Podcasts about epidermal

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I read from epidendrum to epigeal.     If Epidermal Growth Factor was turned into a roller coaster (look at the picture), that would be a fun ride.  https://en.wikipedia.org/wiki/Epidermal_growth_factor     The word of the episode is "epigeal". https://en.wikipedia.org/wiki/Epigeal     Theme music from Tom Maslowski https://zestysol.com/     Merchandising! https://www.teepublic.com/user/spejampar     "The Dictionary - Letter A" on YouTube   "The Dictionary - Letter B" on YouTube   "The Dictionary - Letter C" on YouTube   "The Dictionary - Letter D" on YouTube   "The Dictionary - Letter E" on YouTube     Featured in a Top 10 Dictionary Podcasts list! https://blog.feedspot.com/dictionary_podcasts/     Backwards Talking on YouTube: https://www.youtube.com/playlist?list=PLmIujMwEDbgZUexyR90jaTEEVmAYcCzuq     https://linktr.ee/spejampar dictionarypod@gmail.com https://www.facebook.com/thedictionarypod/ https://www.threads.net/@dictionarypod https://twitter.com/dictionarypod https://www.instagram.com/dictionarypod/ https://www.patreon.com/spejampar https://www.tiktok.com/@spejampar 917-727-5757

Lung cancer is a significant global health issue, being the second most commonly diagnosed cancer and the leading cause of cancer-related death worldwide. Non-small-cell lung cancer (NSCLC) represents the majority of lung cancer cases and is often diagnosed at an advanced stage. Epidermal growth factor receptor (EGFR) mutations are more common in Asian NSCLC populations than in Western populations. Activating EGFR mutations, such as exon 19 deletions and L858R, are predictive of response to tyrosine kinase inhibitors (TKIs) and have revolutionized the treatment landscape for patients with EGFR-mutated NSCLC. However, most clinical trials tend to lack data for the elderly population, even though a significant proportion of lung cancer patients are aged 65 years and older. This underrepresentation of elderly patients in clinical trials limits our understanding of the effectiveness and safety of EGFR-TKIs in this specific population. In this new study, researchers Ling-Jen Hung, Ping-Chih Hsu, Cheng-Ta Yang, Chih-Hsi Scott Kuo, John Wen-Cheng Chang, Chen-Yang Huang, Ching-Fu Chang, and Chiao-En Wu from Chang Gung University and Taoyuan General Hospital conducted a multi-institute retrospective study to investigate the effectiveness and safety of afatinib, gefitinib, and erlotinib for treatment-naïve elderly patients with EGFR-mutated advanced NSCLC. On January 8, 2024, their research paper was published in Aging's Volume 16, Issue 1, entitled, “Effectiveness and safety of afatinib, gefitinib, and erlotinib for treatment-naïve elderly patients with epidermal growth factor receptor-mutated advanced non-small-cell lung cancer: a multi-institute retrospective study.” Full blog - https://aging-us.org/2024/01/efficacy-and-safety-of-egfr-tkis-for-elderly-patients-with-nsclc/ Paper DOI - https://doi.org/10.18632/aging.205395 Corresponding author - Chiao-En Wu - 8805017@cgmh.org.tw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205395 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, elderly patients, epidermal growth factor receptor, tyrosine kinase inhibitor, non-small-cell lung cancer, real-world evidence About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Epidermal necrolysis refers to severe cutaneous reactions that cause extensive necrosis of tissue and detachment of the epidermis. It encompasses three conditions which are on a continuum of severity and how much of the body's surface area is affected: Stevens-Johnson syndrome (SJS): Less than 10% of BSA is detached Toxic epidermal necrolysis (TEN) - More than 30% of BSA is detached SJS/TEN overlap: Between 10 and 30% of BSA is detached In this episode you'll learn:  Epidermal necrolysis pathophysiology and risk factors High risk medications that can cause SJS/TEN Complications of SJS/TEN Signs and symptoms in the prodromal and acute phase Important assessment for a patient with SJS/TEN Key tests utilized to diagnose and evaluate a patient with epidermal necrolysis Treatments for SJS/TEN, including medications Vital education components for patients and families ________ Full Transcript - Read the article and view references Factor - Support our sponsor and get 50% off ready-to-eat meals with code nursemo50 FREE CLASS - If all you've heard are nursing school horror stories, then you need this class! Join me in this on-demand session where I dispel all those nursing school myths and show you that YES...you can thrive in nursing school without it taking over your life! DIC - Learn more about disseminated intravascular coagulation in this episode! Nursing School with a Chronic Illness - Hear more from Christina Brown, RN and how she managed nursing school with a chronic illness. Study Sesh - Change the way you study with this private podcast that includes dynamic audio formats that help you review and test your recall of important nursing concepts on-the-go. Free yourself from your desk with Study Sesh!  Med Surg Solution - Are you looking for a more effective way to learn Med Surg? Enroll in Med Surg Solution and get lessons on 57 key topics and out-of-this-world study guides. LATTE Method Template - Download the free LATTE Method Template so you can streamline how you study and focus on what a nurse needs to know.

BUFFALO, NY- November 30, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Chronological aging impacts abundance, function and microRNA content of extracellular vesicles produced by human epidermal keratinocytes.” The disturbance of intercellular communication is one of the hallmarks of aging. In their new study, researchers Taku Nedachi, Christelle Bonod, Julie Rorteau, Wafae Chinoune, Yuri Ishiuchi, Sandrine Hughes, Benjamin Gillet, Nicolas Bechetoille, Dominique Sigaudo-Roussel, and Jérôme Lamartine from the University of Lyon, Toyo University and Gattefossé SAS aimed to clarify the impact of chronological aging on extracellular vesicles (EVs), a key mode of communication in mammalian tissues. “The present study was therefore conducted to elucidate whether the characteristics of EVs released from cultured human keratinocytes can be modulated during aging process.” The researchers focused on epidermal keratinocytes, the main cells of the outer protective layer of the skin which is strongly impaired in the skin of elderly. EVs were purified from conditioned medium of primary keratinocytes isolated from infant or aged adult skin. A significant increase of the relative number of EVs released from aged keratinocytes was observed whereas their size distribution was not modified. By small RNA sequencing, the researchers described a specific microRNA (miRNA) signature of aged EVs with an increase abundance of miR-30a, a key regulator of barrier function in human epidermis. EVs from aged keratinocytes were found to be able to reduce the proliferation of young keratinocytes, to impact their organogenesis properties in a reconstructed epidermis model and to slow down the early steps of skin wound healing in mice, three features observed in aged epidermis. This work reveals that intercellular communication mediated by EVs is modulated during aging process in keratinocytes and might be involved in the functional defects observed in aged skin. “To conclude, we have shown here that aging modulates EVs abundance, function and microRNA content in human keratinocytes.” DOI - https://doi.org/10.18632/aging.205245 Corresponding author - Jérôme Lamartine - jerome.lamartine@univ-lyon1.fr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205245 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, keratinocytes, microRNA, senescence, exosomes About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.28.550974v1?rss=1 Authors: Peterman, E., Quitevis, E. J. A., Goo, C. E. A., Rasmussen, J. P. Abstract: Skin is often the first physical barrier to encounter invading pathogens and physical damage. Damage to the skin must be resolved quickly and efficiently to maintain organ homeostasis. Epidermal-resident immune cells known as Langerhans cells use dendritic protrusions to dynamically surveil the skin microenvironment, which contains epithelial keratinocytes and somatosensory peripheral axons. The mechanisms governing Langerhans cell dendrite dynamics and responses to tissue damage are not well understood. Using skin explants from adult zebrafish, we show that Langerhans cells maintain normal surveillance activity following axonal degeneration and use their dynamic dendrites to engulf small axonal debris. By contrast, a ramified-to-rounded shape transition accommodates the engulfment of larger keratinocyte debris. We find that Langerhans cell dendrites are richly populated with actin and sensitive to a broad spectrum actin inhibitor. We further show that Rho-associated kinase (ROCK) inhibition leads to elongated dendrites, perturbed clearance of large debris, and reduced Langerhans cell migration to tissue-scale wounds. Altogether, our work describes the unique dynamics of Langerhans cells and involvement of the ROCK pathway in immune cell responses to damage of varying magnitude. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week, we're welcoming back one of the most sought after facialists in the game, Joanna Vargas! Having caught up with us live and in person fresh from her red carpet run-up, Joanna recommends the essential skin tools, ingredients and massage moves we can all use to seriously level-up our skincare routines at home. Plus, as author of the book, Glow From Within, Joanna shares her 360 approach to healthy skin from the inside out.   Mindy Kaling, Rachel Brosnahan and Maggie Gyllenhaal flock to her spas in New York and LA to experience the celebrity esthetician's skilled hands, signature “triple crown facial” and patented LED bed (yep, we said BED).  And this just in, a stand-alone atelier opens in West Hollywood later this month, with plans to open a 10,000 square foot outpost in Brooklyn this fall. Until then, listen in to hear about:   At-home facial massage moves inspired by Joanna's very own triple crown facial, and why she's not a fan of jade rollers Epidermal growth factors - found in Joanna's eponymous line of skincare, Joanna explains all of the benefits behind the buzzy ingredient The most #worthit at-home skin tools, and where to invest in pro treatments Joanna's best tips for treating puffiness – including foods to avoid Rules for getting the most effective, clear skin results, for textured, acne-prone and sensitive skin types The secret Japanese sunscreen we neeeed to protect from hyperpigmentation Joanna's personal routine, including the green smoothie she drinks for lunch every day    Pssst! If you missed Joanna's first appearance on our show, go back and listen to learn all about how to protect and fix your skin's moisture barrier. That's episode 154, January 2021.   Get social with us and let us know what you think of the episode! Find us on Instagram, Tiktok, Twitter. Join our private Facebook group, or give us a call and leave us a voicemail at 1-844-227-0302.    For any products or links mentioned in this episode, check out our website: https://breakingbeautypodcast.com/episode-recaps/ PROMO CODES Sephora Sephora has an amazing selection of Clean makeup brands and products, and the “Clean” seal makes it easy to shop. To learn more visit Sephora.com/clean   Starface If you're ready to start celebrating and decorating your pimples, you can shop the entire Starface collection at Starface.World.  And for a limited time, all Breaking Beauty listeners are getting 15% off their first purchase when you enter the code BREAKINGBEAUTY at checkout.    Blissy Blissy silk pillowcases are the best ones on the market! They have a ton of different prints and colors and they make great gifts because there's an option for literally anyone (men love them too!). Try now risk-free for 60 nights, at Blissy.com/BREAKING and get an additional 30% off.    Fast Growing Trees Join more than 1.5 million happy Fast Growing Trees customers. If you're based in the US, head to FastGrowingTrees.com/ BEAUTY now to get 15% off your entire order.  *Disclaimer: Unless otherwise stated, all products reviewed are gratis media samples submitted for editorial consideration.*   Hosts: Carlene Higgins and Jill Dunn Theme song, used with permission: Cherry Bomb by Saya
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Interview with Benjamin H. Kaffenberger, MD, MS, author of Development of a Skin-Directed Scoring System for Stevens-Johnson Syndrome and Epidermal Necrolysis: A Delphi Consensus Exercise. Hosted by Adewole S. Adamson, MD. Related Content: Development of a Skin-Directed Scoring System for Stevens-Johnson Syndrome and Epidermal Necrolysis

