Podcasts about alveolar

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Dr. Niyati Borkar chats with Dr. Marissa Guttenberg about her article, "Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK-mediated Efferocytosis."

learn to pronounce the alveolar consonants: zh vs ch vs sh vs r

practice the nasal consonants, alveolar vs palatal, n vs ɲ

practice the nasal consonants, bilabial vs alveolar, m vs n

practice the alveolar fricative consonants, s vs z

Dr. Peter Moore chats with Dr. Marilia Zuttion on her article, "Interstitial Macrophages Mediate Efferocytosis of Alveolar Epithelium during Influenza Infection."

After Megan Bugg was diagnosed with Stage 4 Alveolar Rhabdomyosarcoma in late 2014, she underwent a very difficult treatment protocol which included 150 weeks of toxic Chemotherapy , 200 Radiation treatments, 5 trips to the ICU, and 8 surgeries. Even so, Megan fought her disease every day and became an amazing and well known advocate for the cause of Pediatric Cancer before her passing on March 9th of 2022, 7 years and 2 months after her diagnosis.

Dr. Peter Moore chats with Dr. Marilia Zuttion on her article, "Interstitial Macrophages Mediate Efferocytosis of Alveolar Epithelium during Influenza Infection."

BUFFALO, NY- July 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Modulating in vitro lung fibroblast activation via senolysis of senescent human alveolar epithelial cells.” Idiopathic pulmonary fibrosis (IPF) is an age-related disease with poor prognosis and limited therapeutic options. Activation of lung fibroblasts and differentiation to myofibroblasts are the principal effectors of disease pathology, but damage and senescence of alveolar epithelial cells, specifically type II (ATII) cells, has recently been identified as a potential trigger event for the progressive disease cycle. Targeting ATII senescence and the senescence-associated secretory phenotype (SASP) is an attractive therapeutic strategy; however, translatable primary human cell models that enable mechanistic studies and drug development are lacking. In this new study, researchers Joseph S. Spina, Tracy L. Carr, Lucy A. Phillips, Heather L. Knight, Nancy E. Crosbie, Sarah M. Lloyd, Manisha A. Jhala, Tony J. Lam, Jozsef Karman, Meghan E. Clements, Tovah A. Day, Justin D. Crane, and William J. Housley from AbbVie Bioresearch Center and Northeastern University describe a novel system of conditioned medium (CM) transfer from bleomycin-induced senescent primary alveolar epithelial cells (AEC) onto normal human lung fibroblasts (NHLF) that demonstrates an enhanced fibrotic transcriptional and secretory phenotype compared to non-senescent AEC CM treatment or direct bleomycin damage of the NHLFs. “In the current study, we confirm the presence of senescent cell populations within the human IPF lung, as well as assess primary cell reagents for sensitivity to senescent cell targeting therapies.” In this system, the bleomycin-treated AECs exhibited classical hallmarks of cellular senescence, including SASP and a gene expression profile that resembles aberrant epithelial cells of the IPF lung. Fibroblast activation by CM transfer was attenuated by pre-treatment of senescent AECs with the senolytic Navitoclax and AD80, but not with the standard of care agent Nintedanib or senomorphic JAK-targeting drugs (e.g., ABT-317, ruxolitinib). This model provided a relevant human system for profiling novel senescence-targeting therapeutics for IPF drug development. “Taken together, the model described herein provides a physiologically relevant, primary human cell system to study the effects of alveolar epithelial cell senescence on lung fibroblasts in the context of chronic fibrotic lung disease.” DOI - https://doi.org/10.18632/aging.205994 Corresponding author - Tovah A. Day - t.day@northeastern.edu Video short - https://www.youtube.com/watch?v=rpmo2PlGDKc Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205994 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Drs. Nicholas Callahan and Michael Miloro discuss the recent JOMS article on nerve reconstruction. The purpose of this study was to evaluate functional sensory recovery of immediate IAN allograft reconstruction performed during ablative mandibular resection at one year following surgery.

For families facing a cleft lip and palate diagnosis, Nasoalveolar Molding (NAM) can feel like a mysterious first step. Join host Laura Arroyo as she welcomes Alexis Garcia, a parent who's walked the NAM path. Alexis will share her personal NAM experience, offering invaluable firsthand advice and highlighting the transformative power of this treatment. Whether you're about to embark on NAM or seeking reassurance, this episode equips you with knowledge and confidence. Want to share your story? Email us at ourforeversmiles@gmail.com. Want to be a show sponsor? Email us at ourforeversmiles@gmail.com Follow us @ourforeversmiles on social platforms We know you will have questions! Join our FB Community to discuss the weekly episode and speak directly to our guests. https://www.facebook.com/groups/1081522212884073/ This podcast is completely free for you, but if you'd ever consider supporting the show, we truly appreciate it. One way you can do that is by using our affiliate links. These are links to products we've mentioned on the show, and if you make a purchase through one of them, we might earn a small commission at no extra cost to you. It's a great way to show your love for the podcast and help us keep creating content that educates, empowers, and strengthens the cleft lip and palate community! First Bottle to Purchase After Palate Repair - Post Palate Repair Straw Trainer Juselle's Cleft Palate Bottle - Pigeon Bottle Specialty Feeder Sippy Cup for Pre Palate Repair Prep - Munchkin 360 Weigh your Baby at Home - Weighted Feeds Scale Squeezable Straw Training Bottle - Honey Bear Straw Cup Free Flow Cup for Pre palate Repair Prep - Reflo Smart Cup Pacifiers that have Worked for Cleft Lip and Palate Babies - Itzy Ritzy Pacifiers that have Worked for Cleft Lip and Palate Babies - MAM Pacifiers that have Worked for Cleft Lip and Palate Babies - Itzy Ritzy Scar Cream Recommended by Alexis Garcia, Cleft Lip Mom - bioCorneum - Pricey**

