Podcasts about pathobiology

This special live episode of the FemTech Focus was recorded at the Johns Hopkins Bloomberg School of Public Health as part of a women's health innovation event.This panel explores what it actually takes to build in women's health—from identifying unmet clinical needs to navigating customer discovery, commercialization, regulation, fundraising, and equity in femtech innovation.The discussion features four innovators building next-generation solutions across pelvic health, menstrual health, fetal surgery, and digital maternal health.Moderator: Dr. Rosemary Morgan - Associate Professor, Department of International Health Johns Hopkins Bloomberg School of Public HealthDr. Morgan's work focuses on understanding how gender inequities shape health systems, healthcare access, and public health interventions globally. Her research spans sexual and reproductive health, gender analysis, and equity-centered global health systems research.

Description: "When joint pain is present, the diagnosis of psoriatic arthritis needs to be made as soon as possible, ideally within six months to limit joint inflammation" Dr. Vinod Chandran mentions as he discusses efforts to identify a diagnostic test for those at risk of developing psoriatic arthritis.          Join host Jeff Brown as he speaks with leading rheumatologist and clinician scientist Dr. Vinod Chandran, Director of the Gladman Krembil Psoriatic Arthritis Program, Schroeder Arthritis Institute, University Health Network and the Departments of Medicine, Laboratory Medicine and Pathobiology, and the Institute of Medical Science at the University of Toronto to learn more about the progress and promising results towards developing a psoriatic arthritis diagnostic test through multi-omic assays and identifying the distinct differences between psoriasis and psoriatic arthritis.  This episode provides an update on the progress to date of the NPF PsA Diagnostic Test grant initiative which has shown promising results with a potential test entering prospective study in multiple sites soon.   Thank you to Johnson and Johnson for their support of this program activity. Timestamps: (0:00)          Intro to Psoriasis Uncovered & guest welcome rheumatologist Dr. Vinod Chandran.    (0:52)          It is challenging to diagnose psoriatic arthritis with many factors leading to a delay in diagnosis. (4:56)          The start of Dr. Chandran's involvement with the PsA Diagnostic Test Grant project.   (7:55)          The different types of omics and the definition of multi-omic. (9:57)          How the multi-omic approach is used to find biomarkers relative to a specific disease pattern. (11:08)        Development of a predictive or prevention-based test using gene expression.      (13:46)        First year results identify 200 markers across different omic approaches that distinguish psoriatic arthritis from psoriasis.    (14:58)        The significance of MRNA vs mIcroRNA's use in development of a diagnostic test and how critical that is to dissemination of a                     potential test. (17:08)        Identifying the skin-joint axis in relation to different types of arthritis. (20:20)        Next steps to moving the diagnostic test research forward as a prospective study in multiple sites and the cost effectiveness of                  delivering the test.   (23:13)        If you have psoriasis, musculoskeletal, back, and joint pain think of psoriatic arthritis and be diagnosed early to maintain a good                 quality of life. Key Takeaways: ·       Given challenges associated with diagnosing psoriatic arthritis and the impact on quality of life, in 2019 NPF launched the PsA Diagnostic Test Grant project with the goal of developing an early stage test that would identify and diagnose those with psoriatic arthritis before debilitating  joint damage begins.   ·       Progress towards a PsA Diagnostic Test includes the study of multi-omic data sets where 200 distinct biomarkers have been identified leading to a greater understanding of the different pathways between psoriatic arthritis, psoriasis, and the skin joint axis.  ·       A potential diagnostic test is now moving towards the prospective study phase. Until the test is available and if joint pain is present and you have psoriasis, ask your health care provider if it could be psoriatic arthritis and treat appropriately.  Guest Bio: Vinod Chandran, MBBS, MD, DM, PhD is a rheumatologist, clinician scientist, and Director of the Gladman Krembil Psoriatic Arthritis Program, Schroeder Arthritis Institute, University Health Network and the Departments of Medicine, Laboratory Medicine and Pathobiology, and the Institute of Medical Science at the University of Toronto where he is also a Professor of Medicine. His specialties include internal medicine, immunology, rheumatology, and genetic epidemiology. His research focus is on the development of biomarker-based strategies to improve early diagnosis and prognosis of psoriasis and psoriatic arthritis, identification of new treatment targets especially for those who do not respond to current therapies, and strategies to reduce the impact of disease. Dr. Chandran is a Co-Vice President of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis or GRAPPA. He is an active collaborator in a multi-center research consortia such as the International Psoriasis and Arthritis Research Team and the Spondyloarthritis Research Consortium of Canada. Dr. Chandran is the recipient of research funding from the National Psoriasis Foundation for his work in identifying a "Multi-omic Diagnostic Test for PsA in Psoriasis Patients". Resources: "Understanding the NPF Psoriatic Arthritis Diagnostic Test Grant Outcomes" Advance Online. February 18, 2026.  "Managing Chronic Pain with Psoriatic Arthritis" Psoriasis Uncovered podcast episode with physiatrist Dr. Erin Maslowski, LB Herbert who lives with psoriatic disease, and moderator Susan McClelland-Tobert, a retired pediatric cardiologist who also lives with psoriatic disease. Glossary of terms: mRNA: Messenger RNA carries protein information or instructions from the DNA in a cell's nucleus to the cell's interior where the sequence is read and translated into corresponding amino acids for growing protein chains. Micro-RNA (miRNA):  Micro-RNA act as the regulator. They are short and bind to specific target mRNA's to degrade or inhibit production of protein. 

Dr. Adrien Zap was raised in Connecticut. She new from an early age that she wanted to be a veterinarian. She earned her BS in Pathobiology and Veterinary Sciences at the University of Connecticut, a MS in Forensic Toxicology at the University of Florida, and her DVM from St. George's University.After graduation, she entered small animal practice. She has had varied roles in her career; serving as a Zoo Veterinarian, Teaching in a Veterinary Technology Program, as a Veterinarian Responder for both the State of Connecticut and the ASPCA, as a Surgeon and Medical Director in a Spay/Neuter practice, and in Racetrack regulatory work.She became interested in holistic medicine through exposure at veterinary conferences and during a health challenge with her own dog. She is certified in acupuncture, Chinese Herbal Medicine, Rehabilitation, Veterinary Medical Manipulation, and Tui Na. In 2019, she started her own integrative mobile practice serving small, large, and exotic animals.Please enjoy this conversation with Dr. Adrien Zap as we discuss her education, work history, holistic experience, and her successful completion of the AAVA Advanced Certification examination.

In this educational podcast discussion, Carlos M. De Castro, MD, and David Dingli, MD, PhD, FRCP, FRCPEd, FACP, FRCPath, explore paroxysmal nocturnal hemoglobinuria (PNH). They trace the evolution of treatment from early complement inhibitors to today's expanding therapeutic options, emphasizing how these advances have transformed patient outcomes and quality of life. The conversation blends clinical insights with practical considerations for therapy selection and patient care, including:The pathogenesis of PNH and the role of complement activationLandmark therapies such as eculizumab and ravulizumabAdvances in proximal inhibitors (eg, pegcetacoplan, iptacopan, danicopan)Quality-of-life considerations, treatment personalization, and emerging therapiesPresenters:Carlos M. De Castro, MDProfessor of Medicine, DUMCDivision of Malignant Hematology and Cellular TherapyDepartment of MedicineDuke UniversityDuke Cancer InstituteDurham, North CarolinaDavid Dingli, MD, PhD, FRCP, FRCPEd, FACP, FRCPathConsultant Hematologist and Director of Bone Marrow Transplant ProgramProfessor of MedicineDivision of HematologyMayo Clinic College of Medicine and ScienceRochester, MinnesotaLink to full program:https://bit.ly/3Jtjqgr Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

In this podcast, we talk with Dr. Sarah Keating. As an anatomic pathologist for more than 35 years, Sarah worked on staff at a number of hospitals in Ontario as well as at Ontario Forensic Pathology Services. She is recently retired but is passionate about learning as much as possible about tick borne diseases in order to help improve the access to care for suffering patients. She maintains her affiliation with the University of Toronto as an Associate Professor Emeritus in the Department of Laboratory Medicine and Pathobiology. Sarah has been a member of the CanLyme board since 2022 and she is also an active member of ILADS – the International Lyme and Associated Diseases Society.Read morewww.lookingatlyme.cacanlyme.com/sarah-keating/

In this episode of The Poultry Nutrition Blackbelt Podcast, Dr. Taina Lopes, a postdoctoral fellow at Auburn University, explores how nutrition may influence immune responses to Newcastle disease in poultry. She breaks down the impact of viral shedding, immunization challenges, and the role of nutrients like vitamin D and zinc in immune support. Learn how immunity and nutrition intersect in poultry health. Listen now on all major platforms!"Nutritional needs of the immune system differ from those for production and growth in poultry."Meet the guest: Dr. Taina Lopes holds a Ph.D. and M.Sc. in Animal Science from the Federal University of Minas Gerais in Brazil, with a veterinary degree focused on avian pathology and poultry production. Now a postdoctoral fellow in the Department of Pathobiology at Auburn University, her research centers on immune response modulation, viral shedding, and bioinformatics in poultry.Liked this one? Don't stop now — Here's what we think you'll love!What you'll learn:(00:00) Highlight(01:07) Introduction(02:17) Newcastle disease basics(06:15) Immunity gaps(08:42) Future vaccine on immunization(10:27) Immune system nutrition(14:02) Microminerals and immunity(16:59) Closing thoughtsThe Poultry Nutrition Blackbelt Podcast is trusted and supported by innovative companies like:* Kerry* Kemin- BASF- Poultry Science Association- Anitox

Today's guest is Dr. Abby Armwood, an Assistant Professor in the Department of Population Health and Pathobiology at North Carolina State University, College of Veterinary Medicine. Dr. Armwood sat down with us at the 2024 ACVP/ASVCP Annual Meeting in Seattle, WA, to tell us more about the ACVP Student Engagement Committee (SEC) and their commitment to creating fun and educational events. Hear more about Patheletes, kicking off at the 2025 Annual Meeting in New Orleans, LA, and the veterinary student mentoring program. Dr. Armwood also discusses the Pathology Training Committee and its role in enhancing the quality of pathology training programs. And, we hear about her journey in pathology–from an interest in becoming an aquatic veterinarian to expertise in all things aquatic pathology! Grab a snack and join us for a conversation with Dr. Abby Armwood.     If you want to connect with the ACVP SEC, you can find them:  Facebook - ACVP Veterinary Student Engagement Committee ___ More Information on: 2025 ACVP Annual Meeting in NOLA Maintenance of Certification More Information on the ACVP Training Program Accreditation AQUAVET(R) - Cornell University College of Veterinary Medicine ACVP Errors in Publications Portal ___ ACVP Social Media Facebook - ACVP Meetings and Topics Instagram - americancollegevetpath X (Twitter) - @ACVP LinkedIn - AMERICAN COLLEGE OF VETERINARY PATHOLOGISTS  ____ Thank you to Dr. Andrea Kerr, of the MCC Podcast Subcommittee, for editing this episode. Music: Guestlist by Podington Bear, licensed under an Attribution-NonCommercial 3.0 International License.  The contents of this audio do not necessarily reflect the opinions of the American College of Veterinary Pathologists (ACVP) or the participants' affiliations. Spoken audio content and associated photos are the property of the American College of Veterinary Pathologists, 2025. 

This year marks the 50th season of Saturday night live, so today the guys go over their favourite SNL moments from the past half decade (2:37). The guys review their top hosts, top monologues, Top Weekend update anchors, top weekend update correspondents and top 5 SNL skits EVER.    Then the guys discuss how West Nile Virus has been in the news as of late because of Dr. Anthony Fauci's recent battle with this disease (33:44).  Ali asks Asif about what exactly it is and how common it is. Asif goes over the life cycle of the virus and how both birds and mosquitos are involved in transmission. Asif then talks about the symptoms, the limited options for treatment and the prognosis.    The opinions expressed are those of the hosts, and do not reflect those of any other organizations. This podcast and website represents the opinions of the hosts. The content here should not be taken as medical advice. The content here is for entertainment and informational purposes only, and because each person is so unique, please consult your healthcare professional for any medical questions.   Music courtesy of Wataboi and 8er41 from Pixabay   Contact us at doctorvcomedian@gmail.com   Follow us on Social media: Twitter: @doctorvcomedian Instagram: doctorvcomedian   Show Notes: Anthony Fauci: A Mosquito in My Backyard Made Me the Sickest I've Ever Been: https://www.nytimes.com/2024/10/07/opinion/fauci-west-nile-virus.html Anthony Fauci: West Nile virus caught from mosquito ‘nearly took me down': https://www.theguardian.com/us-news/2024/oct/08/anthony-fauci-west-nile-virus West Nile Virus: An Update on Pathobiology, Epidemiology, Diagnostics, Control and “One Health” Implications: https://pmc.ncbi.nlm.nih.gov/articles/PMC7400489/ Transmission of West Nile Virus: https://www.cdc.gov/west-nile-virus/php/transmission/index.html

Remembrance Day: Canada honours veterans' ‘legacy of courage' GUEST: Craig Thomson - President, BC Yukon Command, Royal Canadian Legion Coding for Veterans, a military-focused organization, is celebrating its 5th anniversary. Coding for Veterans will open trading at the TSX on Monday to mark Remembrance Day. Coding for Veterans retrains Canadian military veterans for a second career in cybersecurity.   In that time more than 800 veterans have enrolled in the program.  GUEST: Jeff Musson - Coding for Veterans Executive Director Bird flu: What we know about Canada's 1st human case detected in B.C. GUEST: Allison McGeer - infectious disease specialist in the Sinai Health System, and a professor in the Department of Laboratory Medicine and Pathobiology at the University of Toronto Learn more about your ad choices. Visit megaphone.fm/adchoices

