Podcasts about chds

Send us a textThe journey of raising a child with a critical congenital heart defect (CCHD) involves navigating far more than just medical challenges. Behind every heart surgery and cardiology appointment lies a complex web of developmental considerations that can profoundly shape a child's future.Dr. Dawn Ilardi, a clinical neuropsychologist with over 16 years of experience in cardiac neurodevelopment, brings clarity to this often-overlooked aspect of heart care. Unlike typical developmental patterns, children with CCHDs may present with scattered strengths and weaknesses that don't fit neatly into standard diagnostic categories. While some may develop recognizable conditions like ADHD, autism, or dyslexia, others show unique profiles that require specialized understanding.The conversation explores the fascinating heart-brain connection, revealing how brain development begins simultaneously with heart formation during fetal development. Structural heart defects can affect blood flow patterns to the developing brain, while surgical interventions carry risks of small strokes or other brain injuries. For parents wondering why their child struggles with handwriting, speech delays, or learning difficulties despite excellent medical care, this discussion provides crucial insights.Particularly compelling is the discussion about balancing protection with developmental progress. How do you navigate the tension between keeping a medically fragile child safe while ensuring they develop age-appropriate skills and independence? Dr. Ilardi offers practical strategies for finding this balance, emphasizing the importance of creating a supportive "village" around both the child and parents.Whether you're a parent, medical professional, or educator working with heart warriors, this profound conversation will transform your understanding of the developmental journey these remarkable children face. Most importantly, you'll discover pathways to help them reach their full potential through multisensory learning approaches, compensatory strategies, and family-centered support.Helpful Links:Christy Pace's CHD Connects Hearts: https://chdconnectshearts.com/homeDawn Ilardi's other Heart to Heart with Anna Appearances:Unlocking Neurodevelopmental Breakthroughs: Impact of CHDs and Parental Influence https://www.buzzsprout.com/62761/episodes/15872291What is Normal Child Development in Children with Complex Congenital Heart Defects? https://tinyurl.com/DawnIlardi2014  Dr. Ilardi's website: https://www.pedneurocenter.com  Dr. Ilardi's email: DawnIlardi@pedneurocenter.comGastrointestinal Issues and Feeding Tubes in the CHD Community: https://www.buzzsprout.com/62761/episodes/1999819Sheri Turner is our newest Defender Patron and she also serves as a HUG Volunteer. Thank you so much for your generosity and all you do, Sheri!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Send us a textUnlock the future of heart care and understand how a revolutionary cooperative platform is reshaping the landscape of congenital heart disease treatment. Join us as we explore the groundbreaking innovations at HeartWorks, a transformative program at the Mayo Clinic led by Dr. Tim Nelson. With heartfelt insights from Erin Borkowski, a dedicated heart mom, and Rachel Gott, an inspiring adult living with congenital heart disease, we delve into the challenges and advancements that are redefining patient care and clinical trial processes.Meet the pioneers behind the scenes as Dr. Nelson explains how HeartWorks is bridging the gap between research and real-world applications. By harnessing patient-contributed data, this initiative is overcoming the frustrations of traditional clinical trials, making them more effective and timely. Rachel Gott shares her personal journey with HeartWorks, emphasizing the significant impact of ongoing research and patient empowerment in the fight against congenital heart disease.Discover how HeartWorks is turning obstacles into opportunities through a data-driven cooperative platform. This patient-owned model is not only increasing enrollment in clinical trials but also creating a collaborative network of institutions across the nation. From engineering heart muscle cells from skin biopsies to making clinical trials more accessible, HeartWorks is revolutionizing the way we think about congenital heart disease care. Tune in to learn how you can support these efforts and contribute to a brighter future for individuals of all ages affected by congenital heart conditions.Thanks to our newest HUG Patron, Ayrton Beatty and long-standing Patrons: Laura Redfern, Pam Davis, Michael Liben, Nancy Jensen, Alicia Lynch, Deena Barber, Carlee McGuire, Carter & Faye Mayberry, and Frank Jaworski. We appreciate you!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Send us a textMeet Marina Lohri, a true trailblazer in the world of congenital heart defects (CHDs). Born with tricuspid atresia, a ventricular septal defect, and an atrial septal defect, Marina's journey from a life-saving C-section to being among the first in Switzerland to undergo a modified-Fontan procedure at just 11 months old is nothing short of miraculous. In our conversation, Marina unfolds her inspiring story and shares her passion for working at atHeart Medical, where she is dedicated to promoting innovative solutions for those with similar heart conditions.Navigating the complexities of living with Atrial Fibrillation (AFib) and congenital heart defects is no small feat. Marina opens up about her personal experiences with rapid heart rates and the profound decision to undergo an ablation. As she contemplates the intricate considerations surrounding pregnancy with a congenital heart condition, we delve into the evolving medical advice she received and the diverse perspectives of healthcare professionals. Marina's story is a testament to the importance of specialized care and the expertise found at top hospitals in Switzerland.From finance to the medical field, Marina's career journey is a testament to aligning work with personal values and health needs. As she shares her transition to atHeart Medical, a startup focused on congenital heart defects, Marina highlights the rewards of working in a supportive environment that truly understands the challenges of living with CHD. Her advocacy extends beyond her professional life, as she continues to inspire others with similar heart conditions to pursue their passions and find purpose in their careers. Marina's resilience shines through as she navigates life's challenges with a positive attitude and a commitment to the CHD community.Helpful Links:atHeart Medical website: https://atheartmedical.comSupport Organizations:Mended Hearts: https://mendedhearts.org(In German)Herznetz: https://www.herznetz.ch/Fontanherzen: https://fontanherzen.ch/Swiss Heart: https://swissheart.ch/Thanks to our newest HUG Patron, Ayrton Beatty and long-standing Patrons: Laura Redfern, Pam Davis, Michael Liben, Nancy Jensen, Alicia Lynch, Deena Barber, Carlee McGuire, Carter & Faye Mayberry, and Frank Jaworski. We appreciate you!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Send us a textUnlock the latest in cardiac neurodevelopmental research with Dr. Dawn Ilardi, a distinguished clinical neuropsychologist, as we navigate the complexities of how congenital heart defects (CHDs) impact children's neurodevelopment. Discover the groundbreaking strides made by the Cardiac Neurodevelopmental Outcome Collaborative (CNOC), a global network of over 50 institutions revolutionizing clinical care and research. Explore cutting-edge advancements in brain imaging and gain insight into the often-overlooked influences of non-cardiac factors, such as the placenta, along with the indispensable role of family involvement in enhancing developmental outcomes.Hear a poignant story of parental vigilance that underscores the vital need for early detection and standardized imaging in pediatric cardiology. Despite the challenges faced by families with limited resources, new initiatives are bridging the gap between hospital-based care and private practice, providing essential support and education. Cultural perceptions of disabilities are also on the table, emphasizing the importance of culturally sensitive approaches tailored to diverse communities, ensuring all families receive the understanding and assistance they deserve.Finally, we shed light on the crucial connection between parental mental health and a child's developmental journey. Understand the nuances of capturing accurate baselines in neurodevelopmental assessments for children with CHD and why repeat evaluations are essential. As we discuss the emotional rollercoaster faced by parents, we stress the value of community resources and social media groups in offering support. Join us to appreciate the profound impact of parental well-being on a child's health trajectory and learn strategies for balancing the demands of caregiving with the necessity of self-care.Dr. Ilardi's previous "Heart to Heart with Anna" appearance: https://tinyurl.com/DawnIlardi2014Dr. Ilardi's website: https://www.pedneurocenter.comDr. Ilardi's email: DawnIlardi@pedneurocenter.comThanks to our newest HUG Patron, Ayrton Beatty and long-standing Patrons: Laura Redfern, Pam Davis, Michael Liben, Nancy Jensen, Alicia Lynch, Deena Barber, Carlee McGuire, Carter & Faye Mayberry, and Frank Jaworski. We appreciate you!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Navigating the torrent of emotions that come with being a heart mom to an adult child, Rita Scoggins and I, Anna Jaworski, unfold the layers of our unique journey. Our intimate conversation traverses the evolution of care, from the hands-on nurturing of our children's younger years to the complexities of supporting their maturity and independence. We delve into the potent mix of pride and concern, sharing stories that resonate with anyone who understands the pull of a parent's heartstrings as their children, like Rita's daughter Victoria, and Anna's daughter Hope, carve out lives shaped by both their challenges and triumphs.This episode continues with reading from The Heart of a Heart Warrior Volume One: Survival. In this episode, co-editors Megan Tones and Anna Jaworski, take turns reading essays from the book. In Chapter One we read the narratives of heart warriors who've faced body insecurities and the trials of scoliosis with courage. Laura Ryan's story, in particular, shines as a beacon of hope; her transformative experience at the waterslides in Lancaster, learning to embrace her surgery scars, offers a deep dive into the power of empathy and connection. We hear how individuals like Michael McKelvey and Dajah Scrivner channel their pain and resilience into poignant expressions of life with CHD.Our episode doesn't simply share stories; it offers a lattice of support, exploring how adaptive clothing and familial love can buoy spirits amidst adversity. As we discuss the importance of finding strength in community and the solace of shared experiences, we invite you to join us in a space that celebrates overcoming obstacles and the beauty of human connection. For all who walk the path with heart-defect warriors, this conversation is a testament to the enduring spirit and the ties that bind us all.Rita's other podcast episodes:Rita, Victoria, and Heidi Scoggins on The CHC Podcast: ‘Taking Control of Your Heart Condition' Rita as a Guest Host on Heart to Heart with Anna interviewing Laura Ryan. ‘Heart Warrior Mom Raising Children to Adulthood'Rita and Victoria Scoggins on Heart to Heart with Anna: ‘Congenital Heart Defect Awareness 2015'Learn more about our The Heart of a Heart Warrior Volume One: Survival Book Study and join us to discuss the book and share your stories. Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Blood samples and health records for 15,000 pregnancies provides a wealth of scientific data. Add samples and records from the resultant children and grandchildren, and you have an invaluable cohort with which you can study the long-term results of events that occur during pregnancy. Barbara Cohn with the Public Health Institute is the Director of such a cohort and discusses it with co-hosts Anne Chappelle and David Faulkner, including what she and colleagues have discovered about the generational effects of exposure to DDT and other substances.About the GuestBarbara A. Cohn, PhD, is Director of the Child Health and Development Studies (CHDS) at the Public Health Institute. CHDS is home to a groundbreaking study, which originated in 1959, designed to shed light on the various factors impacting health during pregnancy and early childhood. Between 1959 and 1967, 15,000 pregnant women and their families were enrolled. Researchers continue to study these rich data and conduct important follow-up studies to further examine how events during pregnancy impact the subsequent health of fathers, mothers, and their children and grandchildren. Dr. Cohn consults with researchers around the world on the use of the CHDS data for health research.In addition, Dr. Cohn directs research examining how pregnancy protects against breast cancer and influences other health problems in mothers and their children in order to identify natural protective mechanisms that can be used for prevention. She also investigates whether early life exposure to environmental chemicals during pregnancy affects obesity, immune function, reproductive health, cardiovascular disease, diabetes, neurodevelopment, cancer, and health disparities in mothers and their children across the life span.Dr. Cohn holds a doctorate in epidemiology, a master's degree in city and regional planning, a master's degree in public health planning, and a bachelor's degree in zoology, all from the University of California, Berkeley.

Hello Mumma's! This weeks episode is with the lovely Sarah who is the Mom to 17 month old Ruby. Trigger warning - in this episode we discuss open heart surgery, hospital stays in NICU, PICU, SCBU & Starship so if this is triggering for you I would suggest skipping this episode.Sarah, her partner Rupert & Ruby have been on a journey many of us cannot even fathom. After battling Hyperemisis Gravidarum "HG" in her pregnancy, at Sarah's 20 week scan it was discovered that there was something wrong with Ruby's heart. After the scans were looked over by her Obstetrician and what felt like the longest wait ever, Sarah & Rupert were told that Ruby had a Congenital Heart Disease "CHD" and Tetralogy of Fallot "TOF". CHDs affects 1 in every 100 births, Sarah shares with us her pregnancy experience, the conversations, tests and decisions that had to be made in the lead up to Ruby's birth.After Ruby was born, Sarah shares the experience of what her fourth trimester was like - multiple hospital stays in NICU, SCBU, Starship, helicopter transfers, tests, scans, tubes - hardly the experience Sarah envisioned when she became pregnant. At 12 weeks old, Ruby had open heart surgery to correct the defect in her heart. Sarah takes us through this experience and what life is like for herself, Ruby & Rupert now - spoiler alert Ruby is a thriving, happy, little girl.Sarah opens up about how this whole experience has impacted her own wellbeing including counselling and needing to go back on anti depressants as well as how it impacted her & Rupert's relationship. Sarah found her heart family village online through community groups both within in NZ and overseas. Heart Kids NZ is a nonprofit organisation in Aoteroa that provides lifelong support to the children, teens, adults and whanau impacted by childhood heart conditions and has been an incredibly important part of Sarah's village.All she wanted when she was pregnant was to speak to other families going through something similar who had come out the other side. Sarah's hope in sharing her story is to both raise awareness of CHDs but also so that anyone going through something like this knows that they are not alone.Sarah is happy for people to connect with her on Instagram if they want to chat and you can find her here @sarahkilner. I hope you love this very special episode Mumma's and if you do please rate & review on whichever platform you choose to listen on and follow along on socials @bumptomum.podcast.Enjoy!

With congenital heart defects being the #1 birth defect around the globe, there are many people touched by this condition. At least 1% of the population is born with a heart defect. Many of them will be innocent murmurs that will close up on their own. But some people have more serious heart conditions.In this special mini-series episode for Heart Month 2023, Anna asks her Listeners to identify some famous movies which depict someone with a congenital heart condition (CHC). Since congenital heart conditions are ubiquitous, it's interesting to see how people with these conditions are portrayed in the movies and what role the CHC plays in the movie's plot. Do you think the movies we chose did a good job of showing the world what it's like to have a CHC? Send us an email to Anna@hearttoheartwithanna.com to let us know what you think!Other Links To CHD in Society episodes you may enjoy:CHDs in Society #3: The Musicians https://www.buzzsprout.com/62761/12273541CHDs in Society #2: The Athletes https://www.buzzsprout.com/62761/12209527CHDs in Society #1: The Entertainers https://www.buzzsprout.com/62761/12173766Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

With congenital heart defects being the #1 birth defect around the globe, there are many people touched by this condition. At least 1% of the population is born with a heart defect. Many of them will be innocent murmurs that will close up on their own. But some people have more serious heart conditions.In this special mini-series episode for Heart Month 2023, Anna asks her Listeners to identify some famous musicians who have been touched by CHDs. So many people think that if they have a heart defect, they won't have the stamina to become great at what they love. That's not true, my friends, and the following FOUR people are an example of how people can still excel, despite having a heart defect. Do you know who these people are? See if you can guess!Links to other shows you may enjoy:Paul CardallThe Broken Miraclehttps://www.buzzsprout.com/62761/9193481Heart Dad Sunday -- A Child's Role in Transplant Recovery for a Heart Dadhttps://www.buzzsprout.com/62761/12186961Myles SchweitzerSeizing the Day with Myles Schweitzer!https://www.buzzsprout.com/62761/398954Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Why would a heart dad decide to host a podcast? Why would he write a book for the congenital heart defect community? What has this dad learned from having a child with a heart defect? Tom and Kat Hansen are parents to Audrey and Harding. In 2014, Harding was diagnosed with multiple congenital heart defects in utero, for which he has undergone three open-heart surgeries and multiple other procedures. Inspired by their journey with Harding, Tom and his wife wrote a book and then they started a podcast, The Hope and Courage Podcast for CHD Parents, where they share their insights and interview experts and people with a lived experience of CHD. Their book Hope and Courage: Real-Life Lessons from the Parents of a Child with Congenital Heart Disease was released in 2022. A former high school math teacher, Tom is currently a corporate trainer and instructional designer. Tom's family lives in Cincinnati, Ohio and they enjoy going on adventures together.Links for more information about Tom and Kat Hansen:Their website: https://www.tomandkathansen.com/ (for their podcast, their book, and free resources)Tom and Kat's previous Heart to Heart with Anna episode:  The Tom-Kat Team: Raising Awareness of Congenital Heart Defects:  https://www.buzzsprout.com/62761/9863822Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

How safe is it for a woman born with hypoplastic right heart syndrome to get pregnant and carry a baby to term? What considerations need to be made when Heart Warriors with complex CHDs decide to get pregnant? What advice does a Heart Warrior Mom have for others considering having a baby?Katelynn Scoggins was born with a critical congenital heart defect known as hypoplastic right heart syndrome. Unlike many people born with HRHS, she has not had the Fontan Procedure. She has done very well medically. Katie was homeschooled and she and I have known each other forever! She is a Texan, and she was an intern with Hearts Unite the Globe for a while and I even got her to attend Toastmasters meetings with me in Gatesville. We also worked together with the Texas Chapter of the Children's Heart Foundation. Katie and Christopher Scoggins were married in May 2018. They welcomed their son, Isaiah, into the world in December 2019. She's coming on the show today to tell us about her journey to parenthood. Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