Acil serviste kritik bakının vazgeçilmez bir parçası; Mekanik ventilasyon. Özellikle yoğun bakımlar da doluysa mekanik ventilasyon uygulanan bu hastaların takibini belli bir süre boyunca biz Acil Servislerimizde yapıyoruz. Acil serviste mekanik ventilasyon yönetimini sitemizden okuyabilirsiniz. Tabi ki mekanik ventilasyon kurtarıcı olabildiği gibi çeşitli potansiyel tehlikeler de barındırabiliyor. Her tedavinin kompikasyonu olduğu gibi, mekanik ventilasyon da etkin kullanılmazsa akciğer üzerindeki hasarıyla mortalite ve morbiditeye katkı sağlayabilir. Ventilatör kaynaklı akciğer hasarı (Ventilator-induced Lung Injury-VILI), mekanik ventilasyonun neden olduğu veya ağırlaştırdığı akut akciğer hasarıdır ​1​. Ventilatörün neden olduğu akciğer hasarı kritik hastaların morbidite ve mortalitesine önemli ölçüde katkıda bulunabilir. Mekanik ventilasyon potansiyel olarak hem normal hem de hastalıklı akciğerlere zarar verebilir. Ventilatör ilişkili akciğer hasarı (Ventilator-associated Lung Injury-VALI), akciğer hasarının ventilasyona bağlı olduğu düşünüldüğü ancak bunun kanıtlanmasının zor olduğu durumlarda kullanımı uygun bir tanım. Kanıtlanabilirse, VILI terimi kullanılır. Ancak günlük kullanımda kanıttan bağımsız olarak da VILI ve VALI birbiri yerine kullanılmaktadır. Mekanik ventilasyonda olan yaklaşık 4 hastadan 1'inde VALI gelişir; ARDS hastalarında risk muhtemelen bu oran daha da yüksektir. VALI, normal olan akciğerlerde ortaya çıkabilirken, var olan ARDS'yi de kötüleştirebilir. Mekanik ventilasyonun neden olduğu akciğer hasarı; 1952 yılında çocuk felci salgını sırasındaki araştırmalarla konuşulmaya başlanmıştır. 1967 yılında, mekanik ventilasyon uygulanan ve akciğerlerinde yaygın alveolar infiltrasyon ve hiyalin membran oluşumu görülen hastaların post mortem akciğer patolojisini tanımlamak için “solunum cihazı akciğeri” terimi geliştirilmiştir ​2​. Patogenez Alveoler aşırı gerilme (volutravma), barotravma, atelektravma ve biyotravma mekanik ventilasyon sırasında VALI'nin temel mekanizmalarıdır. Alveoler hasar, yüksek alveolar geçirgenliğe, interstisyel ve alveolar ödeme, alveoler hemorajiye, hiyalin membran oluşumuna, fonksiyonel surfaktan kaybına ve alveolar kollapsa neden olur. Barotravma: Yüksek transalveolar basınçtan dolayı alveoler rüptür oluşmasıdır. Ekstra alveolar dokuya hava sızıntısı, pnömotoraks, pnömomediastinum, pnömoperiton ve deri altı amfizemi gibi durumlara neden olur. Alveolar aşırı gerilme (volutravma): Volutravma, akciğer birimlerinin artan transpulmoner basınçla aşırı gerilmesinden kaynaklanan nonhomojen akciğer hasarını temsil eder. Transpulmoner basınç 30 cmH2O'yu aştığında hücre membranın gerilmesiyle(strain) ve stresiyle oluşur. Strain: inspirasyon sırasında alınan gaz hacminin, havalandırılan akciğerin hacmine oranı olarak tanımlanabilir. Yapılan hayvan çalışmalarında, yüksek havayolu basıncından ziyade yüksek tidal hacimlerin akciğer hasarına neden olduğunu gösterilmiştir ​3​. ARDS dışındaki nedenlerle entübe edilen hastalarda yüksek tidal hacimlerden kaynaklanan aşırı gerilmenin de VALI riskini arttırdığı saptanmıştır ​4​. Alveollerin aşırı gerilmesi için her zaman büyük tidal hacimler gerekli değildir. Heterojen konsolidasyon veya atelektazik akciğerde, her solukta orantısız bir hacim açık alveollere iletilir bu da bölgesel alveolar aşırı gerilmeye ve VILI'ye neden olabilir ​5​. Atelektotravma: Sürfaktan disfonksiyonu ve akciğerin sıvıyla birikmiş bölgelerinin ağırlığı atelektaziye katkıda bulunur. Ventilasyon sırasında bu tür atelektatik olan fakat yeniden kullanılabilir akciğer bölgelerinin döngüsel olarak açılması ve çökmesi, atelektotravma olarak adlandırılan akciğer hasarına katkıda bulunur. Hayvan deneylerinde, her bir solunum döngüsünde atelektatik alveollerin açılıp kapanmasının, yırtılma stresi kuvvetleri nedeniyle komşu atelektatik olmayan alveollere ve hava yollarına zarar verdiği görülmüştür ​6​. Bu mekanizmayı önlemekte en önemli olan parametre,

