Antibody directed against an autogenic protein
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4 episodes with autoantibodies
4 episodes with autoantibodies
3 episodes with autoantibodies
2 episodes with autoantibodies
2 episodes with autoantibodies
3 episodes with autoantibodies
3 episodes with autoantibodies
2 episodes with autoantibodies
3 episodes with autoantibodies
Dr. Prem Premsrirut is the Executive Director and CEO of Micoy Therapeutics, a pioneering biotech company dedicated to combating autoantibodies that transform common illnesses into life-threatening diseases. In this episode, KJ and Dr. Prem discuss the importance of understanding the immune system, the challenges of current diagnostic methods for autoimmune diseases, and the potential future of healthcare driven by innovative research. Key Highlights: 03:46 The Fascination with the Human Body and Disease Prevention 04:39 Exploring Autoantibodies and Autoimmune Diseases 08:50 The Impact of COVID-19 on Autoimmune Research 11:48 The Role of Autoantibodies in Viral Infections 25:03 The Future of Healthcare and AI Quote of the Show (29:00): “Your body is fascinating. It's dynamic, and it's about preventing what tries to take that resilience away.” - Dr. Prem Premsrirut Join our Anti-PR newsletter where we’re keeping a watchful and clever eye on PR trends, PR fails, and interesting news in tech so you don't have to. You're welcome. Want PR that actually matters? Get 30 minutes of expert advice in a fast-paced, zero-nonsense session from Karla Jo Helms, a veteran Crisis PR and Anti-PR Strategist who knows how to tell your story in the best possible light and get the exposure you need to disrupt your industry. Click here to book your call: https://info.jotopr.com/free-anti-pr-eval Ways to connect with Dr. Prem Premsrirut: LinkedIn https://www.linkedin.com/in/prem-premsrirut-36220125/ Company website https://www.micoytherapeutics.com/ How to get more Disruption/Interruption: Amazon Music - https://music.amazon.com/podcasts/eccda84d-4d5b-4c52-ba54-7fd8af3cbe87/disruption-interruption Apple Podcast - https://podcasts.apple.com/us/podcast/disruption-interruption/id1581985755 Spotify - https://open.spotify.com/show/6yGSwcSp8J354awJkCmJlDSee omnystudio.com/listener for privacy information.
In today's episode of The Root Cause Medicine Podcast, Dr. Carrie Jones sits down with Dr. Elroy Vojdani, an expert in autoimmune diseases and author of the book “When Food Bites Back,” to dive deep into the rising prevalence of autoimmune conditions and how lifestyle factors like diet, sleep, and stress management may play a role in supporting overall immune health. You'll hear them discuss: The alarming increase in autoimmune diseases over the past two decades Common autoimmune diseases Environmental triggers of autoimmunity Lab tests for autoimmune disease The importance of diet, sleep, movement, and stress management in addressing autoimmune conditions With a rich background in both scientific research and traditional medicine, Dr. Elroy has dedicated his career to understanding the complexities of autoimmunity, particularly the environmental and genetic factors that contribute to its rise. Dr. Elroy uses his medical training and knowledge, along with state-of-the-art lab testing and scientifically proven methods, to accurately diagnose and develop personalized wellness strategies based on lab testing and functional medicine principles to support overall health and well-being. Order tests through Rupa Health, a resource for functional medicine lab tests from 30+ labs. Speak with your healthcare provider to determine which tests may be most appropriate for you - https://www.rupahealth.com/reference-guide
CME credits: 1.00 Valid until: 17-01-2026 Claim your CME credit at https://reachmd.com/programs/cme/autoantibodies-in-mg-their-role-in-diagnosis-and-treatment/32239/ The burden of generalized myasthenia gravis (gMG) on patients and caregivers is substantial. Current traditional therapies are often effective in the short term but bring with them many debilitating side effects. A more targeted approach to treatment that focuses on inhibition of the neonatal FcRn receptor complex is offering an exciting and different treatment option. Join Drs. Nicholas Silvestri and James Howard, Jr, as they discuss the expanding landscape of gMG treatments.
Immune discusses basophils as regulators of of lung inflammation over space and time, and neoself-antigens as the primary target for autoreactive T cells in human lupus. Hosts: Vincent Racaniello, Cindy Leifer, Steph Langel, and Brianne Barker Subscribe (free): Apple Podcasts, RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Basophils promote asthma (J Exp Med) Basophils regulate lung inflammation (J Exp Med) Neoself antigens are primary T cell targets in lupus (Cell) Time stamps by Jolene. Thanks! Music by Tatami. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv
In this episode Dr. Kharrazian explores the world of chronic infections, such as Epstein-Barr Virus (EBV), Hepatitis C, Covid, and Human Cytomegalovirus (CMV), and their impact on our immune system. He explores how some pathogens hide within our bodies and reemerge when our immunity is compromised.He discusses the latest research linking these infections to autoimmune diseases and even cancer, and emphasizes the importance of enhancing our immune defenses rather than just relying on antiviral treatments. He covers a wide range of topics from the basics of virology, the dynamics of long COVID, and the sobering realities of Hepatitis C and Human Papillomavirus (HPV), to the ripple effects of viral infections on our overall health.Learn more at drknews.comFor patient-oriented courses, visit https://drknews.com/online-courses/For CE and CME practitioner courses, visit https://kharrazianinstitute.com/00:00 MHC proteins activate cells to fight infection.06:16 Long COVID factors: comorbidities, age, severity, inflammation, genetics13:50 Viral infection can trigger chronic inflammatory conditions.17:27 Long COVID linked to persistent antinuclear antibodies.22:53 Autoantibodies may form due to SARS-CoV-2 infection.27:28 Hepatitis B virus vaccine increases MS risk.33:58 Alphaviruses include herpes, 53% exhibit antibodies.39:30 Cytomegalovirus linked to autoimmune diseases, immune manipulation.45:39 Chronic Epstein Barr causes inflammation, cancer risk.52:02 Hepatitis C symptoms: diverse and system-wide impacts.57:33 High treatment costs spark global protests, denials.01:00:33 PCR measures viral load; biomarkers assess liver damage.01:06:08 Identify underlying health issues causing recurring infections.Support this show http://supporter.acast.com/solving-the-puzzle-with-dr-datis-kharrazian. Hosted on Acast. See acast.com/privacy for more information.
Autoimmunity and autoimmune diseases are on the rise. In this episode I look at why this is the case, the mechanisms behind autoimmunity and what we can do to prevent and manage it.Innate vs adaptive immunity (including B and T cells): https://www.ncbi.nlm.nih.gov/books/NBK279396/#Molecular mimicry in autoimmunity: https://www.sciencedirect.com/science/article/pii/S0896841118305365#Hashimoto's - molecular mimicry in action. Gluten mimics the surface proteins of the thyroid gland: https://pubmed.ncbi.nlm.nih.gov/37554764/Autoantibodies: https://pathology.jhu.edu/autoimmune/definitionsThe rise of autoimmunity and autoimmune diseases: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9918670/#Intestinal permeability and autoimmunity: https://academic.oup.com/biohorizons/article/doi/10.1093/biohorizons/hzx015/4670557#'Leaky gut' syndrome: https://www.medicalnewstoday.com/articles/326117Autoimmune protocol diet: https://www.healthline.com/nutrition/aip-diet-autoimmune-protocol-diet#how-it-worksProteus and rheumatoid arthritis; https://www.iomcworld.org/open-access/worldwide-links-between-emproteus-mirabilisem-and-rheumatoid-arthritis-46162.htmlSleep and autoimmunity: https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(22)00311-3/fulltextStress and autoimmunity: https://www.autoimmuneinstitute.org/articles/stress-autoimmune-disease-navigating-the-complex-relationship/An expert opinion on the rise in autoimmunity: https://medicine.yale.edu/news-article/why-are-autoimmune-and-allergic-diseases-rising-andrew-wang/Vitamin D and autoimmunity: https://www.newscientist.com/article/2306132-vitamin-d-supplements-really-do-reduce-risk-of-autoimmune-disease/#ixzz7KF2W0SEL Hosted on Acast. See acast.com/privacy for more information.
David Liew talks to rheumatologist Nicola Cook about the utility of common investigations for suspected inflammatory arthritis in adults. They discuss the notion of pretest probability and how this is used to determine the utility of testing, and the role of specific tests. Nicola also talks about the potential harm of overinvestigation. Read the full article by Nicola and her co-author, Rachelle Buchbinder, in Australian Prescriber.