Explore the critical role of specific blood tests in managing PCOS, focusing on fasting insulin, estradiol, DHEA-S, hs-CRP, and leptin. This episode dives deep into how these tests can guide treatments and lifestyle changes for better health outcomes. 5 KEY TAKEAWAYS  1. Fasting Insulin as a Foundation: Understanding insulin's role in PCOS is crucial, as it affects multiple bodily functions and is often elevated in affected individuals.  2. Importance of Estradiol Levels: Monitoring estradiol is essential for managing PCOS, as it influences ovarian function and overall hormonal balance.  3. Role of DHEA-S: Elevated levels can indicate adrenal involvement in PCOS, influencing the body's androgen levels and contributing to symptoms.  4. Significance of hs-CRP: This inflammatory marker can highlight underlying inflammation associated with PCOS and its impact on cardiovascular health.  5. Monitoring Leptin: Addresses leptin resistance often seen in PCOS, impacting appetite regulation and metabolic functions. FEATURED PRODUCT Liver Boost and Berberine are essential in managing PCOS due to their role in supporting liver health and regulating insulin levels. By enhancing liver function and insulin sensitivity, these supplements can mitigate some of the systemic effects of PCOS, aligning with the insights discussed about the importance of managing insulin and inflammation in PCOS. visit www.mswnutition.com for more info TIMESTAMPS  • 00:00 START  • 00:01:00 Introduction to PCOS and importance of proactive lab testing.  • 00:05:00 Detailed discussion on fasting insulin's role in PCOS.  • 00:10:00 The critical impact of estradiol and its management.  • 00:15:00 Exploring DHEA-S and its implications in adrenal health.  • 00:20:00 Understanding hs-CRP and its link to inflammation.  • 00:25:00 Leptin's role in appetite and weight regulation in PCOS.  • 00:30:00 Summary and key actionable advice on managing PCOS through targeted bloodwork. RESOURCES   1. Title: Insulin Resistance and the Polycystic Ovary Syndrome: Mechanism and Implications for Pathogenesis URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277302/  2. Title: Recent Insights into the Pathophysiology of Polycystic Ovarian Syndrome: A Narrative Review URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9832677/  3. Title: Androgen Excess in Women: Experience with Over 1000 Consecutive Patients URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9705998/  4. Title: The Role of Insulin Resistance in the Polycystic Ovary Syndrome URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676075/  5. Title: Estrogen Signaling in the Pathobiology of Ovarian Cancer URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6830311/  6. Title: Estrogen and Cardiovascular Disease: Is Timing Everything? URL: https://pubmed.ncbi.nlm.nih.gov/29224098/  7. Title: C-Reactive Protein: A Predictive Factor and Marker of Inflammation in Inflammatory Diseases URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6647201/

He has his Ph.D. and is an Associate Professor of Viral Immunology in the Department of Pathobiology, University of Guelph. He went viral in the middle of Covid for discovering the vax crossed the blood brain barrier and since has had his life turned upside down. He will be in Alberta June 17th for the An Injection of Truth town hall. Let me know what you think. Text me 587-217-8500 Substack:https://open.substack.com/pub/shaunnewmanpodcast E-transfer here: shaunnewmanpodcast@gmail.com Website: https://silvergoldbull.ca/ Email: SNP@silvergoldbull.com Text: (587) 441-9100 – and be sure to let them know you're an SNP listener. Ticket for Dr. James Lindsay “Parental Rights Tour”: https://brushfire.com/anv

My friend Hannah Russell (married mother of three, PhD, lives in Cincinnati, active Latter-day Saint) joins us to share her story of being asexual out of a desire to help others not feel alone. Hannah starts realizing she is different and falsely concluding “I am not a divine child of Heavenly Parents” because I don't have any sexual interest. Hannah talks about how being asexual is a real thing and there isn't some backstory “confusing” Hannah to falsely make this conclusion. Hannah talks about learning more about herself at BYU and dating. Hannah is very brave—and without shame—in sharing her feelings about not wanting to be sexually intimate. Hannah talks about getting on with her life (after a broken off engagement) and getting her PhD in Pathobiology and Molecular Medicine. Hannah talks about meeting her husband John and opening up to him about being asexual and how they navigated that road together and decided to get married and start a family. Hannah talks about how their marriage—a beautiful love story—is based on communication and consent. I learned so much from Hannah story about how to better understand and support my asexual friends, and principles to create a stronger marriage and family. Thank you, Hannah, for your courage to share your story so others don't feel alone and all are welcome and needed as we create Zion. You are awesome! Links: Hannah's Facebook: https://www.facebook.com/hannah.russell.1428 Facebook Group to Better Support LGBTQ Latter-Day Saints: https://www.facebook.com/groups/1433556613672143

On April 25, 2024, we met with the 5 speakers for this year's Annual Neuroscience Symposium at UTSA to discuss epigenetics and nervous system development. We discussed the best known molecular mechanisms that control patterns of gene expression and current limitations faced in studies of those mechanisms. We also discussed the promise of epigenetics to explain the differentiation of nervous system cell types, mechanisms of developmental, neuropsychiatric and neurodegenerative disorders. Guests: Melanie Carless, Associate Professor, Department of Neuroscience, Developmental and Regenerative Biology, UTSA Christine Ladd-Acosta, Associate Professor, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health Paulino Ramirez, Postdoctoral Fellow, Department of Cell Systems and Anatomy, UT Health San Antonio Alexey Soshnev, Assistant Professor, Department of Neuroscience, Developmental and Regenerative Biology, UTSA Hehuang "David" Xie, Associate Professor, Department of Biomedical Sciences and Pathobiology, Virginia Tech Host: Charles Wilson, Department of Neuroscience, Developmental and Regenerative Biology, UTSA Thanks to Jim Tepper for original music

Welcome to our podcast episode on diagnostic, prognostic and predictive biomarkers for the treatment of upper GI cancers. In this episode, Dr Brezden-Masley (medical oncologist) and Dr Streutker (pathologist) discuss the latest biomarkers that may inform treatment of upper GI cancer. Our Guests:Dr. Christine Brezden-MasleyDr.  Brezden-Masley is a Medical Oncologist and the Director of the Marvelle Koffler Breast Centre at Mount Sinai Hospital as well as the Medical Director of Cancer Program for Sinai Health System in Toronto, Canada. Dr. Catherine StreutkerDr.  Streutker is a Professor in the Department of Laboratory Medicine & Pathobiology at the University of Toronto.This podcast episode was sponsored by Merck Canada.If you enjoy our podcast, please review and subscribe. For more podcasts and other medical education content, visit our website at: https://www.impactmedicom.com 

Ashley Kalinauskas is the Founder and CEO of Torigen Pharmaceuticals ( https://www.torigen.com/ ), a company dedicated to researching and developing novel immuno-oncology products and services specifically for the veterinary market, with a focus on autologous cancer vaccines. Torigen Pharmaceuticals is a start‑up that resulted from Ashley's graduate thesis project at the University of Notre Dame, as she was working on her Masters in Engineering, Science and Technology Entrepreneurship in collaboration with Dr. Mark Suckow ( https://www.research.uky.edu/staff/mark-suckow ). Ashley also received an undergraduate degree in Veterinary Pathology and Pathobiology from University of Connecticut. Support the show

Dr. Amy Durham, Professor and Assistant Dean at the University of Pennsylvania, joins Dr. Andy Roark on the Cone of Shame podcast to discuss PennVet's new active learning and learner centered curriculum. Together they dive into the driving factors behind this decision and what it's meant to students, faculty and the veterinary industry. LINKS PennVet Article on Curriculum: https://www.vet.upenn.edu/about/news-room/bellwether/bellwether-magazine/bellwether-spring-2023/educating-a-21st-century-veterinarian AAHA Article on Curriculum: Penn Vet transitions from discipline-based to fully integrated curriculum (aaha.org) Today's Veterinary Business Article: https://todaysveterinarybusiness.com/penn-vet-curriculum-121823/?oly_enc_id=5467B7086134E1Y Competency-Based Veterinary Education: https://www.aavmc.org/programs/cbve/ Uncharted Veterinary Conference: https://unchartedvet.com/uvc-april-2024/ Uncharted on the Road: https://unchartedvet.com/on-the-road/ Charming the Angry Client Course: https://drandyroark.com/charming-the-angry-client/ Dr. Andy Roark Swag: https://drandyroark.com/store/ ABOUT OUR GUEST Dr. Amy Durham is a Professor of Anatomic Pathology and Assistant Dean for Education at the University of Pennsylvania School of Veterinary Medicine. She went to Penn for vet school (class of 2005), did a residency in anatomic pathology at Penn, and then have stayed as a faculty member in the Department of Pathobiology. She became the assistant Dean for Education a couple of years ago, and is currently completing an MSEd in medical education.

Mutations in the LRRK2 gene were first linked to Parkinson's disease (PD) risk in 2004. Since then, researchers from around the world have advanced our understanding of the mechanisms through which LRRK2 may contribute to PD, leading to the development of three potential LRRK2-targeted therapies that are now being evaluated in clinical trials. Along with colleagues and collaborators, Dr. Dario Alessi has pioneered new research and approaches that have aided in the development of drugs to inhibit LRRK2 and potentially treat people with Parkinson's disease. In this episode Dario discusses his work developing the LRRK2 kinase assay, LRRK2 Ser935 dephosphorylation assay, and Rab phosphorylation assay, as well as future directions and opportunities in the field. This year, Dario received the 2023 Robert A. Pritzker Prize for Leadership in Parkinson's Research for his substantial research contribution and his commitment to mentoring the next generation of Parkinson's scientists. Dario is the Professor of Signal Transduction and Science Director of the Medical Research Council Protein Phosphorylation and Ubiquitylation Unit at the University of Dundee.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

Mutations in the LRRK2 gene were first linked to Parkinson's disease (PD) risk in 2004. Since then, researchers from around the world have advanced our understanding of the mechanisms through which LRRK2 may contribute to PD, leading to the development of three potential LRRK2-targeted therapies that are now being evaluated in clinical trials. Along with colleagues and collaborators, Dr. Dario Alessi has pioneered new research and approaches that have aided in the development of drugs to inhibit LRRK2 and potentially treat people with Parkinson's disease. In this episode Dario discusses his work developing the LRRK2 kinase assay, LRRK2 Ser935 dephosphorylation assay, and Rab phosphorylation assay, as well as future directions and opportunities in the field. This year, Dario received the 2023 Robert A. Pritzker Prize for Leadership in Parkinson's Research for his substantial research contribution and his commitment to mentoring the next generation of Parkinson's scientists. Dario is the Professor of Signal Transduction and Science Director of the Medical Research Council Protein Phosphorylation and Ubiquitylation Unit at the University of Dundee.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

12 more charges laid against Ontario man accused of aiding suicides Guest: Dr. Tyler Hickey, Assistant Professor, Department of Laboratory Medicine & Pathobiology, University of Toronto and forensic pathologist, Ontario Forensic Pathology Service Poor mental health, violence among threats to children in Canada  Guest: Sara Austin, founder and CEO of Children First Canada BC confirms first Canadian case of new COVID-19 Omicron variant  Guest: Dr. Horacio Bach, a researcher at the Immunity and Infection Research Centre and a clinical assistant professor in the Faculty of Medicine, Division of Infectious Diseases at the University of British Columbia Can the Conservatives translate a surge in the polls to electoral success?  Guest: Ken Boessenkool, founding partner, Meredith Boessenkool Policy Advisors Soccer Canada is a mess ahead of the 2026 World Cup Guest: Alan McDougall, Professor of History, University of Guelph, author of "Contested Fields: A Global History of Modern Football" Wagner chief Yevgeny Prigozhin buried at a St. Petersburg cemetery Guest: Anders Aslund, economist, former economic advisor to Russia, later Ukraine, author of Russia's Crony Capitalism: The Path from Market Economy to Kleptocracy How scientists recreated a famous Pink Floyd song from brain waves Guest: Ludovic Bellier, a computational research scientist at UC Berkeley

In this latest episode of ASTCT Talks, Dr. Tania Jain engages in a conversation with Dr. Richard Jones, the BMT director and co-director of the Hematologic Malignancies Programs at Johns Hopkins University. He shares his journey in the field of oncology and transplantation, reflecting on the life events and experiences that led him to this path. He delves into the groundbreaking development of post-transplant cyclophosphamide (PTCy) and its significant impact on transplant procedures. Gain insights into the behind-the-scenes efforts and the role PTCy has played in expanding donor options and improving graft-versus-host disease prophylaxis. The episode also highlights Dr. Jones' dedication to mentoring and his commitment to family, emphasizing the importance of work-life balance in this profession. About Dr. Rick Jones Richard J. Jones, M.D. is Professor of Oncology, Medicine, and Pathobiology, Associate Director of the Sidney Kimmel Cancer Center for Faculty and Program Development, as well as Director of the Bone Marrow Transplantation (BMT) and co-Director of the Hematologic Malignancies Programs at Johns Hopkins University. His major area of research interest is normal and malignant stem cell biology, especially the translation of promising findings from the laboratory to the clinic to improve the treatment of malignant and non-malignant blood disorders. Examples of his research accomplishments have been the development of the stem cell marker Aldefluor and high-dose cyclophosphamide for auto- and alloimmunity. The latter has led to the ability to safely perform partially mismatched BMT, allowing now everyone in need access to BMT. He has authored over 300 articles and book chapters on hematopoiesis, hematologic malignancies, and transplantation biology. Dr. Jones is a past Stohlman Memorial Scholar of the Leukemia and Lymphoma Society. About Dr. Tania Jain, MBBS Dr. Jain, MBBS, (@TaniaJain11) is a physician scientist in the hematological malignancies and stem cell transplantation division with Sidney Kimmel Comprehensive Cancer Center at the Johns Hopkins. Her academic focus is cellular therapy and transplantation in the treatment of high-risk hematological malignancies especially myeloproliferative neoplasms. Her primary research focus is to develop strategies to improve outcomes and prevent relapse of hematological malignancies following allogeneic stem cell transplantation. She also serves as the Director of the Immune Effector Cell (IEC) Therapy at Johns Hopkins, where they are currently expanding their CAR T program to help patients with advanced hematological malignancies. Her academic interest in this space lies in developing novel IEC strategies and studying aspects of toxicity of CAR T cell therapy with an aim to improve long term outcomes in these patients.