Welcome to PICU Doc On Call, where Dr. Pradip Kamat from Children's Healthcare of Atlanta/Emory University School of Medicine and Dr. Rahul Damania from Cleveland Clinic Children's Hospital delve into the intricacies of Pediatric Intensive Care Medicine. In this special episode of PICU Doc on Call shorts, we dissect the Alveolar Gas Equation—a fundamental concept in respiratory physiology with significant clinical relevance.Key Concepts Covered:Alveolar Gas Equation Demystified: Dr. Rahul explains the Alveolar Gas Equation, which calculates the partial pressure of oxygen in the alveoli (PAO2). This equation, PAO2 = FiO2 (Patm - PH2O) - (PaCO2/R), is essential in understanding hypoxemia and the dynamics of gas exchange in the lungs.Calculating PAO2: Using the Alveolar Gas Equation, the hosts demonstrate how to calculate PAO2 at sea level, emphasizing the influence of atmospheric pressure, fraction of inspired oxygen (FiO2), water vapor pressure, arterial carbon dioxide pressure (PaCO2), and respiratory quotient (R) on oxygenation.A-a Gradient and Hypoxemia: The A-a gradient, derived from the Alveolar Gas Equation, is discussed in the context of hypoxemia evaluation. Understanding the causes of hypoxemia, including ventilation/perfusion (V/Q) mismatch, anatomical shunt, diffusion defects, and hypoventilation, is crucial for clinical diagnosis and management.Clinical Scenarios and A-a Gradient Interpretation: Through a clinical scenario, the hosts elucidate how different conditions affect the A-a gradient and oxygenation, providing insights into respiratory pathophysiology and differential diagnosis.Clinical Implications and Management Strategies: The hosts highlight the clinical significance of the Alveolar Gas Equation in assessing oxygenation status, diagnosing gas exchange abnormalities, and tailoring respiratory management strategies in the pediatric intensive care setting.Key Takeaways:Utility of the Alveolar Gas Equation: Understanding and applying the Alveolar Gas Equation is essential for evaluating oxygenation and diagnosing respiratory abnormalities.Interpreting A-a Gradient: A normal A-a gradient suggests alveolar hypoventilation as the likely cause of hypoxemia, whereas elevated gradients indicate other underlying pathologies.Clinical Relevance: Recognizing the clinical implications of the Alveolar Gas Equation aids in accurate diagnosis and optimal management of respiratory conditions in pediatric intensive care patients.Conclusion:Join Dr. Kamat and Dr. Damania as they unravel the complexities of the Alveolar Gas Equation, providing valuable insights into respiratory physiology and its clinical applications. Don't forget to subscribe, share your feedback, and visit picudoconcall.org for more educational content and resources.References:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter: Physiology of the respiratory system. Chapter 42. Khemani et al. Pages 470-481Rogers textbook of Pediatric intensive care: Chapter 44....

En este episodio 2 de la serie de hipoxemia refractaria hablaremos de la importancia y lo ligados que van la posicion prono y el reclutamiento, adicional mencionaremos el porque el lazo o bucle presion volumen tinen un papel papel tan importante en la evaluacion del reclutamiento alveolar o sobredistencion segun sea el caso, bienvenidos!

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.24.550385v1?rss=1 Authors: Bramey, N., Melo-Narvaez, M. C., See, F., Ballester-Llobell, B., Steinchen, C., Jain, E., Hafner, K., Yildirim, A. O., Koenigshoff, M., Lehmann, M. Abstract: Aging is the main risk factor for chronic lung diseases including idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Accordingly, hallmarks of aging such as cellular senescence are increased in different cell types such as fibroblasts in the lungs of patients. However, whether the senescent phenotype of fibroblasts derived from IPF or COPD differs is still unknown. Therefore, we characterized senescence at baseline and after exposure to disease-relevant insults (H2O2, bleomycin, and TGF-{beta}1) in primary human lung fibroblasts (phLF) from control donors, IPF, and COPD patients. We found that phLF from different disease origins have a low baseline senescence. Moreover, senescence trigger and not disease origin defines their senescence phenotype. Finally, senescent fibroblasts interfere with the stem cell capacity of alveolar progenitors in vitro. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

AfterThoughts: The Teenage Years was created to make visible some of the invisible cancer stories from within the young cancer community.Joining us for Episode Three is the brill Maddie. Maddie was diagnosed with Alveolar soft part sarcoma when she was 18. Shortly after she had primary tumour removed from her left shoulder, it was discovered the cancer had spread to her lungs. While her disease is currently stable, it is incurable and Maddie will be on treatment for life. She joined us to tell her stories about dealing with stomach side-effects at Swiftogeddon (don't let the poo shamers win!), how writing a will can be empowering and how she became more confident talking openly about her cancer over time.  _______________________________________________________________AfterThoughts is hosted by Aiden Grant and Shaumya KularajanFind AfterThoughts on Facebook, Twitter and InstagramAfterThoughts : The Teenage Years is supported by Teenage Cancer Trust. Teenage Cancer Trust support those diagnosed with cancer when they're 13-24 and provide specialised nursing care and support to get them through treatment.As ever, AfterThoughts deals with some conversations you may find tricky to listen to. If you need any further support, please don't hesitate to reach out to a friend, or find support from any of the brilliant charities online.AfterThoughts is produced by Toby Peach and Alice-May Purkiss from Beyond Arts. Sounds by Kieron Lucas and Dinah Mullen.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.22.545997v1?rss=1 Authors: DiGiovanni, G. T., Han, W., Sherrill, T., Taylor, C. J., Nichols, D. S., Geis, N. M., Singha, U. K., Calvi, C. L., McCall, A. S., Dixon, M. M., Lui, Y., Jang, J.-H., Gutor, S. S., Polosukhin, V. V., Blackwell, T. S., Kropski, J. A., Gokey, J. J. Abstract: A hallmark of idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases is dysregulated repair of the alveolar epithelium. The Hippo pathway effector transcription factors YAP and TAZ have been implicated as essential for type 1 and type 2 alveolar epithelial cell (AT1 and AT2) differentiation in the developing lung, yet aberrant activation of YAP/TAZ is a prominent feature of the dysregulated alveolar epithelium in IPF. In these studies, we sought to define the functional role of YAP/TAZ activity during alveolar regeneration. We demonstrate that Yap and Taz are normally activated in AT2 cells shortly after injury, and deletion of Yap/Taz in AT2 cells led to pathologic alveolar remodeling, failure of AT2 to AT1 cell differentiation, increased collagen deposition, exaggerated neutrophilic inflammation, and increased mortality following injury induced by a single dose of bleomycin. Loss of Yap/Taz activity prior to a LPS injury prevented AT1 cell regeneration, led to intra-alveolar collagen deposition, and resulted in persistent innate inflammation. Together these findings establish that AT2 cell Yap/Taz activity is essential for functional alveolar epithelial repair and prevention of fibrotic remodeling. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

