lung disease ( n = 15) or chronic obstructive bronchitis ( n = 19). Results: Pro-SP-B of 25 - 26 kD was commonly abundant in all groups of subjects, suggesting that their presence is not of diagnostic value for processing defects. In contrast, pro-SP-B peptides cleaved off during intracellular processing of SP- B and smaller than 19 - 21 kD, were exclusively found in PAP and cRD. In 4 of 6 children with no SP- B, mutations of SFTPB or SPTPC genes were found. Pro-SP-C forms were identified at very low frequency. Their presence was clearly, but not exclusively associated with mutations of the SFTPB and SPTPC genes, impeding their usage as candidates for diagnostic screening. Conclusion: Immuno-analysis of the hydrophobic surfactant proteins and their precursor forms in bronchoalveolar lavage is minimally invasive and can give valuable clues for the involvement of processing abnormalities in pediatric pulmonary disorders.

Background: In a cross-sectional analysis of cystic fibrosis (CF) patients with mild lung disease, reduced surfactant activity was correlated to increased neutrophilic airway inflammation, but not to lung function. So far, longitudinal measurements of surfactant function in CF patients are lacking and it remains unclear how these alterations relate to the progression of airway inflammation as well as decline in pulmonary function over time. Methods: As part of the BEAT trial, a longitudinal study to assess the course of airway inflammation in CF, we studied lung function, surfactant function and endobronchial inflammation using bronchoalveolar lavage fluid from 20 CF patients with normal pulmonary function ( median FEV1 94% of predicted) at three times over a three year period. Results: There was a progressive loss of surfactant function, assessed as minimal surface tension. The decline in surfactant function was negatively correlated to an increase in neutrophilic inflammation and a decrease in lung function, assessed by FEV1, MEF75/25%VC, and MEF25%VC. The concentrations of the surfactant specific proteins A, C and D did not change, whereas SP-B increased during this time period. Conclusion: Our findings suggest a link between loss of surfactant function driven by progressive airway inflammation and loss of small airway function in CF patients with limited lung disease.

Background: Inhibition of phrenic nerve activity (PNA) can be achieved when alveolar ventilation is adequate and when stretching of lung tissue stimulates mechanoreceptors to inhibit inspiratory activity. During mechanical ventilation under different lung conditions, inhibition of PNA can provide a physiological setting at which ventilatory parameters can be compared and related to arterial blood gases and pH. Objective: To study lung mechanics and gas exchange at inhibition of PNA during controlled gas ventilation (GV) and during partial liquid ventilation (PLV) before and after lung lavage. Methods: Nine anaesthetised, mechanically ventilated young cats ( age 3.8 +/- 0.5 months, weight 2.3 +/- 0.1 kg) ( mean +/- SD) were studied with stepwise increases in peak inspiratory pressure ( PIP) until total inhibition of PNA was attained before lavage ( with GV) and after lavage ( GV and PLV). Tidal volume (V-t), PIP, oesophageal pressure and arterial blood gases were measured at inhibition of PNA. One way repeated measures analysis of variance and Student Newman Keuls-tests were used for statistical analysis. Results: During GV, inhibition of PNA occurred at lower PIP, transpulmonary pressure (Ptp) and Vt before than after lung lavage. After lavage, inhibition of inspiratory activity was achieved at the same PIP, Ptp and Vt during GV and PLV, but occurred at a higher PaCO2 during PLV. After lavage compliance at inhibition was almost the same during GV and PLV and resistance was lower during GV than during PLV. Conclusion: Inhibition of inspiratory activity occurs at a higher PaCO2 during PLV than during GV in cats with surfactant-depleted lungs. This could indicate that PLV induces better recruitment of mechanoreceptors than GV.

Bronchoalveolar lavage (BAL) liquid of 138 children with different inflammatory lung diseases was examined to determine the magnitude of the oxidative stress in the lungs. The content of protein carbonyls was measured by means of a sensitive dot-blot assay as a parameter of protein oxidation. The oxidative stress was highest in the group of the patients with cystic fibrosis (CF). In these patients direct correlations existed between the magnitude of protein oxidation and the content of neutrophil granulocytes in the BAL as well as a reverse proportionality between lung function and protein oxidation. The pattern of distribution and the sensitivity of different proteins to oxidation were determined in samples with different degree of oxidation by means of the 2-D-electrophoresis. Plasma proteins present in BAL fluid, e.g. albumin and transferrin, were especially sensitive to oxidation. Oxidation of the SP-D primary chain was achieved only by relatively strong oxidation in vitro. In contrast to SP-D, SP-A was very sensitive to the oxidative stress. The influence of antioxidative therapy with inhaled glutathione was examined in CF patients by measurement of protein carbonyls, protein thiols and lipid hydroperoxyds in BAL fluid before and after the therapeutic intervention. GSH inhaled for two weeks had no effect on the parameters assessed. Even if the primary chain of SP-D was very resistant towards oxidative influences, oxidation caused nevertheless clear changes of the macromolecular organization of SP-D. It led to the depolimerisation of the SP-D structure which is usually supported by disulfid bridges. SP-D damaged in this way had lost essential functional properties and was no more capable to agglutinate bacteria. Local oxidative stress plays an important role in different lung diseases in childhood and is especially pronounced in the presence of chronic, neutrophilic inflammation. Successful specific therapeutic interventions are nowadays not easily realized.