Dr. Jeffrey Bryan earned his D.V.M. from the University of California - Davis in 1993. He worked as an Associate Veterinarian from 1993-1995 and served as Medical Director from 1995-2002 of the Irving Street Veterinary Hospital in San Francisco, CA. Bryan then completed a medical oncology residency, a Masters of Biomedical Sciences, and a PhD in Pathobiology at the University of Missouri. He received certification by the American College of Veterinary Internal Medicine in Oncology 2005. He is the Director of the Tom and Betty Scott Endowed Program in Veterinary Oncology, the Director of PET Imaging Center of the University of Missouri, Associate Department Chair for Research, and the Associate Director of Comparative Oncology for Ellis Fischel Cancer Center. Dr. Bryan's research focuses on comparative examination of cancers in companion animals to better understand cancers in all species. His particular areas of interest are targeted imaging and therapy, epigenetics, and immunotherapy of cancers. He directs the PET Imaging Center, which seeks to develop novel PET imaging agents for cancer diagnosis, localization, and prognostication. He studies DNA methylation of canine non-Hodgkin lymphoma. He studies immunotherapy in companion dogs including investigating fetal microchimerism. --- What We Do at MIB Agents: PROGRAMS: End-of-Life MISSIONS Gamer Agents Agent Writers Prayer Agents Healing Hearts - Bereaved Parent and Sibling Support Ambassador Agents - Peer Support Warrior Mail Young Adult Survivorship Support Group EDUCATION for physicians, researchers and families: OsteoBites, weekly webinar & podcast with thought leaders and innovators in Osteosarcoma MIB Book: Osteosarcoma: From our Families to Yours RESEARCH: Annual MIB FACTOR Research Conference Funding multiple $100,000 and $50,000 grants annually for OS research MIB Testing & Research Directory The Osteosarcoma Project partner with Broad Institute of MIT and Harvard ... Kids are still dying with 40+ year old treatments. Help us MakeItBetter. https://www.mibagents.org​ Help support MIB Agents, Donate here https://give-usa.keela.co/embed/YAipuSaWxHPJP7RCJ SUBSCRIBE for all the Osteosarcoma Intel

Welcome to our podcast episode on external quality assurance (or eQA) for testing biomarkers in oncology, hosted by Anna Christofides. In this episode,  we discuss with Dr. Emina Torlakovic, the use of eQA to aid in the improvement of biomarker testing in Canada . Our Guest: Dr. Emina Torlakovic is a Professor in Department of Laboratory Medicine and Pathobiology at the University of Toronto. She is also a Staff Hematopathologist and Director of Biomarker Development and Quality Assurance at the University Health Network. Dr. Torlakovic is also a founding member of NordiQC, Canadian Immunohistochemistry Quality Control (CIQC), as well as the International Society for Immunohistochemistry and Molecular Morphology. She is Chair of the Canadian Association of Pathologists' National Standards Committee for High Complexity Testing and also co-directs CIQC. This podcast episode was sponsored by Merck, Canada.If you enjoy our podcast, please review and subscribe. For more podcasts and other medical education content, visit our website at: https://www.impactmedicom.com.

From working with electron microscopes to pioneering a career in fertility treatments, this scientist has led an interesting journey. But the biggest challenge still awaits: will the patients he serves be able to bring home a baby at the end of it all? With a world of unknowns ahead, it will take careful control, talented embryologists and a little luck to make it happen. But will it be enough? In this episode of Meet the Mentor with Dr. Bill Dorfman, you will be able to: Discover the critical effects of age and genetics on fertility treatment outcomes. Uncover the latest breakthroughs in assisted reproductive technology and embryo assessment. Comprehend the crucial role of education and training for embryologists in the IVF process. Learn how savvy financial planning can make IVF more accessible and budget-friendly. Grasp the benefits of enhancing patient experience by minimizing stress and discomfort during IVF. Get ready to be inspired by Dr. David Hill, a leading expert in fertility treatments with nearly four decades of experience. With a doctoral degree in Pathobiology from the University of Connecticut, Dr. Hill has dedicated his career to helping countless couples achieve their dream of parenthood. As the Scientific Director for various top-rated reproductive centers in California, he has contributed immensely to the advancements in assisted reproductive technology. Dr. Hill's expertise in the impact of age and genetics on fertility treatment success has made him a sought-after speaker and mentor in the field. Join us as we learn from Dr. Hill's extensive knowledge and fascinating insights into the world of fertility. The resources mentioned in this episode are: Look into the Leap program for high school and college students aged 15-25 to learn entrepreneurship and life skills. Explore assisted reproductive technology options, such as in vitro fertilization, for those struggling with fertility. Consider freezing eggs in the mid-30s if not ready for parenthood but want to preserve future fertility potential. Research pre-implantation genetic evaluation and testing for embryos to screen for potential hereditary disorders before pregnancy. Stay informed on advancements in the reproductive medicine field and how they may impact future fertility treatments and optioms Reasons Behind Infertility According to experts, the trend of starting families later in life may contribute to the increase in infertility problems, along with the prevalence of heritable disorders. As societal norms have shifted, more individuals and couples are waiting to have children until they achieve certain career or financial milestones. Delaying family planning can place couples at a higher risk of experiencing fertility challenges. Additionally, heritable genetic disorders can cause further barriers to conception and healthy pregnancies, making it essential for medical professionals to develop specialized solutions to address these issues. In his interview with Dr. Bill Dorfman, Dr. David Hill confirms that age is a significant factor when it comes to fertility. Dr. Hill also highlights the importance of advancements in assisted reproductive technology in helping a broader range of patients. For individuals who might have genetic markers or pre-existing health conditions impacting their pregnancy outcomes, their options for successful fertility treatments have significantly improved. Learn more about your ad choices. Visit megaphone.fm/adchoices