We speak to Simblified fan (!) and microbiologist Avraneel Paul on a whole bunch of things related to what happens inside our body! Viruses and bacteria, how vaccines work, how those WBC badasses keep us safe, and so on. Along the way, we also speak about exciting advancements like CRISPR, and explore philosophical questions like whether Covid has changed the field... And what a day in the life of a scientist looks like. There's loads of trivia, loads of simblification and a few bad jokes as well in this two-part episode. We hope you like it and have renewed appreciation for scientists (and your body!) after it! Add one part news, one part bad jokes, one part Wikipedia research, one part cult references from spending too much time on the internet, one part Wodehouse quotes, and one part quality puns, and you get Simblified. A weekly podcast to help you appear smarter, to an audience that knows no less! Your four hosts - Chuck, Naren, Srikeit, and Tony attempt to deconstruct topics with humor (conditions apply). Fans of the show have described it as "fun conversations with relatable folks", "irreverent humor", "the funniest thing to come out of Malad West" and "if I give you a good review will you please let me go". Started in 2016 as a creative outlet, Simblified now has over 300 episodes, including some live ones, and some with guests who are much smarter than the hosts. Welcome to the world of Simblified! You can contact the hosts on: Chuck: http://twitter.com/chuck_gopal  / http://instagram.com/chuckofalltrades Naren: http://twitter.com/shenoyn  / http://instagram.com/shenoynv Tony: http://twitter.com/notytony  / http://instagram.com/notytony Srikeit: http://twitter.com/srikeit  / http://instagram.com/srikeitSee omnystudio.com/listener for privacy information.

This week we will discuss an extremely rare type of cancer that is most often associated with younger children.  When it affects adults it is more difficult to treat. Our guest this week is Wilder McNemar.  Wilder has a decent following on TikTok which is where I found him.  You can follow him here: https://www.tiktok.com/@queerpple?lang=en ​ A Rhabdomyosarcoma is a type of soft tissue sarcoma. A sarcoma is a tumor that starts in the supporting tissues (connective tissues) of the body - for example, bone, muscle, fat, cartilage and ligaments. Rhabdomyosarcomas grow in the muscles of the body. Rhabdomyosarcoma can occur anywhere in the body. There are three types of rhabdomyosarcoma which affect different age groups:   Embryonal Rhabdomyosarcoma (ERMS) This most often affects young children, usually under the age of 6 years. It most often occurs in the head and neck region, especially in the tissues around the eye (called an orbital rhabdomyosarcoma). Embryonal Rhabdomyosarcoma may also occur in the womb, vagina, bladder or the prostate gland. One type of Embryonal Rhabdomyosarcoma is called sarcoma botryoides, which looks like a bunch of grapes and most often occurs in the vagina or bladder. Embryonal Rhabdomyosarcomas usually spread to surrounding tissues. However, the outcome (prognosis) is usually very good and most children with Embryonal Rhabdomyosarcoma are cured of the cancer. Alveolar Rhabdomyosarcoma This tends to occur in older children and young adults. Alveolar Rhabdomyosarcomas (also called ARMS) most often occur in the arms and legs, chest or tummy (abdomen).  This is the type Wilder is working with. ​ARMS typically affects all age groups equally. It makes up a larger portion of RMS in older children, teens, and adults than in younger children (because ERMS is less common at older ages). ARMS most often occurs in large muscles of the trunk, arms, and legs. ARMS tends to grow faster than ERMS, and it usually requires more intense treatment. However, in some cases of ARMS, the cancer cells lack certain gene changes, which makes these cancers act more like ERMS (and allows doctors to give less intense treatment). ​Pleomorphic Rhabdomyosarcoma This tends to occur in middle-aged adults. It is usually treated with chemotherapy, surgery and radiotherapy but treatment is not as effective as for other types of Rhabdomyosarcoma. ​We will keep Wilder in our thoughts and prayers and if you are interested in making a donation, there's a link on Wilder's TikTok account: https://www.tiktok.com/@queerpple?lang=en .  

An interview with Alice P. Chen, MD of the National Cancer Institute.

