Podcasts about alveolar

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/2023.02.27.530122v1?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

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

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]

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.

Join moderators Alice Gallo de Moraes, MD, and Christopher L. Carroll, MD, MS, FCCP, and journal CHEST® authors Zhenmei Zhang, MD, and Hemang Yadav, MBBS, as they discuss the article, "Epidemiology, Risk Factors and Outcomes of Diffuse Alveolar Hemorrhage After Hematopoietic Stem Cell Transplantation," from the June 2021 issue. DOI: https://doi.org/10.1016/j.chest.2021.01.008

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.

Estimated reading time: 5 minutes The prestigious British Medical Journal recently published a study that got little attention from Mainstream Media, probably because it wasn't about getting the COVID-19 vaccine. The study showed that four dietary supplements significantly reduce COVID-19 infection risk. Using an app developed by Zoe Global, in partnership with King's College London, Massachusetts General Hospital, Lund University, Sweden, and Uppsala University, Sweden, researchers reviewed data from more than 400,000 users. To summarize their findings: In the largest observational study on SARS-CoV-2 infection and dietary supplement use to date on over 400,000 app users from three different countries, we show a significant association between users of omega-3 fatty acid, probiotic, multivitamin or vitamin D supplements and lower risk of testing positive for infection with SARS-CoV-2.Louca P, et al. Interestingly, supplement use seemed to be more effective in women than men in relation to COVID-19. What makes these supplements especially effective? Vitamin D One of the many health benefits of vitamin D is its impact on the immune system.  Health care providers have known for decades that low vitamin D levels increase the risk of the flu and other infections. Vitamin D affects the function of T cells and B cells. It's no surprise, then, that low vitamin D levels could increase the risk of COVID-19. In the BMJ study, vitamin D supplementation lowered COVID-19 risk by 9% for United Kingdom participants and by 24% for those in the United States. Another new study, published in The Lancet, also affirmed the protective effects of vitamin D supplementation. In summary, this updated meta-analysis of data from RCTs of vitamin D supplementation for the prevention of ARIs showed a significant overall protective effect of this intervention compared with a placebo control.Joliffe DA, et al. Multivitamins Though I'm a major advocate for multivitamin use, health care practitioners often question the health benefits of multivitamins. Because they include multiple ingredients, and the supplement market includes a wide range of qualities, the research on multivitamins isn't as in-depth as that of the individual ingredients. However, there's no doubt that most people don't get enough of most micronutrients for optimal health. Any micronutrient deficiency has the potential to interfere with immune function, but inadequate zinc, or vitamins A, C, D, and E can all increase the risk of viral infection. In the BMJ study, multivitamin use lowered COVID-19 infection risk by 13% for those in the U.K., and 12% for those in the U.S. Read also: The Best Multivitamins for Men and Women. Omega-3 Fatty Acids (Fish Oil) You might be surprised to see fish oil included in this list. When most people think of fish oil health benefits, they think of heart health, fat loss, brain function, and possibly muscle growth.  Omega-3 fatty acids help support a normal inflammatory response, and inflammation plays a significant role in the immune process. That said, it's unclear exactly how fish oil reduces SARS-CoV-2 infection, but it does. The data from the BMJ shows fish oil supplementation lowers COVID-19 risk in the United States by 21% and in the United Kingdom by 12%. Probiotics It's often said that “70% of your immune system lies in your gut.” Whether that's an accurate percentage or not, the point is that your gut health plays a crucial role in immune function. That doesn't mean your gut only protects you from pathogens that reach your gut. In reality, the bacteria in your intestines produce metabolites and other compounds that enhance immune function throughout the body. In fact, research shows that the balance of good and bad bacteria in the gut impacts the function of immune cells even in the lungs. Alveolar macrophages act as patrols in the lung tissues,

Ortocast #74 – Dats Longos em Área Extra-alveolar

Alveolar consonants are made with the tip of tongue TopDadSadZebraButterNopeLightFrom BBC presentation trainer Peter Stewart (@TweeterStewart), GET A BETTER BROADCAST, PODCAST AND VIDEO VOICE is a short, daily guide to help you become a stronger voice communicator on radio and TV, podcasts, video, voiceovers and webinars.It's the audio version of the book Peter's writing of the same name, both focusing exclusively on your vocal image on audio and video channels with two main aims:· To get you a better voice for audio and video channels.· To show you how to read out loud confidently, convincingly and conversationally.Through these under-5-minute episodes, you can build your confidence and competence with advice on breathing and reading, inflection and projection, the roles played by better scripting and better sitting, mic techniques and voice care tips... with exercises and anecdotes from a career spent in TV and radio studios.And as themes develop over the weeks (that is, they are not random topics day-by-day), this is a free, course to help you GET A BETTER BROADCAST, PODCAST AND VIDEO VOICE.Look out for more details of the book during 2021.Contacts: https://linktr.ee/Peter_Stewart Peter has been around voice and audio all his working life and has trained hundreds of broadcasters in all styles of radio from pop music stations such as Capital FM and BBC Radio 1 to Heart FM, the classical music station BBC Radio 3 and regional BBC stations. He’s trained news presenters on regional TV, the BBC News Channel and on flagship programmes such as the BBC’s Panorama. Other trainees have been music presenters, breakfast show hosts, travel news presenters and voice-over artists.He has written a number of books on audio and video presentation and production (“Essential Radio Journalism”, “JournoLists”, two editions of “Essential Radio Skills” and three editions of “Broadcast Journalism”) and has written on voice and presentation skills in the BBC’s in-house newspaper “Ariel”.Peter has presented hundreds of radio shows (you may have heard him on BBC Radio 2, BBC Radio 4, Virgin Radio or Kiss, as well as BBC regional radio) with formats as diverse as music-presentation, interview shows, ‘special’ programmes for elections and budgets, live outside broadcasts and commentaries and even the occasional sports, gardening and dedication programmes. He has read several thousand news bulletins, and hosted nearly 2,000 podcast episodes, and is a vocal image consultant advising in all aspects of voice and speech training for presenters on radio and TV, podcasts and YouTube, voiceovers and videocalls. See acast.com/privacy for privacy and opt-out information.