Interview with Benjamin H. Kaffenberger, MD, MS, author of Development of a Skin-Directed Scoring System for Stevens-Johnson Syndrome and Epidermal Necrolysis: A Delphi Consensus Exercise. Hosted by Adewole S. Adamson, MD. Related Content: Development of a Skin-Directed Scoring System for Stevens-Johnson Syndrome and Epidermal Necrolysis

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.30.534941v1?rss=1 Authors: Ingram, S., DeCorte, A., Gentry, A. E., Philpott, M. K., Moldenhauer, T., Stadler, S., Steinberg, C., Millman, J., Ehrhardt, C. J. Abstract: Analysis of DNA mixtures from sexual assault evidence is an ongoing challenge for DNA casework laboratories. There is a significant need for new techniques that can provide information as to the source of DNA, particularly for sexual assault samples that do not involve semen. The goal of this study was to develop a new biological signature system that provides additional probative value to samples comprised of mixtures of epidermal and vaginal cells, as may be observed in cases involving digital penetration. Signatures were based on morphological and autofluorescence properties of individual cells collected through Imaging Flow Cytometry (IFC). Comparisons to reference cell populations from vaginal tissue and epidermal cells collected from hands showed strong multivariate differences across greater than 80 cellular measurements. These differences were used to build a predictive framework for classifying unknown cell populations as originating from epithelial cells associated with digital penetration or epidermal tissue. As part of the classification scheme, posterior probabilities of specific tissue group membership were calculated for each cell, along with multivariate similarity to that tissue type. We tested this approach on cell populations from reference tissue as well as mock casework samples involving digital penetration. Many more cells classifying as non-epidermal tissue were detected in digital penetration samples than control hand swabbings. Minimum interpretation thresholds were developed to minimize false positives; these thresholds were also effective when screening licked hands, indicating the potential utility of this method for a variety of biological mixture types and depositional events relevant to forensic casework. Results showed that samples collected subsequent to digital penetration possessed markedly higher numbers of cells classifying as vaginal tissue as well as higher posterior probabilities for vaginal tissue ( greater than or equal to 0.90) compared to cell populations collected from hands without prior contact with vaginal tissue. Additionally, digital penetration cell populations may be resolved from saliva cell populations and other non-target tissue types. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.23.533814v1?rss=1 Authors: Scharaw, S., Sola Carvajal, A., Belevich, I., Webb, A. T., Das, S., Andersson, S., Pentinmikko, N., Villablanca, E. J., Goldenring, J. R., Jokitalo, E., Coffey, R. J., Katajisto, P. Abstract: Cell-to-cell signalling between niche and stem cells regulates tissue regeneration. While the identity of many mediating factors is known, it is largely unknown whether stem cells optimize their receptiveness to niche signals according to the niche organization. Here, we show that Lgr5+ small intestinal stem cells (ISCs) regulate the morphology and orientation of their secretory apparatus to match the niche architecture, and to increase transport efficiency of niche signal receptors. Unlike the progenitor cells lacking lateral niche contacts, ISCs orient Golgi apparatus laterally towards Paneth cells of the epithelial niche, and divide Golgi into multiple stacks reflecting the number of Paneth cell contacts. Stem cells with a higher number of lateral Golgi transported Epidermal growth factor receptor (Egfr) with a higher efficiency than cells with one Golgi. The lateral Golgi orientation and enhanced Egfr transport required A-kinase anchor protein 9 (Akap9), and was necessary for normal regenerative capacity in vitro. Moreover, reduced Akap9 in aged ISCs renders ISCs insensitive to niche-dependent modulation of Golgi stack number and transport efficiency. Our results reveal stem cell-specific Golgi complex configuration that facilitates efficient niche signal reception and tissue regeneration, which is compromised in the aged epithelium. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.23.529672v1?rss=1 Authors: Yang, Y., Yu, C., Le, Y., Gong, W., Ju, J., Zhang, G., Ji, P., Zuo, R., Liu, Z., Zhang, P., Hou, R., Fu, Y. Abstract: Proliferation and migration of epidermal stem cells (EpSCs) are essential for epithelialization during skin wound healing. Angiopoietin-like 4 (ANGPTL4) has been reported to play an important role in wound healing, but the mechanisms involved are not fully understood. Here we investigate the contribution of ANGPTL4 to full-thickness wound re-epithelialization and the underlying mechanisms using Angptl4 knockout mice. Immunohistochemical staining reveals that ANGPTL4 is significantly upregulated in the basal layer cells of the epidermis around the wound during cutaneous wound healing. ANGPTL4 deficiency impairs wound healing. H & E staining shows that ANGPTL4 deficiency significantly reduces the thickness, length and area of regenerated epidermis postwounding. Immunohistochemical staining for markers of EpSCs (alpha 6 integrin and beta 1 integrin) and cell proliferation (PCNA) shows that the number and proliferation of EpSCs in the basal layer of the epidermis are reduced in ANGPTL4-deficient mice. In vitro studies show that ANGPTL4 deficiency impedes EpSC proliferation, causes cell cycle arrest at the G1 phase and reduced the expression of cyclins D1 and A2, which can be reversed by ANGPTL4 overexpression. ANGPTL4 deletion suppresses EpSC migration, which is also rescued by ANGPTL4 overexpression. Overexpression of ANGPTL4 in EpSCs accelerates cell proliferation and migration. Collectively, our results indicate that ANGPTL4 promotes EpSCs proliferation by upregulating cyclins D1 and A2 expression and accelerating cell cycle transition from G1 to S phase, and ANGPTL4 promotes skin wound re-epithelialization by stimulating EpSC proliferation and migration. Our study reveals a novel mechanism underlying EpSC activation and re-epithelialization during cutaneous wound healing. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this radiology lecture, we review the ultrasound appearance of epidermal inclusion cyst! Key teaching points include: Epidermal inclusion cyst The post Case Review: Ultrasound of Epidermal Inclusion Cyst appeared first on Radiologist Headquarters.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.14.528558v1?rss=1 Authors: Clary, R. C., Jenkins, B. A., Lumpkin, E. A. Abstract: As the juncture between the body and environment, epithelia are both protective barriers and sensory interfaces that continually renew. To determine whether sensory neurons remodel to maintain homeostasis, we used in vivo two-photon imaging of somatosensory axons innervating Merkel cells in adult mouse skin. These touch receptors were highly plastic: 63% of Merkel cells and 89% of branches appeared, disappeared, grew, regressed and/or relocated over a month. Interestingly, Merkel-cell plasticity was synchronized across arbors during rapid epithelial turnover. When Merkel cells remodeled, the degree of plasticity between Merkel-cell clusters and their axons was well correlated. Moreover, branches were stabilized by Merkel-cell contacts. These findings highlight the role of epithelial-neural crosstalk in homeostatic remodeling. Conversely, axons were also dynamic when Merkel cells were stable, indicating that intrinsic neural mechanisms drive branch plasticity. Two terminal morphologies innervated Merkel cells: transient swellings called boutons, and stable cups termed kylikes. In Atoh1 knockout mice that lack Merkel cells, axons showed higher complexity than control mice, with exuberant branching and no kylikes. Thus, Merkel cells limit axonal branching and promote branch maturation. Together, these results reveal a previously unsuspected high degree of plasticity in somatosensory axons that is biased, but not solely dictated, by plasticity of target epithelial cells. This system provides a platform to identify intrinsic and extrinsic mechanisms that govern axonal patterning in epithelial homeostasis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.13.528249v1?rss=1 Authors: Jing, J., Chen, S., Wu, X., Yang, J., Liu, X., Wang, J., Wang, J., Li, Y., Zhang, P., Tang, Z. Abstract: Intracerebral hemorrhage (ICH) is an acute cerebrovascular disease with high disability and mortality rates. Recombinant tissue plasminogen activator (rtPA) is commonly applied for hematoma evacuation in minimally invasive surgery (MIS) after ICH. However, rtPA may contact directly with brain tissue during MIS procedure, which makes it necessary to discuss the safety of rtPA. We found that, in the in vivo ICH model induced by VII-type collagenase, rtPA treatment improved the neurological function of ICH mice, alleviated the pathological damage and decreased the apoptosis and autophagy level of the peri-hematoma tissue. In the in-vitro model of ICH induced by hemin, the administration of rtPA down-regulated neuronal apoptosis, autophagy, and endoplasmic reticulum stress of neurons. Transcriptome sequencing analysis showed that rtPA treatment upregulated the PI3K/AKT/mTOR pathway in neurons, and PI3K inhibitor (LY294002) can reverse the protective effects of rtPA in inhibiting excessive apoptosis, autophagy and ER-stress. Epidermal growth factor receptor inhibitor (AG-1487) reversed the effect of rtPA on PI3K/AKT/mTOR pathway, which might indicate that the EGF domain played an important role in the activation of PI3K/AKT/mTOR pathway. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Join DMK Founder and Aesthetic Legend Danné Montague King for AMA With Danné, a podcast continuation of our regular Q&A With Danné series answering all your pressing queries on everything Skin Revision. We've got some surprises up our sleeve in this latest installment; make sure you're tuned in if you don't want to miss it! Got skincare questions? We have the answers. Submit your inquiries for the next episode via Instagram @dmkinternational or at: ask@dannemontagueking.com.New episodes every 3rd Friday of the month. Instagram - Facebook - TikTok - Twitterwww.dannemking.com