Sub influența cântecelor tradiționale, fundație pentru multe din piesele sale, E-an-na ne oferă în 2023 un nou produs discografic lansând "Alveolar" citiţi mai departe

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.27.530149v1?rss=1 Authors: Yao, Y., Miethe, S., Kattler, K., Walter, J., Schneider-Daum, N., Herr, C., Garn, H., Ritzmann, F., Bals, R., Beisswenger, C. Abstract: Alveolar type 2 (AT2) and club cells are part of the stem cell niche of the lung and their differentiation is required for pulmonary homeostasis and tissue regeneration. A disturbed crosstalk between fibroblasts and epithelial cells contributes to the loss of lung structure in chronic lung diseases. Therefore, it is important to understand how fibroblasts and lung epithelial cells interact during regeneration. Here we analyzed the interaction of fibroblasts and the alveolar epithelium modelled in air-liquid interface cultures. Single-cell transcriptomics showed that co-cultivation with fibroblasts leads to increased expression of type 2 markers in pneumocytes, activation of regulons associated with maintenance of alveolar type 2 cells, and trans-differentiation of club cells towards pneumocytes. This was accompanied by an intensified transepithelial barrier. Vice versa, activation of NF{kappa}B pathways and the CEBPB regulon as well as the expression of IL-6 and other differentiation factors (e.g. FGFs) were increased in fibroblasts co-cultured with epithelial cells. Recombinant IL-6 enhanced epithelial barrier formation. Therefore, in our co-culture model, regulatory loops were identified by which lung epithelial cells mediate regeneration and differentiation of the alveolar epithelium in a cooperative manner with the mesenchymal compartment. 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/2023.02.27.530122v1?rss=1 Authors: Lv, Z., Liu, Z., Liu, K., Pu, W., Li, Y., Zhao, H., Xi, Y., Vaughan, A., Gillich, A., Zhou, B. Abstract: Lung injury activates epithelial stem or progenitor cells for alveolar repair and regeneration. However, the origin and fate of injury-induced progenitors are poorly defined. Here, we report that p63-expressing progenitors emerge upon bleomycin-induced lung injury. These p63+ progenitors proliferate rapidly and differentiate into alveolar type 1 (AT1) and type 2 (AT2) cells through distinct trajectories. Dual recombinase-mediated sequential genetic lineage tracing reveals that p63+ progenitors originate from airway secretory cells and subsequently generate alveolar cells. Functionally, p63 activation is required for efficient alveolar regeneration from secretory cells. Our study identifies a secretory cell-derived p63+ progenitor that contributes to alveolar repair, indicating a potential therapeutic avenue for lung regeneration after injury. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Listen to a soundcast of the December 9 and 12, 2022, FDA approvals of Tecentriq (atezolizumab) for unresectable or metastatic alveolar soft part sarcoma, and Krazati (adagrasib) for KRAS G12C-mutated locally advanced or metastatic non-small cell lung cancer”