In this episode, we review the high-yield topic of Autoantibodies in Autoimmune Disease from the MSK section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets
Nils Erik Gilhus, MD, PhD - Disruption at the Neuromuscular Junction: Relevance of Autoantibodies to Therapy in Generalised Myasthenia Gravis
Nils Erik Gilhus, MD, PhD - Disruption at the Neuromuscular Junction: Relevance of Autoantibodies to Therapy in Generalised Myasthenia Gravis
Nils Erik Gilhus, MD, PhD - Disruption at the Neuromuscular Junction: Relevance of Autoantibodies to Therapy in Generalised Myasthenia Gravis
Nils Erik Gilhus, MD, PhD - Disruption at the Neuromuscular Junction: Relevance of Autoantibodies to Therapy in Generalised Myasthenia Gravis
Nils Erik Gilhus, MD, PhD - Disruption at the Neuromuscular Junction: Relevance of Autoantibodies to Therapy in Generalised Myasthenia Gravis
Nils Erik Gilhus, MD, PhD - Disruption at the Neuromuscular Junction: Relevance of Autoantibodies to Therapy in Generalised Myasthenia Gravis
In this week's episode, Jonathan is joined by Stephanie Hanna, a Research Fellow for the Diabetes Research and Wellness Foundation, in the Division of Infection and Immunity, at Cardiff University's School of Medicine, Wales, UK. In this fascinating episode, the pair discuss all things diabetes, including immunotherapy, the future of diagnosis, and how to predict your diabetes risk. Use the following timestamps to navigate the content in this episode: (00:00)-Introduction (01:22)-Getting into Type 1 diabetes (T1D) (02:23)-Stages of T1D (05:04)-Biomarkers of T1D (07:01)-Phenotypic analysis of T and B-cells (08:24)-Diabetes progression (10:11)-Immunotherapy for T1D (14:00)-Challenges in measuring immune response (16:22)-Some thoughts on artificial intelligence (18:11)-How to get involved in a study (19:27)-Checking your own antibody status (23:51)-Thyroid eye disease (25:19)-Risks of overlooking T1D (27:34)-Three wishes for the future of healthcare
1. Understand the ways to screen for T1D risk (Autoantibodies).2. Be aware of the currently FDA approved therapies to prevent/delay T1D progression.3. Refer potential subjects for participation in T1D research studies.**please add the below exam questions for CE credits: 1. More than 90% of newly diagnosed patients with type 1 diabetes do NOT have a first degree family member with type 1 diabetes (T/F) - answer True2. Type 1 diabetes can be delayed with the use of an FDA approved immunotherapy (T/F) - answer True3. Which autoantibodies can be used to detect T1DGADAIAAIA2AZnT8AICAAnswer - all of the above
MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: July 18, 2017 Myasthenia gravis is a disorder characterized by proximal weakness, ptosis, and antibody formation against proteins at the neuromuscular junction. Most commonly, the protein targeted by antibodies is the nicotinic acetylcholine receptor. However, research in the last 2 decades has identified a number of other antibody targets, which we have reviewed here in this BrainWaves brief. BrainWaves podcasts and online content are intended for medical education only and should not be used to guide medical decision-making in routine clinical practice. Any cases discussed in this episode are fictional and do not contain any patient health-identifying information. The content in this episode was vetted and approved by Grant T Liu. REFERENCES Dalmau J, Rosenfeld MR. Paraneoplastic syndromes of the CNS. Lancet Neurol 2008;7(4):327-40. PMID 18339348Evoli A, Lancaster E. Paraneoplastic disorders in thymoma patients. J Thorac Oncol 2014;9(9 Suppl 2):S143-7. PMID 25396312Gilhus NE, Verschuuren JJ. Myasthenia gravis: subgroup classification and therapeutic strategies. Lancet Neurol 2015;14(10):1023-36. PMID 26376969Hurst RL, Gooch CL. Muscle-specific receptor tyrosine kinase (MuSK) myasthenia gravis. Curr Neurol Neurosci Rep 2016;16(7):61. PMID 27170368Koneczny I, Cossins J, Vincent A. The role of muscle-specific tyrosine kinase (MuSK) and mystery of MuSK myasthenia gravis. J Anat 2014;224(1):29-35. PMID 23458718 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.
Hello bug lovers! Today, we're guided by Mike Skvarla into a deep dive on West Nile virus. A mosquito borne illness, West Nile is something the Arthro-Pod crew has learned a lot about over the course of their lives and careers. In fact, one of them even tested positive for it after trying to give blood... Mike was inspired by Episode 1031 of the This Week in Virology podcast, where they discussed a recent paper on the subject. The paper is “Autoantibodies neutralizing type I IFNs underlie West Nile virus encephalitis in ∼40% of patients”, by Gervais et al. published in the Journal of Experimental Medicine. Tune in to learn about the history of WNV and the current research focused on it. The virus of concernQuestions? Comments? Follow the show on Twitter @Arthro_PodshowFollow the hosts on Twitter @bugmanjon, @JodyBugsmeUNL, and @MSkvarla36Get the show through Apple Podcast, Spotify, or your favorite podcatching app!If you can spare a moment, we appreciate when you subscribe to the show on those apps or when you take time to leave a review!Subscribe to our feed on Feedburner!
References Journal of Immunology Research Article ID 8263829 JAMA. 2021 Jun 15; 325(23): 2392–2393. Thyroid. 2014 Feb 1; 24(2): 371–382. Pol Arch Intern Med. 2022 Mar 30; 132(3): 16222. FEBS Letters.1997. (414): 258-262 --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support
Host Roz is joined by AJT Editorial Board Member Kenneth Newell, MD, PhD (Emory University) and AJT Editorial Fellow Kyle Jackson, MD, PhD (Emory University) [2:45] Identifying and understanding variation in population-based access to liver transplantation in the United States [12:44] Intra-graft B cell differentiation during the development of tolerance to kidney allografts is associated with a regulatory B cell signature revealed by single cell transcriptomics [18:21] Single-cell RNA sequencing reveals peripheral blood mononuclear immune cell landscape associated with operational tolerance in a kidney transplant recipient [22:20] Impact of allele-specific anti-HLA class I antibodies on organ allocation [28:12] Autoantibodies against DNA-topoisomerase I promote renal allograft rejection by increasing alloreactive T cell responses
Welcome to the 12th episode of The Brain Podcast - the official podcast of the journals Brain and Brain Communications. In this episode we speak with Nico Melzer, senior author of the article entitled: A genome-wide association study in autoimmune neurological syndromes with anti-GAD65 autoantibodies This article explores expanding entity of GAD-65 associated neurological syndromes, the exciting role of T-cells and potential therapeutic avenues that these findings may bring. Check out the full article on the Brain website: https://doi.org/10.1093/brain/awac119 This episode was co-hosted by Adam Handel and Darshan Pandya , edited and produced by Adam Handel and Xin You Tai; co-produced by Antonia Johnston; original music by Ammar Al-Chalabi.
TWiV notes the passing of virologist Michael BA Oldstone, a study to assess the performance of rapid antigen tests to detect symptomatic and asymptomatic SARS-CoV-2 infection, and the presence of antibodies to type I interferons in ~40% of patients with West Nile virus encephalitis. Hosts: Vincent Racaniello, Rich Condit, and Alan Dove Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode MicrobeTV Discord Server MicrobeTV store at Cafepress Position in Rosenfeld Laboratory (pdf) XKCD on antivaxxers RFK Jr. CDC or FDA head? (Politico) Performance of rapid antigen tests (Ann Int Med) Guidance on rapid antigen tests (FDA) Autoantibodies to IFN in West Nile virus encephalitis (JEM) Letters read on TWiV 1031 Timestamps by Jolene. Thanks! Weekly Picks Rich – The Final Covid-19 Grand Rounds: What Have We Learned? Alan – Teaching biology to Tibetan Buddhist monks Vincent – I got it from Agnes by Tom Lehrer and Why Oppenheimer has important lessons for scientists today Listener Picks Ryan – Paul Offit on PBS Newshour to explain RFK Jr.'s Congressional Hearing Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv
The ANA, anti-CCP, RF, and beyond! We all have ‘rheum' to grow when it comes to making sense of autoantibodies and common markers. We talk through the nuances with rheumatologist Dr. Matthew B. Carroll (biography here!). Our interview covers physical exam tips for inflammatory arthritis, basic interpretation of rheumatologic testing, and what to do with the dreaded ‘vaguely positive' speckled ANA! Claim free CME for this episode at curbsiders.vcuhealth.org! Patreon | Episodes | Subscribe | Spotify | YouTube | Newsletter | Contact | Swag! | CME Show Segments Intro Case 1 History clues Physical exam pearls; what does synovitis look like? Interpreting mixed labs Rheumatoid Factor tips Role for imaging Importance of early diagnosis New testing modalities Case 2 Oh no– a vaguely positive ANA! ANA testing basics Outro Credits Showrunners, Hosts, Producers and Writers: Matthew Watto MD, FACP; Paul Williams MD, FACP Show Notes, Infographic, Cover Art: Beth Garbitelli MD Reviewer: Emi Okamoto MD Technical Production: PodPaste Guest: Matthew B. Carroll MD Sponsor: Brooklinen Visit Brooklinen.com today and get $20 off plus free shipping on orders of $100+ with code [CURB] Sponsor: Grammarly Go to grammarly.com/tone to download and learn more about Grammarly Premium's advanced tone suggestions. Sponsor: Glass Health You can get one month of Glass Pro free by signing up at glass.health and using the code: CURBSIDERS.