This month on Episode 47 of Discover CircRes, host Cynthia St. Hilaire highlights three original research articles featured in the March 31 issue of Circulation Research. We'll also provide an overview of the Compendium on Increased Risk of Cardiovascular Complications in Chronic Kidney Disease published in the April 14 issue. Finally, this episode features an interview with Dr Elizabeth Tarling and Dr Bethan Clifford from UCLA regarding their study, RNF130 Regulates LDLR Availability and Plasma LDL Cholesterol Levels.   Article highlights:   Shi, et al. LncRNAs Regulate SMC Phenotypic Transition   Chen, et al. Bilirubin Stabilizes Atherosclerotic Plaque   Subramaniam, et al. Mapping Non-Obvious cAMP Nanodomains by Proteomics   Compendium on Increased Risk of Cardiovascular Complications in Chronic Kidney Disease   Cindy St. Hilaire:              Hi, and 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 share three articles selected from our March 31st issue of Circulation Research and give you a quick summary of our April 14th Compendium. I'm also excited to speak with Dr Elizabeth Tarling and Dr Bethan Clifford from UCLA regarding their study, RNF130 Regulates LDLR Availability and Plasma LDL Cholesterol Levels.   So first the highlights. The first article we're going to discuss is Discovery of Transacting Long Noncoding RNAs that Regulates Smooth Muscle Cell Phenotype. This article's coming from Stanford University and the laboratory of Dr Thomas Quertermous. Smooth muscle cells are the major cell type contributing to atherosclerotic plaques. And in plaque pathogenesis, the cells can undergo a phenotypic transition whereby a contractile smooth muscle cell can trans differentiate into other cell types found within the plaque, such as macrophage-like cells, osteoblast-like cells and fibroblast-like cells. These transitions are regulated by a network of genetic and epigenetic mechanisms, and these mechanisms govern the risk of disease.   The involvement of long non-coding RNAs, or Lnc RNAs as they're called, has been increasingly identified in cardiovascular disease. However, smooth muscle cell Lnc RNAs have not been comprehensively characterized and the regulatory role in the smooth muscle cell state transition is not thoroughly understood. To address this gap, Shi and colleagues created a discovery pipeline and applied it to deeply strand-specific RNA sequencing from human coronary artery smooth muscle cells that were stressed with different disease related stimuli. Subsequently, the functional relevancy of a few novel Lnc RNAs was verified in vitro.   From this pipeline, they identified over 4,500 known and over 13,000 unknown or previously unknown Lnc RNAs in human coronary artery smooth muscle cells. The genomic location of these long noncoding RNAs was enriched near coronary artery disease related transcription factor and genetic loci. They were also found to be gene regulators of smooth muscle cell identity. Two novel Lnc RNAs, ZEB-interacting suppressor or ZIPPOR and TNS1-antisense or TNS1-AS2, were identified by the screen, and this group discovered that the coronary artery disease gene, ZEB2, which is a transcription factor in the TGF beta signaling pathway, is a target for these Lnc RNAs. These data suggest a critical role for long noncoding RNAs in smooth muscle cell phenotypic transition and in human atherosclerotic disease.   Cindy St. Hilaire:              The second article I want to share is titled Destabilization of Atherosclerotic Plaque by Bilirubin Deficiency. This article is coming from the Heart Research Institute and the corresponding author is Roland Stocker. The rupture of atherosclerotic plaque contributes significantly to cardiovascular disease. Plasma concentrations of bilirubin, a byproduct of heme catabolism, is inversely associated with risk of cardiovascular disease, but the link between bilirubin and atherosclerosis is unknown.   Chen et el addressed this gap by crossing a bilirubin knockout mice to a atherosclerosis prone APOe knockout mouse. Chen et el addressed this gap by crossing the bilirubin knockout mouse to the atherosclerosis-prone APOE knockout mouse, and used the tandem stenosis model of plaque instability to address this question. Compared with their litter mate controls, bilirubin-APOE double knockouts showed signs of increased systemic oxidative stress, endothelial dysfunction, as well as hyperlipidemia. And they had higher atherosclerotic plaque burden.   Hemeatabolism was increased in unstable plaques compared with stable plaques in both of these groups as well as in human coronary arteries. In mice, the bilirubin deletion selectively destabilized unstable plaques and this was characterized by positive arterial remodeling and increased cap thinning, intra plaque hemorrhage, infiltration of neutrophils and MPO activity. Subsequent proteomics analysis confirmed bilirubin deletion enhanced extracellular matrix degradation, recruitment and activation of neutrophils and associated oxidative stress in the unstable plaque. Thus, bilirubin deficiency generates a pro atherogenic phenotype and selectively enhances neutrophil-mediated inflammation and destabilization of unstable plaques, thereby providing a link between bilirubin and cardiovascular disease risk.   Cindy St. Hilaire:              The third article I want to share is titled Integrated Proteomics Unveils Regulation of Cardiac Monocyte Hypertrophic Growth by a Nuclear Cyclic AMP Nano Domain under the Control of PDE3A. This study is coming from the University of Oxford in the lab of Manuela Zaccolo. Cyclic AMP is a critically important secondary messenger downstream from a myriad of signaling receptors on the cell surface. Signaling by cyclic AMP is organized in multiple distinct subcellular nano domains, regulated by cyclic AMP hydrolyzing phosphodiesterases or PDEs.   The cardiac beta adrenergic signaling has served as the prototypical system to elucidate this very complex cyclic AMP compartmentalization. Although studies in cardiac monocytes have provided an understanding of the location and the properties of a handful of these subcellular domains, an overview of the cellular landscape of the cyclic AMP nano domains is missing.   To understand the nanodynamics, Subramanian et al combined an integrated phospho proteomics approach that took advantage of the unique role that individual phosphodiesterases play in the control of local cyclic AMP. They combined this with network analysis to identify previously unrecognized cyclic AMP nano domains associated with beta adrenergic stimulation. They found that indeed this integrated phospho proteomics approach could successfully pinpoint the location of these signaling domains and it provided crucial cues to determine the function of previously unknown cyclic AMP nano domains.   The group characterized one such cellular compartment in detail and they showed that the phosphodiesterase PDE3A2 isoform operates in a nuclear nano domain that involves SMAD4 and HDAC1. Inhibition of PDE3 resulted in an increased HDAC1 phosphorylation, which led to an inhibition of its deacetylase activity, and thus derepression of gene transcription and cardiac monocyte hypertrophic growth. These findings reveal a very unique mechanism that explains the negative long-term consequences observed in patients with heart failure treated with PDE3 inhibitors.   Cindy St. Hilaire:              The April 14th issue is our compendium on Increased Risk of Cardiovascular Complications in Chronic Kidney Disease. Dr Heidi Noels from the University of Aachen is our guest editor of the 11 articles in this issue. Chronic kidney disease is defined by kidney damage or a reduced kidney filtration function. Chronic kidney disease is a highly prevalent condition affecting over 13% of the population worldwide and its progressive nature has devastating effects on patient health. At the end stage of kidney disease, patients depend on dialysis or kidney transplantation for survival. However, less than 1% of CKD patients will reach this end stage of chronic kidney disease. Instead, most of them with moderate to advanced chronic kidney disease will prematurely die and most often they die from cardiovascular disease. And this highlights the extreme cardiovascular burden patients with CKD have.   The titles of the articles in this compendium are the Cardio Kidney Patient Epidemiology, Clinical Characteristics, and Therapy by Nicholas Marx, the Innate Immunity System in Patients with Cardiovascular and Kidney Disease by Carmine Zoccali et al. NETs Induced Thrombosis Impacts on Cardiovascular and Chronic Kidney disease by Yvonne Doering et al. Accelerated Vascular Aging and Chronic Kidney Disease, The Potential for Novel Therapies by Peter Stenvinkel et al. Endothelial Cell Dysfunction and Increased Cardiovascular Risk in Patients with Chronic Kidney Disease by Heidi Noels et al. Cardiovascular Calcification Heterogeneity in Chronic Kidney Disease by Claudia Goettsch et al. Fibrosis in Pathobiology of Heart and Kidney From Deep RNA Sequencing to Novel Molecular Targets by Raphael Kramann et al. Cardiac Metabolism and Heart Failure and Implications for Uremic Cardiomyopathy by P. Christian Schulze et al. Hypertension as Cardiovascular Risk Factor in Chronic Kidney Disease by Michael Burnier et al. Role of the Microbiome in Gut, Heart, Kidney crosstalk by Griet Glorieux et al, and Use of Computation Ecosystems to Analyze the Kidney Heart Crosstalk by Joachim Jankowski et al.   These reviews were written by leading investigators in the field, and the editors of Circulation Research hope that this comprehensive undertaking stimulates further research into the path flow of physiological kidney-heart crosstalk, and on comorbidities and intra organ crosstalk in general.   Cindy St. Hilaire:              So for our interview portion of the episode I have with me Dr Elizabeth Tarling and Dr Bethan Clifford. And Dr Tarling is an associate professor in the Department of Medicine in cardiology at UCLA, and Dr Clifford is a postdoctoral fellow with the Tarling lab. And today we're going to be discussing their manuscript that's titled, RNF130 Regulates LDLR Availability and Plasma LDL Cholesterol Levels. So thank you both so much for joining me today.   Elizabeth Tarling:             Thank you for having us.   Bethan Clifford:               Yeah, thanks for having us. This is exciting.   Cindy St. Hilaire:              I guess first, Liz, how did you get into this line of research? I guess, before we get into that, I should disclose. Liz, we are friends and we've worked together in the ATVB Women's Leadership Committee. So full disclosure here, that being said, the editorial board votes on these articles, so it's not just me picking my friends. But it is great to have you here. So how did you enter this field, I guess, briefly?   Elizabeth Tarling:             Yeah, well briefly, I mean my training right from doing my PhD in the United Kingdom in the University of Nottingham has always been on lipid metabolism, lipoprotein biology with an interest in liver and cardiovascular disease. So broadly we've always been interested in this area and this line of research. And my postdoctoral research was on atherosclerosis and lipoprotein metabolism. And this project came about through a number of different unique avenues, but really because we were looking for regulators of LDL biology and plasma LDL cholesterol, that's sort of where the interest of the lab lies.   Cindy St. Hilaire:              Excellent. And Bethan, you came to UCLA from the UK. Was this a topic you were kind of dabbling in before or was it all new for you?   Bethan Clifford:               It was actually all completely new for me. So yeah, I did my PhD at the same university as Liz and when I started looking for postdocs, I was honestly pretty adamant that I wanted to stay clear away from lipids and lipid strategy. And then it wasn't until I started interviewing and meeting people and I spoke to Liz and she really sort of convinced me of the excitement and that the interest and all the possibilities of working with lipids and well now I won't go back, to be honest.   Cindy St. Hilaire:              And now here you are. Well-   Bethan Clifford:               Exactly.   Cindy St. Hilaire:              ... congrats on a wonderful study. So LDLR, so low density lipoprotein receptor, it's a major determinant of plasmid LDL cholesterol levels. And hopefully most of us know and appreciate that that is really a major contributor and a major risk for the development of atherosclerosis and coronary artery disease. And I think one thing people may not really appreciate, which your study kind of introduces and talks about nicely, is the role of the liver, right? And the role of receptor mediated endocytosis in regulating plasma cholesterol levels. And so before we kind of chat about the nitty-gritty of your study, could you just give us a brief summary of these key parts between plasma LDL, the LDL receptor and where it goes in your body?   Elizabeth Tarling:             Yeah. So the liver expresses 70% to 80% of the body's LDL receptor. So it's the major determinant of plasma lipoprotein plasma LDL cholesterol levels. And through groundbreaking work by Mike Brown and Joe Goldstein at the University of Texas, they really define this receptor mediated endocytosis by the liver and the LDL receptor by looking at patients with familial hypercholesterolemia. So those patients have mutations in the LDL receptor and they either express one functional copy or no functional copies of the LDL receptor and they have very, very large changes in plasma LDL cholesterol. And they have severe increases in cardiovascular disease risk and occurrence and diseases associated with elevated levels of cholesterol within the blood and within different tissues. And so that's sort of how the liver really controls plasma LDL cholesterol is through this receptor mediated endocytosis of the lipoprotein particle.   Cindy St. Hilaire:              There's several drugs now that can help regulate our cholesterol levels. So there's statins which block that rate limiting step of cholesterol biosynthesis, but there's this new generation of therapies, the PCSK9 inhibitors. And can you just give us a summary or a quick rundown of what are those key differences really? What is the key mechanism of action that these therapies are going after and is there room for more improvement?   Bethan Clifford:               Yeah, sure. So I mean I think you've touched on something that's really key about the LDR receptor is that it's regulated at so many different levels. So we have medications available that target the production of cholesterol and then as you mentioned this newer generation of things like PCSK9 inhibitors that sort of try and target LDL at the point of clearance from the plasma.   And in response to your question of is there room for more regulation, I would say that given the sort of continual rate of increased cholesterol in the general population and the huge risks associated with elevated cholesterol, there's always capacity for more to improve that and sort of generally improve the health of the population. And what we sort of found particularly exciting about RNF130 is that it's a distinct pathway from any of these regulatory mechanisms. So it doesn't regulate the level of transcription, it doesn't regulate PCSK9. Or in response to PCSK9, it's a completely independent pathway that could sort of improve or add to changes in cholesterol.   Cindy St. Hilaire:              So your study, it's focusing on the E3 ligase, RNF130. What is an E3 ligase, and why was this particular one of interest to you? How did you come across it?   Elizabeth Tarling:             is predTates Bethan joining the lab. This is, I think, again for the listeners and those people in training, I think it's really important to note this project has been going in the lab for a number of years and has really... Bethan was the one who came in and really took charge and helped us round it out. But it wasn't a quick find or a quick story. It had a lot of nuances to it. But we were interested in looking for new regulators of LDL cholesterol and actually through completely independent pathways we had found the RNF130 locus as being associated with LDL cholesterol in animals. And then it came out in a very specific genome-wide association study in the African American care study, the NHLBI care study. And so really what we started looking at, we didn't even know what it was.   Elizabeth Tarling:             So we asked ourselves, well what is this gene? What is this protein? And it's RNF, so that's ring finger containing protein 130 and ring stands for really interesting new gene. Somebody came up with the glorious name. But proteins that contain this ring domain are very characteristic and they are E3 ubiquitin ligases. And so they conjugate the addition of ubiquitin to a target protein and that signals for that protein to either be internalized and/or degraded through different decorative pathways within the cell. And so we didn't land on it because we were looking at E3 ligases, we really came at it from an LDL cholesterol perspective. And it was something that we hadn't worked on before and the study sort of blossomed from there.   Cindy St. Hilaire:              That's amazing and a beautiful, but also, I'm sure, heartbreaking story because these long projects are just... They're bears. So what does this RNF130 do to LDLR? What'd you guys find?   Bethan Clifford:               As Liz said, this is a long process, but one of the key factors of RNF130 is it's structurally characteristically looked like E3 ligase. So the first thing that Liz did and then I followed up with in the lab is to see is this E3 ligase ubiquitinating in vitro. And if it is going to ubiquitinate, what's it likely to regulate that might cause changes in plasma cholesterol that would explain these human genetic links that we saw published at the same time.   And so because the LDL cholesterol is predominantly regulated by the LDL receptor and the levels of it at the surface of the parasites in the liver, the first question we wanted to see is does RNF130 interact in any way with that pathway? And I'm giving you the brief view here of the LDL receptor. We obviously tested lots of different receptors. We tested lots of different endocytose receptors and lipid regulators, but the LDL receptor is the one that we saw could be ubiquitinated by RNF130 in vitro. And so then we wanted to sort of go on from there and establish, okay, if this E3 ubiquitin ligase, is it regulating LDL receptor? What does that mean in an animal context in terms of regulating LDL cholesterol?   Cindy St. Hilaire:              Yeah, and I guess we should also explain, ubiquitination, in terms of this receptor, and I guess related to Goldstein and Brown and receptor mediated endocytosis, like what does that actually mean for the liver cell and the cholesterol in the LDLR that is binding the receptor?   Bethan Clifford:               So yes, ubiquitination is a really common regulatory mechanism actually across all sorts of different cells, all sorts of different receptors and proteins. And basically what it does is it signals for degradation of a protein. So a ubiquitin molecule is conjugated to its target such as in our case the LDL receptor and that ubiquitin tells the cell that this protein is ready for proteasomal degradation. And that's just one of the many things ubiquitination can do. It can also signal for a trafficking event, it can signal for a protein to protein interaction, but it's most commonly associated with the proteasomal degradation.     Cindy St. Hilaire:              So in terms of... I guess I'm thinking in terms of PCSK9, right? So those drugs are stemming from observations in humans, right? There were humans with gain and loss of function mutations, which caused either more or less of this LDLR receptor internalization. How is this RNF130 pathway different from the PCSK9 activities?   Elizabeth Tarling:             Yeah, so PCSK9 is a secreted protein, so it's made by hepatocyte and actually other cells in the body and it's secreted and it binds to the LDL particle, LDL receptor complex, and signals for its internalization and degradation in the proteasome. So this is not ubiquitination event, this is a completely different trafficking event. And so the RNF130, actually what Bethan showed, is it directly ubiquitinates the LDL receptor itself, signaling for an internalization event and then ultimately degradation of the LDR receptor through a decorative pathway, which we also define in the study.   So these are two unique mechanisms and actually some key studies that we did in the paper were to modulate RNF130 in animals that do not have PCSK9. And so in that system where in the absence of PCSK9 you have a lot of LDR receptor in the liver that's internalizing cholesterol. What happens when you overexpress RNF130? Do you still regulate at the LDL receptor? And you absolutely do. And so that again suggests that they're two distinct mechanisms and two distinct pathways.   Cindy St. Hilaire:              That was one thing I really loved about your paper is every kind of figure or section, the question that would pop up in my head, even ones that didn't pop in my head were beautifully answered with some of these really nice animal models, which is never an easy thing, right? And so one of the things that you brought up was difficulty in making one of the animal models. And so I'm wondering if you could share a little bit for that challenge. I think one thing that we always tend to hide is just science is hard and a lot of what we do doesn't work. And I really think especially for the trainees and really everyone out there, if we kind of share these things more, it's better. So what was one of the most challenging things in this study? And I guess I'm thinking about that floxed animal.   Elizabeth Tarling:             Yeah, so I'll speak a bit about that and then I'll let Bethan address because she was really the one on the ground doing a lot of the struggles. But again, we actually weren't going to include this information in the paper. And upon discussion and actually prompted by the reviewers of the paper and some of the questions that they asked us, we realized, you know what? It's actually really important to show this and show that this happens and that there are ways around it.   And so the first story is before Bethan even arrived in the lab, we had purchased embryonic stem cells that were knockout first condition already. And so this is a knockout strategy in which the exon of interest is flanked with lots of P sites so that you can create a flox animal, but also so you can create a whole body knockout just by the insertion of this knockout first cassette.   Elizabeth Tarling:             And so we got those mice actually in the first year of Bethan joining the lab. We finally got the chimeric mice and we were able to stop reading those mice. And at the same time we tried to generate our flox animals so that we could move on to do tissue-specific studies. And Bethan can talk about the pain associated with this. But over two years of breeding, we never got the right genotypes from the different crosses that you need to do to generate the flox animal.   And it was actually in discussions with Bethan where we decided we need to go back. We need to go back to those ESLs that we purchased five years ago and we need to figure out if all of the elements that the quality control step had told us were in place are actually present. And so Bethan went back and sequenced the whole locus and the cassette to figure out what pieces were present and we found that one of the essential locks P sites that's required for every single cross from the initial animal was absent and therefore we could actually never make the mouse we wanted to make.   And so that's sort of just a lesson for people going down that route and making these tools that we need in the lab to answer these questions is that despite paying extra money and getting all of the sort of QCs that you can get before you receive the ESLs, we should have gone back and done our own housekeeping and sort of a long journey told us when we went back that we didn't have what we thought we had at the beginning. And that was a real sticking point as Bethan can-   Cindy St. Hilaire:              Yeah. And so you know you're not alone. My very first postdoc that I did, I went with a mouse that they had also bought and were guaranteed that it was a knockout and it was not. And it is a painful lesson, but it is critical to... You get over it.   So Bethan, maybe you can also tell us a little bit about what are the other kind of next things you tried? You pivoted and you pivoted beautifully because all the models you used I thought were quite elegant in terms of exactly asking the question you wanted to ask in the right cells. So can you maybe explain some of the in vivo models you used for this study?   Bethan Clifford:               Sure, there are definitely a lot. So I mean I think Liz sort of encapsulated the trouble we have with the knockout really succinctly, but actually I want to just take this moment to sort of shout out to another postdoc in the Tarling lab, Kelsey Jarrett, who was really instrumental in the pivoting to a different model. So for the knockouts when we sort of established we didn't have exactly what we thought we did and then to compound that we also weren't getting the DeLiAn ratios breeding this whole body knockout.   We wanted to sort of look at a more transient knockout model. And that's where Kelsey really stepped in and sort of led the way and she generated AAV-CRISPR for us to target RNF130 specifically in the liver. And that had the added beauty of, one, not requiring breeding to get over this hurdle of the knockout being somewhat detrimental to breeding. But it also allowed us to ask the question of what RNF130 is doing specifically in the liver where the liver regulates LDL receptor and LDL cholesterol.   And so that was one of the key models that really, really helped get this paper over the finish line. But we did a whole barrage of experiments, as you've seen. We wanted to make sure... One of the key facets of the Tarling lab is whenever you do anything, no matter what you show Liz, it will always be, "Okay, you showed it to me one way, now show it to me a different way." Can you get the same result coming at it from different ways? And if you can't, why is that? What is the regulation behind that? And so that's really what the paper is doing is asking the same question in as many ways as we can accurately and appropriately probe what RNF130 does to the LDR receptor.   So we tried gain of function studies without adenovirus overexpression. We tried transient knockdown with antisense oligonucleotides, and then we did, as I said, the AAV-CRISPR knockdown with the help of Kelsey and our whole body knockout. And then we also repeated some of these studies such as the adenovirus and the ASO in specific genetic backgrounds. So in the absence of PCSK9, can we still regulate the LDL receptor? And then we also, just to really confirm this, in the absence of the LDL receptor, do we see a difference? And the answer is no, because this effect was really dependent on that LDL receptor being present. So there was a big combination.   Cindy St. Hilaire:              It was really nice, really a beautiful step-wise progression of how to solidly answer this question. But a lot of, I think, almost all you did was in mice. And so what is the genetic evidence for relevancy in humans? Can you discuss a little bit about those databases that you then went to to investigate, is this relevant in humans?   Bethan Clifford:               I think Liz might be better off answering that question.   Elizabeth Tarling:             And I think this sort of pivots on what Bethan was saying. So when we had struggles in the lab, it was a team environment and a collaboration between people in the lab that allowed us to make that leap and make those next experiments possible to then really answer that question. And to be able to include the antisense oligonucleotides required a collaboration with industry. We were very lucky to have a longstanding collaboration with Ionis, who provided the antisense oligonucleotides.   And for the human genetics side of things, that also was a collaboration with Marcus Seldin, who was a former postdoc with Jake Lusis and is now our PI at UC Irvine. And what he helped us do is dive into those summary level databases and ask from that initial study in the NHLBI care population, do we see associations of RNF130 expression in humans with LDL cholesterol with cardiovascular outcomes. And so one database which I would recommend everybody use, it's publicly available, is the StarNet database. And it's in the paper and the website is there. And that allowed us to search for RNF130.   Elizabeth Tarling:             And what it does is it asks how RNF130 expression in different tissues is associated with cardiometabolic outcomes and actual in CAD cases and controls, so people with and without heart disease. And we found that expression of RNF130 in the liver was extremely strongly correlated with the occurrence of cardiovascular disease in people with CAD. So in cases versus controls. And then we were also able to find many other polymorphisms in the RNF130 locus that were associated with LDL cholesterol in multiple different studies.   And I think the other message from this paper is this, unlike PCSK9 and unlike LDR receptor itself, which are single gene mutations that cause cardiovascular disease, there are many sub genome-wide significant loci that contribute to this multifactorial disease, which is extremely complex. And I think RNF130 falls within that bracket that those sort of just on the borderline of being genome-wide significant still play significant biological roles in regulating these processes. And they don't come up as a single gene hit for a disease, but combinatorialy they are associated with increased risk of disease and they have a molecular mechanism that's associated with the disease. And so that's what Marcus helped us do in terms of the human genetics is really understand that and get down to that level of data.   Cindy St. Hilaire:              Yeah. Yeah, it really makes you want to go back and look at those. Everyone always focuses on that really high peak and those analyses, but what are all those other ones above the noise, right? So it's really important.   Elizabeth Tarling:             I think it's really hard to do that. I think that's one where people... Again, it comes down to team science and the group of people that we brought together allowed us to ask that molecular question about how that signal was associated with the phenotype. I think by ourselves we wouldn't have been able to do it.   Cindy St. Hilaire:              Yeah. So your antisense oligonucleotide experiments, they were really nice. They showed, I think it was a four-week therapy, they showed that when you injected them expression of RNF130 went down by 90%. I think cholesterol in the animals was lowered by 50 points or so. Is this kind of a next viable option? And I guess related to that, cholesterol's extremely important for everything, right? Cell membrane integrity, our neurons, all sorts of things. Is it possible with something that is perhaps really as powerful as this to make cholesterol too low?   Elizabeth Tarling:             I think that what we know from PCSK9 gain and loss of function mutations is that you can drop your plasma cholesterol to very low levels and still be okay because there are people walking around with mutations that do that. I think RNF130 is a little different in that it's clearly regulatory in a homeostatic function in that it's ubiquitously expressed and it has this role in the liver to regulate LDL receptor availability, but there are no homozygous loss of function mutants people walking around, which tells us something else about how important it is in potentially other tissues and in other pathways. And we've only just begun to uncover what those roles might be.   So I think that as a therapy, it has great potential. We need to do a lot more studies to sort of move from rodent models into more preclinical models. But I do think that the human data tell us that it's really important in other places too. And so yeah, we need to think about how best it might work as a therapy. If it's combinatorial, if it's dosed. Those are the types of things that we need to think about.   Cindy St. Hilaire:              Yeah, it's really exciting. Do you know, are there other protein targets of RNF130? Is that related to my next question of what is next?   Elizabeth Tarling:             I mean, so I should point out, so Bethan unfortunately left the lab last year for a position at Amgen where she's working on obesity and metabolic disease. But before she left, she did two very, very cool experiments searching for new targets or additional targets of RNF130. Starting in the liver, but hopefully we'll move those into other tissues. And so she did gain of function RNF130 versus what loss of function we have of RNF130, and she did specific mass spec analysis of proteins that are ubiquitinated in those different conditions. And by overlaying those data sets, we're hoping to carve out new additional targets of RNF130. And there are some, and they're in interesting pathways, which we have yet to completely test, but definitely there are additional pathways, at least when you overexpress and reduce expression. Now, whether they turn out to be, again, bonafide in vivo, actual targets that are biologically meaningful is sort of the next step.   Cindy St. Hilaire:              Yeah. Well, I'm sure with your very rigorous approach, you are going to find out and hopefully we'll see it here in the future. Dr Elizabeth Tarling and Dr Bethan Clifford, thank you so much for joining me today. I really enjoyed this paper. It's a beautiful study. I think it's a beautiful example, especially for trainees about kind of thoroughly and rigorously going through and trying to test your hypothesis. So thanks again.   Elizabeth Tarling:             Thank you.   Bethan Clifford:               Thank you very much.   Cindy St. Hilaire:              That's it for the highlights from the March 31st and April 14th issues of Circulation Research. Thank you for listening. Please check out the Circulation Research Facebook page and follow us on Twitter and Instagram with the handle @CircRes, and #DiscoverCircRes. Thank you to our guests, Dr Liz Tarling and Dr Bethan Clifford.   This podcast is produced by Ishara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. I'm your host, Dr Cindy St. Hilaire, and this is Discover CircRes, you're on-the-go source for the most exciting discoveries in basic cardiovascular research.   This program is copyright of the American Heart Association 2022. The 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.  