With congenital heart defects being the #1 birth defect around the globe, there are many people touched by this condition. At least 1% of the population is born with a heart defect. Many of them will be innocent murmurs that will close up on their own. But some people have more serious heart conditions.In this special mini-series episode for Heart Month 2023, Anna asks her Listeners to identify some famous athletes who have been touched by CHDs. So many people think that if they have a heart defect, they can't participate at an exceptional level in sports. That's not true, my friends, and the following THREE people are an example of how people can still excel, despite having a heart defect. Do you know who these people are? See if you can guess!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Are congenital heart defects hereditary? How might someone born with a hole in his heart choose to live his life? Why might a social worker choose to write a book to help the congenital heart defect community?This is our 2nd Wednesday Writer Chat--a special mini-series during Heart Month, February 2023.Today's show is "Social Worker, Heart Warrior Author" and our Guest is Richard Schwindt. We'll start today's program by learning a bit about Richard and his family in Segment 1. In the second segment, we'll talk about how Richard's book and in the final segment we'll talk about how CHDs have affected another generation of his family, what that has meant to him, and advice for others in the same situation.Richard Schwindt is married and has two children and two grandchildren. For the last 40 years, Richard has worked as a social worker, psychotherapist, and hypnotherapist. He has written 25 books, both fiction and nonfiction. For the congenital heart defect (or CHD) community, one book is especially pertinent–Emotional Recovery from Congenital Heart Disease, which is part of his Emotional Recovery series.Richard's interests include management of anxiety in CHD patients, and helping his teen and adult clients discover how they can live their lives to the fullest.Richard has had multiple heart procedures, two surgeries, and many pacemakers. He is from Kingston, Ontario. Here's a link to Richard's Amazon link: https://www.amazon.com/Emotional-Recovery-Congenital-Heart-Disease-ebook/dp/B0153VEL1E/ref=sr_1_7?crid=2C8B26YNP8WQC&keywords=richard+schwindt&qid=1675810257&sprefix=richard+schwindt%2Caps%2C171&sr=8-7If you enjoyed this episode, we'd love a little love from you! Please consider subscribing to our program on Buzzsprout. Thank you!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

With congenital heart defects being the #1 birth defect around the globe, there are many people touched by this condition. At least 1% of the population is born with a heart defect. Many of them will be innocent murmurs that will close up on their own. But some people have more serious heart conditions.In this special mini-series episode for Heart Month 2023, Anna asks her Listeners to identify some famous entertainers who have been touched by CHDs. Put your thinking cap on and let's see if you can guess who these 4 Entertainers are!Support the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

How do you enjoy the holidays when your heart warrior is in the hospital during the holiday season? What can you do, as a parent, grandparent, or friend, when a child is in the hospital during the holidays? Why is it especially difficult to have a child in the hospital during the holidays?We'll answer these questions and more in this episode which features Jenny Muscatell and Lauren Backe. These heart moms have both faced plenty of hospital time and they have some advice and experiences to share with us.Jenny Muscatell is a Licensed Social Worker, author, and radio host for Christian Mix 106.  She is the Co-founder of Muscatell Ministries, The Heart Community Collection, and serves as Editor in Chief for CHD Magazine. As a licensed social worker, Jenny has established an extensive reservoir of expertise specializing in crisis intervention, health systems, and end-of-life care. Her best-selling book, The Journey of Faith and Open Heart, shares the story of how she found faith battling for her daughter's life against odds in a true but inspirational journey of trial and triumph. Through faith-filled presentations, and heartfelt written words, Jenny's mission is to give voice to the vulnerable, hope to the hurting, and to make way for the unspoken to be told.Lauren Backe is Mom to Jack and Everly. Her daughter Everly was born with a congenital heart defect. Everly was induced at a hospital 65 miles from home after a prenatal diagnosis determined she would need open-heart surgery right after birth. Lauren and Matt Backe decided after their daughter's surgery that they wanted to make life better for children born with CHDs, and other hospitalized children. Lauren currently serves on the Advocate Children's Hospital Family Advisory Council, is a board member for LJ's Healing Hearts and is an active contributor in planning and running LJ's events. She is also a committee member for Children's Heart Foundation Red Tie Ball.Together, Lauren, Matt, Jack (10), and Everly (5) work with Brave Gowns to get soft, comfortable, and fun hospital gowns on kids. They collect pop tabs to benefit Ronald McDonald House Charities, and attend school kickoffs for the American Heart Association: Kids Heart Challenge. The Backe Family also enjoyed writing a book about Everly's CHD journey in 2020 with the foundation, Books that Heal. The Backe Family recently set up a blood drive with the American Red Cross.Helpful Links to Broadcast Episodes Mentioned in the Show:Jenny Muscatell's previous Heart to Heart with Anna appearances:Jenny Muscatell: Heart Mom, and AuthorThe “CHD Magazine”: A Magazine for the Congenital Heart Defect CommunityJenny's bookMatt Backe's episode: Beyond the Scar: Bonding with our CHD ChildrenLJ's Healing Hearts Brave GownsLauren's bookSupport the showAnna's Buzzsprout Affiliate LinkBaby Blue Sound CollectiveSocial Media Pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsite

Why would a doctor recommend parents take their child to a facility to live his life in the 1980s? Is there ever a good reason to take your child out of the hospital and take him to Disney instead? How did Peg trust her gut when it came to her son needing cardiac transplantation during COVID-19?Peg Eitl is a mom of three children: Joe, 40, Jason, 36, and Lacey, 31. Joe was born with Down Syndrome and a single ventricle heart. Due to his medical complexity and intellectual disability, the doctors advised Peg and her husband Craig to put him in a facility but they would have none of it! Fortunately, they met with cardiologist Dr. Black who encouraged them and gave them hope for Joe. Over the next few years, the new parents worked tirelessly with their son, enrolling him in early intervention, therapies, and extra-curricular activities in between cardiac appointments and procedures including a B-T shunt at 11 months, a Modified Glenn and Fontan at 7 years of age. Throughout his health battle, Joe and his parents have worked together to achieve the best outcomes possible: Joe's determination to survive drove him to be the best he could be, and his parents' advocacy in pushing for the best treatment possible resulted in him being listed for a heart/ liver transplant. This was an especially trying time because they also had to deal with the complexities that COVID-19 required.This episode of "Heart to Heart with Anna" features a mom to a special-needs heart warrior who fought valiantly to survive multiple heart procedures, complications, and transplantation. Peg talks candidly with Anna about some of the most significant struggles they've faced, the medical changes their family has seen over the last four decades, and her hopes for the future.Helpful Information about Joe:Facebook - TeamJoeEitlInstagram - @TeamJoe Eitl"Last Chance Transplant" Docuseries on Discovery Plus - Episode 3Joe is also a featured character (DJ Dog) in a children's book on Inclusion called "The Fusion of Inclusion, Where Friends Meat" written by his best friend Mark Graham and Coach Sean Hanleyhttps://www.developmentalfitness.com/meatball-man-and-hoagie-boyThere is an article written by VUMC that can be found here:https://news.vumc.org/2021/12/15/down-syndrome-patient-celebrates-anniversary-of-novel-transplant/Visit our Heart to Heart with Anna Social Media and Podcast pages:Apple Podcasts: https://tinyurl.com/H2HwAnnapodcastFB: https://www.facebook.com/HearttoHeartwithAnna/IG: https://www.instagram.com/hearttoheartwithanna/MeWe: https://mewe.com/i/annajaworskiTwitter: https://twitter.com/AnnaJaworskiWebsite: https://tinyurl.com/4kuckfn7YouTube: https://tinyurl.com/HUGpodcastMusic thanks to the Baby Blue Sound Collective - https://tinyurl.com/BBSCmusicSupport the show

How can a family deal with the loss of a child? What happens when a surviving child needs a transplant? What advice does a long-time Heart Mom have for other heart families?Bridgett Streacker has been married to her husband Brian for 34 years. They have four children: Jacob 33, Chesna (stillborn), Mallory (their Heart Warrior), and Haleigh 24. As a family, they have gone through many surgeries and obstacles, heartbreak and triumphs, which have made them closer.  Bridgett describes her Heart Warrior as one of a kind, who never let her CHD define her and lives like there is no tomorrow. The family faced one of its biggest challenges during COVID when Mallory had a heart transplant and was allowed no visitors for her entire hospital stay.In this episode, Bridgett and Anna discuss what it's like to be a CHD family, how they deal with mental health issues, and some advice for other families facing situations such as the ones they've faced.Please visit our Heart to Heart with Anna Social Media and Podcast pages:Apple Podcasts: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/Instagram: https://www.instagram.com/hearttoheartwithanna/MeWe: https://mewe.com/i/annajaworskiTwitter: https://twitter.com/AnnaJaworskiYouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwMusic thanks to the Baby Blue Sound Collective - https://music.apple.com/us/album/home-tonight-forever/1201349904Support the show

in this episode Will is joined by Dr. Weiland  from the UMMC Pediatric Cardiology department. We will discuss some of what are CHDs, what are some of the management and recognition tricks. How each diagnosis presents can sometimes be a challenge, and some of stuff we discuss is the more "later onset" of these patients two to three weeks after birth. These patients also have several considerations when transporting to a tertiary center, there is some discussion about transport considerations as well.  We also discuss several management techniques and pharmacological management of several of these patients between surgeries and how complex some of those patients can be. 