Junjie from Jason's lab joins TWiN to discuss the observation that the cell gene PNMA2 encodes non-enveloped virus-like capsids that induce autoantibodies which underlie paraneoplastic syndrome. Hosts: Vincent Racaniello, Jason Shepherd, Timothy Cheung, and Junjie Xu Subscribe (free): Apple Podcasts, Google Podcasts, RSS Links for this episode MicrobeTV Discord Server Virus-like capsids in paraneoplastic disease (bioRxiv) Timestamps by Jolene. Thanks! Music is by Ronald Jenkees Send your neuroscience questions and comments to twin@microbe.tv
TWiV reveals how treatment with remdesivir for COVID-19 resolved a chronic poliovirus infection in an immunocompromised patient, and the finding that infection with SARS-CoV-2 leads to an increase in new and preexisting autoantibodies. Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode •Register for ASV 2023 •MicrobeTV Discord Server •Janet Sinsheimer on TWiV 653 •Clearance of chronic poliovirus infection by remdesivir (Front Immunol) •Autoimmunity induced by SARS-CoV-2 infection (Nat Comm) •Letters read on TWiV 993 •Timestamps by Jolene. Thanks! Weekly Picks Brianne – Xkcd: Lymphocytes Kathy – A brief history of Parafilm with video Alan – Mapping and exploring the USS Monitor wreck Vincent – Skype a Scientist Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv
Did you know that there are now over 80 different types of autoimmune diseases that impact multiple organs, tissues, cells and compounds such as enzymes in the body? An autoimmune disease occurs when your body's own immune system starts to attack itself, and as a result of this attack, it causes damage to the body leading to disease.Classifying different autoimmune diseases is no mean feat and requires scrutiny of your symptoms, biochemistry and whether the condition is organ-specific and systemic. And that is why many conditions that we don't class as autoimmune in nature could, in fact, have an element of autoimmunity. One such condition is polycystic ovarian syndrome (PCOS) which I repeatedly see in my clinical practice with my clients living with autoimmune diseases. This led me to investigate some similarities between these conditions and even to question, is PCOS an autoimmune disease?In this episode we will explore the link between autoimmune disease and PCOS and how addressing the root cause may help with symptoms of both conditions. Highlight's from today's episode include:What is PCOS?Autoantibodies and how they affect your body. Insulin resistance and blood sugar dysregulation in PCOS and autoimmune disease.Chronic inflammation in autoimmune disease and PCOS.Do you think PCOS is an autoimmune disease? You can also read my article, 'Is polycystic ovarian syndrome an autoimmune disease?'Tune in today and be sure to share any of your thoughts about the show on my Instagram page: @theautoimmunitynutritionistYou can also download a free copy of The Autoimmunity Recovery Plan here.Book your free discovery call with me here.And if you would like to join my community of strong-willed people thriving with autoimmune disease, join The Autoimmunity Community. Thanks for listening! You can join The Autoimmunity Community on Facebook or find me on Instagram @theautoimmunitynutritionist.Thanks for listening! You can join The Autoimmunity Community on Facebook or find me on Instagram @theautoimmunitynutritionist.
Autoantibodies against post-translationally modified proteins (PTM) are described in various rheumatic diseases and facilitate diagnosis and patient stratification. Researchers from the Leiden University Medical Center analysed the presence of autoantibodies against six different post-translational modifications in a cohort of patients with neuropsychiatric lupus. In this podcast, Leendert Trouw, Rory Monahan and Michelle van den Beukel discuss the results of their study with the ARD/RMDopen social media advisor Caroline Ospelt. Read the Open Access related paper: https://rmdopen.bmj.com/content/8/1/e002079 Listen to more episodes of RMD Open: https://podcasts.apple.com/gb/podcast/rmd-open-rheumatic-and-musculoskeletal-diseases/id1237127864
CME credits: 0.50 Valid until: 10-01-2024 Claim your CME credit at https://reachmd.com/programs/cme/testing-and-screening-for-type-1-diabetes-t1d-genes-antigens-autoantibodies-methodology-and-clinical-utility/14285/ Autoantibody Screening to Identify Risk for Type 1 DiabetesT1D defines a continuum that begins during an asymptomatic prodrome before the disease manifests clinically. One of the challenges of T1D is identifying persons at high risk before the onset of clinical manifestations by screening for pancreatic β cell autoantibodies. Interventions to delay or prevent the underlying autoantibody-mediated loss of pancreatic β cells are now available to delay or potentially prevent the clinical presentation of T1D as diabetic ketoacidosis and mitigate subsequent, longer-term complications.=
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.29.510196v1?rss=1 Authors: Zhou, J., Greenfield, A., Loudermilk, R., Bartley, C., Tran, B., Zhao, C., Wang, H., Wilson, M., Pleasure, S. Abstract: NMDA receptor autoimmune encephalitis (NMDAR-AE) is characterized by cerebrospinal fluid (CSF)-resident anti-NMDA receptor autoantibodies that cause behavioral and neurologic deficits. Although many symptoms are responsive to immunotherapy, for many patients functionally impairing deficits persist. We used patient-derived GluN1 and GluN2A-specific monoclonal antibodies (mAbs) to interrogate the molecular and circuit basis for persistent sensory-motor deficits following NMDAR-AE. During postnatal development, intracortical injection of either mAb disrupted callosal circuit formation with excess callosal projections in primary somatosensory cortex (S1), although the anti-GluN1 antibody provoked the more severe phenotype. S1 circuit disruption during development results in permanent axon morphology alterations and sensory-motor deficits lasting to adulthood. The severity of sensory-motor deficits was correlated with the severity of axon morphology alterations, and these anatomic changes are associated with sensory-motor behavior deficits similar to those in children NMDAR-AE. Our studies provide a molecular, cellular, and circuit basis for persistent neuropsychiatric deficits in NMDAR-AE. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
What is autoimmune-associated epilepsy, and how is it different from acute seizures with an autoimmune cause? How can clinicians best diagnose and treat these conditions? Sharp Waves reporter Dr. Maryam Nabavi-Nouri spoke with Dr. Claude Steriade.Claude Steriade, MD, CM is originally from Quebec City, Canada. She completed medical school at McGill University in Montreal, followed by an adult neurology residency at the University of Toronto. Dr. Steriade then completed a two-year epilepsy fellowship at the Cleveland Clinic before joining the epilepsy center at New York University. Relevant articles:Acute symptomatic seizures secondary to autoimmune encephalitis and autoimmune-associated epilepsy: Conceptual definitionsDiscerning the Role of Autoimmunity and Autoantibodies in Epilepsy: A Review --This episode was reported by Dr. Maryam Nabavi-Nouri, and edited and produced by Nancy Volkers.Sharp Waves content is meant for informational purposes only and not as medical or clinical advice.The International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, Twitter, and Instagram.Contact us with feedback or episode ideas at podcast@ilae.orgILAE website | Facebook | InstagramTwitter feeds: English | French | Japanese | Portuguese | Spanish | ILAE-YES The International League Against Epilepsy invites you to explore the ILAE Academy: Interactive, practice based online courses for health care professionals who diagnose and treat epilepsy. Find more information at ilae-academy.org. Support the showSharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.The International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, Twitter, and Instagram.
Welcome to OC talks, a podcast series exploring the latest advancements in oncology. I'm your host, Jade Parker, Oncology Central's Senior Editor. In this episode, supported by Sengenics, we will be exploring the importance of autoantibodies in the development of cancer as well as how they can be used in the early detection of tumors. Joining me for this episode is Field Application Scientist Joseph Miseirvitch from Sengenics, a precision medicine company working to improve patient outcomes for physiologically relevant, data-guided decision making.
There's a bit of a misunderstanding in the health world that endometriosis is just a hormone problem, but this line of thinking is incomplete. Hormones can absolutely contribute to the endometriosis picture, but they are not the cause of endometriosis. And part of treating endometriosis should include strategies to support the hormones, though that's not where the support should end. Today on the show Erin speaks with Dr. Lara Briden all about endometriosis and why it's such a complex thing to treat. Tune in to hear Lara dive into the immune side of endometriosis, epigenetics, gut dysbiosis, and how all these things can be interconnected. Erin and Lara also discuss testing options and strategies to treat endometriosis, plus and natural remedies you can try at home and lifestyle factors to consider. This episode is important to hear if you've been struggling with endometriosis or suspect you might have it, have been diagnosed with IBS but think there may be more going on, or if you're a practitioner looking to deepen your understanding on the complexities of endometriosis. In this episode: -Lara Briden is kind of a big deal [2:50] -The misunderstanding with endometriosis [4:02] -Looking at endometriosis as a disease of immune dysfunction [7:25] -Lara's philosophy towards women's physiology and women's health [8:57] -What is endometriosis? [13:26] -Retrograde menstruation [16:20] -Autoantibodies associated with endometriosis [20:31] -The link between endometriosis and GI dysfunction [21:47] -The importance of the immune cells macrophages [23:14] -Focusing on bacteria as part of endometriosis treatment [25:30] -The overlap between SIBO, IBS & endometriosis [28:54] -Epigenetic involvement in endometriosis [31:11] -Visceral sensitivity [37:52] -How hormones like estrogen & progesterone can impact endometriosis [39:41] -Why the pill isn't always the best option for endometriosis [44:34] -Progesterone resistance, and what it means for endometriosis [46:26] -Testing options, natural remedies and treatment strategies [48:46] -The role nickel allergy plays [55:13] -The regulating effects of vitamin A [59:20] -Reducing endometriosis lesions [1:00:22] -What to know about taking iodine [1:01:49] FOR OUR FULL LIST OF LINKS + RESOURCES, HEAD TO: https://www.thefunktionalnutritionist.com/podcast/219-endometriosis-hormone-gut-immune-health-lara-briden
The Journal of Rheumatology's Editor-in-Chief Earl Silverman discusses this month's selection of articles that are most relevant to the clinical rheumatologist. Included is an excerpt from this month's Editor's Picks spotlight interview with authors Gregory McDermott, Ritu Gill, Staci Gagne, Suzanne Byrne, Weixing Huang, Xiaosong Wang, Lauren C. Prisco, Alessandra Zaccardelli, Lily W. Martin, Lucy Masto, Vanessa L. Kronzer, Nancy Shadick, Paul F. Dellaripa, Tracy J. Doyle and Jeffrey A. Sparks about their article "Demographic, Lifestyle, and Serologic Risk Factors for Rheumatoid Arthritis (RA)–associated Bronchiectasis: Role of RA-related Autoantibodies" - doi.org/10.3899/jrheum.211242 This month's selections also include: Mortality Rates in Patients With Ankylosing Spondylitis With and Without Extraarticular Manifestations and Comorbidities: A Retrospective Cohort Study - doi.org/10.3899/jrheum.210909 Baseline Disease Activity Predicts Achievement of cDAPSA Treatment Targets With Apremilast: Phase III Results in DMARD-naïve Patients With Psoriatic Arthritis - doi.org/10.3899/jrheum.210906 Tacrolimus in Patients With Interstitial Pneumonia Associated With Polymyositis or Dermatomyositis: Interim Report of Postmarketing Surveillance in Japan - doi.org/10.3899/jrheum.210322 Gout and Hospital Admission for Ambulatory Care–Sensitive Conditions: Risks and Trajectories - doi.org/10.3899/jrheum.220038 IgG4-related Disease With Destructive Nasal Bone Involvement Leading to Saddle Nose Deformity - doi.org/10.3899/jrheum.200621 To read these, and other full articles visit www.jrheum.org. Music by David Hilowitz
Please go to https://academiccme.com/myapodcast/ and complete the evaluation to receive your CE/CME Credit.