Die hydrophilen pulmonalen Surfactantproteine A und D (SP-A, SP-D) gehören zur Gruppe der C-Typ Lektine und spielen bei der angeborenen, primären Immunantwort der Lunge eine Rolle. In mehreren Studien wurde gezeigt, dass SP-A und SP-D mit einer Reihe von Mikroorganismen und pulmonalen Entzündungszellen interagieren. In der vorliegenden Arbeit wurde die Funktion von SP-A und SP-D bei der Immunabwehr Mukoviszidose-assoziierter Keime wie Pseudomonas aeruginosa, Xanthomonas maltophilia, Burgholderia cepacia und Staphylococcus aureus untersucht. Hierzu wurden zunächst insgesamt 57 klinische Isolate der Bakterien, darunter 35 P. aeruginosa Stämme, durch Sero- beziehungsweise Pyozintypisierung, Alginatbildung oder Kollagenase-aktivität charakterisiert. Wir untersuchten, inwiefern Agglutination und Proliferation der Bakterien sowie die Phagozytose speziell von P. aeruginosa durch SP-A und SP-D beeinflusst werden können. Die hier gezeigten Ergebnisse demonstrieren, dass SP-A und SP-D an P. aeruginosa binden. Die Interaktion mit den Bakterien ist kalziumabhängig, wird durch einfache Kohlehydrate gehemmt und somit über die Lektin/Kohlehydrat-Bindungsstellen der Surfactantproteine vermittelt. Trotz Bindung an plastikadhärente P. aeruginosa induziert SP-A keine Agglutination der Bakterien. SP-D hingegen agglutiniert P. aeruginosa. Darüber hinaus hemmt SP-D unabhängig von der Agglutination konzentrationsabhängig das Wachstum von P. aeruginosa. SP-D stimuliert die Phagozytose von Bakterien, indem es als Opsonin die Aufnahme der Keime durch eine humane Makrophagen Zelllinie verstärkt. SP-A beeinflusste die Phagozytose der untersuchten Keime dagegen nicht. Zusammenfassend konnte gezeigt werden, dass SP-A und SP-D unterschiedliche immunmodulatorische Funktionen haben. SP-D stimuliert durch verstärkte Phagozytose unabhängig vom LPS Serotyp die Abwehr Mukoviszidose-assoziierter Keime, speziell nicht mukoider P. aeruginosa. Beide Surfactantproteine binden spezifisch P. aeruginosa, aber nur SP-D induziert deren Agglutination und führt durch die Bildung von größeren Aggregaten möglicherweise zur Steigerung der pulmonalen Clearance der Bakterien.

In den vergangenen zehn Jahren wurden große Fortschritte hinsichtlich einer möglichen Gentherapie angeborener Lungenerkrankungen wie Mukoviszidose oder a1-Antitrypsinmangel erzielt. Dabei spielt die Gentherapie mittels nichtviraler Genvektoren zunehmend eine größere Rolle. Doch trotz ermutigender Ergebnisse aus einer Reihe von klinischen Studien ist die Effizienz des nichtviralen Gentransfers über eine topische Applikation in die Atemwege bis heute zu gering. Ziel dieser Arbeit war es, zu untersuchen, welchen Wechselwirkungen nichtvirale Genvektorkomplexe im Milieu der Atemwege unterliegen. Dabei konnten Veränderungen der inneren Struktur nichtviraler Genvektorkomplexe unter Einfluss von Surfactant bzw. bronchoalveolärer Lavageflüssigkeit mit Hilfe von Fluoreszenz-Quenching-Assays und Fluoreszenz-Resonanz-Energietransfer (FRET) nachgewiesen werden. Auch die Oberflächenladung der kationischen Genvektorkomplexe wurde beeinflusst, wobei in Anwesenheit hoher Konzentrationen von Surfactant eine Ladungsumkehr hin zu negativen Werten gemessen wurde. In Bezug auf die äußere Struktur der kationischen Genvektorkomplexe konnte gezeigt werden, dass in Anwesenheit von Surfactant bei Lipoplexen eine starke Zunahme der Größe beobachtet wurde, während die Größe von Polyplexen sogar leicht abnahm. Ebenfalls konnte gezeigt werden, dass die An- oder Abwesenheit von Salz in physiologischen Konzentrationen bei der Herstellung der Genvektorkomplexe einen Einfluss hat auf die Interaktion von Surfactant mit den Genvektorkomplexen. Um zu ermitteln, inwieweit die Veränderung biophysikalischer Parameter die Funktion der Genvektorkomplexe beeinflusst, wurden das Adhäsionsverhalten der Genvektorkomplexe an der Zelloberfläche und ihre Transfektionseffizienz untersucht. Auch hier waren die Folgen der Interaktion mit Surfactant sehr unterschiedlich ausgeprägt, je nach dem, ob kationische Liposomen oder kationische Polymere als Genvektorsystem verwendet wurden. Um die Effizienz des nichtviralen Gentransfers in die Lunge zu erhöhen, gibt es eine Reihe unterschiedlicher Ansätze. Im Rahmen der vorliegenden Arbeit wurde die Anwendbarkeit der Magnetofektion auf die Transfektion von Atemwegsepithelien untersucht. Die Magnetofektion beruht auf dem Prinzip der Anreicherung von Genvektorkomplexen am Zielgewebe mit Hilfe magnetischer Anziehungskräfte. Es konnte eine deutlich bessere Dosis-Wirkungs-Beziehung der über kationische Polymere vermittelten Magnetofektion verglichen mit dem konventionellen über kationische Polymere vermittelten Gentransfer nachgewiesen werden. Hierfür waren sowohl eine stärkere als auch eine schnellere Anreicherung der Genvektorkomplexe an der Zelloberfläche verantwortlich. Die Effizienz der Magnetofektion war bei gegebener Inkubationszeit der Transfektionseffizienz konventioneller nichtviraler Gentransfersysteme deutlich überlegen. In elektronenmikroskopischen Untersuchungen konnte eine Aufnahme der Genvektorkomplexe in Zellen intakter Atemwegsepithelien mit Hilfe der Magnetofektion nachgewiesen werden.