This month on Episode 39 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the August 5th and 19th issues of the journal. This episode also features an interview with Dr Annet Kirabo and Dr Ashley Pitzer from Vanderbilt University on their article, Dendritic Cell ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension.   Article highlights:   Jain, et al. Role of UPR in Platelets   Orlich et al: SRF Function in Mural Cells of the CNS   Xue et al: Gut Microbial IPA Inhibits Atherosclerosis   Wang et al: Endothelial ETS1 on Heart Development   Cindy St. Hilaire:        Hi, welcome to Discover CircRes, the podcast of the American Heart Association's journal Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'm going to be highlighting articles from our August 5th and August 19th issues of Circulation Research. I'm also going to have a chat with Dr Annet Kirabo and Dr Ashley Pitzer from Vanderbilt University about their study, Dendritic Cell ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension.   But before I get to the interview, I first want to share an article from our August 5th issue, and that article is titled, Unfolded Protein Response Differentially Modulates the Platelet Phenotype. The first author of this study is Kanika Jain and the corresponding author is John Hwa from Yale University. Self-stress can lead to protein misfolding, and the accumulation of misfolded proteins can lead to a reduction in protein translation and may alter gene transcription, a process collectively known as the unfolded protein response, or UPR. UPR is well documented in nucleated cells; however, it has not been studied in platelets, which are anuclear, but do have a rapid response to cellular stress. In this study, they investigated the UPR in anucleate platelets and explore its role, if any, in platelet physiology and function.   They found that treating human and mouse platelets with various stressors caused aggregations of misfolded proteins and induction of UPR-specific factors. Oxidative stress, for example, induced the UPR kinase PERK, while an endoplasmic reticulum stressor induced the transcription of the UPR factor XBP1. The team went on to study the UPR in platelets from people with type II diabetes, which is a population in which platelet mediated thrombosis is a major complication. They showed that protein aggregation and upregulation of the XBP1 pathway in diabetic patient platelets correlated with disease severity. Furthermore, treating the diabetic patient platelets with a chemical chaperone that helps to correct protein misfolding reduced protein aggregations and prevented the cells prothrombotic activation. This work confirms that even without transcription, platelets display stress-induced UPR, and that targeting this response may be a way to reduce thrombotic risk in diabetic patients.   Cindy St. Hilaire:        The second article I want to share with you is from our August 5th issue and is titled, Mural Cell SRF Controls Pericyte Migration, Vessel Patterning and Blood Flow, and it was led by Michael Orlich from Uppsala University in Sweden. Blood vessels are lined with endothelial cells and surrounded by mural cells. Vascular smooth muscle cells are the mural cells in the case of veins and arteries, and pericytes are the mural cells in the case of capillaries. In the capillaries, pericytes maintain blood-brain and blood-retina barrier function and can mediate vascular tone, similar to smooth muscle cells. While these pericytes and smooth muscle cells are related, they have distinct roles and characteristics.   To learn more about the similarities and the differences between pericytes and smooth muscle cells, this group examined how each would be affected by the absence of SRF in the other. SRF is a transcription factor, essential for nonvascular or visceral smooth muscle cell function. In visceral smooth muscle cells, SRF drives expression of smooth muscle actin and other smooth muscle genes. Using mice engineered to lack SRF in mural cells, they show that SRF drives smooth muscle gene expression in these pericytes and smooth muscle cells, and its loss from smooth muscle cells causes atrial venous malformations and diminishes vascular tone. In pericytes, loss of SRF impaired cell migration in angiogenic sprouting. In a mouse model of retinopathy, activation of SRF drove pathological growth of pericytes. This work not only highlights the various functions of SRF in mural cell biology, but it also suggests that it has a role in pathological capillary patterning.   Cindy St. Hilaire:        The third article I want to share is from our August 19th issue of Circulation Research and is titled, Gut Microbially Produced Indole-3-Propionic Acid Inhibits Atherosclerosis by Promoting Reverse Cholesterol Transport and its Deficiency Is Causally Related to Atherosclerotic Cardiovascular Disease. The first authors are Hongliang Xue and Xu Chen, and the corresponding author is Wenhua Ling from Sun Yat-Sen University in Guangzhou, China. Recent studies provide evidence that disorders in the gut microbiota and gut microbiome derived metabolites affect the development of atherosclerosis. However, which and how specific gut microbial metabolites contribute to the progression of atherosclerosis and the clinical relevance of these alterations remain unclear. Gut microbiome derived metabolites, such as short-chain fatty acids and trimethylamine N-oxide, or TMAO, have been found to correlate with atherosclerotic disease severity.   This study has now found that serum levels of indole-3-propionic acid, or IPA, are lower in atherosclerosis patients than controls. The team performed unbiased metagenomic and metabolomic analyses on fecal and serum samples from 30 coronary artery disease patients and found that, compared with controls, patients with atherosclerosis had lower gut bacterial diversity, depletion of species that commonly produce IPA and lower levels of IPA in their blood. Examination of a second larger cohort of atherosclerosis patients confirmed this IPA disease correlation. The team also showed serum IPA was reduced in a mouse model of atherosclerosis, and that supplementing such mice with dietary IPA could slow disease progression. Analysis of the macrophages from these mice showed that IPA increased cholesterol efflux, and the team went on to elucidate the molecular steps involved. The results of this study not only unraveled the details of IPA's influence on atherosclerosis, but suggest boosting levels of this metabolite could slow atherosclerotic disease progression.   Cindy St. Hilaire:        The last article I want to share is also from our August 19th issue, and it's titled, Endothelial Loss of ETS1 Impairs Coronary Vascular Development and Leads to Ventricular Non-Compaction. The first author is Lu Wang and the corresponding author is Paul Grossfeld, and they are at UCSD. Congenital heart defects, or CHDs, are present in nearly 1% of the human population. In some cases, the heart defects result from a genetic error, which can give researchers clues to its etiology. Jacobson syndrome is a complex condition caused by deletions from one end of chromosome 11, and the occurrence of a congenital heart defect in this syndrome has been associated with the loss of the gene ETS1. ETS1 is an angiogenesis promoting transcription factor, but how ETS1 functions in heart development was not known.   Wang and colleagues now show that both global or endothelial-specific loss of ETS1 in mice caused differences in embryonic heart development that ultimately led to a muscular wall defect known as ventricular non-compaction. The mice also had defective coronary vasculogenesis associated with decreased abundance of endothelial cells in the ventricular myocardium. RNA sequencing of ventricular tissue revealed that, compared with controls, mice lacking ETS1 had reduced expression of several important angiogenesis genes and upregulation of extracellular matrix factors, which together contributed to the muscular and vascular defects.   Cindy St. Hilaire:        Today I have with me, Dr Annet Kirabo and Dr Ashley Pitzer, both from Vanderbilt University, and we're going to talk about their paper, Dendritic Cell ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension. This article is in our August 5th issue of Circulation Research. Thank you both so much for joining me today.   Annet Kirabo:             Yeah, thank you so much for having us.   Ashley Pitzer:              Yeah, thank you for having us.   Cindy St. Hilaire:        Yeah, it's a great paper. I think we're all familiar with hypertension and this idea that too much salt is bad for our cardiovascular system. When I was a kid, my grandparents had those salt replacements on their kitchen table, Mrs. Dash and whatever. But, like you said in the start of your paper, the exact mechanism by which salt intake increases blood pressure and also increases cardiovascular risk, it's not really well understood, and you guys are focusing on the contribution of immune responses in this process or in this pathogenesis. Before we dig into the details of your paper, I was wondering if you could give us a little bit of background about what's known regarding the role of inflammation in this salt-sensitive hypertension pathogenesis.   Annet Kirabo:             Yeah. It's difficult to know where begin to from, but the role of inflammation in cardiovascular disease have been known for many, many decades. Right now, Dr David Harrison showed more than 10 years ago that T cells contribute to hypertension, but the mechanisms were not known. Back when I was a post doc in David Harrison's lab, we discovered a new mechanism, how immune cells are activated in inflammation and hypertension, whereby we found that there is increased oxidative stress in antigen-presenting cells. This leads to formation of oxidative products known as arachidonic acid or lipid products known as isolevuglandin, or IsoLGs. These IsoLGs are highly, highly reactive and they adapt to lysines on proteins. This is a covalent binding, which leads to permanent alteration of proteins, and so these proteins act as neoantigens that are presented as self-antigens to T cells, leading to an autoimmune-like state in hypertension.   Annet Kirabo:             We found that these antigen-presenting cells are activated and they start producing a lot of cytokines that paralyze T cells to IL-17 producing T cells that contribute to hypertension. And so, when I started my lab back in 2016, we discovered that excess dietary salt profoundly activates this pathway, and we found for the first time that these antigen-presenting cells, they express ENaC, the epithelial sodium channel, and sodium goes into these antigen-presenting cells and activates the NADPH oxidase, which is an enzyme which produces this reactive oxygen species, leading to this IsoLG formation, which I've talked about, and leading to inflammation.   So, three years ago when Ashley joined my lab, she had extensively studied the inflammasome in her PhD program, and she suggested why don't we look at the role of the inflammasome in this pathway and how IsoLG may contribute to this. In her paper that we are discussing right now, she found that in a dependent manner, sodium enters the cell and activates this pathway, and the NLRP3 inflammasome is involved in this process.   Cindy St. Hilaire:        That's such a wonderful story that fits together so many pieces. One of the things you talk about, which I guess I didn't even appreciate myself is, there are certain individuals out there who are more salt-sensitive than others.   Annet Kirabo:             Yeah.   Cindy St. Hilaire:        What is that difference? Do we know the root cause of that? And then also, how many individuals are we talking about are salt-sensitive?   Annet Kirabo:             Salt-sensitive blood pressure, it is a variable trait and it's normally distributed in the population, but it happens more in some individuals than others. It happens even in 25% of people without any hypertension. These people go to that doctor, that doctor thinks they're normal, they don't have any hypertension, but these people can be at a risk of sudden heart attack or cardiovascular risk or even a stroke, simply because when they eat a salty meal, their blood pressure will go up.   Cindy St. Hilaire:        Yeah, that's one of my questions. How much salt are we talking about here? And not only how much in a meal, but a sustained amount? How bad is a miso soup a day?   Annet Kirabo:             Yes. The American Heart Association and the World Health Organization have recommendations. American Heart Association recommends one spoon per day. We have refused to adapt to this recommendation, but that is the recommendation that they have recommended per day to eat. But this is difficult because most of the salt, as you know, is already in our food through processing in our processed foods and we don't have any control over how much salt we have, and there's also a lot of adding of salt at a table.   Cindy St. Hilaire:        Ashley, your background was more the inflammasome. What were your thoughts entering into this project? Did you have much of a hypertension background?   Ashley Pitzer:              No. My graduate thesis focused mainly on endothelial dysfunction and cardiovascular disease, and so it was a pretty easy segue. But it was just with Annet, so excited about the project and showing me all the data and this robust IL-1 beta production that she was seeing after these immune cells being exposed to high salt, I, with my inflammasome background, was immediately like, this could be playing a role. And so it was, like I said, a pretty easy transition and, as is in the paper, we're doing human studies. All of my research back in grad school was very basic research, so it was very exciting to see how our research was being translated with people having this condition and potentially finding mechanisms where we can target this to help actual people.   Cindy St. Hilaire:        I think a lot of us who are not in the hypertension field, and maybe this was you before you joined Annet's lab, we really only kind of think of the kidneys and the blood vessels when we think about hypertension, but studies like this are changing that. And I think a lot of Annet's earlier work, as well as the work of others, have shown a role for this epithelial sodium channel as an important player in this salt-induced hypertension. New to me, it's not just found in the kidney, which I totally did not appreciate that. And it's this channel sensing the salt that can trigger this IL-1 beta production that does a whole bunch of other things.   Cindy St. Hilaire:        What are those other things? What are those cells that are affected and where is this happening? Obviously it's not just kidney cells, but is it only in the kidney or are these systemic cells? What do we think is happening?   Ashley Pitzer:              That's the question, is, where is this happening? There's been studies at Vanderbilt by Jens Titze and his lab showing, where are these immune cells sensing the salt? And so they've shown that sodium accumulates in the skin, a huge argument is for they're sensing the sodium in the kidney because that's where a lot of it is being processed. But these immune cells travel through the whole body, so they're seeing it where there are the highest amounts of sodium concentration, and so I would argue it's in the kidney.   Annet Kirabo:             Indeed, because we're now collaborating with Tina Kon, and we have recently published with her a paper in the International Journal of Science, where we have done sodium MRI and we find this accumulation of sodium in the kidney even much more than in the skin. And we know that the kidney is where sodium is highly concentrated. So the working hypothesis in the lab is that these immune cells can be activated wherever they are, in the lymph nodes or not, in other tissues, but they can travel to the kidney.   We find that in high salt, if you feed high salt to the mouse, the endothelium in the kidney becomes dysfunctional and it expresses molecules, chemoattractants, that attract these immune cells in the kidney. We think that the high salt accumulation in the kidney can activate these, and then these immune cells are activated and they produce cytokines. Dr Steve Crowley showed that they can produce IL-1 beta, which induces activation of sodium channels that can be induced. We have also actually found that even IL-17 can be produced by these immune cells in the kidney and they can activate sodium channels in the kidney, leading retention of sodium and water and hypertension.   Cindy St. Hilaire:        Very cool. You used a lot of mice in this paper. Can you tell us, I just want to know a little bit about the models you chose to use, but also how similar is hypertension in mouse and humans? Obviously for atherosclerosis, we have to do lots of things to get them to form a plaque. Is hypertension similar in a mouse and do mice also show this salt-sensitive phenotype?   Annet Kirabo:             That is an extremely important point. If you read our paper, we use a slightly different approach. Most people do benchside to bed approach. We did the opposite. We did a bed to benchside approach.   Cindy St. Hilaire:        Always smart.   Annet Kirabo:             Yeah. We first started humans, and then with some references, we went to the mice, because I think when it comes to salt-sensitive blood pressure, mice are different from humans. In fact, if we look in the lab, we find that female mice are protected from salt-sensitive blood pressure, but we find that in the humans, it's the opposite. Females are more prone to salt-sensitive hypertension. Those are studies that we are doing right now. We haven't published. But we know that it can be different.   The model we use most of the time in the lab, the C57 mice, are resistant to salt-sensitive hypertension. These C57 mice would rather die before they raise their blood pressure in response to salt. We can induce salt-sensitivity in these mice like in the paper that we are discussing. When we induce the endothelial dysfunction using L-NAME and we wash it out, then these mice, when you give them, subsequently, salt, suggests that they become salt-sensitive. But we also have a salt-sensitive mouse model that we use, the 129/SV mouse. So we use several models to kind of prove the same thing over and over again with the findings that we found in humans.   Cindy St. Hilaire:        And you used a technique, which I'm a little bit familiar with, but I'd like to hear, A, about it from you, but also your experience in using it, and that is CITE-seq. So, how does that work?   Ashley Pitzer:              That was with our human study where we actually had patients come in, who were hypertensive, took them off medication for 2 weeks. They come in, we get baseline samples, we give them a salt load on one day, and then the next day we completely salt deplete them.   Cindy St. Hilaire:        How much is a salt load? Like a Big Mac? What's a salt load?   Ashley Pitzer:              Yeah, it's pretty much just like eating Lays chips all day. It's a lot of salt. It's a very salty meal.   Annet Kirabo:             And then in addition, we also infuse saline too.   Cindy St. Hilaire:        Oh, wow.   Annet Kirabo:             Because these people, when they come into the hospital, some them have already eating high salt. This approach is to just maximize the whole system so that then when we sort deplete everybody, it's at the same level and it's just to unify the whole process. But sorry, Ashley, you go ahead.   Ashley Pitzer:              With the CITE-seq, we're able to take different patients on different days. So we take samples each day, and we can give each sample a barcode, basically. Give them a barcode, we can pool them all together, process them, and we can sequence their RNA, we can probe for a certain amount of protein expression as well. So then when we analyze, we can look at protein expression, so you get the translation and the transcription for each person on each day, and then you're able to compare. And so you get this huge picture and it's a lot of data.   Cindy St. Hilaire:        How long did it take you to sort through?   Ashley Pitzer:              Well, we have a statistician who does all of that, because my wheelhouse is here and it is on a different planet. So we have somebody who helps us with that who does an unbiased approach. And then once he does an analysis, gives us back what are the things that are changing the most, and one of those was IL-1 beta.   Annet Kirabo:             As you can see, our list is huge, this is a massive input of so many collaborators. We have computational people on there that help us with this. I can't even begin to learn these techniques, but with all this collaboration and the resources at Vanderbilt, these things are possible. And so, this is a really powerful approach where you can combine protein expression and you get the specific cells that express the genes and you couple the channel type to the gene expression.   Annet Kirabo:             We actually found that not all monocytes are the same. There's a specific class that of monocytes, A small class of monocytes that is so angry, and the inflammasome is activated and producing this IL-1 beta, and that is enough to contribute to this phenotype of salt-sensitive hypertension, which dynamically changed according to blood pressure, suggesting that this is a targetable salt-sensitive blood pressure, even in normotensive people, is a targetable trait. And because these monocytes are in blood, can we get a blood sample and routinely diagnose salt-sensitive blood pressure so that doctors are aware and they can appropriately advise patients.   Cindy St. Hilaire:        This was samples obviously taken from a blood draw, right? So they're circulating.   Annet Kirabo:             It was a blood draw, yes.   Cindy St. Hilaire:        What do you think about these immune cells, perhaps, native in the kidney? Do you think the small population of angry cells, like you said, is escaping from the kidney environment? What do you think?   Annet Kirabo:             When I was a post-doc in David Harrison's lab, we found that the most angry dendritic cells that contribute to this inflammation and hypertension are monocyte-derived. So that's why in the human study we focused on monocytes, because there are so many subtypes of dendritic cells, plasmacytoid dendritic, classical dendritic cells. We have studied all of these subtypes, and we have focused on monocyte-derived dendritic cells because they're the ones that seem to be contributing to this phenotype the most.                                     Cindy St. Hilaire:        You guys focused in on the NLRP3 inflammasome, which, obviously it's a really critical component broadly for the innate immune system. Do you think that this is going to be a targetable approach that can be leveraged for hypertension? Or do you think it's too broad? What do you think about that as a therapeutic potential?   Ashley Pitzer:              Even when you look in our paper, and we use a knockout model, where we use a completely global knockout model, put them on high salt, and we give them back only dendritic cells that are from wild-type mice, so they have that NLRP3, that have been exposed to high salt. We were able to increase blood pressure, but I also did, in mice, where I gave them an IL-1 beta neutralizing antibody, similar to canakinumab, which is the CANTOS trial, and there's not much of a difference. There is, but it's minor. It's very minor.   Ashley Pitzer:              So, to be able to target in specific cell types in humans one thing, it's very difficult, and maybe one day we can get there. But I think it at least gives us a better idea of what is the full picture, what's the big mechanism going on with immune cells? In part of our human study, we are looking at something to try and be able to identify who is salt sensitive. So if anything, we're able to sit here and potentially have a way of identifying salt-sensitive patients, where, right now, all we can do is have them come in like we do and do a 3-day study, and not everybody can do that.   Annet Kirabo:             To add onto that, perhaps you know, we are talking about precision medicine. This is an era of precision medicine where you need to really tailor treatments if we can get there, and I think this is one way. CANTOS trial. They had no way of knowing who is salt-sensitive and who is not, it was a global approach, and the lack of differences in blood pressure might be explained that this IL-1 beta pathway is targetable in a specific population whose blood pressure is probably driven by inflammation. There are so many, many mechanisms that drive hypertension, and so perhaps we need to focus this on salt-sensitive people, and maybe we can really use this approach to target. Plus, this is ENaC-dependent.   As you know, amiloride has lost favor in the clinic as a treatment of hypertension, because in the majority, it's not effective. But studies have shown that in Black men, for example, who had been categorized salt-resistant, when they give them amiloride, their blood pressure went down, and yet it's not effective in the majority of the people.   So, can we bring back, can we take another look at amiloride. As our studies indicate that blockade of ENaC is anti-inflammatory and it's also antioxidant agent, can we at least bring back amiloride and look at it again and we focus it for specific populations of people that may be more prone to salt-sensitive hypertension?   Here we have so many targets for potential precision treatment of salt-sensitive potential in this paper. You can target SGK1, which we know is possible, we listed a number of clinical trials that they have used NLRP3 inflammasome inhibitors, you can use amiloride for these people, and you can also potentially scavenge IsoLGs.     Cindy St. Hilaire:        What was the most challenging aspect of this study? There's a lot of moving parts, so what was the biggest challenge? And then, also, what was the most surprising part or the most pleasantly surprising part?   Ashley Pitzer:              You have to think, most of this was going on right when the pandemic hit. And right before that, we had started our human recruitment for the human study. And so that put a little bit of a time damper on it.   Ashley Pitzer:              Other than that, it was just, we were finding one thing, developing a new experiment, doing it again, doing it again. And honestly, what was the most surprising and rewarding was just seeing the same thing in, because we took just PBMCs from normotensive patients, treated them with high salt, and saw the changes that we did with the inflammasome. And to see that exactly again in an in vivo model of giving patients high salt and seeing the same thing, it was very rewarding and confirmed that, okay, we're on the right path. Seeing the same thing over and over and over again, it kind of reaffirms that you had a good idea.   Annet Kirabo:             I might add, one of the most challenging was, initially, the computational. Oh, part of the pandemic I was, the pandemic hit, I had a baby during the pandemic, and it was my time to leave my home, and then all these things were going on. We had a clinical trial where patients had to come in. Vanderbilt was so super supportive ,even checking for COVID-19. Our patients could not have COVID-19. We needed to check them.   Cindy St. Hilaire:        Yeah.   Annet Kirabo:             They also had to check for COVID-19. And so during that time, I realized, wait, I need learn computation analysis. I realized I cannot learn, and then reached out to collaborators that helped. That was extremely challenging. And then the other challenging thing that we faced later during the pandemic is vaccinations. In our criteria, these people cannot be vaccinated for reasons. We've studied inflammation, hypertension, and so vaccination was confounding. And even COVID-19 is even more for confounding. So we had this exclusion criteria where we could not recruit anyone.   Annet Kirabo:             Everybody was having COVID, everybody was being vaccinated, and everybody was in that exclusion criteria, so it was difficult to get people. We have had some slow down, but right now it's beginning to build up.   Cindy St. Hilaire:        So, what's next? What's the next question?   Annet Kirabo:             We have so many.   Cindy St. Hilaire:        That means it was a great study. If you have more, that means it was a great study.   Annet Kirabo:             Yeah. This study and us, it kind of warms. The inside seat just opened up, we have primary data in the genetic regulation of ENaC, we have primary data where we found. We are trying to figure out the specific ENaC channel in these antigen-presenting cells. We don't know. We found that ENaC delta, for example, it's not found in a kidney or you talked about a kidney contribution versus immune cells. ENaC delta is not found in the kidney, but we have primary data that show that ENaC delta is the most correlated with cardiovascular risk, is the most correlated with kidney disease and all forms of hypertension. So now we're like, ENaC delta expressed in the immune cells, not in the kidney, it is the one that is most involved in cardiovascular disease, so how are we going to tell the world that.   Cindy St. Hilaire:        Yeah, very cool.   Annet Kirabo:             Those cells, not necessarily the kidney. The kidney plays a part because the cells are going there, but it's very, very exciting. Plus a number of other lines that we are investigating.   Cindy St. Hilaire:        It's great. Well, congratulations, again, on this publication, on just getting all this done with what sounds like extremely difficult patient recruitment. So, Dr Kirabo and Dr Pitzer, thank you so much for joining me today and I'm looking forward to these next studies on maybe ENaC delta.   Annet Kirabo:             Thank you. Thank you so much.   Ashley Pitzer:              Thank you for having us.   Cindy St. Hilaire:        That's it for the highlights from the August 5th and August 19th issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and hashtag Discover CircRes. Thank you to our guests, Dr Annet Kirabo and Dr Ashley Pitzer.   This podcast is produced by Ashara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Some of the copy text for the highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire, and this is Discover CircRes, your on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. Opinions expressed by speakers in this podcast are their own, and not necessarily those of the editors or of the American Heart Association. For more information, visit ahajournals.org.  