Lauren Phillips is the Chief Product Officer of BioBox Analytics, a techbio startup company for biological data analysis. Lauren attended Toronto Metropolitan University, where she earned her Bachelor of Science in the Biomedical Science program. With an interest in medicine and research, Lauren became interested in paediatric brain cancer research, which led her to her Master of Science degree at the University of Toronto for Laboratory Medicine and Pathobiology. During her master's, Lauren met the co-founders of BioBox and joined the techbio start-up with the mission to help scientists with their biological data. As CPO, Lauren is responsible for designing and testing the software features, as well as communicating with clients' needs and relaying feedback to the BioBox team.   In this conversation, Lauren gives us an inside perspective on what it's like working in a startup. She discusses the many opportunities within the field of biology and how it has led to her current role. Lauren explains what the CPO position entails and how it brings in a diverse skillset from scientific research, design, communications, and even psychology. BioBox Analytics Website: https://biobox.io/BioBox Social Media: @BioboxanalyticsBioTechTO: https://biotechto.com/ Produced by Ment Projects. Follow us on @mentprojects on all social media platforms for updates and more mentorship resources. Visit our website to learn more about our mission and services.  Episode transcript 

We hope you enjoy this conversation between Lesley Moser and previous AASRP Emerging Leader, Mike Pesato. Dr. Pesato is the current chair of the College Liaison Committee for AASRP and an assistant clinical professor in the Department of Pathobiology and Population Medicine at Mississippi State University's College of Veterinary Medicine. As you will appreciate, he is a passionate small ruminant practitioner and educator of veterinary students. In this episode, Dr. Pesato tells us more about the AASRP Student Symposium, an exciting opportunity for students to gain insight into small ruminant and camelid practice from clinicians in the private and public sectors. If you have any questions about this episode, the 2023 AASRP Student Symposium, or opportunities to get involved in AASRP, feel free to contact us: AASRP website: aasrp.orgAnn DiPastina, DVMann.dipastina@gmail.comLesley Moser, DVMtrmvetc@gmail.com

In this week's episode we will first review a new clinical trial evidence that for patients with sickle cell anemia in resource limited settings, both low and moderate dose hydroxyurea are effective for secondary stroke prevention. Next, a research article showing how secreted mutant calreticulin functions as a “rogue cytokine” in myeloproliferative neoplasms, acting in a paracrine manner to promote growth of nearby tumor cells. Finally, we'll review new research on the pathobiology of adult and pediatric Burkitt lymphoma. With the help of whole-genome sequencing, investigators unraveled distinct subgroups, which may provide a new framework for epidemiology, diagnosis, and treatment of these lymphomas.

Dr. Iyad Alnahhas interviews Dr. David Gutmann about the review entitled "T lymphocytes as dynamic regulators of glioma pathobiology", published online in Neuro-Oncology in March 2022.   Read paper

Featuring an interview with Dr Ruben Mesa, including the following topics: Managing myelofibrosis (MF) before the availability of ruxolitinib (0:00) Pathobiology and mutational profile of MF (7:33) Matching treatments to individual patients with MF (13:25) Case: A man in his early 70s with MF and worsening anemia (17:13) Case: A man in his late 60s initially diagnosed with polycythemia vera now with MF requiring therapy (23:15) Case: A woman in her mid 60s with MF that has a suboptimal response to first-line JAK inhibitor therapy (30:25) Efficacy and safety of novel agents and strategies for MF (35:40) CME information and select publications

https://psychiatry.dev/wp-content/uploads/speaker/post-10910.mp3?cb=1669144551.mp3 Playback speed: 0.8x 1x 1.3x 1.6x 2x Download: The Behavioral Mapping of Psychomotor Slowing in Psychosis Demonstrates Heterogeneity Among Patients Suggesting Distinct Pathobiology – Niluja Nadesalingam et al. Schizophrenia Bulletin.Full EntryThe Behavioral Mapping of Psychomotor Slowing in Psychosis Demonstrates Heterogeneity Among Patients Suggesting Distinct Pathobiology –

This week on the show, Petrendologist Charlotte Reed and Michael Fleck, DVM, talk with Heather Zabiecki of Brown Heating & Cooling about the importance of cleaning air ducts and maintaining our HVAC systems; and with Dr. Scott Weese, professor in the Department of Pathobiology at U of G's Ontario Veterinary College (OVC) and the director of the Centre for Public Health and Zoonoses (CPHAZ), about his research on the transmission of COVID-19 between humans and animals.

Drs Vallerie McLaughlin and Paul Forfia discuss the diagnosis of PAH. What are the causes and why does it take so long? Relevant disclosures can be found with the episode show notes on Medscape.com (https://www.medscape.com/viewarticle/968546). The topics and discussions are planned, produced, and reviewed independently of advertiser. This podcast is intended only for US healthcare professionals. Resources Pulmonary Arterial Hypertension https://emedicine.medscape.com/article/303098-overview The 'Great Wait' for Diagnosis in Pulmonary Arterial Hypertension https://onlinelibrary.wiley.com/doi/full/10.1111/resp.13814 Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.116.022362 Management of Coronary Artery Disease and Chronic Stable Angina https://www.medscape.com/viewarticle/881468 What Is Myocardial Ischemia? https://www.medscape.com/answers/352401-192899/what-is-myocardial-ischemia Chronic Obstructive Pulmonary Disease (COPD) https://emedicine.medscape.com/article/297664-overview Group 4 Pulmonary Hypertension https://emedicine.medscape.com/article/2500057-overview Pulmonary Arterial Hypertension in Connective Tissue Disorders: Pathophysiology and Treatment https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6405825 Scleroderma https://emedicine.medscape.com/article/331864-overview Pulmonary Hypertension Phenotypes in Patients With Systemic Sclerosis https://err.ersjournals.com/content/30/161/210053.long Mixed Connective-Tissue Disease (MCTD) https://emedicine.medscape.com/article/335815-overview Systemic Lupus Erythematosus (SLE) https://emedicine.medscape.com/article/332244-overview Sjogren Syndrome https://emedicine.medscape.com/article/332125-overview Pulmonary Arterial Hypertension in Patients Infected With the Human Immunodeficiency Virus https://www.sciencedirect.com/science/article/abs/pii/S0733865121000679?via%3Dihub Portal Hypertension https://emedicine.medscape.com/article/182098-overview Liver Abnormalities in Pulmonary Arterial Hypertension https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8544777/ Pulmonary Hypertension in Adults With Congenital Heart Disease https://www.sciencedirect.com/science/article/abs/pii/S0733865121000692?via%3Dihub Atrial Septal Defect https://emedicine.medscape.com/article/162914-overview Anorexigens and Pulmonary Hypertension in the United States https://linkinghub.elsevier.com/retrieve/pii/S0012-3692(15)32749-5 Methamphetamine and the Risk of Pulmonary Arterial Hypertension https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6880795/ Echocardiography in Pulmonary Arterial Hypertension: Comprehensive Evaluation and Technical Considerations https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8348437/pdf/jcm-10-03229.pdf Echocardiography https://emedicine.medscape.com/article/1820912-overview Echocardiography Can Identify Patients With Increased Pulmonary Vascular Resistance by Assessing Pressure Reflection in the Pulmonary Circulation https://www.ahajournals.org/doi/10.1161/circimaging.109.913467 Pulmonary Resistance https://reference.medscape.com/calculator/189/pulmonary-resistance Right Heart Adaptation to Pulmonary Arterial Hypertension: Physiology and Pathobiology https://www.sciencedirect.com/science/article/pii/S0735109713058701?via%3Dihub RV Systolic Pressure (TR Jet) https://reference.medscape.com/calculator/200/rv-systolic-pressure-tr-jet Modified Bernoulli Formula https://reference.medscape.com/calculator/150/modified-bernoulli-equation Limitations and Strengths of Doppler/Echo Pulmonary Artery Systolic Pressure-Right Heart Catheterization Correlations: A Systematic Literature Review https://onlinelibrary.wiley.com/doi/10.1111/echo.12594