Tue, 29 Oct 2002 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/646/ https://edoc.ub.uni-muenchen.de/646/1/Wiesener_Annegret.pdf Wiesener, Annegret ddc:610, ddc:600, Medizinische Fakultät

Pulmonary surfactant is a multimolecular complex located at the air-water interface within the alveolus to which a range of physical (surface-active properties) and immune functions has been assigned. This complex consists of a surface-active lipid layer (consisting mainly of phospholipids), and of an aqueous subphase. From discrete surfactant sub-fractions one can isolate strongly hydrophobic surf acta nt proteins B (SP-B) and C (SP-C) as well as collectins SP-A and SP-D, which were shown to have specific structural, metabolic, or immune properties. Inborn or acquired abnormalities of the surfactant, qualitative or quantitative in nature, account for a number of human diseases. Beside hyaline membrane disease of the preterm neonate, a cluster of hereditary or acquired lung diseases has been characterized by periodic acid-Schiff-positive material filling the alveoli. From this heterogeneous nosologic group, at least two discrete entities presently emerge. The first is the SP-B deficiency, in which an essentially proteinaceous material is stored within the alveoli, and which represents an autosomal recessive Mendelian entity linked to the SFTPB gene (MIM 1786640). The disease usually generally entails neonatal respiratory distress with rapid fatal outcome, although partial or transient deficiencies have also been observed. The second is alveolar proteinosis, characterized by the storage of a mixed protein and lipid material, which constitutes a relatively heterogeneous clinical and biological syndrome, especially with regard to age at onset (from the neonate through to adulthood) as well as the severity of associated signs. Murine models, with a targeted mutation of the gene encoding granulocyte macrophage colony-stimulating factor (GM-CSF) (Csfgm) or the beta subunit of its receptor (II3rb1) support the hypothesis of an abnormality of surfactant turnover in which the alveolar macrophage is a key player. Apart from SP-B deficiency, in which a near-consensus diagnostic chart can be designed, the ascertainment of other abnormalities of surfactant metabolism is not straightforward. The disentanglement of this disease cluster is however essential to propose specific therapeutic procedures: repeated broncho-alveolar ravages, GM-CSF replacement, bone marrow grafting or lung transplantation.

The function of pulmonary surfactant of a group of 14 preterm neonates (birth weight 907 +/- 60 g) who suffered from severe respiratory distress syndrome (RDS) and who had received exogenous bovine lipid extracted surfactant on the first day of life was compared to that in a second group of 8 neonates (birth weight 940 +/- 110 g) with mild RDS who had not received surfactant treatment. Mechanical respiratory support from day 2 on was the same in both groups. The minimal surface tension (gamma(min)) improved steadily, falling from about 30 mN/m initially to less than 20 mN/m before extubation, A consistent but loose correlation was found between gamma(min) and mechanical respiratory support necessary, as quantitated by the oxygenation index. Total protein was about 0.8 +/- 0.2 mg/mg of phospholipids and did not change during the first week of life. There were no correlations between total protein and gamma(min) or the oxygenation index. The data suggest that inhibition of surfactant function by proteins leaked into the airspaces does not play a major role during recovery from RDS, Instead, endogenous remodelling of surfactant might be of greater relevance.