Why would it be helpful for parents of adults with congenital heart defects (or CHDs) to have group therapy? What kinds of problems might parents of adult Heart Warriors face? Who provides this specialized kind of therapy?Dr. Smorra is passionate about psychotherapy for the CHD community. Being born with CHD herself, she brings experiential knowledge, along with her training, and research when working with clients, families, and medical professionals impacted by CHD. Her research interest is social work services, and therapy for individuals who are born with congenital heart disease. Her experience is counseling individuals who are permanently impacted by automobile accidents, afflicted with chronic disease, and experiencing grief, depression, anxiety, and end of life. She enjoys helping students succeed academically. Dr. Smorra earned her Bachelor's in Business Administration from Western Michigan University, Master's in Social Work from Western New Mexico University, and Doctorate in Social Work from Walden University. Currently, she is an Adjunct Associate Professor, MSW Program at Western New Mexico University, Contributing Faculty, MSW Program at Walden University, as well as Chief Clinical Officer (CCO) for Heart and Mind Counseling, LLC. She is currently licensed in multiple states.Dr. Smorra's Helpful Information:Website: www.heartandmindcounseling.comParents of adults with CHD therapy page: https://heartandmindcounseling.com/congenital-disease-group/Instagram @heartandmindcounselingFacebook: https://www.facebook.com/HeartandMindLLC/ or @heartandmindllcFacebook Group: Congenital Heart Disease and Mental HealthPlease visit our Social Media and Podcast pages:Apple Podcasts: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/Instagram: https://www.instagram.com/hearttoheartwithanna/MeWe: https://mewe.com/i/annajaworskiTwitter: https://twitter.com/AnnaJaworskiYouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwWebsite: https://www.hug-podcastnetwork.com/Music thanks to the Baby Blue Sound Collective - https://music.apple.com/us/album/home-tonight-forever/1201349904If you enjoy this program and would like to be a Patron, please check out our Patreon page: https://www.patreon.com/HeartToHeartSupport the show

This episode deals with a very unusual congenital heart defect (CHD) -- a vascular ring defect. In this episode, we will be learning about what this heart defect is, how it affects the body, how the defect can be surgically managed, and how one mother took this experience and created a children's book to help other children with CHDs.Carli Valentine lives with her husband and their two sons, Finnegan and Lochlan, in Ogden, Utah. Finnegan was born with a heart defect which contributed to other medical challenges. Carli's experiences as a mother have informed her as an author. She has written several children's books that explore themes including congenital heart defects, ADHD, emotional regulation, executive dysfunction, and airway disorders. She hopes to share the magic of books with children to instill a passion for reading. When she's not writing, she enjoys spending time with her family and volunteering at her son's school or with CHD charities.  She is the author of six children's books including Turkey Trot, Bad Habit Rabbit and more. You can learn more about her at Linktree and follow her on Facebook.Link to Carli's author page on The Heart Community CollectionCarli's Facebook linkCarli's Instagram linkCarli's TikTok linkCarli's YouTube channel link Carli's Goodreads link Please visit our Social Media and Podcast pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsiteAnna's Buzzsprout Affiliate Link (we both benefit if you sign up with Buzzsprout with my link - yay!) Support the show

This is the 3rd of 4 episodes of Heart Dad Sunday -- a mini-series developed for Heart Month, February 2022. Heart Dad Frank Jaworski returns in this episode as the Guest Host. He interviews long-time friend, Michael Liben, about what it was like to raise a daughter with a critical congenital heart defect in Israel. Not only did Michael's daughter have double-outlet right ventricle, but she also had autism and she later developed epilepsy as well. Michael is the father of three children: 27-year old Idan, 25-year-old Sapir, and forever 15-year old Liel. Michael and Leora have been married for 34 years and Michael made aliyah to Jerusalem after college.Michael was a former filmmaker, high school teacher, adjunct professor of television and radio production, and he now works in security. For almost 6 years Michael has been working with Frank's wife, Anna, as the Host of a bereavement podcast now entitled, “Bereaved But Still Me.”Links to Michael's other appearances on "Heart to Heart with Anna"Congenital Heart Defects Around the Globe: IsraelLiel and Her Many Gifts: A Family's Decision to Donate One Girl's Lungs, KidneysMichael and Jamie: An Interview with an Organ Recipient and Donor's DadLink to Michael's podcast -- Bereaved But Still MePlease visit our Social Media and Podcast pages:Apple PodcastsFacebookInstagramMeWeTwitterYouTubeWebsiteAnna's Buzzsprout Affiliate Link (we both benefit if you sign up with Buzzsprout with my link - yay!) Support the show (https://www.patreon.com/HearttoHeart)

What is being done in 2022 to help children born with hypoplastic left heart syndrome (HLHS)? Is it possible to consider there may be a day when heart defects can actually be cured? What event is occurring on February 3, 2022 to raise funds to stamp out congenital heart defects?Dr. Timothy Nelson is the director of the Todd and Karen Wanek Family Program for HLHS at Mayo Clinic. Dr. Nelson's research work is focused on cardiovascular regeneration using bioengineered stem cells to improve the ability to discover, diagnose, and ultimately treat mechanisms of degenerative diseases. As director of the program, Dr. Nelson and his team are specifically interested in the cause of HLHS and finding ways to delay and prevent heart failure for individuals with HLHS. To better understand and treat this congenital heart disease, the program has taken a multifaceted approach that includes research into stem cells, genetics, imaging tools, and the creation of a biorepository. The program has launched clinical trials using autologous stem cells, also known as stem cells collected from an individual's own body.In June 2020, “HeartWorks” was created to accelerate and expand the product development undertaken by the program at the Mayo Clinic. This episode includes discussion about Dr.  Timothy Nelson's research as well as a conversation about an important, upcoming fundraising event. Links mentioned in the podcast:Jennifer Gutman on "Heart to Heart with Anna" talking about her HLHS child's participation in the Mayo Clinic's stem cell research project  Dr. Timothy Nelson on "Heart to Heart with Anna" in Season 9.A Cure is in the Works CelebrationTodd and Karen Wanek Family Program for HLHSPlease visit our Social Media and Podcast pages:Apple Podcasts -- https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook -- https://www.facebook.com/HearttoHeartwithAnna/Instagram -- https://www.instagram.com/hearttoheartwithanna/MeWe -- https://mewe.com/i/annajaworskiTwitter -- https://twitter.com/AnnaJaworskiYouTube -- https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwWebsite -- https://www.hug-podcastnetwork.com/Anna's Buzzsprout Affiliate Link (we both benefit if you sign up with Buzzsprout with my link - yay!) Support the show (https://www.patreon.com/HearttoHeart)

How can having an atrial septal defect, or ASD, affect a baby's growth and development? Specifically, could an ASD be responsible for feeding issues? What are the dangers of surgeons operating on a baby too soon if their congenital heart defect (CHD) is an ASD?Amna Saeed Salman is the author of Style Stripped, a prominent fashion and lifestyle blog in Pakistan. She is also Mom to beautiful 4-year-old twin boys. One of the boys was diagnosed with a 24mm atrial septal defect at age 1. Amna researched surgery options in England, Pakistan, and America and received differing opinions. Watching her son struggle to keep up with his brother, she decided to go for the surgery when he was 20 months of age. Amna noticed an immediate improvement in her son and today he is thriving.  In this episode of "Heart to Heart with Anna," Amna talks with Anna about her son's medical journey, some of the differences between medical treatment of CHDs in Pakistan and abroad, and how she has become a CHD advocate.Here is a link to an article referencing Amna's blog: https://tribune.com.pk/story/439325/make-way-for-pakistan%E2%80%99s-fashion-bloggersHere is an article about another team having a medical mission to Pakistan: https://www.hmpgloballearningnetwork.com/site/cathlab/content/humanitarian-spotlight-medical-mission-pakistan Please visit our Social Media and Podcast pages:Apple Podcasts -- https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2 Facebook -- https://www.facebook.com/HearttoHeartwithAnna/ Instagram -- https://www.instagram.com/hearttoheartwithanna/ MeWe -- https://mewe.com/i/annajaworski Twitter -- https://twitter.com/AnnaJaworski YouTube -- https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwWebsite -- https://www.hug-podcastnetwork.com/ Anna's Buzzsprout Affiliate Link (we both benefit if you sign up with Buzzsprout with my link - yay!) Support the show (https://www.patreon.com/HearttoHeart)

How does having obstacles to playing sports affect a boy's feelings of self-worth when growing up? In what ways can a young man feed his desire for sports and athletics, even if his body isn't able to do what his mind wishes he could do? How can an adult Heart Warrior enjoy a passion for sports when he only has half a heart?Michael Hills was born in February of 1998 in Ontario, Canada. He was diagnosed with Hypoplastic Left Heart Syndrome when he was five and a half months old. He has had three surgeries: a Norwood at nearly six months, a Glenn at nine months, and a Fontan at two years and four months of age. Ever since the last surgery, he has enjoyed good health. Michael has a passion for sports and played on several sports teams during his school days. Since leaving school, he has studied sports management and sport and event marketing and currently works for a variety of sports clubs and teams. He also enjoys traveling to different countries. Michael wants to share his story about how sports allowed him to live a life with joy and a sense of normalcy, and to show a healthy, active life with complex CHD is possible. Links mentioned in the episode:Links Michael sent me to better understand curlingJoanne Courtney Explains Curling Shoe Grippershttps://www.youtube.com/watch?v=igG5WyPvyDoSuper Sweeper Joanne Courtney critiques sweeping techniquehttps://www.youtube.com/watch?v=1iZbrteHx1oPlease visit our Social Media and Podcast pages:Apple Podcasts: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/Instagram: https://www.instagram.com/hearttoheartwithanna/MeWe: https://mewe.com/i/annajaworskiTwitter: https://twitter.com/AnnaJaworskiYouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwWebsite: https://www.hug-podcastnetwork.com/Anna's Buzzsprout Affiliate Link: https://www.buzzsprout.com/?referrer_id=16817 (we both benefit if you sign up with Buzzsprout with my link - yay!)Support the show (https://www.patreon.com/HearttoHeart)

Anna Jaworski is an author, publisher and public speaker. Most importantly, Anna Jaworski is the mother of two sons -- one who has a severe, congenital heart defect (CHD) known as "hypoplastic left heart syndrome."Anna has written two books: Hypoplastic Left Heart Syndrome: A Handbook for Parents and My Brother Needs an Operation. She is a contributor to The Heart of a Mother -- an anthology of stories by mothers affected by CHDs. Anna also edited both The Heart of a Mother and The Heart of a Father (the companion book to The Heart of a Mother.) Anna Jaworski has also contributed to two medical textbooks on hypoplastic left heart syndrome and a nursing magazine.Anna Jaworski is not a nurse or a doctor. She is a mother who has made it her goal in life to help other families of children with CHDs. To do so, in addition to producing helpful resources through her publishing company Baby Hearts Press, she has also worked with Sue Dove (another "heart mom") to create two websites: www.babyheartspress.com and www.congenitalheartdefects.com******************************************************************To listen to all our XZBN shows, with our compliments go to: https://www.spreaker.com/user/xzoneradiotv*** AND NOW ***The ‘X' Zone TV Channel on SimulTV - www.simultv.comThe ‘X' Chronicles Newspaper - www.xchroniclesnewspaper.com ******************************************************************

Hypoplastic Left Heart Syndrome - Anna Jaworski is an author, publisher and public speaker. Most importantly, Anna Jaworski is the mother of two sons -- one who has a severe, congenital heart defect (CHD) known as "hypoplastic left heart syndrome."Anna has written two books: Hypoplastic Left Heart Syndrome: A Handbook for Parents and My Brother Needs an Operation. She is a contributor to The Heart of a Mother -- an anthology of stories by mothers affected by CHDs. Anna also edited both The Heart of a Mother and The Heart of a Father (the companion book to The Heart of a Mother.) Anna Jaworski has also contributed to two medical textbooks on hypoplastic left heart syndrome and a nursing magazine.Anna Jaworski is not a nurse or a doctor. She is a mother who has made it her goal in life to help other families of children with CHDs. To do so, in addition to producing helpful resources through her publishing company Baby Hearts Press, she has also worked with Sue Dove (another "heart mom") to create two websites: www.babyheartspress.com and www.congenitalheartdefects.com For Your Listening Pleasure all the radio shows available on The 'X' Zone Broadcast Network with our compliments, visit - https://www.spreaker.com/user/xzoneradiotv. Our radio shows archives and programming include: A Different Perspective with Kevin Randle; Alien Cosmic Expo Lecture Series; Alien Worlds Radio Show; America's Soul Doctor with Ken Unger; Back in Control Radio Show with Dr. David Hanscom, MD; Connecting with Coincidence with Dr. Bernard Beitman, MD; Dick Tracy; Dimension X; Exploring Tomorrow Radio Show; Flash Gordon; Imagine More Success Radio Show with Syndee Hendricks and Thomas Hydes; Jet Jungle Radio Show; Journey Into Space; Know the Name with Sharon Lynn Wyeth; Lux Radio Theatre - Classic Old Time Radio; Mission Evolution with Gwilda Wiyaka; Paranormal StakeOut with Larry Lawson; Ray Bradbury - Tales Of The Bizarre; Sci Fi Radio Show; Seek Reality with Roberta Grimes; Space Patrol; Stairway to Heaven with Gwilda Wiyaka; The 'X' Zone Radio Show with Rob McConnell; Two Good To Be True with Justina Marsh and Peter Marsh; and many other! That's The ‘X' Zone Broadcast Network Shows and Archives - https://www.spreaker.com/user/xzoneradiotv

Hypoplastic Left Heart Syndrome - Anna Jaworski is an author, publisher and public speaker. Most importantly, Anna Jaworski is the mother of two sons -- one who has a severe, congenital heart defect (CHD) known as "hypoplastic left heart syndrome."Anna has written two books: Hypoplastic Left Heart Syndrome: A Handbook for Parents and My Brother Needs an Operation. She is a contributor to The Heart of a Mother -- an anthology of stories by mothers affected by CHDs. Anna also edited both The Heart of a Mother and The Heart of a Father (the companion book to The Heart of a Mother.) Anna Jaworski has also contributed to two medical textbooks on hypoplastic left heart syndrome and a nursing magazine.Anna Jaworski is not a nurse or a doctor. She is a mother who has made it her goal in life to help other families of children with CHDs. To do so, in addition to producing helpful resources through her publishing company Baby Hearts Press, she has also worked with Sue Dove (another "heart mom") to create two websites: www.babyheartspress.com and www.congenitalheartdefects.comFor Your Listening Pleasure all the radio shows available on The 'X' Zone Broadcast Network with our compliments, visit - https://www.spreaker.com/user/xzoneradiotv.Our radio shows archives and programming include: A Different Perspective with Kevin Randle; Alien Cosmic Expo Lecture Series; Alien Worlds Radio Show; America's Soul Doctor with Ken Unger; Back in Control Radio Show with Dr. David Hanscom, MD; Connecting with Coincidence with Dr. Bernard Beitman, MD; Dick Tracy; Dimension X; Exploring Tomorrow Radio Show; Flash Gordon; Imagine More Success Radio Show with Syndee Hendricks and Thomas Hydes; Jet Jungle Radio Show; Journey Into Space; Know the Name with Sharon Lynn Wyeth; Lux Radio Theatre - Classic Old Time Radio; Mission Evolution with Gwilda Wiyaka; Paranormal StakeOut with Larry Lawson; Ray Bradbury - Tales Of The Bizarre; Sci Fi Radio Show; Seek Reality with Roberta Grimes; Space Patrol; Stairway to Heaven with Gwilda Wiyaka; The 'X' Zone Radio Show with Rob McConnell; Two Good To Be True with Justina Marsh and Peter Marsh; and many other!That's The ‘X' Zone Broadcast Network Shows and Archives - https://www.spreaker.com/user/xzoneradiotv

Hypoplastic Left Heart Syndrome - Anna Jaworski is an author, publisher and public speaker. Most importantly, Anna Jaworski is the mother of two sons -- one who has a severe, congenital heart defect (CHD) known as "hypoplastic left heart syndrome."Anna has written two books: Hypoplastic Left Heart Syndrome: A Handbook for Parents and My Brother Needs an Operation. She is a contributor to The Heart of a Mother -- an anthology of stories by mothers affected by CHDs. Anna also edited both The Heart of a Mother and The Heart of a Father (the companion book to The Heart of a Mother.) Anna Jaworski has also contributed to two medical textbooks on hypoplastic left heart syndrome and a nursing magazine.Anna Jaworski is not a nurse or a doctor. She is a mother who has made it her goal in life to help other families of children with CHDs. To do so, in addition to producing helpful resources through her publishing company Baby Hearts Press, she has also worked with Sue Dove (another "heart mom") to create two websites: www.babyheartspress.com and www.congenitalheartdefects.com For Your Listening Pleasure all the radio shows available on The 'X' Zone Broadcast Network with our compliments, visit - https://www.spreaker.com/user/xzoneradiotv. Our radio shows archives and programming include: A Different Perspective with Kevin Randle; Alien Cosmic Expo Lecture Series; Alien Worlds Radio Show; America's Soul Doctor with Ken Unger; Back in Control Radio Show with Dr. David Hanscom, MD; Connecting with Coincidence with Dr. Bernard Beitman, MD; Dick Tracy; Dimension X; Exploring Tomorrow Radio Show; Flash Gordon; Imagine More Success Radio Show with Syndee Hendricks and Thomas Hydes; Jet Jungle Radio Show; Journey Into Space; Know the Name with Sharon Lynn Wyeth; Lux Radio Theatre - Classic Old Time Radio; Mission Evolution with Gwilda Wiyaka; Paranormal StakeOut with Larry Lawson; Ray Bradbury - Tales Of The Bizarre; Sci Fi Radio Show; Seek Reality with Roberta Grimes; Space Patrol; Stairway to Heaven with Gwilda Wiyaka; The 'X' Zone Radio Show with Rob McConnell; Two Good To Be True with Justina Marsh and Peter Marsh; and many other! That's The ‘X' Zone Broadcast Network Shows and Archives - https://www.spreaker.com/user/xzoneradiotv