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.19.524655v1?rss=1 Authors: Burgess, C. L., Huang, J., Bawa, P., Alysandratos, K.-D., Minakin, K., Morley, M. P., Babu, A., Villacorta-Martin, C., Hinds, A., Thapa, B. R., Wang, F., Matschulat, A. M., Morrisey, E. E., Varelas, X., Kotton, D. N. Abstract: In the distal lung, alveolar epithelial type I cells (AT1s) comprise the vast majority of alveolar surface area and are uniquely flattened to allow the diffusion of oxygen into the capillaries. This structure along with a quiescent, terminally differentiated phenotype has made AT1s particularly challenging to isolate or maintain in cell culture. As a result, there is a lack of established models for the study of human AT1 biology, and in contrast to alveolar epithelial type II cells (AT2s), little is known about the mechanisms regulating their differentiation. Here we engineer a human in vitro AT1 model system through the directed differentiation of induced pluripotent stem cells (iPSC). We first define the global transcriptomes of primary adult human AT1s, suggesting gene-set benchmarks and pathways, such as Hippo-LATS-YAP/TAZ signaling, that are enriched in these cells. Next, we generate iPSC-derived AT2s (iAT2s) and find that activating nuclear YAP signaling is sufficient to promote a broad transcriptomic shift from AT2 to AT1 gene programs. The resulting cells express a molecular, morphologic, and functional phenotype reminiscent of human AT1 cells, including the capacity to form a flat epithelial barrier which produces characteristic extracellular matrix molecules and secreted ligands. Our results indicate a role for Hippo-LATS-YAP signaling in the differentiation of human AT1s and demonstrate the generation of viable AT1-like cells from iAT2s, providing an in vitro model of human alveolar epithelial differentiation and a potential source of human AT1s that until now have been challenging to viably obtain from patients. 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/2023.01.12.523571v1?rss=1 Authors: Iezza, D., Predella, C., NI, K., Murray, J. W., Liu, H.-Y., Saqi, A., Glasser, S. W., Dorrello, N. V. Abstract: Childhood interstitial lung disease (chILD) secondary to pulmonary surfactant deficiency is a devastating chronic lung disease in children. Clinical presentation includes mild to severe respiratory failure and fibrosis. There is no specific treatment, except lung transplantation, which is hampered by a severe shortage of donor organs, especially for young patients. Repair of lungs with chILD represents a longstanding therapeutic challenge but cellular therapy is a promising strategy. As surfactant is produced by alveolar type II epithelial (ATII) cells, engraftment with normal or gene-corrected ATII cells might provide an avenue to cure. Here we used a chILD disease-like model, Sftpc-/- mice, to provide proof-of-principle for this approach. Sftpc-/- mice developed chronic interstitial lung disease with age and were hypersensitive to bleomycin. We could engraft wild-type ATII cells after low dose bleomycin conditioning. Transplanted ATII cells produced mature SPC and attenuated bleomycin-induced lung injury up to four months post-transplant. This study demonstrates that partial replacement of mutant ATII cells can promote lung repair in a mouse model of chILD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.20.521114v1?rss=1 Authors: Kastlmeier, M. T., Gonzalez Rodriguez, E., Cabanis, P., Guenther, E. M., Koenig, A.-C., Han, L., Hauck, S., Stoeger, T., Hilgendorff, A., Voss, C. Abstract: Fibrotic interstitial lung disease (ILD) is a group of lung disorders characterized by the accumulation of extracellular matrix, ultimately resulting in the destruction of the pulmonary scaffold. Continuous mesenchyme-derived profibrotic signaling perpetuates the remodeling process, specifically targeting the epithelial cell compartment, thereby destroying the gas exchange area. Studies that address this detrimental crosstalk between lung epithelial cells and fibroblasts are key to understanding ILD. With the aim of identifying functionally relevant targets that drive lung mesenchymal-epithelial crosstalk and their potential as new avenues to therapeutic strategies, we developed a 3D organoid co-culture system based on human induced pluripotent stem cell (hiPSC)-derived alveolar epithelial type 2 cells (iAT2s) and lung fibroblasts from ILD patients as well as IMR-90 controls. While organoid formation capacity and organoid size was comparable in the presence of ILD or control lung fibroblasts, metabolic activity was significantly increased in ILD co-cultures. Alveolar organoids cultured with ILD fibroblasts further demonstrated reduced stem cell function supported by reduced Surfactant Protein C (SFTPC) gene expression together with an aberrant basaloid-prone differentiation program indicated by elevated Cadherin 2 (CDH2), Bone Morphogenic Protein 4 (BMP4) and Vimentin (VIM) transcription. In order to identify key mediators of the misguided mesenchymal-to-epithelial crosstalk with a focus on disease-relevant inflammatory processes, we used secretome mass spectrometry to identify key signals secreted by end stage ILD lung fibroblasts. Over 2000 proteins were detected in a single-shot experiment with 47 differentially upregulated proteins when comparing ILD and non-Chronic Lung Disease (CLD) control fibroblasts. The secretome profile was dominated by chemokines of the C-X-C motif family, including CXCL1, CXCL-3, and -8, all interfering with (epithelial) growth factor signaling orchestrated by Interleukin 11 (IL11), steering fibrogenic cell-cell communication, and proteins regulating extracellular matrix remodeling including epithelial-to-mesenchymal transition (EMT). When in turn treating 3D monocultures of iAT2s with IL11 we recapitulated the co-culture results obtained with primary ILD fibroblasts including changes in metabolic activity as well as organoid formation capacity and size. In summary, our analysis identified mesenchyme-derived mediators likely contributing to the disease-perpetuating mesenchymal-to-epithelial crosstalk in ILD by using sophisticated alveolar organoid co-cultures indicating the importance of cytokine-driven aberrant epithelial differentiation and confirmed IL11 as a key player in ILD using an unbiased approach. 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/2022.11.11.516088v1?rss=1 Authors: Kortekaas, R. K., Geillinger-Kaestle, K. E., Borghuis, T., Belharch, K., Webster, M., Timens, W., Burgess, J. K., Gosens, R. Abstract: IL-11 is linked to the pathogenesis of idiopathic pulmonary fibrosis (IPF), since IL-11 induces myofibroblast differentiation and stimulates their excessive collagen deposition in the lung. The alveolar architecture is disrupted in IPF, yet the effect of IL-11 on dysregulated alveolar repair associated with IPF remains to be elucidated. We hypothesized that epithelial-fibroblast communication associated with lung repair is disrupted by IL-11. Thus, we studied whether IL-11 affects the repair responses of alveolar lung epithelium using mouse lung organoids and precision cut lung slices (PCLS). Additionally, we assessed the anatomical distribution of IL-11 and IL-11 receptor in human control and IPF lungs using immunohistochemistry. IL-11 protein was observed in human control lungs in airway epithelium, macrophages and in IPF lungs, in areas of AT2 cell hyperplasia. IL-11R staining was predominantly present in smooth muscle and macrophages. In mouse organoid co-cultures of epithelial cells with lung fibroblasts, IL-11 decreased organoid number and reduced the fraction of pro-SPC expressing organoids, indicating dysfunctional regeneration initiated by epithelial progenitors. In mouse PCLS alveolar marker gene expression declined, whereas airway markers were increased. The response of primary human fibroblasts to IL-11 on gene expression level was minimal, though bulk RNA-sequencing revealed IL-11 modulated a number of processes which may play a role in IPF, including unfolded protein response, glycolysis and Notch signaling. In conclusion, IL-11 disrupts alveolar epithelial regeneration by inhibiting progenitor activation and suppressing the formation of mature alveolar epithelial cells. The contribution of dysregulated fibroblast - epithelial communication to this process appears to be limited. 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/2022.10.28.514255v1?rss=1 Authors: Chioccioli, M., Magruder, S., McDonough, J. E., Nouws, J., Gonzalez, D., Borriello, L., Traub, B., Ye, X., Hendry, C. E., Entenberg, D., Kaminski, N., Krishnaswamy, S., Sauler, M. Abstract: Tissue repair requires a highly coordinated cellular response to ensure the correct balance of replacement cells to lost cells. In the lung, alveolar type 2 (AT2) cells act as stem cells and can replace both themselves and alveolar type 1 cells (AT1); however, the complex orchestration of AT2 stem cell activity following lung injury is poorly understood owing to the inability to track individual stem cells and their dynamic behavior over time. Here, we apply live time lapse imaging to ex vivo mouse precision cut lung slice (PCLS) culture and in vivo mouse lung to track individual GFP-labeled AT2 cells for 72h following intra-tracheal administration of bleomycin. We observe highly dynamic movement of AT2 cells, including migration within and between alveoli, as well as the emergence of at least three distinct morphokinetic AT2 cell states. Small molecule-based inhibition of Rho-associated protein kinase (ROCK) pathway significantly reduced motility of AT2 stem cells following injury and reduced expression of Krt8, a known marker of intermediate progenitor cells. Together, our results uncover motility of alveolar stem cells as a new injury response mechanism in the lung and uncover properties of stem cell motility at high cellular resolution. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Article discussed in this episode:Autoimmune Pulmonary Alveolar Proteinosis

In this week's episode we'll discuss an undescribed role for NOX2 in maintaining lung homeostasis through suppression of alveolar macrophage activation. We'll also cover results of a phase 3 randomized trial that compares the safety and efficacy of hydroxyurea and peginterferon alfa-2a in patients with high-risk polycythemia vera and essential thrombocythemia (or PV and ET, respectively). Finally, we'll go more in depth on the emerging treatment landscape for PV, and the limits of current clinical trial endpoints.