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/

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/

Listen as Dr. London Smith (.com) and his producer Cameron discuss Pulmonary Alveolar Proteinosis with special guest Sean Curry (Alex Bozinovic). Not so boring! https://www.patreon.com/join/jockdocpodcast Hosts: London Smith, Cameron Clark Guest: Alex Bozinovic. Produced by: Dylan Walker Created by: London Smith

ligamento periodontal e osso alveolar

This episode covers pulmonary alveolar proteinosis! --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

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".

Join us as we discuss best practices and protocols for Ridge Preservation after tooth extraction with Prof Simon Wright. 

Ortocast #68 – Mini-implantes em Mucosa Alveolar

Dr. Maor Sauler is joined by Drs. Kalinichenko, Greenberg, and Jobe to discuss their article "Nanoparticle Delivery of Proangiogenic Transcription Factors into the Neonatal Circulation Inhibits Alveolar Simplification Caused by Hyperoxia".

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.

استمعوا للبودكاست الخاص بي " الاحياء الدقيقة في دقيقة" ارجو ان ينال اعجابكم . ادعموني على منصة patreon من خلال مساهماتكم على الرابط التالي www.patreon.com/microinmin #podcast #microbiology_in_aminute شرح ال Pathogenesis of 2019_nCoV : ١_ بعد دخول الفايروس الى الجسم، يحتاج الى مستقبل خاص (receptors) ليساعده على دخول الخلية، هذا ال receptor يسمى Angiotensin Converting Enzymes_2 إنزيمات الأنجيوتنسين المحولة يرمز له ب ACE_2 . ٢_ ال ACE_2 موجود على سطح خلايا الحويصلة الهوائية "alveolar cells" الموجودة في الرئة . لدينا ٣ أنواع من alveolar cells : _النوع الأول "type1" : يكون مسؤول عن تبادل الغازات مع الأوعية الدموية (gas exchange ). _النوع الثاني "type2" : يكون مسؤول عن إنتاج مادة ال "surfactant" و هو عبارة عن مزيج من البروتينات و الدهون التي تقلل الشد السطحي للحويصلة الهوائية. _النوع الثالث"type3" : خلايا مناعية "dust cell" و هي عبارة عن macrophages .البلاعم *ال ACE_2 موجود على النوع الثاني"type2" من هذه الخلايا. ٣_ غلاف فايروس كورونا يحتوي على بروتينات تسمى spikes.المسامير و خاصة (S_Spike) تساعد الفايروس على الارتباط ب ACE_2 . عندما يحدث الارتباط اعلاه، تدخل المادة الوراثية للفايروس الى داخل الخلية و تسخر الخلية لإنتاج بروتينات الفايروس و بالتالي يتكاثر الفايروس و تموت الخلية. ٤_ عندما تموت type 2 alveolar cells ف أنها تقوم ب طرح مواد تسمى specific inflammatory mediators وسطاء التهابات محددة هذه المواد تعمل على تحفيز الخلايا المناعية الموجودة "macrophages" و عندما تتحفز ال macrophages" ف أنها تفرز ٣ مواد مناعية تسمى ب " cytokines"السيتوكينات و هي: Interleukin_1 "IL_1"إنترلوكين Interleukin_6 "IL_6" Tumor Necrosis Factor "TNF_α" .عامل نخر الورم هذه المواد الثلاث عندما تصل الى مجرى الدم فإنها تسبب الاعراض المصاحبة للاصابة ب فايروس كورونا. #الأعراض: اولاً _ على مستوى ال lungs:الرئتين ١_ هذه المواد تسبب توسع بالاوعية الدموية المحيطة بالحويصلة و كذلك زيادة نفاذية جدار هذه الأوعية _ Vasodilation توسع الأوعية _ Capillary permeability increased .زيادة النفاذية الشعرية و بالتالي يؤدي الى "alveolar edema".الوذمة السنخية. التي تؤدي الى نقص الأوكسجين "Hypoxia"نقص الأكسجة و ضيق التنفس. ٢_ فقدان ال surfactant يؤدي الى زيادة الشد السطحي ل الحويصلة و بالتالي يؤدي إلى Alveolar collapse .انهيار سنخي. و تؤدي أيضاً الى Hypoxia و ضيق التنفس. ٣_ كذلك هذه المواد الثلاث تؤدي الى زيادة تدفق خلايا "neutrophils" الى مكان الإصابة الفايروسية ك استجابة مناعية، خلايا neutrophils تقوم بقتل بعض الفايروسات عن طريق إفراز مادتين مثل : _Reactive Oxygen Species "ROS". _ أنواع الأكسجين التفاعلية "ROS" _Proteases. البروتياز لكن المادتين أعلاه أيضاً تقوم ب تحطيم بعض ال alveolar cells المسؤولة عن التبادل الغازي وتسبب حالة تسمى consolidation الدمج. التي تسبب أعراض السعال "cough" . ثانياً: على مستوى ال CNS : الجهاز العصبي المركزي المواد الثلاث "IL_1, IL_6, TNF" تذهب الى ال "hypothalamus".الغدة النخامية. و بالتالي تعمل على زيادة درجة حرارة الجسم و تسبب أعراض ال "Fever" .الحمى ثالثاً: في حالة severe. شديدة. ستحدث ال " SIRS " Systemic inflammatory response syndrome . متلازمة الاستجابة الالتهابية الجهازية. التي تؤدي الى septic shock . الصدمة الإنتانية و كذلك "MODS" Multiple organ dysfunction syndrome. متلازمة ضعف الأعضاء المتعددة. و خاصة الكلية و بالتالي يحصل فشل كلوي.