Anti-aging compound improves muscle glucose metabolism in people Washington University School of Medicine in St. Louis, April 26, 2021   A natural compound previously demonstrated to counteract aspects of aging and improve metabolic health in mice has clinically relevant effects in people, according to new research at Washington University School of Medicine in St. Louis. A small clinical trial of postmenopausal women with prediabetes shows that the compound NMN (nicotinamide mononucleotide) improved the ability of insulin to increase glucose uptake in skeletal muscle, which often is abnormal in people with obesity, prediabetes or Type 2 diabetes. NMN also improved expression of genes that are involved in muscle structure and remodeling. However, the treatment did not lower blood glucose or blood pressure, improve blood lipid profile, increase insulin sensitivity in the liver, reduce fat in the liver or decrease circulating markers of inflammation as seen in mice. The study, published online April 22 in the journal Science, is the first randomized clinical trial to look at the metabolic effects of NMN administration in people. Among the women in the study, 13 received 250 mg of NMN orally every day for 10 weeks, and 12 were given an inactive placebo every day over the same period. "Although our study shows a beneficial effect of NMN in skeletal muscle, it is premature to make any clinical recommendations based on the results from our study," said senior investigator Samuel Klein, MD, the William H. Danforth Professor of Medicine and Nutritional Science and director of the Center for Human Nutrition. "Normally, when a treatment improves insulin sensitivity in skeletal muscle, as is observed with weight loss or some diabetes medications, there also are related improvements in other markers of metabolic health, which we did not detect in our study participants." The remarkable beneficial effects of NMN in rodents have led several companies in Japan, China and in the U.S. to market the compound as a dietary supplement or a neutraceutical. The U.S. Food and Drug Administration is not authorized to review dietary supplement products for safety and effectiveness before they are marketed, and many people in the U.S. and around the world now take NMN despite the lack of evidence to show clinical benefits in people. The researchers studied 25 postmenopausal women who had prediabetes, meaning they had higher than normal blood sugar levels, but the levels were not high enough to be diagnosed as having diabetes. Women were enrolled in this trial because mouse studies showed NMN had the greatest effects in female mice. NMN is involved in producing an important compound in all cells, called nicotinamide adenine dinucleotide (NAD). NAD plays a vital role in keeping animals healthy. Levels of NAD decline with age in a broad range of animals, including humans, and the compound has been shown to contribute to a variety of aging-associated problems, including insulin resistance in studies conducted in mice. Supplementing animals with NMN slows and ameliorates age-related decline in the function of many tissues in the body.  Co-investigator Shin-ichiro Imai, MD, PhD, a professor of developmental biology and of medicine who has been studying NMN for almost two decades and first reported on its benefits in mice said, "This is one step toward the development of an anti-aging intervention, though more research is needed to fully understand the cellular mechanisms responsible for the effects observed in skeletal muscle in people." Insulin enhances glucose uptake and storage in muscle, so people who are resistant to insulin are at increased risk for developing Type 2 diabetes. But the researchers caution that more studies are needed to determine whether NMN has beneficial effects in the prevention or management of prediabetes or diabetes in people. Klein and Imai are continuing to evaluate NMN in another trial involving men as well as women.     N-acetylcysteine for depression in adolescents and young adults at risk for bipolar disorder University of Cincinnati, April 23, 2021 According to news reporting originating from Cincinnati, Ohio, by NewsRx correspondents, research stated, “To investigate the mechanism of action of N-acetylcysteine (NAC) in depressive symptoms in young individuals at familial risk for bipolar disorder. We conducted an 8-week open label clinical trial of NAC 2400 mg/days in 15-24 years old depressed offspring of a bipolar I disorder parent, with baseline and endpoint proton magnetic resonance spectroscopy acquired within the left ventrolateral prefrontal cortex (VLPFC).” Our news editors obtained a quote from the research from the University of Cincinnati, “Nine participants were enrolled and finished the study. NAC significantly improved depressive and anxiety symptom scores, and clinical global impression (all p< .001). There was a non-significant reduction in glutamate levels in the left VLPFC. Reduction in depressive symptom scores was positively associated with reduction in glutamate levels in the left VLPFC (p = .007).” According to the news editors, the research concluded: “This pilot study suggests that NAC might be efficacious for depressive symptoms in at-risk youth, and that its mechanism of action involves the modulation of glutamate in the left VLPFC.” This research has been peer-reviewed.     Soda consumption linked to accelerated aging and increased mortality risk University of California at San Francisco, April 26, 2021 A recent study by researcher from the University of California, San Francisco says that drinking soda can increase the risk of all-cause mortality and accelerate aging. The findings build on mounting evidence of the adverse effects drinking soda and other sugary beverages have on the body, which include obesity, Type 2 diabetes, heart disease, kidney disease, non-alcoholic fatty liver disease, dental caries and gout. The team collated data from the National Health and Examination Surveys, an annual program for assessing the health and nutrition of American adults and children. They gathered data from over 5,300 participants between 1999 and 2002, all of whom had no history of diabetes or cardiovascular disease.  In particular, they looked at stored DNA data from the participants – measuring telomere length and comparing it with their consumption of sugar-sweetened soda. The researchers found that those who regularly drank sugar-sweetened soda had shorter telomeres than those who didn’t. Research has shown that telomeres have been previously associated with lifespan. Having shorter telomere length, for instance, has been linked to cardiovascular disease, diabetes and even certain types of cancer. The team reported in their study that consuming even just eight ounces of soda every day can accelerate aging by nearly two years. Meanwhile, 20 ounces of soda can accelerate aging by up to 4.6 years when consumed daily. In fact, drinking sugar-sweetened soda can reduce telomere length at a rate similar to smoking. The UCSF study is also the first to link regular consumption of sugar-sweetened soda to telomere shortening. According to study co-author Elissa Epel, drinking sugar-sweetened soda adds strain to the body by metabolizing these sugars and accelerates cellular aging in tissues. “This finding held regardless of age, race, income and education level. Telomere shortening starts long before disease onset,” Epel added. ” Although we only studied adults here, it is possible that soda consumption is associated with telomere shortening in children, as well.” Sugary sodas linked to rising all-cause deaths In another study, European experts revealed that drinking sugary sodas and other sweetened drinks increases the risk of all-cause deaths. The researchers collected data from more than 450,000 individuals enrolled in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, a large-scale cohort study for biochemical and genetic markers for cancer and other chronic diseases. A follow-up revealed that more than 40,000 participants from the original study had already died. Using their data, the team found a strong link between regular soda consumption and all-cause mortality. Those who regularly drank more than two glasses of sugary drinks increased their risk of dying from circulatory diseases, while those who drank at least one glass of sugary drinks increased their risk of dying from digestive diseases and Parkinson’s disease. “Our results … provide additional support for the possible adverse health effects of sugar-sweetened soft drinks and to replace them with other healthier beverages, preferably water,” explained co-author Neil Murphy. “For artificially-sweetened soft drinks, we now need a better understanding of the mechanisms that may underlie this association and research such as ours will hopefully stimulate these efforts.” The findings appeared in JAMA Internal Medicine.     Curcumin concoction could combat colitis: Study Baylor University, April 25, 2021 A formula that blends curcumin and turmeric oils can prove effective against the activity and inflammatory burden of colitis, a study has determined. Published in Nature Scientific Reports, the study identifies the efficacy of a specific curcumin preparation containing essential turmeric oils (ETO-curcumin) in reducing colitis symptoms. These turmeric oils, aromatic-tumerones (ar-tumerones), alpha-turmerones, beta-turmerones, alpha-santalene and aromatic curcumene, appear to be responsible for an anti-inflammatory and anti-oxidant action, the study suggests. The combination also appeared to exert higher bioactivity than stand-alone curcumin – a feature that could prove valuable in using turmeric for other intestinal conditions. “The therapeutic benefits of turmeric can be attained at its best by combining curcumin with turmerone, an active compound derived from essential oil of turmeric,” said P.J. Kunjachan, chairman and managing director for Arjuna Natural Extracts “This new finding provides our customers an added value for promoting their BCM-95-based formulations in an increasingly crowded curcumin market,” added Dr Benny Antony, joint managing director for Arjuna. BCM-95 often combines curcumin with other turmeric compounds as its poor bioavailability has been cited as a barrier to its use in other disorders. Obstacles are not limited to curcumin's chemical properties. Despite the 17 claims for its anti-inflammatory and digestive health properties, there are currently no approved health claims for curcumin in the EU. These claims are featured on the 2000+ list of on-hold botanical claims yet to be processed by the European Food Safety Authority (EFSA). As well as Arjuna, other manufacturers with an interest in curcumin include herbal manufacturers Sabinsa and Italian botanicals firm Indena. Led by Dr Shusuke Toden, research associate from Baylor University in the US, the trial compared ETO-curcumin preparations  against standard curcumin at three specific doses (0, 5, 25 or 50 milligrams per kilogram (mg/kg)). These doses were administered to an animal model with induced colitis for seven days. The research team found that ETO-curcumin improved disease activity index (DAI) dose-dependently, while the anti-inflammatory efficacy of standard curcumin remained constant. “This suggests that ETO-curcumin may provide superior anti-inflammatory efficacy compared to standard curcumin,” the study explained. “ETO-curcumin associated anti-inflammatory effects were particularly pronounced at higher doses.” Further findings revealed that anti-inflammatory proteins produced included IL-10 and IL-11 as well as FOXP3, which increased in number in the colon by ETO-curcumin.   Study examines association between lifestyle patterns and BMI in early childhood Results support obesity prevention efforts early in life Deakin University (Australia), April 26, 2021   A new Australian study reveals that changes in lifestyle patterns were longitudinally associated with concurrent changes in body mass index (BMI) z scores, and maternal pre-pregnancy BMI, maternal dietary patterns and television viewing time are significant determinants, according to a paper published online in Obesity, The Obesity Society's (TOS) flagship journal. This is the first study that used multi-trajectory modeling to examine the longitudinal relationship between concurrent changes in lifestyle patterns and BMI z scores in early childhood.  "The findings will inform early childhood obesity prevention intervention and policy, and will be of great interest to pediatricians, researchers, policymakers and the general public," said Miaobing Zheng of the Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, in Geelong, Australia. Zheng is the corresponding author of the study.  Experts explain that longitudinal studies investigating the association between lifestyle patterns and obesity in children are scarce. An association between a healthy lifestyle pattern and lower obesity risk has, however, been previously reported in a few cross-sectional studies. In the present study, the co-occurrence of stable healthy lifestyle patterns along with a concurrent normal BMI z score trajectory of one unit from 18 to 60 months in about half of the children provides new longitudinal evidence supporting that children with healthy lifestyles were more likely to concurrently have normal BMI z score development.  Data of 439 children were used from the Melbourne Feeding Activity and Nutrition Trial (InFANT) program. This longitudinal cohort of children commenced in 2008 as a 15-month parent-focused cluster randomized controlled trial aiming to reduce obesity risk behaviors in children until 18 months. Additional follow-ups without interventions occurred for children aged 42 and 60 months. Multi-trajectory modeling identified groups of children following similar lifestyle patterns and BMI z score trajectories and multi-nomial logistic regression assessed the determinants of the trajectory groups.  Three trajectory groups of child lifestyle patterns and BMI z scores were identified and distinguished, showing a mixture of healthy and unhealthy lifestyle behaviors and BMI zscores. Compared to Groups 1 "Unhealthy lifestyle pattern, Low BMI z" and 3 "Unhealthy lifestyle pattern, High BMI z", Group 2 "Healthy lifestyle pattern, Mid BMI z" revealed the most distinctive trajectories across lifestyle patterns and BMI z scores. Group 2 comprised nearly 53 percent of children and followed a stable and low trajectory for an unhealthy lifestyle pattern characterized by energy-dense and nutrient poor discretionary food consumption and television viewing time and a high and rising trajectory for a healthy lifestyle pattern of fruit and vegetable intakes and time outdoors, along with a mean BMI z score of +1 unit over time. Groups 1 and 3 shared similar high trajectories for an unhealthy lifestyle pattern of discretionary food consumption and television viewing time, and low trajectories for a healthy lifestyle pattern of fruit and vegetable intakes and time outdoors. The two groups however differed in BMI z score trajectories, showing stable patterns but at mean scores of 0 and +2 units, respectively. Child sex, breastfeeding duration and maternal physical activity were not associated with the identified trajectory groups. The study's authors note that the co-occurrence of stable lifestyle patterns and BMI z score trajectories in early childhood highlight the importance of initiating lifestyle obesity prevention early in life, and such interventions could target both children and the mother. A multi-behavior approach to simultaneously target healthy diet, physical activity and sedentary behaviors could be adapted. "Young children learn by imitating that which they see daily. There is no doubt that children copy the behaviors observed in the presence of parents: healthy and unhealthy," said Liliana Aguayo, PhD, MPH, a childhood obesity expert, TOS member and research assistant professor from the Hubert Department of Global Health at Emory University in Atlanta, Ga. "Evidence from this study highlights the importance of early childhood as a critical period for development of obesity. More research is needed to identify effective approaches to simultaneously address parent and child health behaviors." Aguayo was not associated with the research.     DDT exposure in grandmothers linked to obesity, earlier periods in granddaughters Young women today may face increased health risks linked to breast cancer due to effects from the banned toxic pesticide lasting over three generations University of California at Davis, April 16, 2021 In the first study to report on the health effects of exposure to a toxic environmental chemical over three human generations, a new study has found that granddaughters whose grandmothers were exposed to the pesticide DDT have higher rates of obesity and earlier first menstrual periods. This may increase the granddaughters' risk for breast cancer as well as high blood pressure, diabetes and other cardiometabolic diseases.  The research by the Public Health Institute's Child Health and Development Studies (CHDS) and the University of California at Davis was published today in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research. It suggests that effects from the pesticide DDT -- despite being banned in the U.S. nearly 50 years ago -- may contribute to the falling age of first periods and increases in obesity rates among young women today. The study found that the risk of obesity in young adult granddaughters was 2 to 3 times greater when their grandmothers (who were not overweight) had higher levels of o,p'-DDT (a contaminant of commercial DDT) in their blood during or just after pregnancy. Granddaughters were twice as likely to have earlier first menstrual periods when their grandmothers had higher o,p'-DDT blood levels. DDT and its related chemicals, including o,p'-DDT, are known to be endocrine disrupting chemicals, compounds that can alter and interfere with natural hormones that are essential for development.  "We already know that it's nearly impossible to avoid exposures to many common environmental chemicals that are endocrine disruptors. Now our study shows for the first time in people that environmental chemicals like DDT may also pose health threats to our grandchildren," said Barbara Cohn, director of CHDS and senior author of the study. "In combination with our on-going studies of DDT effects in the grandmother's and mother's generations, our work suggests we should take precautionary action on the use of other endocrine disrupting chemicals, given their potential to affect generations to come in ways we cannot anticipate today."  The Child Health and Development Studies is a unique project that has followed 20,000 pregnant women and their families for more than 60 years. CHDS enrolled and began following pregnant women in the Bay Area between 1959 and 1967, a time of high pesticide use before DDT was banned in 1972. These "founding grandmothers" in the study gave blood samples at each trimester during pregnancy and one sample shortly after birth. The blood samples were tested for levels of DDT and its related chemicals, including active ingredients, contaminants and their metabolites. The study today focused on o,p'-DDT as it has previously been linked to breast cancer, obesity and other harmful health effects in daughters, and is believed to be the most sensitive biomarker for exposures before and immediately after birth. Since granddaughters' exposure would occur via their mothers' in utero egg cell development, o,p'-DDT levels are a potential predictor of granddaughters' exposure outcomes.  "These data suggest that the disruption of endocrine systems by DDT initiates in immature human eggs, decades before the eggs are fertilized," said Michele La Merrill, associate professor at UCD who was co-lead author of the study. The CHDS study included interviews, home visits and questionnaires from the daughters and granddaughters of the original enrollees. During home visits, blood pressure and height and weight measurements were taken. The study today is based on 365 adult granddaughters who completed questionnaires, participated in a home visit, had available DDT measures from grandmothers' serum, and (for 285 of them) had available information on body mass index (BMI) in all three generations. Information on the age of first period for all three generations was available from 235 granddaughters. Previous CHDS studies have shown that mothers' DDT exposure during pregnancy or immediately after birth correlates with increased daughters' risk of breast cancer and the prevalence of breast cancer risk factors, including obesity, among adult daughters. Other prior studies have linked DDT exposure to birth defects, reduced fertility and an increased risk of diabetes. A commentary in the journal Reproductive Toxicology last year called CHDS "a national treasure that keeps on giving" and noted that "There are no other U.S. studies as well defined, sampled, and followed as the CHDS....The CHDS provides unique and essential value in understanding health effects of environmental exposures as they relate to life-stage sensitivity."       Capsaicin analog could help treatment-resistant lung cancer Small cell lung cancer cells exposed to synthetic analog of chili pepper compound responded better to chemotherapy Marshall University, April 27, 2021 A new study found that non-pungent synthetic analog of capsaicin -- the compound that makes chili peppers hot -- made small cell lung cancer cells more responsive to treatment. Small cell lung cancer is a very aggressive form of cancer with a low survival rate.  Cisplatin-based combination chemotherapy is typically the first-line treatment for small cell lung cancer patients. Although patients initially respond very well to this chemotherapy, the tumor usually comes back within a year in a form that doesn't respond to treatments. Patients with relapsed small cell lung cancer have very few treatment options.  "Irinotecan is the only FDA approved second-line drug for small cell lung cancer, but less than 3% of patients respond to it," said research team leader Piyali Dasgupta, PhD, from Marshall University. "Therefore, agents that improve the anti-cancer activity of irinotecan would be of great value to these patients." Jamie Friedman, a former doctoral student in Dasgupta's lab will present the new findings at the American Society for Investigative Pathology annual meeting during the virtual Experimental Biology (EB) 2021 meeting, to be held April 27-30.  The natural compound capsaicin has been shown to have anti-cancer effects, but its heat can also cause a burning sensation, stomach cramps, gut pain and nausea. In the new work, the researchers studied arvanil, a synthetic capsaicin analog without capsaicin's undesirable side effects.  When the researchers exposed two cisplatin-resistant lung cancer cell lines to a low concentration of arvanil, they saw no growth-inhibitory activity. However, when they treated the cells with varying concentrations of SN38 -- the active ingredient irinotecan -- they observed that the presence of arvanil greatly enhanced the ability of SN38 to slow cancer cell growth. Statistical analysis showed that the interaction between arvanil and SN38 was synergistic in nature.  "Because arvanil enhanced the anti-cancer activity of SN38 in human small cell lung cancer cells, arvanil-based combination therapies may be useful for patients with relapsed small cell lung cancer cells," said Friedman. "We hope that this work will pave the way for novel therapies for relapsed and cisplatin-resistant small cell lung cancer."     Five Therapeutic Properties of Medicinal Mushrooms GreenMedInfo, April 25, 2021   Mushrooms have recently gained popularity in culinary circles, but their far-reaching therapeutic properties should get your attention for a longer and healthier life. Although mushrooms have been part of the healer’s toolbox since ancient times, the medicinal power of mushrooms is gaining momentum in evidence-based journals. Medicinal mushrooms come in a wide variety and shapes such as white button, reishi, maitake, shiitake, oyster, cordyceps, cauliflower, tiger tail and lion’s mane, and most have health benefits that range from fighting cancer and boosting your immunity and memory to preventing diseases like diabetes and arthritis. 1. Anticancer Reishi (in Japanese) or lingzhi (in Chinese) mushrooms are well known in Asia for their anticancer properties. In a meta-analysis by scientists of 23 trials involving 4,246 cancer patients, reishi mushrooms enhanced longevity and quality of life in cancer patients.[i] Therapy with white button mushrooms impacted prostate-specific antigen (PSA) levels and inhibited prostate cancer by decreasing immunosuppressive factors.[ii] Polysaccharides from Cordyceps cicadae mushrooms inhibited the growth of cancer cells and induced cancer cell deaths showing its effectiveness as a low cost and safe treatment for cervical cancer.[iii] A peptide from the shiitake mushroom showed promising results in growth arrest, cell death and cleaning out damaged cells in a breast cancer in vitro study.[iv] In both in vitro and in vivo studies, results showed that mice with induced testicular cancer treated with the Cordyceps sinensis mushroom had significantly smaller and fewer tumors than the control group.[v] Cordyceps cicadae mushroom treatment prevented testicular damage and tumors caused by the chemotherapy drug cisplatin via inhibition of oxidative stress and inflammation in rats.[vi] In a lung cancer-induced study of mice, treatment with reishi mushrooms inhibited cell viability and mobility of lung cancer cells in vitro.[vii] In a cell study of reishi mushroom extract, the treatment offered high antitumor and liver protection with low toxicity on human liver cancer cells.[viii] 2. Immunomodulatory In a meta-analysis of 20 animal disease studies, grifola frondosa, or maitake mushroom, polysaccharide showed strong immune function by enhancing T cells, natural killer cells and macrophages in mice and increasing the secretion of two important immune factors, TNF-α and INF-γ.[ix] In a clinical study of 105 cancer patients undergoing chemotherapy or radiation treatments, a combination of reishi mushroom extract and geraniums improved immunity and fought the cancer and secondary infections that could have compromised treatment and health.[x] In a study of 18 patients diagnosed with low and intermediate myelodysplastic syndrome, which can lead to leukemia if not managed well, maitake mushroom extract treatment of three milligrams (mg) twice a day for 12 weeks increased immunity, positively affecting neutrophil, monocyte and free radical production.[xi] In a clinical study of asymptomatic children from 3 to 5 years old, treatment with beta glucans from reishi mushrooms showed increased immune system cells in the peripheral blood — signaling a strong defense against childhood infections.[xii] Reviewing in vivo and in vitro studies on mice and human cell lines using lion’s mane (Hericium erinaceus) and tiger tail (Trametes versicolor) mushrooms, treatments showed immunomodulatory, anticancer, anti-inflammatory and neuroregenerative effects.[xiii] 3. Antioxidant Polysaccharide beta glucan extracted from reishi mushroom was shown to be a powerful antioxidant in 37 high risk and 34 stable angina patients; those who were treated with 750 mg per day for three months had significantly decreased oxidative radicals and improved progression of atherosclerosis.[xiv] In a study of 42 healthy subjects, another intervention with beta glucan from reishi mushrooms of 225 mg per day for three months demonstrated its antioxidative effects — enhanced total antioxidant capacity and enzyme activities as well as reduced mild fatty liver condition to normal by suppressing oxidative stress were observed.[xv] 4. Anti-inflammatory  Crohn’s disease is a chronic inflammatory disease of the gastrointestinal tract. Treatment with a triterpene compound from reishi mushrooms showed that the inflammatory cytokines were significantly inhibited in a study of children with Crohn’s disease.[xvi] Sixty patients with moderate persistent asthma were studied and those who took the cordyceps sinensis mushroom capsule for two months had reduced airway inflammation caused by their chronic asthma.[xvii] Cordycepin from medicinal mushrooms showed strong effects on many anti-inflammatory diseases.[xviii] In a study of 32 patients with active rheumatoid arthritis, supplementation of medicinal mushroom and Chinese herbs — reishi (4 grams) and San Miao San (2.4 grams) daily — lowered arthritic pain for patients.[xix] The data in a mice study support a model where white button mushrooms regulate immunity in vitro and protect the colon from inflammation-induced injuries in vivo.[xx] The brain is susceptible to inflammation as well. In an Alzheimer’s disease model of rats, treatment with medicinal mushroom extracts delayed disease progression, improved learning and memory functions and stopped neural cell deaths and brain atrophy.[xxi] Chaga mushrooms administered to mice successfully protected against Alzheimer’s disease by modulating oxidative stress, Nrf2 signaling and mitochondrial cell deaths while improving memory and cognition.[xxii] Cordycepin from the Cordyceps sinensis mushroom alleviated Parkinson’s disease motor disorder symptoms by lowering oxidative stress and inflammation in vivo and in vitro.[xxiii] Lion’s mane mushrooms were supplemented for 12 weeks and were effective in preventing dementia and cognitive decline.[xxiv] Lion’s mane supplementation for four weeks in a study of 30 females also reduced depression and anxiety.[xxv] 5. Antidiabetic Dyslipidemia, high blood cholesterol and triglycerides is often a harbinger of future diabetes. In a rat model, white button mushrooms and a probiotic were found to lower dyslipidemia and decrease oxidative stress.[xxvi] In a study of 89 diabetic patients, oyster mushroom consumption significantly reduced blood glucose, blood pressure, triglycerides and cholesterol without ill effects on the liver or kidneys.[xxvii] Polyphenols from Phellinus igniarius, or willow bracket, mushroom extract were used in vitro and in vivo studies of induced Type 2 diabetes mice and showed improved glucose tolerance, reduced hyperglycemia and normalized insulin levels.[xxviii] Diabetic nephropathy, kidney disease caused by Type 2 diabetes, was studied in vitro with disease-induced rats and treatment with Cordyceps cicadae resulted in improved insulin resistance and glucose tolerance, suppressed inflammation and balanced gut microbiome thus stopping the diabetes-related progression of renal disease and tumors.[xxix] In an animal study, maitake mushroom prevented the progression of kidney fibrosis in diabetic nephropathy rats, significantly decreased fasting blood glucose levels, reduced inflammatory cytokines and lowered renal fibrosis indexes indicating its effectiveness in the treatment or prevention of nephropathy.[xxx] In their meta-analysis of 623 articles and 33 randomized controlled experiments using cauliflower mushroom extract (S. Crispa), researchers found statistically significant differences in diabetic symptoms including decreased serum insulin levels and wound rates and an increase in nutrient intake content.[xxxi] Mushrooms and Their Medicinal Powers Medicinal mushrooms are widely researched and used as treatment in the prevention and progression of many diseases from cancer and asthma to diabetes and dementia. Mushrooms protect you due to their anti-inflammatory, antitumor, antidiabetic, immune boosting and antioxidant activities. To learn more, see GreenMedInfo.com’s database on mushrooms.          