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.24.523981v1?rss=1 Authors: O'Brien, J., Niehaus, P., Remark, J., Salimian, M., Kevas, Y., Rubin, S., Kristian, T., Chandrasekeran, K., Lu, C. P.-J., Russell, J., Ho, C.-Y. Abstract: Diabetic neuropathy (DN) is a debilitating disorder characterized by mechanical allodynia and sensory loss. It has traditionally been considered a small-fiber neuropathy, defined by the loss of free nerve endings in the epidermis. Free nerve endings, however, are nociceptors which may not be the only sensor for mechanical pain. To investigate the role of mechanoreceptors, specifically Meissner corpuscles, in the development of diabetic mechanical allodynia, our study focused on the keratinocyte-secreted brain-derived neurotrophic factor (BDNF) and its transcriptional regulator sirtuin 1 (SIRT1). Wild-type DN mice demonstrated decreased SIRT1 deacetylase activity, leading to a decrease in BDNF expression and Meissner corpuscle densities in foot skin. Epidermal SIRT1 knockout (KO) mice developed exacerbated DN phenotypes including severe mechanical allodynia, markedly reduced Meissner corpuscles, and subcutaneous A-beta axon degeneration. Among the major skin-derived neurotrophic factors, only BDNF was down-regulated in epidermal SIRT1 KO mice. With similar KO phenotypes, epidermal BDNF appeared to belong to the same pathway as SIRT1 in modulating diabetic mechanical allodynia. Furthermore, mice overexpressing epidermal SIRT1 showed BDNF up-regulation and improved DN phenotypes, supporting an important role of epidermal SIRT1 and BDNF in skin sensory apparatus regeneration and functional recovery in the setting of diabetes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.28.522133v1?rss=1 Authors: Rathod, M., Franz, H., Beyersdorfer, V., Wanuske, M.-T., Fischer, K. L., Stüdle, C., Zimmermann, A., Spindler, V. Abstract: Glycosylation is an essential mediator of cell-cell adhesion and epidermal differentiation. We used CRISPR/Cas9-based gene editing to determine the role of dolichol phosphate mannosyltransferase 1 (DPM1), a key enzyme for N- and O-glycosylation. DPM1 loss resulted in weakening of cell-cell adhesion, impaired localization of the desmosome components desmoplakin and desmoglein 2, and cytoskeletal organization defects in human keratinocytes. In a 3D organotypic human epidermis model, loss of DPM1 resulted in impaired differentiation with abnormally increased cornification, reduced thickness of non-corneal layers, and the formation of intercellular gaps in the epidermis. Using proteomic approaches, SERPINB5 was identified as novel interaction partner of desmoplakin, ameliorating the effects of DPM1 loss on cell-cell adhesion and epidermal differentiation. Further analysis showed that the changes induced by DPM1 and SERPINB5 loss were at least in part dependent on elevated TGF-{beta} signalling. Together, we identify DPM1 through SERPINB5 as a novel regulator of cell-cell adhesion and differentiation. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.06.519291v1?rss=1 Authors: Cai, Y., Zhang, X., Li, C., Ghashghaei, T., Greenbaum, A. Abstract: Tissue clearing renders entire organs transparent to enable combination with light sheet fluorescence microscopy and accelerate whole tissue imaging. Yet, challenges remain in analyzing the large resulting 3D datasets that consist of terabytes of images and information on millions of labeled cells. Previous work has established pipelines for automated analysis of tissue cleared mouse brains. However, they have focused on single color channels and/or detection of nuclear localized signals, in relatively low-resolution images. To address this gap, we present an automated workflow to map labeled neurons and astrocytes in the genetically distinct Mosaic Analysis with Double Markers (MADM) mouse forebrains. We named the workflow COMBINe (Cell detectiOn in Mouse BraIN) as it combines modules from multiple pipelines. With RetinaNet in its core, we quantitatively analyzed the regional and subregional effects of MADM-based deletion of the Epidermal growth factor receptor on neuronal and astrocyte populations in the mouse forebrain. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.31.514487v1?rss=1 Authors: Nedachi, T., Bonod, C., Rorteau, J., Chinoune, W., Ischiuchi, Y., Hugues, S., Gillet, B., Sigaudo-Roussel, D., Lamartine, J. Abstract: The disturbance of intercellular communication is one of the hallmarks of aging. The goal of this study is to clarify the impact of chronological aging on extracellular vesicles (EVs), a key mode of communication in mammalian tissues. We focused on epidermal keratinocytes, the main cells of the outer protective layer of the skin which is strongly impaired in the skin of elderly. EVs were purified from conditioned medium of primary keratinocytes isolated from infant or aged adult skin. A significant increase of the relative number of EVs released from aged keratinocytes was observed whereas their size distribution was not modified. By small RNA sequencing, we described a specific microRNA (miRNA) signature of aged EVs with an increase abundance of miR-30a, a key regulator of barrier function in human epidermis. EVs from aged keratinocytes were found to be able to reduce the proliferation of young keratinocytes, to impact their organogenesis properties in a reconstructed epidermis model and to slow down the early steps of skin wound healing in mice, three features observed in aged epidermis. This work reveals that intercellular communication mediated by EVs is modulated during aging process in keratinocytes and might be involved in the functional defects observed in aged skin. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.31.514582v1?rss=1 Authors: Rybak, J. A., Sahoo, A. R., Kim, S., Pyron, R. J., Pitts, S. B., Guleryuz, S., Smith, A. W., Buck, M., Barrera, F. N. Abstract: The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (RTK) commonly targeted for inhibition by anti-cancer therapeutics. Current therapeutics target the kinase domain or extracellular region of EGFR. However, these types of inhibitors are not specific for tumors over healthy tissue and therefore cause undesirable side effects. Our lab has recently developed a new strategy to regulate RTK activity by designing a peptide that specifically binds to the transmembrane (TM) region of the RTK to allosterically modify kinase activity. These peptides are acidity-responsive, allowing them to preferentially target acidic environments like tumors. We have applied this strategy to EGFR and created the PET1 peptide. We observed that PET1 behaves as a pH-responsive peptide that modulates the configuration of the EGFR TM through a direct interaction. Our data indicated that PET1 inhibits EGFR-mediated cell migration. Finally, we investigated the mechanism of inhibition through molecular dynamics simulations, which showed that PET1 sits between the EGFR TM dimer. We propose that the resulting disruption of native TM interactions disrupts the conformation of the kinase domain, inhibiting the ability of EGFR to send migratory cell signals. This study is a proof-of-concept that acidity-responsive membrane peptide ligands can be generally applied to RTKs. In addition, PET1 constitutes a viable approach to therapeutically target the TM of EGFR. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.07.511265v1?rss=1 Authors: Yoshino, J., Mali, S., Williams, C., Morita, T., Emerson, C., Arp, C., Sophie, M., Yin, C., The, L., Chikaya, H., Motoyoshi, M., Ishii, K., Emoto, K., Bautista, D. M., Parrish, J. Z. Abstract: Somatosensory neurons (SSNs) that detect and transduce mechanical, thermal, and chemical stimuli densely innervate an animal's skin. However, despite the fact that epidermal cells provide the first point of contact for sensory stimuli. our understanding of roles that epidermal cells play in SSN function, particularly nociception, remains limited. Here, we show that stimulating Drosophila epidermal cells elicits activation of SSNs including nociceptors and triggers a variety of behavior outputs, including avoidance and escape. Further, we find that epidermal cells are intrinsically mechanosensitive and that epidermal mechanically evoked calcium responses require the store-operated calcium channel Orai. Epidermal cell stimulation augments larval responses to acute nociceptive stimuli and promotes prolonged hypersensitivity to subsequent mechanical stimuli. Hence, epidermal cells are key determinants of nociceptive sensitivity and sensitization, acting as primary sensors of noxious stimuli that tune nociceptor output and drive protective behaviors. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