TWiV reviews recent cases of monkeypox, presence of SARS-CoV-2 RNA but not infectious virus in feces, and the association of autoantibodies to interferons with severe COVID-19. Hosts: Vincent Racaniello, Dickson Despommier, Rich Condit, Kathy Spindler, and Brianne Barker Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Monkeypox in MA (ProMed Mail) Possible monkeypox in NYC (NY Times) Occupational monkeypox, Wisconsin (Emerg Inf Dis) SARS-CoV-2 in feces (Nature) IFN autoantibodies and severe COVID-19 (PNAS) Letters read on TWiV 902 Timestamps by Jolene. Thanks! Weekly Picks Dickson – How to grow food on the moon Brianne – APod May 16: Milky Way over French Alp Hoodoos Kathy – Covid Nationwide data visualization Rich – NIH All of Us Research Program Vincent – Physicians Spreading Misinformation on Social Media — Do Right and Wrong Answers Still Exist in Medicine? Listener Pick Lisa – E.H. Danner Museum of Telephony Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv
Please go to https://academiccme.com/myapodcast/ and complete the evaluation to receive your CE/CME Credit.
Could better understanding of the role of autoantibodies hold the key to personalised treatments in itchy and blistering diseases? This week we bring together experts Prof. Kridin and Dr. Meijer to discuss their recent JEADV publications concerning the role of autoantibodies in itchy and blistering diseases. Prof. Kridin talks about the pathophysiology and therapeutic approaches to treat patients with bullous pemphigoid and comorbid psoriasis, followed by Dr. Meijer's explanation regarding the role of IgE autoantibodies in serum and skin of non-bullous and bullous pemphigoid patients. References https://onlinelibrary.wiley.com/doi/10.1111/jdv.17013 https://onlinelibrary.wiley.com/doi/full/10.1111/jdv.16996 Not an EADV Member? Click Here for more information on the advantages and opportunites that only EADV Members have.
Distinguishing between type 1 and type 2 diabetes is critical, because delayed diagnosis of type 1 diabetes is associated with 20% or more risk of diabetic ketoacidosis, a major cause of death in children. Differentiating between type 1 and type 2 diabetes is also extremely important for choice of appropriate therapy. While the clinical presentation of a patient may not allow an unambiguous discrimination between type 1 and type 2 diabetes, the presence of one or more islet autoantibodies can support the diagnosis of type 1 diabetes, according to William Winter, MD, FCAP, the director of the UF Health Pathology Laboratories' Endocrinology Unit. Because islet autoantibodies can also predict the development of type 1 diabetes, once safe and effective therapies are available to prevent this disease, islet autoantibody testing will become routine in medical practice, as Dr. Winter explains in this CAPcast. Dr. Winter led the development of a Clinical Pathology Improvement Program or CPIP course on this topic.
TWiN explains how anti-DNA antibodies present in lupus patients bind to GluN2A-containing NMDA receptors, act as positive allosteric modulators, and impair spatial memory. Hosts: Vincent Racaniello, Ori Lieberman, Jason Shepherd, Timothy Cheung, and Vivianne Morrison Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiN! Links for this episode Lupus autoantibodies bind GluN2A-containing NMDA receptors (Nat Commun) Timestamps by Jolene. Thanks! Music is by Ronald Jenkees Send your neuroscience questions and comments to twin@microbe.tv
In part two of a four-part series, Dr. Justin Martello discusses a controversy in autoimmune neurology
In part one of a four-part series, Dr. Justin Martello discusses a controversy in autoimmune neurology
A few articles in each issue are chosen by the EIC for their interest. The issue highlights include: laminin-521 –a novel GBM autoantigen, iron biomarkers & mortality in nondialysis kidney disease, & disparities among hemodialysis patients with COVID-19.
CME credits: 0.50 Valid until: 09-07-2022 Claim your CME credit at https://reachmd.com/programs/cme/changing-treatment-paradigms-in-type-1-diabetes-role-of-anti-cd3-targeted-therapy-screening-for-islet-autoantibodies-in-children-and-adolescents-to-preventdelay-t1d/12695/ Experts in the immunopathology of type 1 diabetes review data showing that clinical presentation is preceded by an asymptomatic phase, characterized by the presence of one or more islet autoantibodies. Screening children for islet autoantibodies during the two preclinical stages can identify those with multiple autoantibodies and high-risk antibody phenotypes who may be candidates for preventive interventions before developing dysglycemia or the clinical onset of type 1 diabetes.
CME credits: 0.50 Valid until: 09-07-2022 Claim your CME credit at https://reachmd.com/programs/cme/changing-treatment-paradigms-in-type-1-diabetes-role-of-anti-cd3-targeted-therapy-screening-for-islet-autoantibodies-in-children-and-adolescents-to-preventdelay-t1d/12695/ Experts in the immunopathology of type 1 diabetes review data showing that clinical presentation is preceded by an asymptomatic phase, characterized by the presence of one or more islet autoantibodies. Screening children for islet autoantibodies during the two preclinical stages can identify those with multiple autoantibodies and high-risk antibody phenotypes who may be candidates for preventive interventions before developing dysglycemia or the clinical onset of type 1 diabetes.
Interview with Carsten Finke, MD, and Frederik Bartels, MD, authors of Association Between Neuronal Autoantibodies and Cognitive Impairment in Patients With Lung Cancer
Interview with Carsten Finke, MD, and Frederik Bartels, MD, authors of Association Between Neuronal Autoantibodies and Cognitive Impairment in Patients With Lung Cancer
Main website: https://mehlmanmedical.com/ Instagram: https://www.instagram.com/mehlman_medical/ Facebook: https://www.facebook.com/mehlmanmedical Anchor: https://anchor.fm/mehlmanmedical Audio Qbank - Q306 – A 42F with progressive fatigue See full post on our website: https://mehlmanmedical.com/audio-qbank-q306-a-42f-with-progressive-fatigue
Host: Pallav Mehta, MD What is the role of autoantibodies in breast cancer detection? Dr. Pallav Mehta, the Director of Integrative Oncology and Practice Development at the MD Anderson Cancer Center at Cooper University Health Care, shares the latest research on autoantibodies as potential biomarkers in the early detection of breast cancer?
Host: Pallav Mehta, MD What is the role of autoantibodies in breast cancer detection? Dr. Pallav Mehta, the Director of Integrative Oncology and Practice Development at the MD Anderson Cancer Center at Cooper University Health Care, shares the latest research on autoantibodies as potential biomarkers in the early detection of breast cancer.
Welcome to EndoPod's Revision Series! Each episode will cover bitesize revision material for those preparing for exams or even just for those who are interested in learning the basics of Endocrinology. This episode covers the pathophysiology of diabetes and how it comes about. Voice - Hepsi Xavier Transcript - Hepsi Xavier Editor - Serena Shoker Aberdeen University Endocrinology Society are a student lead organisation. All information provided in this podcast are intended for educational purposes. This podcast is not intended to replace the advice of a qualified health professional. The students involved in the making of this episode are in the 1st and 3rd year of their medical education. Resources: https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_Diabetes_Guide/547013/all/Autoantibodies_in_Type_1_Diabetes https://www.diabetes.org.uk/resources-s3/2017-11/diabetes_in_the_uk_2010.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774991/ University of Aberdeen - Y2 MBChB Lecture - Pathology of Diabetes Mellitus by Dr Paul Brown
In this edition of the World Shared Practice Forum podcast, Dr. Petter Brodin, Consultant in Pediatric Immunology at the Karolinska Institute, discusses new and emerging knowledge regarding the immune response to SARS-CoV-2 infection. He also provides perspective on the immunology of the COVID-19 vaccine response, as well as the Multisystem Inflammatory Syndrome in Children (MIS-C). After this podcast, listeners will be able to: • Discuss the current understanding of COVID-19 immunology • Understand immune system responses that may influence COVID-19 disease burden and severity • Describe current theories of the immunology of the COVID-19 Multisystem Inflammatory Syndrome in Children (MIS-C) Initial publication: February 22, 2021. Speakers: Petter Brodin, MD, PhD Consultant in Pediatric Immunology, Karolinska University Hospital Professor of Pediatric Immunology, Karolinska University Jeffrey Burns, MD, MPH Chief and Shapiro Chair, Critical Care Medicine, Executive Chair, International Health Services, Director, OPENPediatrics, Senior Associate in Critical Care Medicine, Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children's Hospital Professor of Anesthesia, Harvard Medical School Citation: Brodin P, Zackin B, Daniel D, Burns JP. Immune determinants of COVID-19 disease presentation and severity. 2/2021. Online Podcast. OPENPediatrics. https://youtu.be/dFA68r40UMU. Resources: • Brodin P. Immune determinants of COVID-19 disease presentation and severity. Nature Medicine. 2021 Jan;27(1):28-33. • Consiglio CR, Cotugno N, Sardh F, Pou C, Amodio D, Rodriguez L, Tan Z, Zicari S, Ruggiero A, Pascucci GR, Santilli V, Brodin P. The immunology of multisystem inflammatory syndrome in children with COVID-19. Cell. 2020 Nov 12;183(4):968-81. • Bastard P, Rosen LB, Zhang Q, Michailidis E, Hoffmann HH, Zhang Y, Dorgham K, Philippot Q, Rosain J, Béziat V, Manry J, Brodin P, et al. Autoantibodies against type I IFNs in patients with life-threatening COVID-19. Science. 2020 Oct 23;370(6515). • Rodriguez L, Brodin P. Unraveling the Immune Response in Severe COVID-19. Journal of clinical immunology. 2020 Oct;40(7):958-9. This recording is intended to be used as an educational resource for healthcare providers. It is in no way a substitute for the independent decision making and judgment of a qualified healthcare professional. It should not be used to make a diagnosis, or to overrule the advice of a qualified health care provider, nor should it be used to provide advice for emergency medical treatment. Please visit: www.openpediatrics.org OPENPediatrics™ is an interactive digital learning platform for healthcare clinicians sponsored by Boston Children's Hospital and in collaboration with the World Federation of Pediatric Intensive and Critical Care Societies. It is designed to promote the exchange of knowledge between healthcare providers around the world caring for critically ill children in all resource settings. The content includes internationally recognized experts teaching the full range of topics on the care of critically ill children. All content is peer-reviewed and open access-and thus at no expense to the user. For further information on how to enroll, please email: openpediatrics@childrens.harvard.edu
Dr. Helen Su, Chief of the Human Immunological Diseases Section at the National Institute of Allergy and Infectious Diseases (part of the NIH) and co-leader of the COVID Human Genetic Effort, joins host Lauren Richardson to discuss the results and implications of the articles "Inborn errors of type I IFN immunity in patients with life-threatening COVID-19" and "Autoantibodies against type I IFNs in patients with life-threatening COVID-19", both published in Science.