Welcome back to another episode of oralmaxfax. Today we are diving into another orthognathic complications-alveolar necrosis. We review the literature and talk about what is known including the rule of HBO treatment. Happy Tuning " Music from https://filmmusic.io: "Movement Proposition" by Kevin MacLeod (https://incompetech.com) Licence: CC BY (http://creativecommons.org/licenses/by/4.0/)" Music from https://filmmusic.io "Your Call" by Kevin MacLeod (https://incompetech.com) License: CC BY (http://creativecommons.org/licenses/by/4.0/)

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

In this inaugural podcast episode, John Van Aalst, Joseph Incorvia, Stacey Francis, Jack Yu, and Carolyn Rogers-Vizena discuss the article, "Racial Disparities Affect Timing of Alveolar Bone Grafting for Patients With Cleft Lip and Palate: An Analysis of the 2012 Kids' Inpatient Database," with senior author Matthew Grieves.

What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]

What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]

What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]

What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]

What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]

What are the obstacles that stand between us and engineering functional lungs? Laura Niklason, MD, PhD outline the promises and challenges of lung regeneration. She details current studies that may unveil a roadmap for building functional lung aveolus. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 37580]

Please support us on our Patreonhttps://www.patreon.com/anaesthesiaAll proceeds will go to Fund a Fellow to help train anaesthetists in developing countries whilst acknowledging the work it takes to keep creating this educational resource.This podcast is all aboutNORMAL VALUES: PvCO2 45mmHg         CO2 content 52ml CO2/100ml bloodMEASUREMENT: sampled from a pulmonary artery catheter.1. Alveolar ventilation2. Increased CO2 production 3. Carbonic anhydrase inhibitors i.e. acetazolamide4. Tissue blood flow5. Haldane EffectIf you enjoyed this content please like and subscribePlease post any comments or questions below. Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group for other content.Any questions please email lahiruandstan@gmail.comDisclaimer: The information contained in this video/audio/graphic is for medical practitioner education only. It is not and will not be relevant for the general public.Where applicable patients have given written informed consent to the use of their images in video/photography and aware that it will be published online and visible by medical practitioners and the general public.This contains general information about medical conditions and treatments. The information is not advice and should not be treated as such. The medical information is provided “as is” without any representations or warranties, express or implied. The presenter makes no representations or warranties in relation to the medical information on this video. You must not rely on the information as an alternative to assessing and managing your patient with your treating team and consultant. You should seek your own advice from your medical practitioner in relation to any of the topics discussed in this episode' Medical information can change rapidly, and the author/s make all reasonable attempts to provide accurate information at the time of filming. There is no guarantee that the information will be accurate at the time of viewingThe information provided is within the scope of a specialist anaesthetist (FANZCA) working in Australia.The information presented here does not represent the views of any hospital or ANZCA.These videos are solely for training and education of medical practitioners, and are not an advertisement. They were not sponsored and offer no discounts, gifts or other inducements. This disclaimer was created based on a Contractology template available at http://www.contractology.com.

Show notes at: Dr. Tessa Balach @tbalachMD is a board-certified orthopaedic surgeon. She earned her medical degree from New York Medical College and later on completed her internship, residency and fellowship at University of Medicine Chicago. Dr. Balach specializes in Orthopaedic Surgery and Oncology with multiple areas of expertise on Bone and Soft Tissue Cancers and Knee/Hip Replacement, where she treats both adults and children with malignant tumors. She is also the residency director at UChicago Orthopaedic residency program and founder of Ortho Access Info ! She is also a researcher who is currently leading and participating in clinical studies aimed at improving the treatment and management of bone illnesses and injuries. Dr. Balach works with medical students, residents, and fellows as a mentor and educator. She has also published multiple articles in peer-reviewed journals and medical journals, as well as giving speeches at a variety of professional conferences. Also, Dr. Balach works together with experts in the Medical Center where they provide highly specialized care for patients with both common and rare bond and soft tissue tumors. Moreover, she also treats patients with metastatic bone disease to strengthen weak bones to avoid fractures caused by breast, lung, prostate and kidney metastases.  Goal of episode: To develop a baseline knowledge on Soft Tissue Sarcoma. We cover: Presentation Predisposing factors Imaging Diagnosis Mets Treatment Fibrous tumors Fatty Tissue tumors Neural tissue tumors Muscle Tissue tumors Vascular tumors Synovial disorders Synovial sarcoma Epithelioid sarcoma Clear cell sarcoma Alveolar cell sarcoma