David Pharis, MD, FAAD interviewed by Abel Torres, MD, JD, MBA, FAAD

Infants in the NICU are patients that require specialized care with unique clinical considerations. Specific recommendations must be considered for all systems of NICU patients and the skin is not any different. Infants who are being cared for in the NICU, especially those that were born premature have an increased risk for skin trauma. On this episode, we review some of the skin care guidelines and recommendations available for clinical practice of NICU patients. As NICU clinicians, is is important to not only be aware of the anatomical variations of a term and preterm infant's skin, but to also know how that guides their clinical care and treatment plan. Many of the topics we cover on this episode have been standards of care for years, but there are also new recommendations for practice and products available based on recent research findings. NICU clinicians will hear a great review as well as up-to-date clinical recommendations for skin care of our specialized population in the NICU. The episode will also be beneficial for parents to hear the clinical practice guidelines and recommendations for term and preterm infants as well as some of the variations that may exist between different institutions. Our NICU Roadmap: A Comprehensive NICU Journal: https://empoweringnicuparents.com/nicujournal/NeoTech Free Samples: neotechneoshades.comNICU Mama Hats: https://empoweringnicuparents.com/hats/NICU Milestone Cards: https://empoweringnicuparents.com/nicuproducts/Empowering NICU Parents Show Notes: https://empoweringnicuparents.com/episode35Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group: https://www.facebook.com/groups/empoweringnicuparentsPinterest Page: https://pin.it/36MJjmH

You hear dermatologists mention the "multimodal approach to allergies" but what does that mean beyond prescribing an anti-itch therapy? Find out why the epidermal barrier matters and how you can help restore it for your itchy patients.

Welcome To Blue Presents A Podcast! Today my guests are Siggi and Stefan of Epidermal Veil. Join us as we discuss their debut single "My Wish Your Veil Of Flesh". We also discuss the formation of Epidermal Veil and how Stefan and Siggi met. CHECK OUT LINKSlinktr.ee/bluepresentsCHECK OUT EPIDERMAL VEIL:https://www.instagram.com/epidermalveil/https://distrokid.com/hyperfollow/epidermalveil/my-wish-your-veil-of-flesh

Suiting Ao, MD and Wang Fang, MD interviewed by Steven Chen, MD, FAAD

A Systematic Review of Efficacy and Safety of Monotherapy and Combination Therapy With Biologic for Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis Kirk Barber is joined by Dr Marisa Ponzo to discuss her article in the Nov/Dec issue of the Journal of Cutaneous Medicine and Surgery, a deep and thorough investigation of treatments for Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. Dr Ponzo runs a specialty clinic that reviews these cases and is responsible for the treatment of this very rare disease, at St Paul's Hospital in Vancouver, which has become a referral centre for this condition. She's also the division head of Dermatology at St. Paul's and a community dermatologist at West Dermatology. Dr Ponzo's co-authors on this article are Dr Muskaan Sachdeva and Dr Khalad Maliyar, both from the faculty of medicine at the University of Toronto.This article is open access at the JCMS website for three weeks after this episode is posted.JCMS Author Interviews is produced by David McGuffin of Explore Podcast Productions in Ottawa.Our theme music was composed by Lee Rosevere.Be sure to also check out the CDA's Residents Podcast, Dermalogues, hosted by Dr Kerri Purdy, available at the CDA website or wherever you listen.For more on the work of the CDA, please visit our website: www.dermatology.ca

A Systematic Review of Efficacy and Safety of Monotherapy and Combination Therapy With Biologic for Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis Kirk Barber is joined by Dr Marisa Ponzo to discuss her article in the Nov/Dec issue of the Journal of Cutaneous Medicine and Surgery, a deep and thorough investigation of treatments for Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. Dr Ponzo runs a specialty clinic that reviews these cases and is responsible for the treatment of this very rare disease, at St Paul's Hospital in Vancouver, which has become a referral centre for this condition. She's also the division head of Dermatology at St. Paul's and a community dermatologist at West Dermatology. Dr Ponzo's co-authors on this article are Dr Muskaan Sachdeva and Dr Khalad Maliyar, both from the faculty of medicine at the University of Toronto.This article is open access at the JCMS website for three weeks after this episode is posted.JCMS Author Interviews is produced by David McGuffin of Explore Podcast Productions in Ottawa.Our theme music was composed by Lee Rosevere.Be sure to also check out the CDA's Residents Podcast, Dermalogues, hosted by Dr Kerri Purdy, available at the CDA website or wherever you listen.For more on the work of the CDA, please visit our website: www.dermatology.ca

In the previous episode, Dr. Nagourney discussed targeted cancer therapy. One particular class of targeted agents are called epidermal growth factors. The epidermal growth factor receptor protein is involved in cell signaling pathways that control cell division and survival. Drugs that block epidermal growth factor receptor proteins can be used for certain kinds of cancer.

In this episode, we review the high-yield topic of Epidermal Inclusion Cyst from the Hand section. Follow Orthobullets on Social Media: Facebook: www.facebook.com/orthobullets Instagram: www.instagram.com/orthobulletsofficial Twitter: www.twitter.com/orthobullets LinkedIn: www.linkedin.com/company/27125689 YouTube: www.youtube.com/channel/UCMZSlD9OhkFG2t25oM14FvQ --- Send in a voice message: https://anchor.fm/orthobullets/message

This ep is all about dermaplanning and what it is!! I really hope you enjoyed this episode and I'm super happy to be back recording!! Ps. To get 50% off my course; Upgrade your Skin Science Knowledge in 10 Days, use code SLU50 & follow this link: www.skin-queen.com/skin-science-knowledge Thank you for listening and stay moisturized xx