How do you observe Black History Month? Thinking of your (or your child's/friend's/relative's) school, was it celebrated at an individual or school-wide level? In a time when so many are unsure of what to do, Capitol Hill Day School (CHDS) has figured out ways for all students and faculty to participate in month-long activities and celebrating, that's woven into the curricula. Meet Leslie Sinsay and Jamayca Williams of CHDS, a place where participating in BHM is not optional, where every teacher and class takes part, where they take BHM seriously, SO SERIOUSLY that planning for it starts in October! Leslie & Jamayca share some of what they do, how and why they do it, and tips to help other educators do the same. We'll also hear what some experts and professors think of BHM, including educators Rebecca Horwitz-Willis and Anri Wheeler and parent Adelle Harris, plus a statement from NAIS VP of Equity and Justice, Caroline Blackwell. from a CHDS parent, and I'll read a statement provided on this topic by the VP of Equity and Justice for the NAIS. Let this episode help you think ways to approach heritage months and other days to recognize. --- Send in a voice message: https://anchor.fm/dailybordercrossings/message

I never thought we'd need to know what CHD stands for. Turns out it stands for Congenital Heart Defect... or a heart defect that is present at birth! Genevieve, our daughter with Down syndrome had a CHD, and did have open heart surgery to correct it. As we went through this process, we found out there was a lot we didn't know about CHDs, and we want to share some of those facts with you! Listen in for a quick fact spotlight on CHD for American Heart Month. Thank you for being part of The Upside Down Family!

Today we have a role reversal with Mark Longbottom being interviewed about his dual roles as CEO of Heart Kids New Zealand as well as founder and host of Purposely Podcast. The interviewer is the impressive Dhivya O'Connor (charity leader and podcaster) who is based in the UK. Show notes “Less about egos and logos and let's think more about mission and (those) whose lives we are trying to help and change... People first, mission always.” Mark has 25 years of nonprofit experience both in the UK and New Zealand, leading fundraising, events, service delivery, community engagement, and commercial functions in well known charities such as The Prince's Trust, MS Society, Terrence Higgins Trust, Auckland City Mission, New Zealand Aids Foundation and the Auckland Foundation. Mark is currently Chief Executive of Heart Kids New Zealand, a charity providing lifelong care and support to children, young people and families impacted by childhood heart defects or CHDs. Previous to that, he was Head of the St. James's Place Charitable Foundation for over a decade. The Foundation is the seventh largest corporate foundation in the UK and is the charitable arm of St. James's Place Wealth Management. Mark is also the Founder of the Purposely Podcast, interviewing inspirational people. Purposely was set up to amplify the stories of founders and leaders of nonprofits, charities, for-purpose businesses, as well as social entrepreneurs. Mark's hope is that Purposely will inspire other people to make a positive and lasting difference to the lives of people living in our communities and those who need the help the most. https://heartkids.org.nz/ https://www.purposelypodcast.com/ Dhivya O'Connor is a charity leader, who has over 20 years' experience across the charity and commercial sectors. Most recently, Dhivya served as CEO of Children with Cancer UK. She is also a Trustee and Chair of the Development Board of the international development organisation, Book Aid International. Dhivya has deep knowledge of the charity sector, with expertise in fundraising and philanthropy. She has also volunteered with NGOs in India, South Africa and Cambodia. A passionate advocate for the work of charities, she launched The Charity CEO Podcast in August 2020, whilst on Maternity break with her second child. www.thecharityceo.com --- Send in a voice message: https://anchor.fm/mark-longbottom2/message

“Less about egos and logos and let's think more about mission and (those) whose lives we are trying to help and change... People first, Mission always.” With 12 babies every week born with Congenital Heart Defects in New Zealand and just one specialist hospital in the entire country that can provide treatment, Heart Kids New Zealand provides a lifeline of vital care and support for children, young people and families affected by these incurable conditions. Mark Longbottom is CEO of Heart Kids New Zealand by day and podcast host of the Purposely Podcast by night. Mark lived in the UK and worked in the UK voluntary sector for nearly 20 years before moving back to his home country of New Zealand in 2019. In this episode we talk about the differences between the charity sectors in New Zealand and the UK, the work of Heart Kids, and of course Jacinda Arden! We share our experiences podcasting and why we think its a good idea for charities to consider launching their own podcasts. Recorded Decemeber 2020.