On this episode of TWiV, mRNA vaccines from Moderna and Pfizer show over 90% efficacy, prothrombotic auto-antibodies in serum of COVID-19 patients, and the whereabouts of SARS-CoV-2 in the human body. Hosts: Vincent Racaniello, Rich Condit, Kathy Spindler, and Brianne Barker Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Efficacy of Moderna and Pfizer mRNA vaccines Longer shelf life of Moderna vaccine (Moderna) Prothrombotic antibodies in COVID-19 serum (Sci Trans Med) Where is SARS-CoV-2 in the human body? (PLoS Path) Letters read on TWiV 683 Timestamps by Jolene. Thanks! Weekly Picks Brianne – Picture a Scientist Kathy – Colors of the Moon and Word that hasn’t changed Rich – NASA YouTube channel Vincent – Laura Splan science art Listener Pick Mona – Ad5 vector and podcast with ImmunityBio founder Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv
On this episode of TWiV, mRNA vaccines from Moderna and Pfizer show over 90% efficacy, prothrombotic auto-antibodies in serum of COVID-19 patients, and the whereabouts of SARS-CoV-2 in the human body. Hosts: Vincent Racaniello, Rich Condit, Kathy Spindler, and Brianne Barker Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Efficacy of Moderna and Pfizer mRNA vaccines Longer shelf life of Moderna vaccine (Moderna) Prothrombotic antibodies in COVID-19 serum (Sci Trans Med) Where is SARS-CoV-2 in the human body? (PLoS Path) Letters read on TWiV 683 Timestamps by Jolene. Thanks! Weekly Picks Brianne – Picture a Scientist Kathy – Colors of the Moon and Word that hasn’t changed Rich – NASA YouTube channel Vincent – Laura Splan science art Listener Pick Mona – Ad5 vector and podcast with ImmunityBio founder Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv
Pemphigus is an uncommon intraepidermal blistering disease occurring on the skin and mucous membranes. It is caused by autoantibodies to adhesion molecules expressed in the skin and mucous membranes. The cause is unknown. The bullae appear spontaneously and are tender and painful when they rupture. Drug induced pemphigus from penicillamine, captopril, and others have been reported. There are several forms of pemphigus: pemphigus vulgaris and its variant, pemphigus vegetans; and the more superficially blistering pemphigus foliaceus and its variant, pemphigus erythematosus. All forms may occur at any age, but most present in middle age. The foliaceus form is especially apt to be associated with other autoimmune diseases, or it may be drug induced. Paraneoplastic pemphigus, a unique form of the disorder, is associated with numerous types of benign and malignant neoplasms (typically non-Hodgkin lymphoma). Pemphigus is characterized by an insidious onset of flaccid bullae, crusts, and erosions in crops or waves. In pemphigus vulgaris, lesions often appear first on the oral mucous membranes. These quickly become erosive. The scalp is another site of early involvement. Practitioners can rub a cotton swab or finger laterally on the surface of uninvolved skin which may cause easy separation of the epidermis (this is Nikolsky's sign). The diagnosis is made with light microscopy and by direct and indirect immunofluorescence (IIF) microscopy. Autoantibodies to intercellular adhesion molecules can be detected with ELISA assays and have replaced the use of IIF in some centers. When the condition is severe, patients should be hospitalized at bed rest and given antibiotics/intravenous feedings. Anesthetic troches used before eating ease painful oral lesions. While pemphigus requires systemic therapy as early as possible, ironically, the main morbidity here is side effects from treatment. Initial therapy with systemic corticosteroids can consist of prednisone (60-80 mg daily). In most cases, a steroid sparing agent is added at the beginning at treatment (ex. azathioprine 100-200 mg daily, mycophenolate mofetil 1-1.5 twice daily). Treatment courses can be repeated in patients who do not achieve complete remission or relapse (ex. monthly IVIG at 2 g/kg intravenously over 3-4 days). In refractory cases, cyclophosphamide plus intravenous corticosteroids and plasmapheresis are also used. In patients who have a limited form of the disease, skin and mucous membrane lesions should be treated with topical corticosteroids. Complicating infection requires appropriate systemic and local antibiotic therapy. As far as complications are concerned, secondary infection can occur. This is a major cause of morbidity and mortality. Disturbances of fluid, electrolyte, and nutritional intake can occur as a result of painful oral ulcers. One in three patients will experience remission and, infection from S. aureus is the most frequent fatality cause. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app
FA 2020 - p114-115 blood transfusion reactions and autoantibodies
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.06.240101v1?rss=1 Authors: St Clair, R., Teti, M., Pavlovic, M., Hahn, W., Barenholtz, E. Abstract: Computer-aided rational vaccine design (RVD) and synthetic pharmacology are rapidly developing fields that leverage existing datasets for developing compounds of interest. Computational proteomics utilizes algorithms and models to probe proteins for functional prediction. A potentially strong target for such a computational approach is autoimmune antibodies which are the result of broken tolerance in the immune system where it cannot distinguish self from non-self resulting in attack of its own structures (proteins and DNA, mainly). The information on structure, function and pathogenicity of autoantibodies may assist in engineering RVD against autoimmune diseases. Current computational approaches exploit large datasets curated with extensive domain knowledge, most of which include the need for many computational resources and have been applied indirectly to problems of interest for DNA, RNA, and monomer protein binding. Here, we present a novel method for discovering potential binding sites. We employed long short-term memory (LSTM) models trained on FASTA primary sequences directly to predict protein binding in DNA-binding hydrolytic antibodies (abzymes). We also employed CNN models applied to the same dataset. While the CNN model outperformed the LSTM on the primary task of binding prediction, analysis of internal model representations of both models showed that the LSTM models highlighted sub-sequences that were more strongly correlated with sites known to be involved in binding. These results demonstrate that analysis of internal processes of recurrent neural network models may serve as a powerful tool for primary sequence analysis. Copy rights belong to original authors. Visit the link for more info
Dr. Rae Bacharach discusses the article, "Drebrin Autoantibodies in Patients with Seizures and Suspected Encephalitis". Show references: https://onlinelibrary.wiley.com/doi/full/10.1002/ana.25720
Between the latest online fads and the crazy media headlines, it’s easier than ever to get confused about your health. If you want to make better decisions about your health today so you can feel better and live longer, you’ve come to the right place. Today is the first episode of a three part series that examines the effect of grains on health. I’m joined today by the Gluten-Free Warrior — Dr. Peter Osborne, the founder of the Gluten-Free Society who works to help people with autoimmune and degenerative diseases. He shares some of the experiences and citations that have led him to work so passionately to educate people about the effect of grains on our overall health. Dr. Osborne has helped over 5,000 patients regain overall health and wellness with a grain-free diet, and his approach to healing is focused on individuals with auto-immune diseases. If you’ve ever suspected that you might have gluten intolerance but aren’t sure if you have Celiac disease, if you’re wondering what environmental factors might be affecting your health, or if you are looking for ways to eliminate painful reactions to gluten, you need to listen to this conversation to help you decide which steps you need to take next. Key Takeaways: [1:10] Today’s topic is grains — are they harmful to people who don’t have Celiac’s disease? [2:00] Introducing Dr. Peter Osborne, who shares his overall thoughts on the effects of grains on human health, the quality of studies that have been conducted about grains, and the importance of identifying autoimmune diseases when healing for chronic disease. [5:48] Dr. Osborne reacts to the statement that reduced-grain diets contribute to worse health outcomes, including cardiovascular death, and explains how the quality of the diet is a greater factor than the gluten intake itself. [9:52] The correlation between a grain-free diet and autoimmune disease, and a snapshot of the overall history and changing health factors that have an influence on a person's weakened health status. [15:00] The danger of not controlling for variables in a patient, the importance of believing that you can feel better again, and the value of overall body-fuel balance. [18:10] How can you tell if you have non-Celiac gluten sensitivity, and what can you do about it? Dr. Osborne suggests starting with diet change and supporting nutritional deficit. [22:30] Understanding the prevalence of non-Celiac gluten sensitivity and the environmental factors that accelerate it including exposure to pesticides, plastics, antibiotics, chemicals and medications. [27:04] Should all people with a gluten sensitivity be tested for Celiac’s disease? Dr. Osborne says that it is not necessary, and he explains why. [29:40] What are the pitfalls of making dietary changes that are not accurate relative to the symptoms that are actually present? A look at the variables that affect overall health regardless of gluten-sensitivity. [37:04] If variables such as molds, pesticides and hybridization are present, it becomes increasingly difficult to separate individual aspects of the diet. Here’s what to do about it. [39:24] A list of conditions for non-Celiac gluten sensitivities that are actually caused by gluten and the next steps you should take to begin healing. [43:41] Dr. Osborne’s number one tip for enhancing overall health starts with self observation — pay attention to how your body responds to activity, exercise and food before you decide that your condition is irreversible. [47:14] Do you have a topic you’d like me to cover? Contact me on Facebook or Instagram using #medicalmyths. To learn more: www.drchristianson.com Dr. Christianson on Instagram Dr. Christianson on Facebook Integrative Healthcare No Grain, No Pain: A 30-Day Diet for Eliminating the Root of Chronic Pain by Dr. Peter Osborne Gluten-Free Society Glutenology on YouTube Article References: 1. Arbuckle MR, James JA, Kohlhase KF, et al. Development of anti-dsDNA auto-antibodies prior to clinical diagnosis of systemic lupus erythematosus. Scand J Immunol. 