This month on Episode 36 of Discover CircRes, host Cynthia St. Hilaire highlights original research articles featured in the April 29 and May 13 issues of Circulation Research. This episode also features a conversation with Dr Patricia Nguyen and Jessica D'Addabbo from Stanford University about their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self.   Article highlights:   Zanoli, et al. COVID-19 and Vascular Aging   Wang, et al. JP2NT Gene Therapy in a Mouse Heart Failure Mode   Harraz, et al. Piezo1 Is a Mechanosensor in CNS Capillaries   Zhao, et al. BAT sEVs in Exercise Cardioprotection   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cyndy St. Hilaire, from the Vascular Medicine Institute at the University of Pittsburgh. And today, I'll be highlighting the articles from our April 29th and May 13th issues of Circulation Research. I also will speak with Dr Patricia Nguyen and Jessica D'Addabbo from Stanford University about their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self.   Cindy St. Hilaire:        The first article I want to share is titled Vascular Dysfunction of COVID 19 Is Partially Reverted in the Long-Term. The first author is Agostino Gaudio and the corresponding author is Luca Zanoli. And they're from the University of Catania. Cardiovascular complications, such as endothelial dysfunction, arterial stiffness, thrombosis and heart disease are common in COVID 19. But how quickly such issues resolve, once the acute phase of the illness has passed, remains unclear. To find out, this group examined aortic and brachial pulse wave velocity, and other measures of arterial stiffness in 90 people who, several months earlier, had been hospitalized with COVID 19. These measurements were compared with data from 180 controls, matched for age, sex, ethnicity and body mass index, whose arterial stiffness had been assessed prior to the pandemic. 41 of the COVID patients were also examined 27 weeks later to assess any changes in arterial stiffness over time. Together, the data showed arterial stiffness was higher in COVID patients than in controls. And though it improved over time, it tended to remain higher than normal for almost a year after COVID.   Cindy St. Hilaire:        This finding could suggest residual structural damage to the arterial walls or possibly, persistent low-grade inflammation in COVID patients. Either way, since arterial stiffness is a predictor of cardiovascular health, its potential longterm effects in COVID patients deserves further longitudinal studies.   Cindy St. Hilaire:        The second article I want to share is titled Gene Therapy with the N-Terminus of Junctophilin-2 Improves Heart Failure in Mice. The first author is Jinxi Wang and the corresponding author is Long-Sheng Song from the University of Iowa. Junctophilin-2 is a protein with a split personality. Normally, it forms part of the heart's excitation contraction coupling machinery. But when the heart is stressed, JP2 literally splits in two, and sends its N-terminal domain, JP2NT, to the nucleus, where it suppresses transcription of genes involved in fibrosis, hypertrophy, inflammation and other heart failure related processes. However, if this stress is severe or sustained, the protective action of JP2NT is insufficient to halt the progressive failure. This group asked. "What if this N-terminal domain could be ramped up using gene therapy to aid a failing mouse heart?"   Cindy St. Hilaire:        To answer this question, they injected adenoviral vectors encoding JP2NT into mice either before or soon after transaortic constriction, or TAC, tack, which is a method of experimentally inducing heart failure. They found, in both cases, that the injected animals fared better than the controls. Animals injected before TAC showed less severe cardiac remodeling than control mice, while those treated soon after TAC exhibited slower loss of heart function with reduced ventricle dilation and fibrosis. These data suggest that supplementing JP2NT, via gene therapy or other means, could be a promising strategy for treating heart failure. And this data provides a basis for future translational studies.   Cindy St. Hilaire:        The third article I want to share is titled Piezo1 Is a Mechanosensor Channel in Central Nervous System Capillaries. The first and corresponding author is Osama Harraz from the University of Vermont. Neurovascular coupling is the process whereby transient activation of neurons leads to an upsurge in local blood flow to accommodate the increased metabolic needs of the cell. It's known that agents released from active neurons trigger changes in local capillaries that prompt vasodilation, but how these hemodynamic changes are sensed and controlled is not entirely clear. This group suspected that the mechanosensory protein Piezo1, a calcium channel that regulates dilation and constriction of other blood vessels, may be involved. But whether Piezo1 is even found in the microcirculation of the CNS was unknown. This group shows that Piezo1 is present in cortical capillaries of the brain and the retina of the mouse, and that it responds to changes in blood pressure and flow.   Cindy St. Hilaire:        Ex vivo preparations of mouse retina showed that experimentally induced changes in hemodynamics caused calcium transients and related currents within capillary endothelial cells, and that these were dependent on the presence of Piezo1. While it is not entirely clear how Piezo1 influences cerebral blood flow, its pressure induced activation of CNS capillary endothelial cells suggest a critical role in neurovascular coupling.   Cindy St. Hilaire:        The last article I want to share is titled Small Extracellular Vesicles from Brown Adipose Tissue Mediate Exercise Cardioprotection. The first authors are Hang Zhao and Xiyao Chen. And the corresponding authors are Fuyang Zhang and Ling Tao from the Fourth Military Medical University. Regular aerobic exercise is good for the heart and it increases the body's proportion of brown adipose tissue relative to white adipose tissue. This link has led to the idea that brown fat, possibly via its endocrinal activity, might somehow contribute to exercise related cardioprotection. Zhao and colleagues now show that, indeed, brown fat produces extracellular vesicles that are key to preserving heart health. While mice subjected to four weeks of aerobic exercise were better protected against subsequent heart injury than their sedentary counterparts, blocking the production of EVs prior to exercise significantly impaired this protection. Furthermore, injection of brown fat derived EVs into the hearts of mice lessened the impact of subsequent cardiac injury.   Cindy St. Hilaire:        The team went on to identify micro RNAs within the vesicles responsible for this protection, showing that the micro RNAs suppressed an apoptosis pathway in cardiomyocytes. In identifying mechanisms and molecules involved in exercise related cardio protection, the work will inform the development of exercise mimicking treatments for people at risk of heart disease or who are intolerant to exercise.   Cindy St. Hilaire:        Lastly, I want to bring up that the April 29th issue of Circulation Research also contains a short Review Series on pulmonary hypertension, with articles on: The Latest in Animal Models of Pulmonary Hypertension and Right Ventricular Failure, by Olivier Boucherat; Harnessing Big Data to Advance Treatment and Understanding of Pulmonary Hypertension, by Christopher Rhodes and colleagues; New Mutations and Pathogenesis of Pulmonary Hypertension: Progress and Puzzles in Disease Pathogenesis, by Christophe Guignabert and colleagues; Group 3 Pulmonary Hypertension From Bench to Bedside, by Corey Ventetuolo and colleagues; and Novel Approaches to Imaging the Pulmonary Vasculature and Right Heart, by Sudarshan Rajagopal and colleagues; and Understanding the Pathobiology of Pulmonary Hypertension Due to Left Heart Disease, by Jessica Huston and colleagues.   Cindy St. Hilaire:        Today, Dr Patricia Nguyen and Jessica D'Addabbo, from Sanford University, are with me to discuss their study, Human Coronary Plaque T-cells are Clonal and Cross-React to Virus and Self. And this article is in our May 13th issue of Circulation Research. So, Trisha and Jessica, thank you so much for joining me today.   Jessica D'Addabbo:    Thank you for having us.   Patricia Nguyen:         Yes. Thank you for inviting us to your podcast. We're very excited to be here.   Cindy St. Hilaire:        Yeah. And I know there's lots of authors involved in this study, so unfortunately we can't have everyone join us, but I appreciate you all taking the time.   Patricia Nguyen:         This is like a humongous effort by many people in the group, including Roshni Roy Chowdhury, and Xianxi Huang, as well as Charles Chan and Mark Davis. So, we thank you.   Cindy St. Hilaire:        So atherosclerosis, it stems from lipid deposition in the vascular wall. And that lipid deposition causes a whole bunch of things to happen that lead to a chronic inflammatory state. And there's many cells that can be inflammatory. And this study, your study, is really focusing on the role of T-cells in the atherosclerotic plaque. So, before we get into the nitty gritty details of your study, can you share with us, what is it that a T-cell does normally and what is it doing in a plaque? Or rather, let me rephrase that as, what did we know a T-cell was doing in a plaque before your study?   Patricia Nguyen:         So, T-cells, as you know, are members of the adaptive immune system. They are the master regulators of the entire immune system, secreting cytokines and other proteins to attract immune cells to a diseased portion of the body, for example. T-cells have been characterized in plaque previously, mainly with immunohisto chemistry. And their characterization has also been recently performed using single cell technologies. Those studies have been restricted to mainly mirroring studies, studies in mice in their aortic walls, in addition to human carotid arteries. So, it is well known that T cells are found in plaque and a lot of attention has been given to the macrophage subset as the innate immune D. But let's not forget the T-cell because they're actually composed about... 50% in the plaque are T-cells.   Patricia Nguyen:         And we were particularly interested in the T-cell population because we have a strong collaboration with Dr Mark Davis, who's actually the pioneer of T-cell biology and was the first to describe the T-cell receptor alpha beta receptor in his lab in the 1970s. So, he has developed many techniques to interrogate T-cell biology. And our collaboration with him has allowed us and enabled us to perform many of these single cell technologies. In addition, his colleague, Dr Chen, also was pivotal in helping us with the interrogation and understanding of the T-cells in plaque.   Cindy St. Hilaire:        And I think one of the really neat strengths of your study is that you used human coronary artery plaques. So, could you walk us through? What was that like? I collect a lot of human tissue in my lab. I get a lot of aortic valves from the clinic. And it's a lot of logistics. And a lot of times, we're just fixing them, but you are not just fixing them. So, can you walk us through? What was that experimental process from the patient to the Petri dish? And also, could you tell us a little bit about your patient population that you sampled from?   Jessica D'Addabbo:    So, these were coronary arteries that we got from patients receiving a heart transplant. So, they were getting a heart transplant for various reasons, and we would receive their old heart, and someone would help us dissect out the coronary arteries from these. And then, we would process each of these coronary arteries separately. And this happened at whatever hour the hearts came out of the patient.   Jessica D'Addabbo:    So sometime, I was coming in at 3:00 AM with Dr Nguyen and we would be working on these hearts then, because we wanted the samples to be as fresh as possible. So, we would get the arteries. We would digest out the tissue. And then, we would have certain staining profiles that we wanted to look at so that we could put the cells on fax to be able to sort the cells, and then do all the downstream sequencing from there.   Cindy St. Hilaire:        So, in terms of, I don't know, the time when you get that phone call that a heart's coming in to actually getting those single cells that you can either send a fax or send a sequencing, how long did that take, on a good day? Let's talk only about good days.   Jessica D'Addabbo:    Yeah. A lot of factors went into that, sometimes depending on availability of things. But usually, we were ready with all of the materials in advance. So, I'd say it could be anywhere from six to 12 hours, it would take, to get everything sorted. Then, everything after that would happen. But that was just that critical period of making sure we got the cells fresh.   Patricia Nguyen:         So we have to credit the CT surgeons at Stanford for setting up the program or the structure, infrastructure, that enables us to obtain this precious tissue. That is Jack Boyd and Joseph Woo of CT surgery. So, they have enabled human research on hearts by making these tissues available. Because as you know, a transplant... They can say the transplant's happening at 12:00 AM, but it actually doesn't happen until 4:00 AM. And I think it's very difficult for a lab to make that happen all the time. And I think having their support in this paper was critical. And this has allowed us, enabled us, to interrogate kind of the spectrum of disease, especially focusing on T-cells, which are... They make a portion of the plaque, but the plaque itself has not like a million cells that are immune. A lot of them are not immune. So, enabling us to get the tissue in a timely fashion where they're not out of the body for more than 30 minutes enables us to interrogate these small populations of cells.   Cindy St. Hilaire:        That's actually the perfect segue to my next question, which is, how many cells in a plaque were you able to investigate with the single cell analysis? And what was the percentage again of the T-cells in those plaques or in... I guess you looked at different phases of plaque. So, what was that spectrum for the percentage of T-cells?   Patricia Nguyen:         So, for 10X, for example, you need a minimum of 10,000 captured cells. You could do less, but the utility of the 10X is maximized with 10,000. So, many times before the ability to multiplex these tissues, we were doing like capturing 5,000 for example. And the number of cells follows kind of the disease progression, in the sense that as a disease is more severe, you have more immune cells, in general. And it kind of decreases as it becomes more fibrotic and scarred, like calcified. So, it was a bit challenging to get very early just lipid-only cells. And a lot of those, we captured like 3000 or something like that. And efficiency is like 80% perhaps. So, you kind of capture…   Cindy St. Hilaire:        And also, how many excised hearts are going to have early athero? So, it's...   Patricia Nguyen:         Well, there are... nonischemics will have...   Cindy St. Hilaire:        Oh, okay. Okay.   Patricia Nguyen:         So, the range was nonischemic to ischemic.   Cindy St. Hilaire:        Oh great.   Patricia Nguyen:         So, about a portion... I would say one third of the total heart transplants were ischemic. And a lot of them were non ischemic. But as you know, the nonischemic can mix with ischemia. And so, they could have mild to moderate disease in the other arteries, for example, but not severe like 70%/90% obstruction.   Cindy St. Hilaire:        Wow. That's so great. That's amazing. Amazing sample size you have. So T-cell, it's kind of an umbrella term, right? There's many different types of T-cells. And when you start to get in the nitty gritty, they really do have distinct functions. So, what types of T-cells did you see and did you focus on in this study?   Jessica D'Addabbo:    So, the two main types of T-cells are CD4 positive T-cells and CD8 positive T-cells. And we looked at both of these T-cells from patients. We usually sorted multiple plates from each. And then, with 10X, we captured both. But our major finding was actually that the CD8 positive t-cell population was more clonally expanded than the CD4 population, which led us to believe that these cells were more important in the coronary artery disease progression and in the study that we were doing because for a cell to be clonally expanded, it means it was previously exposed to an antigen. And so, if we're finding these T-cells that are clonally expanded in our plaques, then we're hypothesizing that they were likely exposed to some sort of antigen, and then expanded, and then settled into the plaque.   Cindy St. Hilaire:        And when you're saying expansion, are you talking about them being exposed to the antigen in the plaque and expanding there? Or do you think they're being triggered in the periphery and then honing in as a more clonal population?   Patricia Nguyen:         So, that's a great question. And unfortunately, I don't have the answer to that. So basically-   Jessica D'Addabbo:    Next paper, next paper.   Patricia Nguyen:         Exactly. So, we... Interesting to expand on Jessica's answer. Predominantly what was found, as you said, was memory T-cells, so memory T-cells expressing specific markers, so memory versus naive. And these were effector T-cells. And memory meaning they were previously expanded by antigen engagement, and just happened to be in the plaque for whatever reason. We do not know why T-cells specifically are attracted to the plaque, but they are obviously there. And they're in a memory state, if you will. And some of them did display activation markers, which suggested that they clonally expanded to an antigen. What that antigen is, is the topic of another paper. But certainly, it is important to understand that these patients that we recruit, because they were transplant patients, they're not actively infected, right? That is a exclusionary criteria for transplants, right?   Patricia Nguyen:         So, that means these T-cells were there for unclear reasons. Why they're there is unclear. Whether they are your resident T-cells also is unclear, because the definition of resident T-cell still remains controversial. And you actually have to do lineage tracking studies to find out, "Okay, where... Did they come from the bone marrow? Did they come from the periphery? How did they get there?" Versus, "Okay. They were already there and they just expanded, for whatever reason, inside the plaque."   Cindy St. Hilaire:        So, your title... It was a great title, with this provocative statement, "T-cells are clonal and cross react to virus and self." So, tell us a little bit more about this react to virus and self bit. What did your data show?   Jessica D'Addabbo:    So, because of the way we sequenced the T-cell receptor, we were able to have paired alpha and beta chains. And because we knew the HLA type of the patients, we were able to put the sequences that we got out after we sequenced these through an algorithm called GLIPH, which allows us to look at the CDR3 region of the T cell receptor, which is the epitope binding region. And there are certain peptide. They're about anywhere from three to four amino acids long. These are mapped to certain binding specificities to known peptides. And so, basically, we were able to look at which epitopes were most common in our plaques. And we found that after comparing these to other epitopes, that these were actually more binding to virus. Patricia Nguyen:         So let me add to what Jessica stated, and kind of emphasize the value of the data set, if you will. So, this is, I believe, the first study that provides the complete TCR repertoire of coronary plaque, and actually any plaque that I know of, which is special because we know that there is specificity of TCR binding. It's more complicated than the antibody that binds directly from B cells to the antigen, because the T-cells bind processed antigen. So, the antigens are processed by antigen presenting cells like Dendritic cells and macrophages. And they have a specific HLA MHC class that they need to present to. And they need both arms, the antigen epitope and the MHC, to activate the T-cell. So unfortunately, it's not very direct to find the antigen that is actually activating the T-cell because we're only given a piece of it. Right?            Patricia Nguyen:         But we have provided a comprehensive map of all the TCRs that we find in the plaque. And these TCRs have a sequence, an immuno acid sequence. And luckily, in the literature, there is a database of all TCR specificities. Okay. So, armed with our TCR repertoire, we can then match our TCR repertoire with an existing database of known TCR specificities. Surprisingly, the matching TCRs are specific to virus, like flu, EBV and CMB. And also, because this was done in the era of COVID, we thought it would be important to look at the coronavirus database. We did find that there were matches to the coronavirus database. Even though our finding is not specific to SARS, it does lend to some potential mechanistic link there as well.   So, because this is all computational, it is important to validate. So, the importance of validation requires us to put the TCR alpha beta chain into a Jurkat cell, which is a T-cell line that does not have alpha beta chains on it, and then expose it to what we think is the cognate antigen epitote, with the corresponding HLA MHC APC. Because you don't have all those pieces, it will not work. Yes. So importantly, we did find that what we predicted to have the specificity of a flu peptide had specificity to a flu peptide.   Patricia Nguyen:         So then, the important question was, "Okay, these patients aren't infected, right? Why are these things here? Is there a potential cross reactivity with self peptides?"   Patricia Nguyen:         So luckily, our collaborator, Dr Charles Chan, was able to connect us with another computational algorithm that he was familiar with, whereby we were able to take the peptide sequences from the flu and match them with peptide sequencing from proteins that are self and ubiquitous. And we demonstrated, again, these T-cells were activated in vitro. That is why we concluded that there's a potential cross reactivity between self and virus that can potentially lead to thrombosis associated with viral infections. Of course, this all needs to be proved in vivo.   Cindy St. Hilaire:        Sure, sure.   Patricia Nguyen:         It's that first step for other things.   Cindy St. Hilaire:        The other big immune cell that we know is in atherosclerotic plaques and that's macrophages. And they can help to present antigens and things like that. And they also help to chew up the necrotic bits. And so, do you think that this T-cell component is an earlier, maybe disease driving, process or an adaptive process that goes awry as a secondary event? Patricia Nguyen:         So, I'm a fan of the T-cell. So... I'm with team T cell. I would like to think that it is playing an active role in pathology in this case and not a reactive role, in the sense of just being there. I think that the T-cell is actively communicating with other cells within the plaque, and promoting pro fibrotic and pro inflammatory reactions, depending on the T-cell. So, a subset of this paper was looking at kind of the interactions between the T-cell and other cells within the plaque, like macrophages and smooth muscle cells. And as we know, T-cells are activated and they produce cytokines. Those cytokines then communicate to other cells. And we found that, computationally, when you look at the transcriptome, there is a pro-inflammatory signature of the T-cell that resides in the more complex stage. And then, there's an anti-inflammatory signature that kind of resides in the transition between lipid and fibro atheroma, if you will.   Cindy St. Hilaire:        So, do you know, or is it known, how dynamic these populations are? Obviously, the hearts that you got, the samples you got, didn't have active infections. But do you know perhaps even how long ago they happened, or even how soon after there might be an infection or an antigen presented that you could get this expansion? And could that be a real driver of rupture or thrombosis?   Patricia Nguyen:         So, in theory, you would suppose that T-cells expanding and dividing and producing more and more cytokines would then lead to more macrophages coming, more of their production of proteinases that destroy the plaque. Right? So yes, in theory, yes. I think it's very difficult to kind of map the progression of T cell clonality in the current model that we have, because we're just collecting tissues. However, in the future, as organoids become more in science and kind of a primary tissue, where we can... For example, Mark Davis is making organoids with spleen, and also introducing skin to that.   Patricia Nguyen:         And certainly, we could think of an organoid involving the vasculature with immune cells introduced. And so, I think, in the next phase, project 2.0, we can investigate what... like over time, if you could model atherosclerosis and the immune system contribution, T-cells as well as macrophages and other immune cells, you can then kind of map how it happens in humans. Because obviously, mice are different. We know that mice... Actually, the models of transgenic mice do not rupture. It's very hard to make them rupture. Right?   Cindy St. Hilaire:        Well, if you stop feeding them high fat diet, the plaque goes away.   Patricia Nguyen:         For sure, for sure. So I think.. I mean, Mark Davis is a huge proponent of human based research, like research on human tissue. And as a physician scientist, obviously I'm more inclined to do human based research. And Jessica's going to be a physician someday soon. And I'm sure she's more inclined to do human based research. And certainly, the mouse model and in vitro models are great because you can manipulate them. But ultimately, we are trying to cure human diseases.   Cindy St. Hilaire:        Mice are not little humans. That's what we say in my lab. I similarly do a lot of human based stuff and it's amazing how great mice are for certain things, but still how much is not there when we need to really fully recapitulate a disease model.   So, my last question is kind of regarding this autoimmune angle of your findings. And that is, women tend to have more autoimmune diseases than men, but due to the fact that you are getting heart transplants, you've got a whole lot more men in your study than women. I think it was like 31 men to four women. But, I mean, what can you do? It's the nature of heart transplants. But I'm wondering, did you happen to notice...Maybe the sample size perhaps is too small, but were there any differences in the populations of these cells between women and men? And do you think there could be any differences regarding this more prevalence of autoimmune like reactions in women?   Patricia Nguyen:         So, that's an interesting question, but you hit it on the nose when you said "Your sample is defined mainly by men." And in addition, the samples that were women tend to have less disease. And they tend to be nonischemic in etiology. So, I think that kind of restricts our analysis. And perhaps, I guess, future studies could model using female tissues, for example, instead of only male. But the limitation of all human studies is sample availability. And perhaps, human organoid research can be less limited by that. And certainly, mouse research has become more evenly distributed of male and female mice.   Cindy St. Hilaire:        Yeah. Suffice it to say, human research is hard, but you managed to do an amazing and really important study. It was really elegant and well done. Congratulations on what is an epic amount of time. 12-hour experiments are no joke, and really beautiful data. So, thank you so much for joining me today, Dr Nguyen and Miss almost Dr D'Addabbo. Congrats and I'm really looking forward to seeing your future work.   Jessica D'Addabbo:    Thank you so much.   Patricia Nguyen:         Thanks so much.   Jessica D'Addabbo:    Thank you for having us. This is wonderful.   Cindy St. Hilaire:        That's it for the highlights from the April 29th and May 13th issues of Circulation Research. Thank you so much for listening. Please check out the Circ Res Facebook page and follow us on Twitter and Instagram with the handle @Circres and #Discover CircRes. Thank you to our guests: Dr Patricia Nguyen, and soon to be Doctor, Jessica D'Addabbo, from Stanford University.   This podcast was produced by Ishara Ratnayaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Copy text for the highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Haler. And this is Discover CircRes, you're on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. The opinions expressed by the speakers of this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, visit aha journals.org.  