Merhabalar, bu yazımızda sizlere acil serviste nadir de olsa karşılaştığımız Steven-Johnson sendromu (SJS) ve toksik epidermal nekrolizden (TEN) bahsedeceğim. Ufacık bir patofizyolojiden sonra SJS ve TEN ayrımından daha sonra da skorlama sistemi, mortalite oranları ve tedavi yaklaşımından bahsederek konuyu sonlandırağız. Stevens-Johnson sendromu (SJS) ve toksik epidermal nekroliz (TEN), en yaygın olarak ilaçlarla tetiklenen, ateş, yoğun nekroz ve epidermisin ayrılması ile karakterize şiddetli mukokutanöz advers reaksiyonlardır. Mukoza zarları, hastaların yüzde 90'ından fazlasında, genellikle iki veya daha fazla farklı bölgede (oküler, oral ve genital) etkilenir.1 Yaygın epidermis hasarının nedeni keratinositlerin apotozisidir. İlaçlar ya da metabolitlerinin, hapten görevi görerek keratinositlerin yüzeyine bağlanmasının ve onları antijenik hale getirmesinin olayı başlattığı düşünülmektedir. İlaca özgül CD8 (+) sitotoksik T hücrelerinin Fas/FasL ve perforin/granzim B yolağı ile keratinosit apotozisini tetikleyerek hastalığı başlattığı düşünülür.2 SJS ve TEN, bir hastalık sürekliliği olarak kabul edilir ve esas olarak, cilt dekolmanı ile ilgili vücut yüzeyinin yüzdesine dayalı olarak ayırt edilir: ●SJS, cilt dekolmanının vücut yüzeyinin yüzde 10'undan az olduğu, daha az şiddetli durumdur.  SJS Deri Değişiklikleri ●TEN, vücut yüzey alanının yüzde 30'undan fazlasının ayrılmasını içerir. Toksik Epidermal Nekroliz ●SJS/TEN örtüşmesi, vücut yüzey alanının yüzde 10 ila 30'u, cilt dekolmanı olan hastaları tanımlar. SJS/TEN örnekleri3 Şiddet ve Prognozun Hızla Değerlendirilmesi SJS ve TEN olduğundan şüphelenilen hastalar hastaneye yatırılmalıdır. SJS veya TEN tanısı konur konmaz, uygun tıbbi ortamı tanımlamak için hastalığın şiddeti ve prognozu hızla belirlenmelidir. Bireysel hastaların prognozu, SCORTEN (Score of toxic epidermal necrolysis) adı verilen prognostik skorlama sistemi kullanılarak başvuru anında hızla değerlendirilebilir.3 SCORTEN, yedi bağımsız ve kolayca ölçülebilen klinik ve laboratuvar değişkenine dayanmaktadır ve SJS/TEN için hastaneye yatışın birinci ve üçüncü günlerinde kullanım için onaylanmıştır. Parametreler SkorSkor aralığı Mortalite hızı(%)Yaş ≥ 4010-13,2Malignite1212,1Tutulan vücut yüzeyi ≥ %101335,3Taşikardi ≥1201458,3BUN >10 mmol/L ( >28 mg/dL)1≥590Serum Glukoz >14 mmol/L (>252 mg/dL) 1Serum Bikarbonat < 20 mmol/L1Skor7Stevens-Johnson Sendromu/Toksik Epidermal Nekroliz için SCORTEN Skoru11 SCORTEN skoru, aşağıda açıklanacağı gibi, her bir hastanın tedavisi için hangi klinik ortamın (yoğun tedavi/yanık ünitesi veya uzman olmayan servis) uygun olduğunu belirlemek için kullanılabilir.  Yoğun Tedaviye veya Yanık Ünitesine Sevk  Hastayı yoğun bakım veya yanık ünitesine sevk etme kararı, cilt tutulumunun kapsamına ve komorbiditelerin varlığına bağlı olarak vaka bazında verilmelidir. Hızla ilerlemeyen sınırlı cilt tutulumu olan, ve SCORTEN skoru 0 veya 1 olan hastalar, bu alanda uzmanlaşmamış servislerde tedavi edilebilir. Daha şiddetli hastalığı (cilt dekolmanı > vücut yüzey alanının % 30'u) veya SCORTEN skoru ≥2 olan hastalar, varsa yoğun bakım ünitelerine, yanık ünitelerine veya özel dermatoloji ünitelerine transfer edilmelidir. Birkaç çalışma, yanık bakım ünitesine veya yoğun bakım ünitesine hemen nakledilen hastalarda prognozun daha iyi olduğunu göstermektedir.4 Neden Olan İlaçların Hemen Kesilmesi İlaçların neden olduğu SJS ve TEN şüphesi olan hastalar için, kusurlu ajanın erken tanımlanması ve geri çekilmesi prognozu iyileştirebilir. Kesinlikle İlişkiliİlişkiliŞüpheli İlişik/Düşük RiskAllopurinolDiklofenakPantopazolLamotrijinDoksisiklinGlikokortikoidlerSülfametoksazolAmoksisilin/AmpisilinOmeprazolKarbamazepinSiprofloksasinTetrazepamFeniotinLevofloksasinDipiron (metamizol)NevirapinAmifostinTerbinafinSülfasazalinOkskarbazepinLevetirasetamDiğer SülfonamidlerRifampin (rifampisin) Oksikam NSAID'lerFenobarbitalEtorikoksibStevens-Johnson Sendromu/...

Stevens-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe skin and other body system manifestations of immune hypersensitivity, typically in response to medications and, more commonly in kids, infections. They used to be thought of as different conditions but now we think of them as occurring on a spectrum, according to how much of the body surface is affected. Toxic epidermal necrolysis is the most severe disorder in the spectrum, but both TEN and SJS can be fatal if not managed.   Links and resources: Follow us on Instagram @yourekiddingrightdoctors Facebook: https://www.facebook.com/yourekiddingrightpod-107273607638323/ Our email is yourekiddingrightpod@gmail.com Make sure you hit SUBSCRIBE/FOLLOW so you don't miss out on any pearls of wisdom and RATE if you can to help other people find us! (This isn't individual medical advice, please use your own clinical judgement and local guidelines when caring for your patients)

FDA approvals of Verzenio (abemaciclib) for adjuvant treatment of hormone receptor-positive, human epidermal growth factor receptor 2-negative, node-positive, early breast cancer, & Keytruda (pembrolizumab) for persistent, recurrent or metastatic cervical cancer whose tumors express PD-L1 (CPS ≥

Initially, I was a little thrown off when I heard Douxo® was changing their main active ingredient from phytosphingosine to ophytrium. Why change it now? But, as I learned more about the upgrades that were being made to the new Douxo® S3 line, I was really excited hear about the thought and innovation that went into upgrading this line.On this episode of the podcast, I got to talk to two amazing ladies from Ceva Animal Health: Dr. Christine Mullins (veterinary services manager) and Jacqueline Hodges (associate key account manager). They walk though the steps to this upgrade to assessing its effect on new canine skin models, a human skin model (to assure safety for owners) and in real canine patients. Not only were the ingredients considered but the user experience with the bottle, smell and lather. Enjoy learning all about this new line of topicals!