2001;54(1–2):211–219. [PubMed] [Google Scholar] 2. Arbuckle MR, McClain MT, Rubertone MV, et al. Development of autoantibodies before the clinical onset of systemic lupus erythematosus. N Engl J Med. 2003;349(16):1526–1533. [PubMed] [Google Scholar] 3. Arslan S, Erkut B, Ates A, et al. Pseudoaneurysm of left ventricular following left ventricular apical venting. Clin Res Cardiol. 2009;98(4):280–282. [PubMed] [Google Scholar] 4. Majka DS, Deane KD, Parrish LA, et al. Duration of preclinical rheumatoid arthritis-related autoantibody positivity increases in subjects with older age at time of disease diagnosis. Ann Rheum Dis. 2008;67(6):801–807. [PMC free article] [PubMed] [Google Scholar] 5. Majka DS, Holers VM. Can we accurately predict the development of rheumatoid arthritis in the preclinical phase? Arthritis Rheum. 2003;48(10):2701–2705. [PubMed] [Google Scholar] 6. Rantapaa-Dahlqvist S, de Jong BA, Berglin E, et al. Antibodies against cyclic citrullinated peptide and IgA rheumatoid factor predict the development of rheumatoid arthritis. Arthritis Rheum. 2003;48(10):2741–2749. [PubMed] [Google Scholar] 7. Eriksson C, Kokkonen H, Johansson M, et al. Autoantibodies predate the onset of systemic lupus erythematosus in northern Sweden. Arthritis Res Ther. 2011;13(1):R30. [PMC free article] [PubMed] [Google Scholar]
Lupus isn’t well known, but the currently incurable autoimmune disease often marked by a ‘butterfly’ rash on the face, is highly prevalent, affecting five million people globally. Treatments are few and far between and few researchers are focused on it. But award winning medical researcher Professor Fabienne Mackay has concentrated much of her career on tackling lupus, and in 2011 her genetic research work led to the approval of the first new treatment for the disease in more than 50 years. And while that is good news for some patients, the treatment isn’t effective for all patients, and she says more research work and breakthroughs are needed. “I would love the public to realise that lupus is actually very prevalent; that the therapies we have at the moment, even though I worked towards one, are not serving everybody. It helps some patients but not all of them,” says Professor Mackay who in October 2019 received a Distinguished Innovator Award from the US-based Lupus Research Alliance. The good news is that we are still unravelling the secrets of the human body, which means there continues to be research leads to follow, including for instance the potential role of diet and the gut microbiome – the bacteria in our digestive system. “There is a whole story we didn’t realise was there and now it’s excitement all over again finding out how these layers are working on top of the layers we’ve already unravelled,” says Professor Mackay. “That is what fascinates me – you think you know it all and then there’s always something that comes and surprises you.” And her advice to her medical research students is to think big. “Always be bold. Think blue sky. It is a bit of risk and I know it’s never something that students are comfortable to do, but I think that where you find the most valuable discoveries.” Episode recorded: November 11, 2019. Interviewer: Dr Andi Horvath. Producer, audio engineer and editor: Chris Hatzis. Co-producers: Silvi Vann-Wall and Dr Andi Horvath. Image: Getty Images.
Dr. Andrew Mammen talks about what clinicians need to know about this subtype of dematomyositis.
If you are being treated for a blood disorder, it is time to look deeper and explore the underlying cause. Rather than simply addressing iron- or B12-deficiency anemia in isolation, ask WHY you have a deficiency in the first place. It is possible that damage to your intestines caused by gluten is preventing your body from absorbing the nutrients necessary to grow your red blood cells and keep your immune system healthy. And anemia is not the only blood disorder associated with celiac disease and non-celiac gluten sensitivity! The Gluten Free RN is taking a closer look at the hematologic manifestations of celiac disease from anemia to hyposplenism. She explains the connection between disorders of the blood and bones, offering insight around why men with both anemia and osteoporosis are also likely to have celiac disease. Nadine discusses the danger in taking H2 blockers or proton pump inhibitors for GERD long-term, describing how those medications decrease the gastric acid necessary for breaking down food. She also addresses what you can do to identify any nutritional deficiencies in your blood and reminds us why celiac patients have difficulty absorbing the nutrients necessary to form red blood cells. Listen in to understand how the skin reflects what’s happening internally and learn how to prevent a number of blood disorders with a gluten-free diet! What’s Discussed: The hematologic manifestations of celiac disease Anemia secondary to malabsorption of iron, folate and vitamin B12 Thrombocytosis, thrombocytopenia, leukopenia, venous thromboembolism Hyposplenism, IgA deficiency and increased risk of lymphoma Why iron supplements didn’t solve Nadine’s anemia Couldn’t absorb supplements due to undiagnosed celiac disease The connection between anemia, osteoporosis and celiac disease B12 forms red blood cells made in long bones The danger of taking H2 blockers and PPIs long-term Decreases levels of gastric acid necessary to liquify food Leads to bacterial overgrowth, gastritis How to uncover potential nutrient deficiencies in your blood CBC with differential (breakdown of red blood cells) The conclusions of the 2007 study in Blood Anemia and hyposplenism are most common complications of celiac disease Obtain small-bowel biopsy in all patients with iron-deficiency anemia The fat-soluble vitamins A, D, E and K Deficiency in one indicates malabsorption, potential celiac disease The connection between DH and celiac disease Skin disorders begin in intestines Resources: ‘Hematologic Manifestations of Celiac Disease’ in Blood Celiac Disease and Your Spleen Dr. Ben Lynch: Folic Acid vs. Folate ‘The Thrombophilic Network of Autoantibodies in Celiac Disease’ in BMC Medicine ‘Hematologic Manifestations of Celiac Disease’ in Celiac Disease— From Pathophysiology to Advanced Therapies ‘Sarcoidosis, Celiac Disease and Deep Venous Thrombosis: A Rare Association’ in Balkan Medical Journal ‘Celiac Disease Manifesting with Deep Venous Thrombosis: A Case Report’ in Govaresh ‘Deep Venous Thrombosis and Bilateral Pulmonary Embolism Revealing Silent Celiac Disease’ in Case Reports in Gastrointestinal Medicine ‘How Often Do Hematologists Consider Celiac Disease in Iron-Deficiency Anemia?’ in Clinical Advances in Hematology & Oncology ‘Deep Vein Thrombosis Associated with Celiac Disease’ in Bratislavske Lekarske Listy ‘Celiac Disease Presenting with Immune Thrombocytopenic Purpura’ in Case Reports in Hematology ‘Lower Extremity Deep Vein Thrombosis Associated with Gluten-Sensitivity Celiac Disease’ in Terapevticheskii Arkhiv Connect with Nadine: Instagram Facebook Contact via Email ‘Your Skin on Gluten’ on YouTube Melodies of the Danube Gluten-Free Cruise with Nadine Books by Nadine: Dough Nation: A Nurse's Memoir of Celiac Disease from Missed Diagnosis to Food and Heal
Guest: Robert A. Baldor, MD Guest: Chadwick R. Johr, MD This innovative, 45-minute, case-based CME activity features two prominent faculty covering important, timely issues and data related to the detection of autoimmune (AI) disorders. Using case studies, the faculty will explore diagnosis and management strategies to maximize patient care. In addition to the analysis of AI cases, key topics will be covered, including: Evaluation for suspected RA Combination serological assessment 14-3-3eta as a marker for joint damage Autoantibodies in SLE diagnosis and classification ANA IFA and subserologies Diagnosis of RA, Sjögren’s, Lupus, and Systemic Sclerosis
Today, we discuss highly tested autoantibodies and their associated disease states. In the second half of the show, we review ribs and rib dysfunction. Musical Guest: Colby Deitz Band
The September 2017's JNNP podcast is a double episode. The first conversation is with Professor Michael Hornberger from the Norwich Medical School, University of East Anglia, UK. The cerebellum is often overlooked when looking at neurodegenerative diseases, a practice which Professor Hornberger and his team are challenging. Their recent JNNP paper looks at patterns of grey matter atrophy in the cerebellum across neurodegenerative diseases. What they found may surprise some listeners. Read the paper here: http://jnnp.bmj.com/content/88/9/780. Elizabeth also speaks with Dr Ester Coutinho from the Nuffield Department of Clinical Neurosciences, University of Oxford, UK. Dr Coutinho & colleagues have been looking into maternal transfer of autoantibodies during pregnancy. In particular, their research has focused on antibodies which may be linked to disorders of psychological development in children. Read the paper here: http://jnnp.bmj.com/content/88/9/718.