Our seventh episode of the AMR Action Podcast features Dr. Larissa Matukas, an Associate Professor in the Department of Laboratory Medicine and Pathobiology at the University of Toronto, Head of the Division of Microbiology and an Infectious Disease Consultant at St. Michael's Hospital, Unity Health Toronto.  Dr. Matukas speaks about stewardship, surveillance and the use of diagnostic technologies to help combat antimicrobial resistance.

Guest: Tara Moriarty, Associate Professor at the University of Toronto in the Faculty of Dentistry with cross appointment to the Department of Laboratory Medicine and Pathobiology in the Faculty of Medicine, head of the Moriarity Laboratory

The challenge with ticks and Lyme Disease , Lessons learned from being in the Kremlin's crosshairs for more than a decade,  Marianas Trench lead singer Josh Ramsay & Is Canada doing enough to help Ukrainians hoping to come to this country?   - April 26th, 2022   The challenge with ticks and Lyme Disease   Guest: Tara Moriarty, Associate Professor at the University of Toronto in the Faculty of Dentistry with cross appointment to the Department of Laboratory Medicine and Pathobiology in the Faculty of Medicine, head of the Moriarity Laboratory   Lessons learned from being in the Kremlin's crosshairs for more than a decade   Guest: Bill Browder, financier and author of Freezing Order:    Marianas Trench lead singer Josh Ramsay  Guest: Josh Ramsay, lead singer of Marianas Trench   Is Canada doing enough to help Ukrainians hoping to come to this country?  Guest: Sean Fraser, Federal Immigration Minister and MP for Central Nova

Winnipeg braces for April blizzard, Remembering Gilbert Gottfried, The inspiration behind the Pay Gap App & Canada's COVID 6th Wave and what lies ahead  - April 12th, 2022   Winnipeg braces for April blizzard Guest: Richard Cloutier, co-host of The News CJOB   Remembering Gilbert Gottfried and his comedic legacy  Guest: Mark Breslin, co-founder and CEO of Yuk Yuks, comedian, author, and producer   The inspiration behind the Pay Gap App and calling out companies for hypocrisy on gender pay equity   Guest: Francesca Lawson, co-creator of the gender pay gap bot @paygapapp   Canada's COVID 6th Wave and what lies ahead  Guest: Dr. Tara Moriarity, Associate Professor, Faculty of Dentistry with cross appointment to the Department of Laboratory Medicine and Pathobiology in the Faculty of Medicine, University of Toronto.

Guest: Dr. Tara Moriarity, Associate Professor, Faculty of Dentistry with cross appointment to the Department of Laboratory Medicine and Pathobiology in the Faculty of Medicine, University of Toronto.