An interview with Dr. Beverly Moy from Massachusetts General Hospital, co-chair on “Chemotherapy and Targeted Therapy for Patients With HER2-Negative Metastatic Breast Cancer That is Either Endocrine-Pretreated or Hormone Receptor-Negative: ASCO Guideline Update.” Updated guidance addresses optimal sequence of therapy & indications for treatment regimens. Read the guideline at asco.org/breast-cancer-guidelines. Suggest a topic for guideline development at surveymonkey.com/r/ascoguidelinesurvey.   TRANSCRIPT [MUSIC PLAYING] SPEAKER: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. [MUSIC PLAYING] BRITTANY HARVEY: Hello and welcome to the ASCO Guidelines podcast series brought to you by the ASCO Podcast Network, a collection of nine programs covering a range of educational and scientific content and offering enriching insight into the world of cancer care. You can find all the shows, including this one, at podcast.asco.org. My name is Brittany Harvey. And today I'm interviewing Dr. Beverly Moy from Massachusetts General Hospital in Boston, Massachusetts, co-chair and lead author on chemotherapy and targeted therapy for patients with HER2 negative metastatic breast cancer that is either endocrine pre-treated or hormone receptor negative ASCO guideline update. Thank you for being here, Dr. Moy. BEVERLY MOY: Thanks for having me, Brittany. BRITTANY HARVEY: First, I'd like to note that ASCO takes great care in the development of its guidelines and ensuring that the ASCO conflict of interest policy is followed for each guideline. The full conflict of interest information for this guideline panel is available online with the publication of the guideline in the Journal of Clinical Oncology. Dr. Moy, do you have any relevant disclosures that are directly related to this guideline topic? BEVERLY MOY: I do not have any relevant disclosures related to this guideline topic. BRITTANY HARVEY: Great. Thanks so much. Then let's get into what this update covers. So first, what prompted the update of this ASCO guideline and what does the scope of this guideline update? BEVERLY MOY: So this guideline update was developed to address both chemotherapy and targeted therapy for women with advanced HER2 negative breast cancer that is either endocrine pre-treated or hormone receptor negative. So it really focuses on chemo and targeted therapy. The original ASCO clinical treatment guideline was published in 2014 and really focused on chemotherapy, since that was generally the standard of care at that time. Since 2014, however, there have been several important new therapies that have become available based on robust evidence from numerous clinical trials. These include, but are not limited to, BOLERO-6 and PEARL trials for hormone receptor positive HER2 negative metastatic breast cancer, the ASCENT and EMBRACE trials for triple negative metastatic breast cancer, and the EMBRACA trial for metastatic breast cancer associated with germline BRCA1 or 2 mutations. So it really was important to update the guideline in a fairly urgent matter. BRITTANY HARVEY: Great. Well, then this guideline addresses four overarching clinical questions. For each of these, I'd like to review the key recommendations for our listeners. So starting with question one, is there an optimal sequence of chemotherapy and/or targeted therapy for patients with triple negative metastatic breast cancer either with or without BRCA1 or BRCA2 germline mutations? BEVERLY MOY: So clinical question one really focused on patients with metastatic triple negative breast cancer. So for patients with metastatic triple negative disease, the first key question is, what is the Programmed cell Death Ligand 1, or what we call PD-L1 status? If the disease is PD-L1 positive, then patients may be offered first line therapy with an immune checkpoint inhibitor plus chemotherapy. And that's a very important development. If the disease, however, is PD-L1 negative, patients should be offered single agent chemotherapy rather than combination chemotherapy, unless they have symptomatic or immediately life-threatening disease, and you really need to get a response more quickly. In those cases, combination chemotherapy can be used. After the first line, if patients with metastatic triple negative breast cancer have received at least two prior therapies, then they should be offered treatment with the new antibody drug conjugate called sacituzumab govitecan, which is a very exciting development in the treatment of metastatic triple negative breast cancer. If the patient has a germline BRCA1 or 2 mutation and has metastatic triple negative disease and have been previously treated with chemotherapy, then they may be offered treatment with an oral PARP inhibitor rather than chemotherapy, also a very exciting development that this guideline update addresses. BRITTANY HARVEY: Great. Thank you for reviewing those recommendations for triple negative metastatic breast cancer. So then next for clinical question two, what are the indications for chemotherapy versus endocrine therapy in endocrine pre-treated estrogen receptor positive metastatic breast cancer? BEVERLY MOY: So clinical question two focuses on women or patients with metastatic hormone receptor positive breast cancer who have developed progressive disease on a prior endocrine therapy with or without targeted therapy. So really is focusing on patients with metastatic hormone receptor positive breast cancer that have become fairly resistant to endocrine therapy alone. These patients may be offered treatment with either endocrine therapy with or without a targeted therapy or single agent chemotherapy. Brittany, I think it's important for listeners to realize that there is another important clinical practice guideline update that's being released simultaneously with this guideline. And that one is called endocrine therapy and targeted therapy for hormone receptor positive metastatic breast cancer. This other guideline update will describe in detail recommendations for the various targeted therapies that can be used with endocrine therapy, such as CDK4/6 inhibitors, PI 3-kinase inhibitors, and others. So I encourage everyone to read this guideline as well. Importantly, both guidelines state that treatment choice should be based on individualized patient and provider assessment of preferences, risks, and benefits. BRITTANY HARVEY: Great. And thank you for pointing out that companion guideline. Listeners can also listen to a podcast episode with Dr. Burstein on that particular guideline, which will be available in our podcast feed. So then next, what are the key recommendations for the third question in the guideline, which is, is there an optimal sequence of non-endocrine agents for patients with hormone receptor positive but HER2 negative metastatic breast cancer who are no longer benefiting from endocrine therapy, either with or without BRCA1 or BRCA2 germline mutations? BEVERLY MOY: So this third question really focuses on patients with hormone receptor positive HER2 negative disease and the optimal sequence. Essentially what we recommend is that germline BRCA1 or 2 patients with metastatic hormone receptor positive HER2 negative breast cancer who are no longer benefiting from endocrine therapy, those patients may be offered an oral PARP inhibitor in the first through third line setting rather than chemotherapy. And that is evidence that is evolving and important, and that's what the guideline recommends at this time. BRITTANY HARVEY: Great. And then clinical question four was the last question addressed in this guideline update. And what did the panel say regarding at what point should a patient be transitioned to hospice or best supportive care only? BEVERLY MOY: So this obviously is an incredibly important question for clinicians and oncologists to consider. The current literature and evidence does not allow us, at this time, to make a firm recommendation regarding at which point a patient's care should be transitioned to hospice or best supportive care only. When to transition is a decision that really needs to be shared between the patient and clinician in the context of an ongoing conversation regarding goals of care. The conversation of that integration of supportive care and eventual consideration of hospice care really should start early in the management of metastatic breast cancer. And these conversations have to occur throughout. I would also refer listeners to other important clinical treatment guidelines on the ASCO website about incorporation of palliative and supportive care for patients with metastatic cancer. I think those are incredibly valuable guidelines. BRITTANY HARVEY: And then you've touched on this a bit as you've talked about the recommendations, but in your view, what is the importance of this guideline update? And how will these updated recommendations impact both clinicians and patients? BEVERLY MOY: I think that this is an extremely important guideline update. It provides really important clinical guidance about the new use of immune checkpoint inhibitors, which really is the first time immune checkpoint inhibitors are clearly recommended for the treatment of breast cancer. It also provides important clinical guidance about this new antibody drug conjugate, sacituzumab govitecan, and PARP inhibitors for the treatment of metastatic breast cancer. These are all important and effective new treatments for breast cancer. And every clinician should be aware of their optimal uses. I will point out that many unanswered questions remain. And that was really an exciting part of doing this guideline update to look at these unanswered questions, such as what we described earlier, the optimal time to transition to best supportive care only and the widespread use of molecular tumor profiling. As treatments get more complicated and the entire oncology community are increasingly tasked to absorb new data, ASCO guidelines are enormously helpful in giving people an easy to access tool that takes into account the latest data. BRITTANY HARVEY: Great. Thank you so much for your work on this guideline update and for taking the time to speak with me today, Dr. Moy. BEVERLY MOY: Thank you. BRITTANY HARVEY: And thank you to all of our listeners for tuning in to the ASCO Guidelines podcast series. To read the full guideline, go to www.asco.org/breast cancer guidelines. Additionally, our annual survey for guideline topics is open for submissions. Suggest a topic for guideline development at surveymonkey.com /r/ascoguidelinesurvey. The link is also available in the episode notes of this podcast. If you've enjoyed what you've heard today, please rate and review the podcast and be sure to subscribe so you never miss episode. [MUSIC PLAYING]