Commentary by Dr. Valentin Fuster
Myasthenia gravis is a disorder characterized by proximal weakness, ptosis, and antibody formation against proteins at the neuromuscular junction. Most commonly, the protein targeted by antibodies is the nicotinic acetylcholine receptor. However, research in the last 2 decades has identified a number of other antibody targets, which we have reviewed here in this BrainWaves brief. BrainWaves podcasts and online content are intended for medical education only and should not be used to guide medical decision making in routine clinical practice. Any cases discussed in this episode are fictional and do not contain any patient health identifying information. The content in this episode was vetted and approved by Grant T. Liu. REFERENCES 1. Gilhus NE and Verschuuren JJ. Myasthenia gravis: subgroup classification and therapeutic strategies. The Lancet Neurology. 2015;14:1023-36. 2. Hurst RL and Gooch CL. Muscle-Specific Receptor Tyrosine Kinase (MuSK) Myasthenia Gravis. Current neurology and neuroscience reports. 2016;16:61. 3. Koneczny I, Cossins J and Vincent A. The role of muscle-specific tyrosine kinase (MuSK) and mystery of MuSK myasthenia gravis. J Anat. 2014;224:29-35. 4. Dalmau J and Rosenfeld MR. Paraneoplastic syndromes of the CNS. The Lancet Neurology. 2008;7:327-40. 5. Evoli A and Lancaster E. Paraneoplastic disorders in thymoma patients. J Thorac Oncol. 2014;9:S143-7.
Dermatomyositis and Autoantibodies by Dr. Andrew L. Mammen. This is part three of a three part series on immune-mediated myopathies and autoantibodies.
Dermatomyositis and Autoantibodies by Dr. Andrew L. Mammen. This is part three of a three part series on immune-mediated myopathies and autoantibodies.
Dermatomyositis and Autoantibodies by Dr. Andrew L. Mammen. This is part three of a three part series on immune-mediated myopathies and autoantibodies.
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 17/19
Myelin Oligodendrocyte Glycoprotein (MOG) is one of the few proteins known to be localized on the outermost sheath of central nervous system (CNS) myelin. Due to this localization, MOG is accessible to antibodies. Anti-MOG antibodies are demyelinating and enhance clinical symptoms in a number of animal models of CNS inflammation. Autoantibodies recognizing conformationally intact MOG are found in different inflammatory diseases of the CNS, but their antigenic epitopes had not been mapped. In this work, 9 variants of MOG with an intracellular enhanced green fluorescent protein (EGFP) tag were expressed on the cell surface of human HeLa cells and used to analyze sera from 111 patients (104 children, 7 adults), who had antibodies recognizing cell-bound human MOG. These patients had different diseases, namely acute disseminated encephalomyelitis (ADEM), one episode of transverse myelitis or optic neuritis, multiple sclerosis (MS), anti-aquaporin-4 (AQP4)–negative neuromyelitis optica (NMO), and chronic relapsing inflammatory optic neuritis (CRION). The expression levels of the mutants were comparable and cells with a defined expression level (fluorescence intensity in the EGFP channel of 102-103) were gated. Each MOG-mutant was recognized by at least one MOG-specific mAb. This allowed the comparison of binding to the different mutants. In order to assess the reproducibility of the system, binding of the 111 sera to the mutants was analyzed up to three times in independent experiments, yielding a very good reproducibility of the binding percentage with an absolute SD of 7.8% in the case of low recognition of a mutant and a relative SD of 20% in the case of high recognition of a mutant. The applied variants of MOG gave insight into epitope recognition of 98 patients. All epitopes identified in this work were located at loops connecting the ß-strands of MOG. The immunodominant epitope of human anti-MOG antibodies was at the membrane-proximal CC’-loop containing aa42, which is not present in rodent MOG. This loop was recognized by about half of all patients. Overall, seven epitope patterns were distinguished, including the one mainly recognized by mouse mAbs at the FG-loop around aa104. Evidence from mouse models of CNS inflammation shows that anti-MOG antibodies recognizing different epitopes can be demyelinating and thus pathogenic. This suggests that not only those antibodies recognizing the same epitope of MOG as the pathogenic mAbs (i.e. the FG-loop), but also the ones recognizing the CC'-loop are pathogenic in humans, as both epitopes allow for the recognition of cell-bound MOG. In half of the patients, the anti-MOG response was directed to a single epitope. To analyze the effect of glycosylation on the recognition of MOG by human autoantibodies, a “non-glycosylation mutant” N31D was made. Digestion with PNGaseF and Western blot analysis confirmed that N31 was the only used N-glycosylation site of the MOG constructs in HeLa cells. Glycosylation of MOG was not needed for antibody binding, but 8% of the patients recognized deglycosylated MOG at least two-fold better. The epitope specificity was not linked to certain disease entities. The individual epitope recognition patterns stayed constant in 11 analyzed patients over an observation period of up to 5 years without evidence for intramolecular epitope spreading. Some patients with acute syndromes had anti-MOG IgG at disease onset, but rapidly lost their anti-MOG IgG reactivity. These patients were able to generate a long-lasting IgG response to measles and rubella virus vaccine indicating that the loss of anti-MOG reactivity was not reflective of a lack of capacity for longstanding IgG responses. Human anti-MOG antibodies are mainly of the IgG1 isotype, which can activate complement and antibody dependent cellular cytotoxicity. Upon binding to MOG in the CNS, human anti-MOG antibodies are hence expected to cause demyelination. Transfer experiments with purified human anti-MOG antibodies have not been performed yet. The fact that the majority of human anti-MOG antibodies did not recognize rodent MOG has implications for animal studies. Using the described assay will help to identify patient samples appropriate for these transfer experiments and finally lead to the formal proof of the pathogenicity of human anti-MOG antibodies. This work also gives important information for future detection of potential mimotopes and the development of anti-MOG antibody detection assays and might pave the way to antigen-specific depletion.
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 17/19
Tue, 8 Jul 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/17144/ https://edoc.ub.uni-muenchen.de/17144/1/Kaiser_Cora.pdf Kaiser, Cora ddc:610, ddc:600, Medizinische Fakultät
Type 1 diabetes is a chronic progressive autoimmune disorder with complex, polygenic susceptibility. Environmental factors which are poorly defined also contribute to the pathogenesis. This disease is characterized by lymphocyte infiltration into the islets of Langerhans in the pancreas, leading to inflammation and selective destruction of the insulin-producing beta cells resulting in hyperglycemia.
MDS presents the latest research and findings from the field of Movement Disorders. Abstracts of articles from the Society Journal, Movement Disorders, are taken from the January 2014 (Vol. 29, Issue 1) issue.
Measurement of serum thyroglobulin may be complicated by the presence of endogenous anti-thyroglobulin auto-antibodies which have the potential to interfere with immunoassays and cause false negative results.
Interview with Sean J. Pittock, MD, author of Autoimmune Epilepsy: Clinical Characteristics and Response to Immunotherapy and Gregory K. Bergey, MD author of Autoantibodies in the Patient With Drug-Resistant Epilepsy: Are We Missing a Treatable Etiology?
B cells and antibodies constitute an important element in different inflammatory diseases of the central nervous system (CNS). Autoantibodies can serve as a biomarker to identify disease subgroups and may in addition contribute to the pathogenic process. One candidate autoantigen for multiple sclerosis (MS) is myelin oligodendrocyte glycoprotein (MOG). MOG is localized at the outermost surface of myelin in the CNS and has been the focus of extensive research for more than 30 years. Its role as an important autoantigen for T cells and as a target of demyelinating autoantibodies has been established in several variants of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. The literature regarding antibodies to MOG in MS patients is confusing and contradictory. Recent studies, however, have described high levels of antibodies to conformationally correct MOG in pediatric acquired demyelination, both acute disseminated encephalomyelitis (ADEM) and MS. In adult MS, such antibodies are rarely found and then only at low levels. In this review, we summarize key findings from animal models and patient studies, discuss challenges in detecting anti-MOG antibodies in patients and present recent approaches to identifying new autoantigens in MS.
The occurrence of SOX2-specific autoantibodies seems to be associated with an improved prognosis in patients with monoclonal gammopathy of undetermined significance (MGUS). However, it is unclear if SOX2-specific antibodies also develop in established multiple myeloma (MM). Screening 1094 peripheral blood (PB) sera from 196 MM patients and 100 PB sera from healthy donors, we detected SOX2-specific autoantibodies in 7.7% and 2.0% of patients and donors, respectively. We identified SOX2211-230 as an immunodominant antibody-epitope within the full protein sequence. SOX2 antigen was expressed in most healthy tissues and its expression did not correlate with the number of BM-resident plasma cells. Accordingly, anti-SOX2 immunity was not related to SOX2 expression levels or tumor burden in the patients' BM. The only clinical factor predicting the development of anti-SOX2 immunity was application of allogeneic stem cell transplantation (alloSCT). Anti-SOX2 antibodies occurred more frequently in patients who had received alloSCT (n = 74). Moreover, most SOX2-seropositive patients had only developed antibodies after alloSCT. This finding indicates that alloSCT is able to break tolerance towards this commonly expressed antigen. The questions whether SOX2-specific autoantibodies merely represent an epiphenomenon, are related to graft-versus-host effects or participate in the immune control of myeloma needs to be answered in prospective studies.