Today's guest is an oral and maxillofacial surgeon who specializes in alveolar cleft grafting, cleft orthognathic surgery, and distraction. Through these life-changing procedures, Dr. Chris Viozzi is doing his part to give back, and he does this not only through treating patients within the US, but also those outside of it during 10-day mission trips he was doing twice a year prior to the pandemic. In today's episode, Chris explains the variation that exists amongst the patients he treats, as well as amongst the techniques that can be used for the procedures he does. We also discuss donor sites, follow-ups, and common concerns relating to cleft surgeries. Chris is not fellowship-trained, and his OMS basic training was more than enough to get him to his current position on the Mayo Clinic's Cleft and Craniofacial Clinic team. Key Points From This Episode:The craniofacial team that Chris is a part of, and his niche within the team.Other medical professionals who make up the craniofacial team.Diversity amongst the patients that Chris and his team treat at the clinic.  Vital understandings that anyone doing alveolar cleft grafting must have. Elements of alveolar cleft grafting that have evolved over time. Examples of the variety of techniques for alveolar cleft grafting that exist. Why the iliac crest is usually the best donor site. Common concerns around allografts.  Chris shares why Infuse was black-boxed by the FDA, and his opinion on using it for alveolar cleft grafting.Timing of follow-ups post alveolar cleft grafting.Why Chris avoids corticocancellous blocks whenever possible. The approximate percentage of alveolar cleft grafting patients that need cleft orthognathic surgery later in life. Differences between Asian and Caucasian children in terms of the likelihood of requiring orthognathic surgery.Where Chris acquired the majority of his cleft surgery skills. Chris's experience doing mission trips, and the perspective he gained as a result. The lack of continuity of care in many countries outside of the US.Challenges to OMS involvement in cleft surgery. Book recommendations from Chris.Chris's favorite OMS tool.  Links Mentioned in Today's Episode:Dr. Chris Viozzi — The Immortal Life of Henrietta Lacks — http://rebeccaskloot.com/the-immortal-life/ Quiet — https://www.quietrev.com/quiet-the-book-2/ Medical Missions for Children — https://www.mmfc.org/ Dr. Grant Stucki Email — grantstucki@gmail.comDr. Grant Stucki Phone — 720-441-6059

Riley and Shaw go over and practice concepts such as Relevant Lung Anatomy, Alveolar Compliance-Elastance, O2/CO2 Diffusion Gradients, and more.

Getting the air to our lungs in the first place can be challenging enough. How do we get the oxygen out of the air once we have it in our lungs? This huge job comes down to one tiny unit: the alveoli-capillary unit. In this brick, we take a look at how the exchange of gases takes place. After listening to this AudioBrick, you should be able to: Describe the features, dimensions, and components of the respiratory membrane. List the components and explain the function of surfactant. List the factors that affect the rate of gas exchange across the respiratory membrane. Describe the alveolar gas equation and explain how it is used. Define respiratory quotient. You can also check out the original brick from our Respiratory collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/ from our Musculoskeletal, Skin, and Connective Tissue collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology.

On this week's episode of Fast Facts - Perio Edition your host, Katrina Sanders, RDH talks to us about the Alveolar Bone Crust!   Quotes:    “For most of us we're utilizing dental radiographs to evaluate our approximate what that bone level looks like. So know that when we're looking at the shape of that bony crust, we're looking at several influential factors, things like what is the width of the interdental space? Do we have a close contact? Do we have a diastema or do we have a completely open contact?”   “Now, from a composition standpoint, the alveolar process itself really is a dense collagenous fiber and it's important for us to understand that. These collagen fibers provide that ground substance or that ground matrix and then we have inorganic salts of bone, primarily calcium and phosphate, that permit the remineralization or mineralization itself of the bone within the bone itself.”   Resources:   DentistRX: https://www.dentistrx.com  More Fast Facts: https://www.ataleoftwohygienists.com/fast-facts/    Katrina Sanders Website: https://www.katrinasanders.com  Katrina Sanders Instagram: https://www.instagram.com/thedentalwinegenist/

Here Vikram answers questions on Minimum Alveolar Concentration. Many thanks to Vikram and Sanjana for creating this resource. If you are preparing for the Primary FRCA why not consider joining https://videovivaclub.com/ This resource should be used as a supplement to existing resources. It was recorded live and intends to give an example of a mock viva question. Please do not depend on this resource in isolation to provide a "model answer".

Part 2: Mark describes the clinical factors of space closure and an method of maintaining bone in space opening using miniscrews Space closure aesthetic challenges 1. Gingival height: Canine's height is superior to lateral incisor's 2. Torque: Canine is of buccal root torque, and a lateral is palatal root torque 3. Morphology: Canine is wider and thicker than a lateral incisor. 1. Gingival height solution: a. Bracket placement · Canine bracket placed gingical = extrude gingival margin · Premolar / bicuspid bracket placed incisal = ,intrude gingival margin 2. Torque · Using a lower contralateral 2nd premolar bracket inverted:a achieves 17 degrees of palatal root torque and fits onto the surface of the canine · Mophology · Minimal prep veneer · Narrow buccal lingual via reduction Mechanics – tips for space closure · Always push mechanics · If pull mechanics– distort archform, and alter centreline · TADs can be usedfor anterior anchorage Space closure advantages over space opening · Stable · immediately finish, no 2 stages · Predictable periodontal health · Possible in all malocclusions · Maintains bone · No prosthesis · No evidence of functional problems Space opening miniscrew to maintain bone Does it work? Miniscrews: increase density Al Maaitah AJODO · 3/12 after placement Follow up for 5 years = maintained bone and prosthesis, Ciarlantini 2017 How to insert? o Lateral insertion = as vertical insertion of miniscrew shows infraocclusion o Use of spring to maintain prosthesis References Al Maaitah, E.F., Safi, A.A. and Abdelhafez, R.S., 2012. Alveolar bone density changes around miniscrews: a prospective clinical study. American journal of orthodontics and dentofacial orthopedics, 142(6), pp.758-767. Ciarlantini, R. and Melsen, B., 2017. Semipermanent replacement of missing maxillary lateral incisors by mini-implant retained pontics: A follow-up study. American Journal of Orthodontics and Dentofacial Orthopedics, 151(5), pp.989-994.