An interview with Dr. Harold Burstein from Dana Farber Cancer Institute in Boston, MA, chair on “Endocrine Treatment and Targeted Therapy for Hormone Receptor-Positive, HER2-Negative Metastatic Breast Cancer: ASCO Guideline Update.” This guideline updates recommendations on use of alpelisib, and the role of biomarkers and CDK4/6 inhibitors. Read the guideline at asco.org/breast-cancer-guidelines. Suggest a topic for guideline development at surveymonkey.com/r/ascoguidelinesurvey.   TRANSCRIPT [MUSIC PLAYING] SPEAKER: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. [MUSIC PLAYING] BRITTANY HARVEY: Hello and welcome to the ASCO Guidelines podcast series brought to you by the ASCO Podcast Network, a collection of nine programs covering a range of educational and scientific content and offering enriching insight into the world of cancer care. You can find all the shows, including this one, at podcasts.asco.org. My name is Brittany Harvey. And today I'm interviewing Dr. Harold Burstein from Dana-Farber Cancer Institute in Boston, Massachusetts, chair and lead author on endocrine treatment and targeted therapy for hormone receptor-positive HER2 negative metastatic breast cancer ASCO guideline update. Thank you for being here, Dr. Burstein. HAROLD BURSTEIN: Glad to be with you. BRITTANY HARVEY: First I'd like to note that ASCO takes great care in the development of its guidelines in ensuring that the ASCO conflict of interest policy is followed for each guideline. The full conflict of interest information for this guideline panel is available online with the publication of the guideline in the Journal of Clinical Oncology. Dr. Burstein, do you have any relevant disclosures that are related to this guideline topic? HAROLD BURSTEIN: I do not. BRITTANY HARVEY: Great, thank you. Then let's delve into the content of this guideline. So first, what prompted the update of this guideline and what is the focus of this update? HAROLD BURSTEIN: So this guideline focuses on metastatic breast cancer, and in particular, estrogen receptor-positive HER2 negative metastatic breast cancer. Worldwide in 2021, actually breast cancer became the most commonly diagnosed cancer in the world, excepting superficial skin cancers. And so it is a true global health problem. And the most common type of breast cancer is estrogen receptor-positive HER2 negative breast cancer, which accounts for 70% to 75% of all cancer diagnoses in the breast cancer space, and as a consequence, also accounts for 70% to 75% of the cases of metastatic breast cancer. So it's really important from a public health point of view and a quality point of view, both in the United States and globally, to have current up-to-date guidance for the management of this most common form of breast cancer that we have. In addition, there have been several innovations in the way of targeted therapies that are coming into place for advanced ER-positive breast cancer. And increasingly, we are using genomic tests to help us understand how best to treat patients with advanced ER-positive breast cancer. So those two initiatives-- the interest in genomic testing and the use of targeted therapies-- all warranted and justified an update to the guidelines. BRITTANY HARVEY: Great. Thank you for reviewing that landscape of where we are in clinical practice for this guideline. So then I'd like to review the key recommendations that this guideline addresses. So first, should alpelisib be given to post-menopausal women and to male patients with hormone receptor-positive HER2 negative PIK3CA-mutated advanced or metastatic breast cancer? HAROLD BURSTEIN: So alpelisib, as you indicated, is a new drug. It is now FDA approved. And it is a protein kinase targeted inhibitor. And it goes after the PIK3CA-mutated tumors. And in a seminal study called the SOLAR-1 study, there was randomization to endocrine therapy alone with fulvestrant or endocrine therapy plus alpelisib for ER-positive HER2 negative breast cancer. And that study showed two important things. First was that in women whose tumors did not have a PIK3CA mutation, there was no benefit for alpelisib. However, in the women whose tumors did have a PIK3CA mutation, there was an improvement in progression-free survival with the use of this targeted drug alpelisib. So based on that, the guidelines now incorporate alpelisib into the treatment algorithm. And as a corollary, it means that all patients who have ER-positive metastatic breast cancer now need testing of the tumor to see if they have a PIK3CA mutation because that's going to guide therapy. In the guideline, we now suggest that this be a standard thing to do-- to test all tumors for PIK3CA mutation. And in those cases where there is a PIK3CA mutation to add alpelisib-based therapy with endocrine treatment typically in second or subsequent lines of therapy. BRITTANY HARVEY: Great. And thank you for reviewing the evidence base behind that recommendation. So next, what is recommended regarding the role of biomarkers in treatment selection for patients with hormone receptor-positive metastatic breast cancer? HAROLD BURSTEIN: So there are two different ways of thinking about biomarkers. One is traditional biomarkers, such as estrogen receptor, progesterone receptor, and HER2. Those are familiar to all clinicians who have been dealing with breast cancer. The second is to think about some of the newer technologies, including tumor genomic sequencing and the kind of mutational analysis we just discussed with the PIK3CA mutations. So in the breast cancer space, there are some important innovations in that latter genomic or genetic testing. One, of course, is the PIK3CA mutation testing that we now recommend for all cancers. That can be done on the primary tumor, or it can be done on cell-free or circulating tumor DNA samples from the bloodstream in most cases. The other kind of testing we do relates to ESR1 mutations. And one of the reasons that tumors become resistant to aromatase inhibitors is that they acquire mutations in the estrogen receptor itself, so-called ESR1 activating mutations. Those mutations mean that the estrogen receptor is on even in the absence of estrogen. And that accounts for probably 50% to 60% of the resistance that we see in treatment with aromatase inhibitors. So the panel really struggled with this because, on the one hand, this is not a uniformly accepted way to decide how to treat patients. On the other hand, there are a lot of data that women whose tumors have ESR1 mutations get negligible benefit from ongoing use of aromatase inhibitor therapy. So this recommendation fell into sort of our practice suggestions, which is that if you have the information on ESR1, then it probably is the case that there's very little, if any, role for ongoing aromatase inhibitor treatment. This fell short of the highest level in endorsement because, first, it's not a uniformly tested assay. And secondly, it's important to remember that these tumors can still benefit from ongoing anti-estrogen therapy with different anti-estrogens like fulvestrant. And finally, and perhaps this is the most practical issue, the way you become ESR1 mutated is usually through exposure to aromatase inhibitors. And if you've already had a patient with extensive exposure to AIs, and they need ongoing anti-estrogen therapy in the metastatic setting, it usually means you're switching treatment anyway. So that's an example of where we're sort of on the frontier of thinking about dynamic changes in the tumor as a way to select treatment for ER-positive metastatic disease. BRITTANY HARVEY: Great. That's helpful for a clinical interpretation of the recommendations and incorporating these into practice. So the final question that was addressed in this focused update was, what is the role of CDK4/6 inhibitors in the treatment of patients with hormone receptor-positive metastatic breast cancer? HAROLD BURSTEIN: So CDK4/6 inhibitors are another tyrosine kinase inhibitor class of drugs that has really emerged as an important part of first-line therapy for ER-positive metastatic disease. There have been multiple randomized trials looking at either first-line therapy with an aromatase inhibitor with or without a CDKI4/6 inhibitor, or second-line treatment typically with fulvestrant with or without a CDKI4/6 inhibitor in the metastatic setting. And the panel was able to update the guidance here based on the maturation of multiple randomized trials, as well as extensive subset analyses that have been performed by investigators associated with the individual pharmaceutical-led studies and by the FDA itself. So here are some important takeaways. The first is that in long-term follow-up, these drugs as a class are improving overall survival for women with ER-positive HER2 negative metastatic breast cancer. And for that reason, they are a very important part of the standard armamentarium for ER-positive disease. It's important to say that they also delay the onset of need for chemotherapy, and in general, are associated with a very well preserved quality of life. So this is a big win for patients with ER-positive metastatic breast cancer. We typically recommend them in the first-line setting. So if a patient has de novo metastatic disease, then they should get an endocrine therapy such as an aromatase inhibitor with a CDK4/6 inhibitor. If they've previously had adjuvant aromatase inhibitor treatment or recur while on adjuvant endocrine therapy, we often move to fulvestrant plus a CDKI4/6 inhibitor. Both settings have shown substantial benefit for this class of drugs. It's important that clinicians understand the side effects of these drugs. Neutropenia and diarrhea are common side effects associated with the various drugs. And because of the prevalence of ER-positive metastatic disease, it's really important for clinicians and all those who care for advanced breast cancer patients to know how to manage those side effects carefully. The panel discussed controversial issues, I suppose you might say, in the management. What about patients who have truly minimal metastatic disease? There aren't a lot of data on how best to think about those patients. And we all can imagine on a case-by-case basis an individual who might not need a CDK4/6 inhibitor at a given moment in time. But what was impressive when we pulled all the data was that in subset analyses, it's really hard to find a group of patients that does not benefit from the incorporation of these drugs. So that included premenopausal women who also get concurrent ovarian suppression and then endocrine therapy plus the CDK4/6 inhibitor. It included women with bone-only metastatic disease. It included women whose tumors were ER-positive but PR negative, or had other variations in ER expression. It included patients who had less rather than more metastatic cancer, including visceral disease. So in the literature, one is hard-pressed to see a subset that does not benefit meaningfully from this class of drugs. So we really wanted to reiterate in the algorithms just how important these are. They should be the standard first-line treatment for metastatic disease either paired with an AI or with fulvestrant. And so one of the other nice things that the update gave us was the opportunity to put in some fresh sort of algorithm flow sheets. I would very much encourage people to look at that. They make fantastic PowerPoint or downloadable Twitter documents if you are so inclined. But it's very clear the way the treatment should flow, which is the initial therapy is endocrine treatment plus a CDK4/6 inhibitor. While the patients are getting that, we typically test for PIK3CA mutations. In second line, if it's a PIK3CA mutated, you have the option of using alpelisib. You also might consider an older drug for PIK3CA wild type tumors called everolimus. We reiterated that recommendation in the guideline. Finally, one more thing to touch on that is emerging in the guidelines we generated and in the parallel guideline process for the ASCO guidance on chemotherapy-resistant or refractory breast cancer is the importance of genetic testing all patients who have metastatic breast cancer to look for the possibility of a BRCA1 or BRCA2 deleterious mutation, because there now is FDA approval for PARP inhibitors in the setting of metastatic disease. And one of the interesting things is that as we test more and more, we're seeing that not all the patients who are found to have a BRCA1 or 2 mutation meet the classic criteria for genetic testing-- strong family history, or say, triple-negative breast cancer. So it's really important to test, because that class of drugs, the PARP inhibitors, can be immensely helpful in women with ER-positive metastatic disease when they harbor a BRCA1 or 2 mutation. One of the things the guideline panel wrestled with and ended up putting into the sort of clinical discussion, as opposed to the strong guidance, was the 1% of patients who have PALB2 mutations. So PALB2 mutation, another hereditary predisposing factor for breast cancer. Most tumors that arise in PALB2 mutation carriers are in fact estrogen receptor positive. And a very small study, now published in the JCO, has suggested that those patients have a very high likelihood of response to PARP inhibitors. Because there were only like 15 patients in that cohort, we didn't feel that this warranted clear endorsement in the guidelines. But at the same time, everyone on the panel acknowledges that this is an active drug in that rare subset of tumors with PALB2 mutations in addition to the BRCA1 or 2 mutations. So the takeaway here is that genetic testing should be standard for all patients with advanced metastatic breast cancer to see if the patient is a candidate for a PARP inhibitor-based therapy. BRITTANY HARVEY: Definitely. Well, thank you for reviewing all of those updated recommendations and highlighting some of the ones that were still relevant to this guideline. HAROLD BURSTEIN: Work in progress. BRITTANY HARVEY: Yeah, definitely. And then finally, what is the importance of this guideline update? And how will it impact both clinical practice and what does it mean for patients? HAROLD BURSTEIN: Well, I think guidelines like this have multiple purposes. The first is to sort of describe the state of the art. And while breast cancer is a very common disease, and most clinicians who take care of a lot of cancer patients will see a lot of advanced breast cancer, I think it's still helpful to articulate the rationale for these treatment recommendations. And one of the great things about the ASCO guideline process is the thoroughness of the literature review, the thoroughness of the search to make sure we're including all important publications, and the thoughtfulness that the panel, which includes experts, patient advocates, quality of life expertise, all those things bring to bear on really thinking through what makes sense and what does not for our patients based on the best science available. So I think it is an important activity to really sort of benchmark where we're at. The second thing we've tried to do in the guideline is to introduce areas of nuanced discussion, because not every patient is the same. And I think for those who are interested and take the time to read the guideline, there really is a very nice discussion about how our panel thought about when best to use this approach and when to use a different approach. Third, there's extensive discussion of the side effects and the appropriate management of the side effects. These are drugs that do carry risks. And while by oncology standards, many of them are, quote, "well tolerated," unquote, there's no doubt that there are side effects to these drugs. And it's important for clinical teams to know how to manage them. Finally, I think by putting forward all the evidence, you make clear to investigators, to drug companies, to patients and advocates, and others who are involved in the review of new drugs what the benchmarks are and what the criteria should be for designing clinical trials and for approving new drugs. And I think we've done a nice job of framing that discussion quite handsomely in this guideline and to all of the ASCO guidelines. BRITTANY HARVEY: Great. Well, thank you so much for your work on this guideline update and for taking the time to speak with me today, Dr. Burstein. HAROLD BURSTEIN: Happy to join you and thanks very much. BRITTANY HARVEY: And thank you to all of our listeners for tuning in to the ASCO Guidelines podcast series. To read the full guideline, go to www.asco.org/breast cancer guidelines. Additionally, our annual survey for guideline topics is open for submissions. Suggest a topic for guideline development at SurveyMonkey.com /r/ascoguidelinesurvey. The link is also available in the episode notes of this podcast. If you've enjoyed what you've heard today, please rate and review the podcast and be sure to subscribe so you never miss an episode. [MUSIC PLAYING]