Fakultät für Biologie - Digitale Hochschulschriften der LMU - Teil 04/06
The electrical activity of the brain is the result of a complex interaction between excitation and inhibition mediated by several types of neurotransmitters. As the majority of neurons in the brain utilize either the inhibitory neurotransmitter γ-aminobutyric acid (GABA) or the excitatory neurotransmitter glutamate, the interplay of these two neurotransmitters principally controls brain excitability and, hence, imbalance between these two neurotransmitters may cause severe pathological conditions. Inhibition of glutamic acid decarboxylase (GAD), the rate-limiting enzyme of GABA synthesis, is believed to change neuronal network activity caused by impaired GABAergic inhibition. Recordings of intrinsic optical signals (IOSs) and whole-cell patch-clamp measurements of GABAA receptor-mediated miniature postsynaptic currents (GABAA Minis) and spontaneous excitatory postsynaptic currents (sEPSCs) were performed in the motor cortex in acute brain slices to unveil the effects of GAD inhibitors at the network level. The first project of this PhD thesis was to prove the IOS technique for its capability of monitoring neuronal network activity over several hours. Concurrently, new software for the analysis of IOS data was developed, which facilitates and significantly accelerates data analysis. Afterwards, changes in neuronal network activity after impairing GAD activity with the well-known GAD inhibitor semicarbazide (SMC) were observed with the IOS technique. If compared to the values of sham-drug application, a stable and reversible increase in both signal intensity and signal area was observed after 2 h of 2 mM SMC application. Consistent with these findings of IOS recordings, patch-clamp measurements of GABAA Minis revealed an SMC-induced reduction in the strength of GABAergic inhibition. The results are in line with the assumption that SMC impairs GABA synthesis by blocking GAD activity. SMC application, however, did not alter spontaneous excitatory neuronal network activity. The final aim of this study was to investigate potential effects of Anti-GAD autoantibodies-containing immunoglobulin G (IgG) derived from patients with stiff-person syndrome (SPS-IgG) on motor cortical neuronal network activity. IOS recordings do not reveal differences in neuronal network activity during SPS-IgG application and control IgG application. However, run-down of IOSs was significantly decelerated during IgG application, which possibly indicates a diminished neuronal cell death caused by an unspecific IgG effect. Compared to brain slices preincubated with IgG-free artificial cerebrospinal fluid, control IgG did not affect GABAA Mini amplitude and frequency as well as sEPSC amplitude. The sEPSC frequency, however, was significantly reduced under these conditions. This decreased excitatory transmitter release might explain the beneficial effect of immunoglobulin treatment in some forms of epilepsy. Similar to SMC, patch-clamp measurements of GABAA Minis revealed a reduction in the strength of GABAergic inhibition after preincubation with SPS-IgG. Consistent with this finding, application of SPS-IgG enhanced sEPSC frequency. This shows that IgG of SPS patients is indeed capable of altering GABAergic synaptic transmission, thus further supporting the hypothesis of an autoimmune origin of the stiff-person syndrome.
DLS from November 9, 2009
Aims: An association between inflammatory bowel disease (IBD) and spondyloarthropathies (SpA) has repeatedly been reported. The aim of the present study was to investigate whether serologic markers of IBD, e. g. antibodies against Saccharomyces cerevisiae (ASCA), antibodies against exocrine pancreas (PAB) and perinuclear antineutrophil cytoplasmic antibodies (pANCA) are present in HLA-B27-associated SpA. Methods: 87 patients with HLA-B27-positive SpA and 145 controls were tested for ASCA, PAB and pANCA employing ELISA or indirect immunofluorescence, respectively. Antibody-positive patients were interviewed regarding IBD-related symptoms using a standardized questionnaire. Results/Conclusion: When compared to the controls, ASCA IgA but not ASCA IgG levels were significantly increased in patients with SpA, in particular in ankylosing spondylitis (AS) and undifferentiated SpA (uSpA). pANCA were found in increased frequency in patients with SpA whereas PAB were not detected. The existence of autoantibodies was not associated with gastrointestinal symptoms but sustains the presence of a pathophysiological link between bowel inflammation and SpA. Copyright (C) 2004 S. Karger AG, Basel.
A novel prokaryotic expression vector pGEX-6T was designed for high-level expression of recombinant fusion protein with a histidine-hexapeptide and glutathione-S-transferase at its N-terminus and the recombinant human preproinsulin at its C-terminus. Efficiency of expression was investigated in the Escherichia coli strain CAG456. The synthesized protein was sequestered in an insoluble form in inclusion bodies and was purified to homogeneity by one-step affinity chromatography based on the specific complex formation of the histidine-hexapeptide and a chelating matrix which was charged with Ni2+ ions. The antigenic nature of the purified recombinant preproinsulin fusion protein was evaluated by ELISA screening for insulin autoantibodies in selected sera from patients with recent-onset type 1 (insulin-dependent) diabetes mellitus classified by the existence of additional autoantibodies reactive against glutamic acid decarboxylase. 14% of the tested sera (n=43) conttained insulin autoantibodies which strongly recognized the recombinant human preproinsulin. Comparable measurements with both recombinant human preproinsulin and mature insulin suggested that the observed autoantigenicity of preproinsulin was mediated by the C-peptide or/and signal peptide.
The first human monoclonal islet cell antibodies of the IgG class (MICA 1-6) obtained from an individual with Type 1 (insulin-dependent) diabetes mellitus were cytoplasmic islet cell antibodies selected by the indirect immunofluorescence test on pancreas sections. Surprisingly, they all recognized the 64 kDa autoantigen glutamate decarboxylase. In this study we investigated which typical features of cytoplasmic islet cell antibodies are represented by these monoclonals. We show by double immunofluorescence testing that MICA 1-6 stain pancreatic beta cells which is in agreement with the beta-cell specific expression of glutamate decarboxylase. In contrast an islet-reactive IgM monoclonal antibody obtained from a pre-diabetic individual stained all islet cells but lacked the tissue specificity of MICA 1-6 and must therefore be considered as a polyreactive IgM-antibody. We further demonstrate that MICA 1-6 revealed typical features of epitope sensitivity to biochemical treatment of the target tissue which has been demonstrated for islet cell antibodies, and which has been used to argue for a lipid rather than a protein nature of target antigens. Our results provide direct evidence that the epitopes recognized by the MICA are destroyed by methanol/chloroform treatment but reveal a high stability to Pronase digestion compared to proinsulin epitopes. Conformational protein epitopes in glutamate decarboxylase therefore show a sensitivity to biochemical treatment of sections such as ganglioside epitopes. MICA 1-6 share typical features of islet cell and 64 kDa antibodies and reveal that glutamate decarboxylase-reactive islet cell antibodies represent a subgroup of islet cell antibodies present in islet cell antibody-positive sera.
We investigated the presence of autoantibodies to baculovirus-expressed human recombinant 65- and 67-kD isoforms of glutamate decarboxylase (GAD65 and GAD67) in insulin-dependent diabetes mellitus (IDDM). In the immunoprecipitation test using [35S]methionine-labeled GADs antibodies to GAD65 were detected in 13/15 (87%) islet cell antibody (ICA)-positive and in 1/35 (2.9%) ICA-negative first-degree relatives of patients with IDDM, in 6/11 (54.5%) ICA-positive nondiabetic schoolchildren, and in 35/50 (70%) patients with newly diagnosed IDDM. GAD67 antibodies were positive only in five (33%) of the ICA-positive relatives (P < 0.05) and in nine (18%) IDDM patients at onset (P < 0.00001). After onset of IDDM antibodies to GAD65 and GAD67 declined but were still positive in 25 and 9.4% of subjects with long-standing IDDM (> 10 yr). In all study groups antibodies to GAD67 were only detected in GAD65 antibody-positive sera. An immunotrapping enzyme activity assay for GAD65 antibodies was positive in 64/75 (85.3%) of sera that were GAD antibody positive in the immunoprecipitation test (r = 0.870, P < 0.0001). In two (2.7%) sera GAD65 antibodies that block GAD enzyme activity were found. Our data suggest that antibodies to GAD65 but not to GAD67 represent sensitive markers for preclinical and overt IDDM. The immunotrapping assay here described represents a valuable technique for specific and sensitive screening for GAD antibodies.
Wed, 1 Jan 1992 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8880/1/8880.pdf Scriba, Peter Christian; Müller-Kunert, E.; Brühmann, A.; Schlumberger, W.; Olb
Out of a random population of 4208 non-diabetic pupils without a family history of Type I diabetes 44 (1.05%) individuals had islet cell antibody (ICA) levels greater or equal to 5 Juvenile Diabetes Foundation (JDF) units. 39 of these ICA-positives could be repeatedly tested for circulating insulin autoantibodies (CIAA) using a competitive radiobinding assay. The results were compared with the insulin responses in the intravenous glucose tolerance tests (IVGTT) and with HLA types. Six pupils were positive for CIAA. All of them had complement-fixing ICA, and 5 of them were HLA-DR4 positive. Three of the 6 showed a first-phase insulin response below the first percentile of normal controls. Our data indicate that in population-based studies CIAA can be considered as a high risk marker for impaired beta-cell function in non-diabetic ICA-positive individuals.
Mon, 1 Jan 1990 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8612/1/8612.pdf Scriba, Peter Christian; Kömpf, D.; Vieregge, P.; Schuhose, C.; Schaper, J.; Stöcker, W.
Mon, 1 Jan 1990 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8614/1/8614.pdf Scriba, Peter Christian; Kaiser, Doris; Horbach, E.; Otte, M.; Stöcker, W.; Rögener, W.
Tue, 1 Jan 1985 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8835/1/8835.pdf Scriba, Peter Christian; Berndt, H.; Geusendam, G.; Gutekunst, R.; Finkbeiner, H.; Stöcker, W.
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