Stand Up is a daily podcast. I book,host,edit, post and promote new episodes with brilliant guests every day. Please subscribe now for as little as 5$ and gain access to a community of over 800 awesome, curious, kind, funny, brilliant, generous souls Check out StandUpwithPete.com to learn more  Indeed.com/STANDUP 30 mins Eugene Linden is an award-winning journalist and author on science, nature, and the environment. He is the author of nine books of non-fiction and one novel. His previous book on climate change, Winds of Change, explored the connection between climate change and the rise and fall of civilizations, and was awarded the Grantham Prize Special Award of Merit. His celebrated works on animal intelligence include Apes, Men, and Language, the New York Times “Notable Book” Silent Partners, and the bestselling The Parrot's Lament. For many years, Eugene wrote about nature and global environmental issues for TIME where he garnered several awards including the American Geophysical Union's Walter Sullivan Award. He has also contributed to the New York Times, Foreign Affairs, and National Geographic, among many other publications. 50 mins Dr. Meghan May was appointed in the Department of Biomedical Sciences at the University of New England College of Medicine in 2013. She was previously appointed in the Department of Biological Sciences at Towson University from 2010-2013, and held the Fisher Endowed Chair of Biological Sciences from 2012-2013, and was appointed as a postdoctoral fellow and then a research assistant professor in the Department of Infectious Diseases and Pathology at the University of Florida. Dr. May earned her B.S. degree in Microbiology from the University of New Hampshire, and her M.S. and Ph.D. degrees in Pathobiology and Bacteriology (respectively) from the University of Connecticut. Her research focus is on the evolution of virulence, not only to determine how new diseases appear and where they come from but also how to predict what new disease might arise next — pathogen forecasting Follow her on Twitter  All things Jon Carroll  Follow and Support Pete Coe Pete on YouTube Pete on Twitter Pete On Instagram Pete Personal FB page Stand Up with Pete FB page

Today my guest is Dr Jennifer Sanders What we discuss with Dr Sanders: How she decided to study cell biology, molecular biology, and biochemistry Her post doctoral fellowship in gastroenterology How she developed her skills in teaching How she became co-director of the pathobiology graduate program Pathobiology and how it differs from pathology Her research in liver transplantation and regeneration Her involvement in the American Society for Investigative Pathology Women In Pathology and her role in this organization The importance of mentorship Links for this episode: Health Podcast Network  LabVine Learning The ConfLab from LabVine Dress A Med scrubs   Dr Jennifer Sanders on Twitter American Society for Investigative Pathology Women In Pathology Pathobiology Graduate Program at Brown University Dr Sanders Publications   People of Pathology Podcast: Website Twitter

Happy Black History Month! Lift Every Voice and Sing, till earth and heaven ring! Happy American Heart Month, as well. In this episode of Scientifically Sound, I'm hanging out with Dre'Von Dobson as we talk about our time as black scientists in our love of Ernest Everett Just and discuss The Bee Gees' hit, Al Green classic, "How Can You Mend A Broken Heart". We are tying this song to Dre'Von's research on fibrinogen, a key protein complex circulating in our cardiovascular system. And oh, Dre'Von has a surprise for you and me. For more information about Dre'Von Dobson, read below.  Dre'Von Dobson is a multi-instrumentalist (specializing in the saxophone, bass, and piano) who studied at North Carolina A&T State University, graduating with a B.S. in Biology and minoring in Music Performance. He is currently a PhD student in the Pathobiology and Translational Sciences Program at UNC Chapel Hill studying hemostasis and thrombosis. His current project is identifying genes that regulate the expression of the coagulation protein, fibrinogen. Dre' is also the co-founder of The Society for Black Biomedical Sciences (SBBS) at UNC, an organization that works to promote and support the recruitment, retention, and success of black biomedical scientist. While pursuing his PhD, Dre' continues to provide live music for weddings, festivals, churches, and private functions across North Carolina. Dre' hopes to use his scientific findings and career to improve the cardiovascular health and scientific literacy in black communities. Dre'Von Dobson Social MediaInstagram: @superfly_bamTwitter: @BloodBiologySong of the Sound : High Blues Pressure by Freddie HubbardFollow Scientifically Sound----Twitter: 4theSci_SoundInstagram: scientificallysoundTikTok: scientificallysoundemail: 4thescientificallysound@gmail.com

Disease prevention is a very important aspect of successful swine management but sometimes, no matter how good your biosecurity is, diseases find a way to infect the herd. This is why it is helpful to have effective plans in place to minimize the damage done. In today's talk Dr. Greiner, Dr. Gustavo Machado discusses how swine disease models work, what they will look like in the future, and how they can be effective to prepare for diseases such as ASF infecting our swine herds. "

This week, we talk with Milton Levin '04 Ph.D., Associate Research Professor in the Department of Pathobiology and Veterinary Science, about his research work, but also about the thing UConn's roughly 90,000 Instagram followers will recognize instantly: his breathtaking pictures of campus locations, especially Horsebarn Hill. Professor Levin tells us how he got interested in photography, what it's like to teach yourself to pilot a drone, and what he looks for when he goes for a walk and brings his camera along.

Nicole Chu from the University of Ottawa speaks with Dr. Annie Huang. Dr. Annie Huang holds a Tier 1 Canada Research Chair and is a Professor of Paediatrics with Laboratory Medicine and Pathobiology at the University of Toronto. She is also the Associate Chair of Research of the Department of Paediatrics at The Sickkids Hospital. Dr. Huang founded The Rare Brain Tumor Consortium (RBTC), an international network of physicians and scientists dedicated to improving the survival of children diagnosed with rare brain tumors. Tune in to this episode to learn more about how the RBTC brings families and researchers across the world together, sharing the common goal of making rare brain tumours a curable disease. Learn more: https://lab.research.sickkids.ca/annie-huang/rbtc/

SDG 15: Life on Land, focuses on sustainable management of forests, combatting desertification, halting and reversing land degradation, and halting biodiversity loss. In this episode, Ophelia Michaelides speaks to two researchers that are working towards improving our understanding of zoonotic diseases, or, diseases transmitted between animals and humans. Discussions focus on unpacking what zoonotic diseases are; how social and environmental factors impact their spread; and the actions we can take at individual, national, and global scales to develop more sustainable prevention and mitigation strategies for managing zoonotic disease emergence. Dr. Samira Mubareka is a virologist, medical microbiologist and infectious disease physician at Sunnybrook Health Sciences Centre in Toronto, Ontario, Canada and in the Department of Laboratory Medicine and Pathobiology at the University of Toronto.  Samira has been working on SARS-CoV-2 since the outset of the pandemic in North America with a focus on virus biology, bioaerosols and exposure, genomics and diagnostics through close and cross-disciplinary collaborations across engineering, computational biology, molecular virology and animal health. Samira serves on the Chief Science Advisor of Canada, Dr. M. Nemer's COVID-19 Expert Panel, the Implementation Committee of the Genome Canada-led Canadian COVID-19 Genomics Network (CanCOGeN) VirusSeq project, and the Ontario COVID-19 Science Advisory Table.  She is currently focused on understanding the biology and transmission of SARS-CoV-2 variants of concern and on coronavirus zoonotic spillover. Samira holds an MD from Dalhousie University, completed training in Internal Medicine at McGill University, and specialized in Infectious Diseases and Medical Microbiology at the University of Manitoba. Isha Berry is a PhD Candidate in Epidemiology at the University of Toronto Dalla Lana School of Public Health. She is also a Fellow in the Emerging Leaders in Biosecurity Initiative at the Johns Hopkins Centre for Health Security. Isha has expertise in infectious disease epidemiology and mathematical modelling and has experience conducting infectious disease research in low-, middle-, and high-income settings. Her primary area of research is understanding the socio-behavioral drivers of global emerging infectious diseases at the human-animal interface. She holds an MSc in Epidemiology from the London School of Hygiene and Tropical Medicine and a BSc in Environmental Science from McGill University.CREDITS: This podcast is co-hosted by Dr. Erica Di Ruggiero, Director of the Centre for Global Health, and Ophelia Michaelides, Manager of the Centre for Global Health, at the DLSPH, U of T, and produced by Elizabeth Loftus. Audio editing is by Sylvia Lorico. Music is produced by Julien Fortier and Patrick May. It is made with the support of the School of Cities at U of T. 

Peter is a 5th-year PhD student from the Pathobiology program at Johns Hopkins School of medicine.As part of Dr. Laura D. Wood's lab, his thesis is focused on to understanding new mechanisms of invasion of pancreatic cancer by using patient derived samples in organoid models.The decision to follow the Academic or Industry path has been always in his mind. During his undergrad Peter worked in industry as a chemist and during his PhD, he worked as pro bono consultant at the Johns Hopkins Graduate Consulting Club (JHGCC) as well as participated in consulting competitions.We were happy to hear that he recently accepted a position as Consultant for after his PhD! Join us to hear about how is to work in a cancer research lab in close contact with the hospital and patient samples as well as the journey to pursue a career as a Consultant. Episode hosted by Gustavo Carrizo. We are looking for PhD students from Hopkins, as well as other Institutions in and outside the US!If you are interested in being interviewed for MyPhD please complete the following form and we will get in touch with you: MyPhD podcast application form: https://docs.google.com/forms/d/e/1FAIpQLScNA8TVvuajm9PeNJT9J0KnOLhOWluCegECALe_XSEWFQBWSQ/viewform?usp=sf_link

Stand Up is a daily podcast. I book,host,edit, post and promote new episodes with brilliant guests every day. Please subscribe now for as little as 5$ and gain access to a community of over 800 awesome, curious, kind, funny, brilliant, generous souls Check out StandUpwithPete.com to learn more I have a great news recap for you on all things Omnicron and more then at 32 minutes my interview with Dr Meghan May starts and I begin with JL Cauvin at 1:05   On today's show I  announced my first Stand Up Comedy date with Ophira Eisenberg and Christian Finnegan for Saturday January 15 2021 in King of Prussia PA   Please support my sponsors  All this month and next I will be promoting GiveWell.org and I hope you will consider sending them a donation. They will match new donors up to $250! Please go to GiveWell.org/StandUp TommyJohn.com/STANDUP  GetQuip.com/STANDUP  Indeed.com/STANDUP Dr. Meghan May was appointed in the Department of Biomedical Sciences at the University of New England College of Medicine in 2013. She was previously appointed in the Department of Biological Sciences at Towson University from 2010-2013, and held the Fisher Endowed Chair of Biological Sciences from 2012-2013, and was appointed as a postdoctoral fellow and then a research assistant professor in the Department of Infectious Diseases and Pathology at the University of Florida. Dr. May earned her B.S. degree in Microbiology from the University of New Hampshire, and her M.S. and Ph.D. degrees in Pathobiology and Bacteriology (respectively) from the University of Connecticut. Her research focus is on the evolution of virulence, not only to determine how new diseases appear and where they come from but also how to predict what new disease might arise next — pathogen forecasting Follow her on Twitter  JL Cauvin is the best Trump impersonator in the world. He is also a very talented Stand Up Comic with who I have known for a long time. JL has recorded 6 stand up albums! J-L's act is incredibly diverse and has led to six stand up albums: 2006′s Racial Chameleon, 2008′s Diamond Maker, 2012′s Too Big To Fail and 2013′s Keep My Enemies Closer, 2016's Israeli Tortoise, which hit #1 on the iTunes comedy chart and his 2018 double album Thots & Prayers. He has also released two albums as Donald Trump: 2017's Fireside Craps, an entire album as Donald Trump which hit #1 on the iTunes comedy chart and 2020's Fireside Craps: The Deuce which went #1 on both Amazon and iTunes' comedy charts and broke into the Top 40 on iTunes' overall album charts. JL is the host of 2 podcasts "Righteous Prick" and "Making Podcasts Great Again" ----------------- Check out all things Jon Carroll Follow and Support Pete Coe   Pete on YouTube Pete on Twitter Pete On Instagram Pete Personal FB page

Researchers around the world are busy trying to develop a vaccine for COVID-19. How safe is the vaccine research? How many vaccines will we eventually get, and how effective will they be? How will the vaccines be distributed? Three leading scientists from the Pacific Northwest will help us understand the vaccine research and development process. Lucy Savits is Director of the Center for Health Research at Kaiser Permanente Northwest. Corey Casper is CEO of the Infectious Disease Research Institute, and Jacob Estes is Chief of the Pathobiology and Immunology division at OHSU.

Myeloproliferative neoplasms (MPNs) are a group of hematopoietic stem cell diseases characterized by the excessive production of one or more... The post The MPN Sessions: pathobiology, therapeutic strategies & clinical trials appeared first on VJHemOnc.

This week we present two stories about people who sprung to action to help a dad.Part 1: To cheer up her ailing father, Victoria Ruiz decides to smuggle a turtle into his hospital room.Part 2: Stacey Bader Curry finally meets a nice guy -- the only catch is, he needs a liver.Dr. Victoria Ruiz is an Assistant Professor in Biology at St. Francis College and Adjunct Assistant Professor at NYU Langone medical center. She obtained her PhD in Pathobiology from Brown University, and she completed her postdoctoral work at New York University Langone Medical Center. Her primary research focuses on the effects of environmental perturbations of microbial communities on host immunity. In addition to research, she is passionate about increasing equity and inclusion in STEM and developing new and innovative pedagogical strategies to improve learning outcomes for undergraduate students interested in pursuing STEM fields.Stacey Bader Curry has a BA in art history and political science from Rutgers University. Naturally, she began her career by selling laboratory equipment at Weill Cornell Medical College. She now sells apartments but can still get you a good deal on a centrifuge. Stacey is also a writer and storyteller and has appeared on PBS' Stories From the Stage, Yum's the Word with Mo Rocca, and has won several Moth slams, including a Grand Slam. Stacey lives in Manhattan with her four children, husband, a dog named Pip, and cases of powder-free nitrile gloves. Learn more about your ad choices. Visit megaphone.fm/adchoicesSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.