This episode covers Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).Written notes can be found at https://zerotofinals.com/paediatrics/dermatology/sjs/ or in the dermatology section of the Zero to Finals paediatrics book.The audio in the episode was expertly edited by Harry Watchman.

Experts explain the benefits of using epidermal growth factor in skin care — here's what to know about the wrinkle-smoothing powerhouse.

Dallas facial plastic surgeon Dr. Sam Lam talks about why he uses much longer epidermal sutures and shorter dermal sutures, which is the reverse of what he used five years ago.

This episode is also available as a blog post: http://biopatrika.com/2021/05/11/interview-serum-media-alternative-culture-human-dermal-fibroblasts-and-epidermal-keratinocytes/

Interview with Robert Gil Micheletti, MD, author of Long-term Physical and Psychological Outcomes of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis

Interview with Robert Gil Micheletti, MD, author of Long-term Physical and Psychological Outcomes of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis

Dr Sarah Walsh of the EADV Education Committee sits down and speaks with prominent researchers Dr Pauline O'Reilly and Prof. Jean-Pascal Lefaucheur to discuss two previously poorly-explored aspects of SJS/TEN. Prof Lefaucheur gives insights in to the prevalence of chronic skin pain and possible pathomechanisms, and Dr O'Reilly discusses her research in the area of post-traumatic stress disorder and other psychological consequences of this devastating disease, for patients themselves, their families and their care-givers.   Articles referenced in this episode can be found in the JEADV: Patients', family members' and healthcare practitioners' experiences of Stevens–Johnson syndrome and toxic epidermal necrolysis: a qualitative descriptive study using emotional touchpoints https://www.onlinelibrary.wiley.com/doi/10.1111/jdv.16958   Involvement of small‐diameter nerve fibres in long‐term chronic pain after Stevens–Johnson syndrome or toxic epidermal necrolysis. A neurophysiological assessment https://www.onlinelibrary.wiley.com/doi/10.1111/jdv.16940   Chronic pain: a long‐term sequela of epidermal necrolysis (Stevens–Johnson syndrome/toxic epidermal necrolysis) – prevalence, clinical characteristics and risk factors https://www.onlinelibrary.wiley.com/doi/10.1111/jdv.16891

Today's interview is with Lindsay Passodelis, who has a rare disease called CLOVES Syndrome (Congenital, Lipomatous, Overgrowth, Vascular malformations, Epidermal nevi, and Spinal/Skeletal anomalies and/or Scoliosis), and works at an outpatient transplant center in Pittsburgh as a social worker. She is also a blogger, an ambassador for Allstripes, and is on the CLOVES Family Advisory Council, so she basically lives to advocate! She talks about the specifics of her case, how a physical rare condition affects body image, how important support systems are in a rare disease journey, and much more! Be sure to subscribe to R is for Rare on Apple Podcasts, Spotify, or wherever you get your podcasts! Share the podcast on social media (can post from Spotify to your Instagram story), and leave a review and let me know what you think of the podcast! Follow Lindsay on Instagram - @lindsayy_lovie Lindsay's blog - peaceloveheal.org CLOVES Syndrome Community - https://clovessyndrome.org --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/annie-watson/message

Episode 3 features Dr. April Schachtel and Dr. Katherine Stiff reviewing the following recent publications:Lian et al. Spectrum of Nail Sequelae in Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. JAMA Dermatol. 2021;157(1):117-119. ​Mejbel et al. Prognostic Significance of Subungual Anatomic Site in Acral Lentiginous Melanoma. Arch Pathol Lab Med 20200 [Online Head of Print].

Kirsten is the Clinical Educator for Candela Medical ANZ, which despite being based in Melbourne, has clientele across Australia and New Zealand. Kirsten obtained a Bachelor of Dermal Science and has been an influence in the industry for the past 25 years, specialising in Beauty and Aesthetics devices. Kirsten is responsible for the education and training of the medical devices in Victoria, South Australia, and Tasmania with Candela medical and today she shares with us an insightful look into the cause and condition of epidermal versus dermal pigmentation. A valuable episode for all treating therapists, clinicians and aestheticians who are wanting to gain further treatment results with their clients when using devices for the management of pigmentation. With the purchase of a Candela device, you receive a 3-year service warranty, clinical training for you and your team, as well as access to their comprehensive marketing resources. Your success is their success. Find out more on their website. Don't forget to join our online Facebook community here where thousands of like-minded business owners you like keep each other supported and connected with the latest in the professional beauty industry. If you would like to stay up to date with the latest from Beaute Industrie you can subscribe to our monthly newsletter here. Beaute Industrie Podcast is an independent podcast that operates with the support of our listeners (that's you!) So if you would like to support the show, we would very much appreciate that. Hit 'subscribe' on Apple Podcasts or 'follow' on Spotify, and leave a review if you're feeling especially generous. Your host for the podcast is @tamarareidbeaute and we're at @beauteindustrie --- Send in a voice message: https://anchor.fm/beaute-industrie/message

In this episode, Bryan talks with Kristen about how he has been feeling lately knowing that his dad is moments away from getting a very long, somewhat-safe, and yet still very frightening surgery. Life Level 1 is a general topic podcast about life from the humorous perspective of Bryan and his broad, Kristen. Bryan has a background in video game development and Kristen has a background in life. The thoughts and opinions expressed on this podcast are those of the individual contributors alone and are not a reflection of their employers.

A look at this deadly mucocutaneous reaction and how to best manage these patients in the ED https://media.blubrry.com/coreem/content.blubrry.com/coreem/SJS.mp3 Download Leave a Comment Tags: Critical Care, Dermatology Show Notes Episode Produced by Audrey Bree Tse, MD Rash with dysuria should raise concern for SJS with associated urethritis Dysuria present in a majority of cases SJS is a mucocutaneous reaction caused by Type IV hypersensitivity Cytotoxic t-lymphocytes apoptose keratinocytes → blistering, bullae formation, and sloughing of the detached skin Disease spectrum SJS = 30% TBSA SJS/ TEN Overlap = 10-30% TBSA Incidence is estimated at around 9 per 1 million people in the US Mortality is 10% for SJS and 30-50% for TEN Mainly 2/2 sepsis and end organ dysfunction. SJS can occur even without a precipitating medication Infection can set it off especially in patients with risk factors including HIV, lupus, underlying malignancy, and genetic factors SATAN for the most common drugs Sulfa, Allopurinol, Tetracyclines, Anticonvulsants, and NSAIDS Anti-epileptics include carbamazepine, lamictal, phenobarb, and phenytoin Can have a curious course Hypersensitivity reaction can develop while taking medication, or even one to four weeks after exposure In pediatric population, mycoplasma pneumonia and herpes simplex have been identified as precipitating infections Patients often have a prodrome 1-3 days prior to the skin lesions appearing May complain of fever,