This month on Episode 17 of the Discover CircRes podcast, host Cindy St. Hilaire highlights four featured articles from the September 25 and October 9 issues of Circulation Research. This episode features an in-depth conversation with Drs David Dichek, Sina Gharib and Tomáš Vaisar regarding their study titled Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture. Article highlights: Cai, et al. Single Cell RNA-Seq in Arteriosclerosis Schuhmann, et al. CD84 in Ischemic Stroke VanOudenhove, et al. Gene Regulatory Dynamics of Developing Human Heart Nie, et al. Periostin is a Target to Treat PH Dr Cindy St. Hilaire: Hi, welcome to Discover CircRes, the podcast of the American Heart Association's journal Circulation Research. I'm your host, Dr Cindy St. Hilaire, from the Vascular Medicine Institute at the University of Pittsburgh, and today I'll be highlighting four articles selected from the late September and early October issues of CircRes. I'll also be interviewing Drs David Dichek, Sina Gharib, and Tomáš Vaisar regarding their study titled Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture. The first article I want to share is titled Single Cell RNA Sequencing of Allograft Cells in Transplant Arteriosclerosis. The first author is Jingjing Cai and the corresponding author is Qingbo Xu from Zhejiang university in Hangzhou, China. Arteriosclerosis is a major contributor to organ transplant failure. The thickening and stiffening of arteries within the grafts results in diminished blood flow supplies and diminished organ function. While it is well understood that atherosclerosis is an inflammatory disease, the details of the cellular and molecular players on this transplant-specific pathology are lacking. Now, Cai and colleagues used single cell RNA sequencing to identify a consensus of cells and cytokines in sclerotic transplanted aortas in mice. Two weeks after transplant, the grafted vessels exhibited signs of arteriosclerosis and by four weeks, this remodeling had worsened significantly. Analyzing the RNA transcripts of over 12,000 individual cells isolated at both two and four weeks, the team discovered that the number of T-cells was greatly increased throughout the process. An early abundance of macrophages gave way to a later wave of B cells and there was also evidence of the development of tertiary lymphoid tissue. They further found that chemokine CCL121 was up regulated after transplant, both the mRNA in the tissues, as well as the protein levels in the animal's blood. The authors then went on to show that blocking CCL121 or its attracting partner, CXC3, significantly delayed arteriosclerosis in the grafted vessel. Hence, this work not only defines the cellular and molecular drivers of arteriosclerosis in grafted vessels, but highlights potential molecular targets for future therapeutic interventions. The second article I want to share is titled CD84 Links T-cell and Platelet Activity in Cerebral Thrombo-inflammation in Acute Stroke. The first author is Michael Schuhmann and the corresponding author is David Stegner, and the work was completed at University of Würzburg in Germany. Ischemic stroke is caused by the occlusion of cerebral blood vessels and it is a leading cause of death and disability worldwide. Despite treatments to degrade or remove clots such as mechanical thrombectomy, infarct size itself can continue to grow even when blood perfusion is re-established. Thrombo-inflammatory processes are thought to mediate this worsening injury, with both T-cells and activated platelets playing a role. Because both T-cells and activated platelets express CD84, which is a self-binding adhesion molecule involved in lymphocyte activation, this team tested the hypothesis that CD84 might mediate stroke inflammatory processes. They went on to show that mice lacking CD84 have smaller infarct sizes with reduced T-cell inflammation after stroke than wild-type animals. Furthermore, mice that specifically lack CD84 in either T-cells or platelets also experienced smaller infarcts. The team went on to show that CD84 promotes T cell migration in vitro. And then in patients with stroke, high expression of CD84 in platelets was associated with poor outcomes. Together, these results suggest that activated CD84-secreting platelets encourage inflammatory T cell migration to the infarct site. And that blocking CD84 activity could be a novel therapeutic strategy for minimizing inflammatory injury after stroke. The third article I want to share is titled Epigenomic and Transcriptomic Dynamics During Human Heart Organogenesis. The first author is Jennifer VanOudenhove and the corresponding author is Justin Cotney. And they're from the University of Connecticut. Congenital heart defects, or CHDs, are common birth abnormalities and while some genes have been linked to congenital heart defects, the majority, close to 60%, have unknown etiologies. It's thought that multiple genetic and environmental factors contribute to congenital heart defects. One of which could be variations in both cis and trans regulatory regions of the genome. To find such heart specific regulatory regions, this team examined heart tissue from human embryos obtained four to eight weeks after conception. They performed chromatin immunoprecipitation experiments to scour the heart genomes for histone modifications associated with increased or decreased gene transcription. They also performed transcriptome analysis to see whether the genomic regions identified by chip corresponded with the activity status of nearby genes. In total, the team found more than 12,000 previously unknown enhancers that were enriched for binding sites for heart specific transcription factors, some of which included GATA, MEF2 and Nkx. These binding sites tended to be close to genes activated in the heart. Many of the regions also contain sequence variations that have been associated with atrial fibrillation. These newly identified sites are potential congenital heart defect candidate loci and the authors have now made their data readily available so that other investigators may study it. The last article I want to share with you before we switch to our interview is titled Periostin: a Potential Therapeutic Target for Pulmonary Hypertension? The first author is Xiaowei Nie from the Shenzhen Third People's Hospital and the corresponding authors are Jingyu Chen and Jin-Song Bian from the Wuxi People's Hospital and the National University of Singapore, respectively. Pulmonary hypertension, or PH for short, is a life-threatening disease where an excess in the proliferation of vascular smooth muscle cells and the deposition of extracellular matrix thickens the walls of the lung vasculature, which leads to an increase in pulmonary blood pressure and ultimately contributes to right heart failure. Vasodilatory medications can be used to treat the symptoms of the disease. However, these medications do not prevent or reverse the underlying pathogenic remodeling. This study now suggests that drugs targeting the secreted extracellular matrix protein, periostin, might be a potential therapeutic strategy for the treatment of pulmonary hypertension. Periostin is an abundant protein in the lung arteries of pulmonary hypertension patients. And it is thought to be involved in cell adhesion and wound healing mechanisms, such as the proliferation and the migration of smooth muscle cells. The team confirmed increased production of periostin in patient lungs, and also found the same to be true for mice with an induced model of pulmonary hypertension. They also showed that genetic deletion of periostin attenuated pulmonary hypertension in mice, while suppression of periostin via RNA inhibition could even reverse pathological vessel thickening and the subsequent right ventricle hypertrophy. The team went on to identify factors HIF-1a and TrkB as factors that mediate periostin's effects in cultured arterial cells. And they suggest that blocking either of these factors or by blocking periostin itself could be a novel strategy for the treatment of pulmonary hypertension patients. Drs Tomáš Vaisar, Sina Gharib, and David Dichek from the University of Washington in Seattle, Washington are here with me today and we're going to discuss their recent study titled Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture. Thank you all so much for joining me today and congratulations on this beautiful and interesting study. So this is an atherosclerotic study, but unlike many in the field, it's really looking at the end stage event called plaque rupture. So for those listeners who are unfamiliar with the term, plaque rupture is when an atherosclerotic plaque degrades and its contents are exposed to the circulation, which can then induce a clotting event and lead to all sorts of adverse pathologies, myocardial infarction, transient ischemic events, stroke. So I'm wondering if we if maybe you can give us a little bit of background about what's known and what really is unknown at least before your study regarding plaque rupture. Dr David Dichek: So the pathogenesis of acute myocardial infarction and stroke was really unknown for many years. And the idea that it was due to acute thrombosis was really confirmed by a study probably 30 years ago, that did angioscopy in the coronary arteries, proximal to a myocardial infarction, and visualized actual clot so that the clot was confirmed to be associated with the acute event. At that point, the question became why would a coronary artery form a clot? And that led to identification of, or histologic studies that identified ruptured caps of atherosclerotic plaques, exposure of the blood to the thrombogenic contents of the lesion, and a thrombus. However, it was not known what the initiating event was in rupture of the plaque cap. And there were a lot of hypotheses and a lot of nice work, but it does still remain an unknown. A significant amount of focus has been devoted to the possibility that proteolysis is the initiating event. And that was sort of the takeoff point from our study because we had developed a mouse model where proteolysis clearly was associated with rupture of plaque caps. And we decided we wanted to get more into the biochemistry of what was going on and go beyond the histology. So that was really what led up to our study. Dr Cindy St. Hilaire: It's really interesting. So, mice are really good and obviously really useful, very well-known model systems to study atherosclerosis and particularly the initial drivers and maybe the mechanisms of the disease pathogenesis, but like many models systems, they're not perfect. So I'm wondering if you could discuss the limitations of murine model systems and specifically for this study, how you were able to overcome some of those limitations. Dr David Dichek: So the limitations of mouse models of plaque rupture are that essentially none of them duplicate the histology of human plaque rupture, particularly the thrombus that occurs on top of the plaque rupture. So there are various mouse models where caps are disrupted, but there's not acute thrombosis. It has been argued in the vascular community as to whether these models are authentic models of plaque rupture, because they don't have the superimposed thrombosis. And the counter argument is well, mice aren't people, they have different hemostatic and coagulation factors that may be differentially regulated. The hemodynamics of small mouse arteries is different from human mouse arteries. And the fact that you don't get a thrombus doesn't necessarily mean that you're not modeling the process that would cause it. So we really accepted that argument as being valid and felt that the occurrence of frank plaque rupture, and that was in our Circulation paper in 2010, in these lesions in the mice, really validated it as an authentic model of cap disruption. And so I agree it's arguable, whether this is an authentic model. But we actually took that issue head on by saying, well, is the biochemistry of the ruptured plaque similar to the biochemistry of a ruptured human plaque? And that if there were similarities that we would gain more confidence in our model being an authentic model of plaque rupture and that it matched not only the histology, but also the biochemistry. Dr Cindy St. Hilaire: One of the main tools you used, you used shotgun proteomics, which I think is just a great name for it. And also a algorithmic learning tool or analysis tool called proteomaps. I was wondering if you could give us a little bit of background about the proteomic aanalysis involved, what does that entail? Especially, when you're comparing a teeny tiny mouse plaque to a larger human plaque and then how that analysis was done? Dr Tomáš Vaisar: So the shotgun proteomics term was coined by John Yates, but way back in the early 1990s. And it's essentially the way how you enumerate the proteins and in more recent forms, you even quantify the abundance of the proteins in a very complex mixture. So shotgun proteomics essentially takes a protein sample. And in this case it was an extract of the tissue and uses protease, trypsin typically, to cut the proteins down to peptides, which are relatively small and relatively well behaved compared to intact proteins. And then using tandem mass spectrometry combined with liquid chromatography separation, basically aims to sequence every single of those peptides or majority of the peptides. And then based from the identification of the sequence of individual peptides piece back together like a jigsaw puzzle, what was the protein present in the original mixture? Dr Cindy St. Hilaire: That's so interesting. I know it's been around for a while. I'm always impressed by it. Dr Tomáš Vaisar: And then the other approach we use it's called Proteomap developed by Ben Cravatt, collaborator on this paper at La Jolla. And that approach uses basically the shotgun approach but as a first step uses gel electrophoresis, SDS PAGE electrophoresis to fractionate the very complex mixture to size segments. Dr Tomáš Vaisar: So you run your complex mixture on a gel, you slice it by size and then run shotgun proteomics experiment on each of those slices after gel digestion. And then Ben developed a set of tools where you identify the proteins and their abundance in each of the bands based on the size and the way it's applied to formation or mapping of proteolytic events is based on the idea of that intact protein will show up at the molecular weight of the intact protein but if it was cleaved by a protease, it will also show up at the molecular weight, which is smaller corresponding to the fragments formed by proteolysis. Then you use set of bioinformatics tools to piece this all together and generate the Proteomaps. Dr Cindy St. Hilaire: You pick it apart, throw it in the machine and then put it back together. That's so cool. It's so amazing. So what were the main findings that you were able to pull out of your comparisons? And I think you had three main groups, if I understood it right? There's the transgenic mouse that has the plaques that don't rupture, and then there's the atherosclerotic mouse that had the transgenic bone marrow, and then you had the human. Can you tell us a little bit about the different groups you compared and then what ultimately you found? Dr David Dichek: Sure. Yes. You are absolutely right. We had what we refer to as the straight transgenic mice that are either transgenic for macrophage overexpressed uPA or not. We also had older mice who had advanced atherosclerosis and receive bone marrow transplants from mice that either had uPA overexpression in bone marrow or not and then we had the human plaque. So those were the three groups. So what we found was that looking at the proteome of those three groups, we were able to find some common biological processes, and this was really Sina's work, but taking the proteomics data and analyzing it with sophisticated bioinformatics tools. We looked not only at the overlap in specific proteins among the models, but the overlap in biological processes, because it may be in different species that there are different proteins, different actors carrying out the same roles. And that's been described in other systems as well. So we were able to identify not only common biological processes, but surprisingly, we were able to identify decreases in specific category of proteins, basement membrane proteins that were common to two of the models, the straight transgenic and the human model and loss of these proteins certainly has a plausible role in precipitating plaque rupture. So I think one aspect of the analysis that's worthy of note is that we initially thought we would observe more profound changes in the bone marrow transplant mice because they had more advanced atherosclerosis. And in fact, we found fewer changes than in the straight transgenic mice, but thinking about it after letting the data talk to us, rather than trying to impose our own on the data- Dr Cindy St. Hilaire: Always a good idea. Dr David Dichek: ... was that the straight transgenic mice were telling us we've been overexpressing urokinase for 20 weeks since we were conceived, and the bone marrow transplant mice had it for only eight weeks. And indeed they had far less loss of basement membrane proteins and far fewer changes in their plaques than the mice that had expressed it for a longer time. And so when one placed the three groups in a chronology of exposure to protease activity with the bone marrow transplant mice, being the shortest exposure than the straight transgenic mice, and then the humans who've had decades of exposure, it really tells you a nice chronological story about the biological processes leading to plaque rupture. And I think that's a generally applicable lesson and can be applied to other problems in cardiovascular biology. And that is when you have a biological process for which you can't get human tissue until after it's occurred because you can't go in and biopsy. Dr Cindy St. Hilaire: I have that problem with valve calcifications that you can't take your valve out early. Dr David Dichek: If you can get a mouse model that duplicates the pathology, then you have access to the steps leading up to the event. And that's what we tried to construct in this study. And really it was really Sina’s analyses that allowed us to make those connections. Dr Sina Gharib: Yeah. Of course, David was kind of the mastermind behind the design of the experiments on the developing of genetic models and Tomáš is a renowned expert in proteomics analysis. And I kind of joined more on the bioinformatics component of this study, tried to put some of the large data that was being generated together. And as David and Tomáš mentioned, of course atherosclerosis is a very complex disease with many, many components. And then of course the mouse model doesn't quite capture all the different pathophysiological events that happen. So one of the aims of this study was to try to integrate and merge the findings from these model without coming a priori with a bias or a pathway or a candidate gene, we decided to do a relatively unbiased shotgun proteomics approach, we actually do for everything. So the challenge then was how to put it all together. And as Tomáš mentioned, there are statistical tools to try to identify a relative abundance of proteins. But, a few things that pure biologists often don't have to encounter is, you're not one or two different proteins, you're looking at thousands of proteins. So there are issues, statistical issues, such as multiple comparisons. If you looked for changes, you're going to find changes just by random chance. So a lot of statistical adjustments had to be made to ensure that those were adjusted for. This are also pathways and processes that were coming out of these results. There's many different pathways that were interrogated. And again, statistically, you want to adjust for the fact that many of those could have been there by random chance. So there's a fair amount of statistical methods that need to be applied for this data. We also did somewhat more sophisticated pathway analysis where we develop networks based on the differential expressed proteins between the ruptured and unruptured plaques to identify connection among these proteins and identify hubs which are highly connected nodes that could potentially drive the biology of a network. So other types of kind of deeper statistical analysis was done, which are maybe more hypothesis-generating because we actually did not follow up on some of these candidates, but I think they really do provide a map or framework to then pursue more mechanistic experiments to see what happens if we knocked out this highly connected node at the plaque rupture site to see if we can either stabilize or manipulate the biology as plaque rupture. Dr Cindy St. Hilaire: Yeah. I mean, that's really the strength of these unbiased approaches is you can come up with so many more novel targets and pathways that might be contributing. So they're just really great. So one thing I found really interesting, you mentioned that you saw a clear distinction in the proteome and I think it was specifically talking about the human samples because they were large enough to see ruptured area versus non ruptured area, but you really saw a distinct difference in the proteomes of the ruptured area of the plaque versus the non ruptured area of the plaque. And obviously the models you were using are overexpressing a protease. So of course there's a role for proteolysis in this process, which you've now firmly established, but I'm wondering if there are other processes that might also erode the basement membrane. And did you pull up anything that might suggest of other things that are happening or even are there other hypothesis out there that we could test with an approach like yours? Dr David Dichek: I think the pathways that came up have probably all been implicated previously. We have processes like inflammation and complement activation, immune response, thrombosis. That's a post-hoc event. I think what was most unexpected was the decrease in the abundance to basement membrane proteins rather than collagens. So collagen has become the sort of signature protein of stable and unstable plaques and used as a surrogate, people do Picrosirius red staining. It's easy to detect with a histochemical stain, you don't even need an antibody. And surprisingly, we found very few differences in collagens and actually no differences in the type 1 or type 3 collagen, which are thought to be the primary stabilizers of the plaque cap. They weren't significantly different in between ruptured and stable areas of the same plaque. So that was certainly a big surprise. Dr Cindy St. Hilaire: Yeah. Because that would indicate that it's not necessary... We always say thinning of the cap, which obviously we know that there's remodeling, it can get thinner. But you kind of found that the contents were the same, but it's the basement really that was eroded. Dr David Dichek: Yeah. The basement membrane proteins were lost. It used to be said in physiology that if you discovered something new, you should just go to the German literature and go back 30 years and it had already been described. And so, looking back in the literature, there are actually the work of Jean-Baptiste Michelle in France and a scientist in Finland, Petri Kovanen, have actually focused on the potential role of basement membrane in unstable atherosclerosis many years ago, but it was kind of buried in the collagen hypothesis. And I think it needs resurrection. Dr Cindy St. Hilaire: Well, I think this paper has done that so well done there. That's great. Dr Tomáš Vaisar: Would be worthwhile to know that of course, the way you prepare the samples may affect what exactly you're seeing. But we've done very careful characterization of the sample preparation of the extraction procedure to focus, to enrich the exosomal matrix proteins because of this collagen hypothesis. And even with that, we basically saw no difference. Dr David Dichek: Yeah. I think that's an excellent point. If we hadn't found collagen in our extracts, we would not be able to conclude a lot about it. And how you do the extraction, how you process the samples here can really influence what you find. We call it unbiased, but there are technical biases that enter, especially in sample preparation, but our extraction process really was able to extract collagens as well as elastin, which is really infamous for being a- Dr Cindy St. Hilaire: Difficult. Dr David Dichek: ... I really think we were getting a good sampling of the matrix here. Dr Cindy St. Hilaire: I don’t know iif there is an answer for this question, but it's something I'm always thinking about. We always talk about athero being so prevalent because there's no kind of evolutionarily the way to tamp it down, it happens later in life. But can you think of any advantage that the vasculature would have in eroding the basement membrane or altering proteases in a response? I was just trying to think, is this just harnessing a wound healing process that's gone awry or could this ever be protective at all in any way? Dr David Dichek: Well, I think you hit the nail on the head, at least according to my bias. It's a healing response gone awry and that you can really draw out the pathways, basement membrane digestion release of chemotactic peptides as part of the inflammatory response, attraction of more inflammatory cells and then a potential healing response that unfortunately results in digestion of the matrix, which has a morbid or fatal consequence rather than physiologic remodeling. And you're right, that's not selected against. It's selected for, in settings in earlier life infections, for example, perhaps neoplasia, but it's not selected against in late life because people are post reproductive. Dr Cindy St. Hilaire: So what's next for these studies? What questions are you going to attack next with either these models or with some of your proteomic findings? Dr David Dichek: Well, we were just talking about that recently, Tomáš and I, and I think we'd like to look at... For one study, we're interested in doing, plaques that are high risk based on MRI imaging, which is really very well developed here at the University of Washington. And many of those patients have endarterectomies and they don't have ruptured plaques. So they are in a high risk group. So they undergo a endarterectomy for that. Not because they've had a plaque rupture and those plaques might be particularly instructive because they're pre event and won't have the healing response to thrombotic response. And it would be really interesting to see if our studies were confirmed. So that's one direction we're going in. Dr Cindy St. Hilaire: That would be amazing. Luckily, you have access to a whole bunch of human tissue for those kinds of really high impact studies. Dr Sina Gharib: I just wanted to point out that one of the advantages of doing proteomics and being part of the scientific community is that we made all this data available in the manuscript for other researchers to access and confirm. So, really probably the best way to procced with this is to have other investigators replicate our findings and expand on it. So I just want to bring that up because all of that data that was generated has been included within the supplements of this manuscripts and it's accessible to any scientist who wants to pursue further. Dr David Dichek: Yeah, I would add one other direction we'd like to go is we still like to know what the substrates are. We think their disappearance based on their abundance is due to proteolysis. But boy, would it be exciting if we could detect fragments. We were unable to do that in the study, probably because they were lost either in vivo or in processing. Technical advancements in that area, and maybe Tomáš can speak to that, might enable us to actually find more direct evidence of proteolysis. Dr Tomáš Vaisar: Yeah, I mean, to start with, it's really hard to determine physiological substrates of proteases. There's a huge amount of literature identifying proteolytic substrates in vitro, but the physiological substrates are really extremely hard to determine, and especially physiologic in vivo confirming that because in vitro, in a tube, you can mix whatever you want and you modify the ratio of proteins to protease substrate, and you can cleave almost everything with anything. It's a little exaggeration, but it's close. While the physiology substrates in the really complex milia of tissues is extremely hard. And so there has been several approaches developed and one of them is the Proteomaps. The other one is an approach called TAILS developed by Chris Overall at UBC that uses the idea of formation of the neo termini and then tagging the neo termini. So that in the actual sample, you can specifically detect these neo termini formed. But even with that approach, it's really hard to determine what are actual physiological substrates. And on top of that, what are the cleavage sites of the proteases? Dr Cindy St. Hilaire: And I guess the third being, if those substrates are cleaved, are they circulating and can we detect them in a blood sample? That would be, I guess, the gold standard. Well, thank you all so much for joining me today. Congratulations on this really very cool study. Being into human and translational work, I always love mouse studies that bring in lots of human samples. So congratulations on that. And I look forward to your future publications on this. Dr Tomáš Vaisar: Thanks a lot. Dr David Dichek: Thanks. Dr Cindy St. Hilaire: That's it for the highlights from the late September and early October issues of Circulation Research. Thank you so much for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and #DiscoverCircRes. Thank you to our guests, Drs David Dichek, Sina Gharib, and Tomáš Vaisar. This podcast is produced by Rebecca McTavish and Ishara Ratnayake, edited by Melissa Stoner and supported by the editorial team of Circulation Research. Some of the copy texts for the highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire. And this is Discover CircRes, your on-the-go source for the most up-to-date and exciting discoveries in basic cardiovascular research.

What was it like to be born in 1965 with a severe congenital heart defect in Venezuela? What kind of care was available there? What was a parent to do?Tune in to this week's episode of "Heart to Heart with Anna" to hear Belen Blanton talk with Anna about her heart journey, how she made it to the USA, and why she has started a nonprofit organization to help children with congenital heart defects in her native country - Venezuela.Here is the foundation Belen has started for children with CHDs in Venezuela on Facebook:@Fundacion Estrellita de Belenand on the Internet: www.fundacionestrellitadebelen.orgFind Belen on Instagram:@youdonthavetolooksickLinks to 'Heart to Heart with Anna' Social Media and Podcast Pages:Apple Podcasts (https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2)Facebook (https://www.facebook.com/HearttoHeartwithAnna/)YouTube (https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5Zw)Instagram (https://www.instagram.com/hugpodcastnetwork/)If you enjoy this program and would like to be a Patron, please check out our Patreon page (https://www.patreon.com/HeartToHeart)Support the show (https://www.patreon.com/HearttoHeart)

Do you know how many children are born every single year around the world with the most common birth defect? What percentage of children born with this condition actually live in a country where appropriate care is available? What are non-government organizations (NGOs) doing to bridge the gap between in care for these most vulnerable people?Tune in to this episode of "Heart to Heart with Anna" to meet Bistra Zheleva - an advocate for children born in low-resource countries who need live-saving surgeries for their congenital heart defects. Bistra has a wealth of information about what CHDs look like worldwide, what problems people in countries like Malaysia, Brazil, China, Vietnam, and India face on a daily basis, what organizations have come together to assist people worldwide, and how even a common person with no medical training can still be part of a world-wise voice for the CHD community.Non-government organizations (NGOs) and 501(c)(3)s mentioned in this episode:Children's HeartLink – follow, join our mailing list, donatewww.childrensheartlink.orgFacebook https://www.facebook.com/childrensheartlink/Twitter @CHeartlinkYouTube https://www.youtube.com/user/CHeartLinkInstagram https://www.instagram.com/childrensheartlink/Global ARCH – follow, join our mailing list, donatehttp://www.global-arch.org/https://www.facebook.com/GlobalARCH18/Twitter @GlobalARCH18Novick Cardiac Foundation: https://cardiac-alliance.org/Newborn Foundation: http://www.newbornfoundation.org/Links to our Social Media and Podcast Pages:Apple Podcasts (https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2)Facebook (https://www.facebook.com/HearttoHeartwithAnna/)YouTube (https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5Zw)Links to our Social Media and Podcast Pages:Apple Podcasts (https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2)Facebook (https://www.facebook.com/HearttoHeartwithAnna/)YouTube (https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5Zw)Instagram (https://www.instagram.com/hugpodcastnetwork/)If you enjoy this program and would like to be a Patron, please check out our Patreon page (https://www.patreon.com/HeartToHeart)Support the show (https://www.patreon.com/HearttoHeart)

Ten years ago, Chelsea King discovered that the twins she carried had a potentially deadly secret. The months that followed were full of doctor's appointments, a move to another city, bed rest, and concern. Tune in to hear Chelsea King talk with Host Anna Jaworski about what it was like for her to go from diagnosis through surgeries, and into 2020. Since Chelsea's twin was born with two major congenital defects (tetralogy of Fallot and Duane's Syndrome), she has had many medical procedures and she understands the importance of support. In this episode, she talks with Anna about where she found support, how she's giving support today, and the support she believes she still needs to find.Pages and Episodes mentioned in this program:CongenitalHeartDefects.com Camp Information PageSiblings in the CHD Community -- "Heart to Heart with Anna" featuring Don Meyer and SibShopsSibShops informationPlease visit our Social Media and Podcast pages:Apple PodcastsFacebookYouTubeInstagramIf you enjoy this program and would like to be a Patron, please check out our Patreon page Support the show (https://www.patreon.com/HearttoHeart)Support the show (https://www.patreon.com/HearttoHeart)Support the show (https://www.patreon.com/HearttoHeart)

Mr. Glen Woodbury, Center for Homeland Defense and Security (Episode #1) In this episode of “Listen, Learn, Lead,” President Rondeau meets with Glen Woodbury, Director of NPS' Center for Homeland Defense and Security (CHDS). As the nation's first advanced graduate education program in the field, CHDS has created a cadre of more than 3,000 local, state and federal leaders who think critically about homeland security.

According to Corience: An Independent European Platform on Congenital Heart Defects, "As many as 40–60% of children with congenital heart defects are undernourished." https://www.facebook.com/HearttoHeartwithAnna/Healthy babies double their weight in 6 months; however, children with congenital heart defects put on weight more slowly. Their growth is also affected by the heart defect.Why do children with congenital heart disease not grow as other children do? The answer is because the heart defect makes them need more energy. Their diagnosis might also complicate feeding for several different reasons. Heart failure makes them too tired to feed. Some of them might have trouble keeping down their feeds. Others seem to have difficulty in coordinating breathing and nursing.This episode will investigate what kinds of equipment might be needed to help a babe with a congenital heart defect if that baby cannot nurse or feed normally. Listen as one mother shares her experience with her baby -- who needed a feeding tube. We'll also talk with a clinical psychologist who specializes in early infancy and childhood as well as eating disorders and tube feeding. She works for the NoTube Limited Liability Corporation, which was founded to help children all over the world to overcome the severe condition of tube dependency. Discover how one mother and a company over six thousand miles apart helped one little boy wean successfully from his feeding tube without ever leaving home! The show originally aired on 7/8/14. Please keep in mind that prices quoted may be quite different now!Links mentioned in our show:http://www.corience.org/living-with-a-heart-defect/parents/heart-childrens-health/feeding-problems/ (Corience: An Independent European platform on congenital heart defects: For patients, parents, doctors, and scientists)www.notube.com (NoTube) To write to someone at NoTube, use this email: support@notube.comPlease take a moment to follow us on your preferred social media platforms:iTunes: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/YouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwInstagram: https://www.instagram.com/hugpodcastnetwork/If you enjoy this program and would like to be a Patron, please check out our Patreon page: https://www.patreon.com/HeartToHeartSupport the show (https://www.patreon.com/HearttoHeart)

In this Chaitime, we talk to Dr. Kanwaljeet Anand about the upcoming concert Heart to Heart: Healing thru Music on July 20 7:00 pm - 10:00 pm at the Cemex Auditorium, Graduate Business School, 655 Knight Way, Stanford. More information about the program can be found here: https://arts.stanford.edu/event/84299/ It is a free concert with Jazz and Carnatic Fusion, and it is being organized for raising awareness of Congenital Heart Disease (CHD) and the work done by the H2H Foundation. H2H Foundation (https://www.h2h.foundation/) is a non-profit organization that is dedicated to saving the lives of children born with congenital heart defects (CHDS) by providing free pediatric cardiac surgeries. Dr Anand is a professor of pediatrics(Pediatric critical care) and anesthesiology, perioperative and pain medicine at the Stanford University Medical Center.

Premiering August 6, 2019, Silent Cries: Breaking Through CHD Awareness is Phillip Wolf's latest documentary. With over forty types of CHDs, Silent Cries: Breaking Through CHD Awareness is produced to focus on children and adults born with heart defects and how they have inspired other families and individuals to never give up and continue their fight. There is hope, and advancements in technology are evolving rapidly, yet a cure seems elusive. Many CHDs (congenital heart defects) go undetected until later in adult life.Join Anna today as she interviews the creator and producers of Silent Cries. Phillip Wolf was inspired to create this documentary due to the death of his son, Jeremiah, from his congenital heart defect. Executive Producer/Producer Nicole Vickery was born with a congenital heart, as was Co-Producer David Franco. They share with Anna why they became involved with this project and why it's important for everyone to watch this documentary.Silent Cries: Breaking Through CHD Awareness will be available on Amazon Prime Video. For more information, check out Phillip Wolf's website: http://www.pwfilms.net/Please take a moment to follow us on your preferred social media platforms:iTunes: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/YouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwInstagram: https://www.instagram.com/hugpodcastnetwork/If you enjoy this program and would like to be a Patron, please check out our Patreon page: https://www.patreon.com/HeartToHeartSupport the show (https://www.patreon.com/HearttoHeart)

  In this NPS-CHDS Viewpoints, CHDS alumni Dr. Michael Larranaga and Dr. John Comiskey discuss the results of their examination of the potential threats that climate change could have on the nation’s homeland security... The post The Effects of Climate Change on Homeland Security appeared first on CHDS/Ed.

Dr. Ami Bhatt is the featured Guest on this episode of Heart to Heart with Anna. Dr. Ami Bhatt is an active clinical cardiologist, clinical investigator, and educator. She has developed a robust multidisciplinary curriculum at Mass General to provide requisite ACHD education to cardiovascular fellows. Dr. Bhatt is dedicated to patient advocacy groups including the AHA and Adult Congenital Heart Association and empowering individuals with CHD to lead full and productive lives.In this episode, Anna talks with Dr. Bhatt about becoming an adult congenital cardiologist specializing in the care of adults with CHDs, why she developed a telemedicine program for her patients and where she believes the future of medicine is headed. You won't want to miss this show which discusses an up-and-coming trend to prevent Heart Warriors from being lost to follow-up care.Support the show (https://www.patreon.com/HearttoHeart)

Aubrey Byrnes is a rare mom - she's the mother of Wyatt Nathan Arthur Byrnes, aged 5, and Colton Paul Byrnes, aged 4. Wyatt was born 13 weeks premature and had a rough medical journey. Colton, AKA Superman without a Cape, was born with VACTERL Association, a disorder that affects many body systems. VACTERL stands for vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula, renal anomalies, and limb abnormalities. As part of his condition, Colton has multiple CHDs including truncus arteriosus, ventricular septal defect, atrial septal defect, pulmonary stenosis, and right aortic arch. During his short life Colton has had 52 procedures, including 6 heart catheterizations and 4 open-heart surgeries. Aubrey is married to Rick and together they have a unique, rare outlook on life which has helped them stay together. Aubrey studied American Sign Language Interpreting at Augustana University and works as a freelance interpreter/translator.Support the show (https://www.patreon.com/HearttoHeart)

Anita Moreno Marcelo, as the mother of a son with a congenital heart defect (CHD), penned a poem that touched many lives in the CHD community. In this episode of "Heart to Heart with Anna" she talks about why she wrote the poem entitled "The Presence of Greatness," what it meant to her and why she feels it's important for us to talk about how adults with CHDs are treated in medical settings and what we, as a community, can do to improve our Heart Warriors' medical experiences.Support the show (https://www.patreon.com/HearttoHeart)

Boys born with critical congenital heart defects are frequently not able to participate in sports like their heart-healthy peers. Because of the multiple surgeries needed, the frequent need for pacemakers or the concern about arrhythmias and the other complications that can accompany critical congenital heart defects, survivors of these defects frequently have to avoid contact sports or sports that are intensely aerobic in nature. How does this affect sons' relationships with their fathers? How can they still enjoy sports together despite medical restrictions? This show will feature the father of a young son as well as a father/son pair who have experience with this topic.Support the show (https://www.patreon.com/HearttoHeart)

The birth of a child is one of life's greatest experiences; the emotional and lasting impact has consequences that will last a lifetime and beyond. When that birth becomes compromised with a life-threatening birth defect, your world is immediately forced into a tailspin of unimaginable emotions. This is a story of two lives on two different paths that would come together with a shared goal and vision of helping countless families not just survive, but thrive in some of the most challenging circumstances. They met under the most unusual circumstances while attending a National Congenital Heart Defects fundraising event in the fall of 2015, a meeting that would change their world forever. The first path, Leslee and Jason Schneider, their daughter Lexi was born with a rare heart condition; Hypoplastic left heart syndrome. Without surgery soon after birth, the condition would be fatal. They were given three options: abort the baby, let it develop within its natural life span or take surgical measures to address the defect. They chose to fight for the survival of their daughter. It would be a journey of hope, persistence and faith that would test them like never before. The other path, Brittany and Brady Griffith had just minutes as they rushed into the operating room to hold their newborn son Liam. He was born with Transposition of the Great Arteries (TGA), Double Outlet Right Ventricle (DORV), Ventricular septal defect (VSD) and Pulmonary Stenosis. 21 hours old after enduring open heart surgery, Liam's life was cut short. Brittany explains the driving principle of Romans 5:3-5 changed everything for her. "We rejoice in our sufferings, because we know that suffering produces perseverance; perseverance, character; and character, hope. And hope does not disappoint us, because God has poured out his love into our hearts by the Holy Spirit, whom he has given us." Their story continues on the Brink of Greatness Podcast… The Next Leap Forward Life has a way of connecting like-minded people with a common goal. As you will discover, the work that Leslee and Brittany and their families are doing is remarkable. They have turned their tragedy into their life’s purpose. The Lexiam Heart Foundation was founded in February 2018, to encourage and help other families affected by Congenital Heart Defects (CHDs). Their goal is to comfort and provide support to children and their families that have been impacted by CHDs. DONATE TO LEXIAM HERE TO MAKE AN IMPACT For Further Insight: Website: http://lexiamheartfoundation.org/ Follow on Twitter: https://twitter.com/lexiamheart

Congenital Heart Defect (or CHD) Awareness is an extremely important issue. Congenital heart defects (heart defects present at birth) are the #1 Birth Defect. While a commonly reported statistic is 1 in 100 babies are born with a heart defect, that statistic does NOT include the most common CHD – bicuspid aortic valve. In fact, that statistic does NOT include a number of CHDs. That means that more than 1 baby in 100 is born with a CHD. Congenital heart defects also kill more babies than any other birth defect. In the United States, there are 40,000 babies born every year with a CHD. There will be one million babies born worldwide with a CHD and 100,000 of them will not live to see their 1st birthday. While these numbers are staggering, there are still many people who are unaware of the fact that babies can be born with CHDs. We must raise awareness to stress the importance of funding research to prevent future generations of children from dying and suffering from this birth defect.Support the show (https://www.patreon.com/HearttoHeart)

With more children with complex, congenital heart defects, or CHDs, living beyond their first year of life than ever before, parents and the professionals working with those children need to know what normal development is for this group of survivors. What kind of behaviors are normal or common? Is it to be expected that the majority of these children will be labeled “Failure to Thrive”? Is it common for children with major heart defects to need feeding tubes? How does the use of feeding tubes affect speech and language development? What can parents and the professionals working with them do to help these smallest survivors have a good quality of life? Who should be part of children’s care team? When should parents seek outside help? These questions and more are answered in today’s episode: What is Normal Child Development for Children with Complex Congenital Heart Defects?Support the show (https://www.patreon.com/HearttoHeart)