The story of the secret guardian of New Molar -- THE ALVEOLAR! Written by: JONATHAN A. GOLDBERG Music by: DAVID ORIGLIERI Read by: AMANDA JONES To learn more about Amanda check out this: http://www.amandajones.biz/ To learn more about Fuzztown check out this: www.podmusical.com

Alveolar Oxygen

Law of Laplace

Alveolar compliance curve

Alveolar recruitment Maneuver

In this episode, we cover one check box on your bilateral airspace opacification differential diagnosis. Come take a listen for Diffuse alveolar hemorrhage and pulmonary vasculitis in the ICU. -Imaging findings -Bronch? -What labs to order (you can't just write "vasculitis work up")

This week we discuss some pretty interesting articles from the Journal of Oral & Maxillofacial Surgery the first one discussing the Akinosi nerve block technique versus the inferior alveolar nerve block technique for beginners to see whether there's an ease in learning and decrease complication rates for beginners.   I didn't ask us the use of recombinant human bone morphogenetic protein for use in grafting of the  Alveolar cleft. I then proceeded on to discuss where there's a correlation between an impacted mandibular third molar, the type of impaction and mandible fractures and then the type of mandible fractures and believe me when I tell you there is. You're going to have to listen to this episode to find out what that correlation is.

Dental podcast hosted by Dr. Phil Klein: This Viva Podcast will discuss preserving and augmenting the alveolar bone following an extraction. Our guest is Dr. Veronique Benhamou, a certified Specialist in Periodontics and Implantology and associate professor and Past Director of the Division of Periodontics at McGill University Dental School. Dr. Benhamou has been a recipient of many prestigious teaching and clinical awards and is currently in private practice in downtown Montreal. Dedicated to teaching, she is very involved with continuing dental education worldwide.

Dental podcast hosted by Dr. Phil Klein: This Viva Podcast will discuss alveolar requirements for successful long-term dental implants. We are joined by Dr. Isaac Tawil, President of AIE Advanced Implant Educators. AIE courses offer real world execution of implant placement, alveolar ridge expansion and crestal and lateral wall sinus graft augmentation. Dr. Tawil lectures around the world and teaches live surgical seminars on advanced dental implant procedures using the latest technology.

This podcast is going to dive into the topic of TIME CONSTANT. Have you ever wondered how we truly determine the exhalation time for our ventilator patients? Time Constant is the concept that guides our care and determines the time needed for proper alveolar filling or emptying. We couple this podcast with a downloadable worksheet for practice that can be found in the show notes on the FlightBridgeED website under this podcast. The worksheet gives calculation examples, practice questions, and answers to check your work. I promise this podcast will challenge you, bring insight on problems you've encountered in the transport environment and ultimately give you new tools that will make you better as a clinician. We couldn't make this podcast without. Please rate, and review wherever you download the podcast. Thanks for listening!See omnystudio.com/listener for privacy information.

This podcast is going to dive into the topic of TIME CONSTANT. Have you ever wondered how we truly determine the exhalation time for our ventilator patients? Time Constant is the concept that guides our care and determines the time needed for proper alveolar filling or emptying. We couple this podcast with a downloadable worksheet for practice that can be found in the show notes on the FlightBridgeED website under this podcast. The worksheet gives calculation examples, practice questions, and answers to check your work. I promise this podcast will challenge you, bring insight on problems you've encountered in the transport environment and ultimately give you new tools that will make you better as a clinician. We couldn’t make this podcast without. Please rate, and review wherever you download the podcast. Thanks for listening!

In this episode I discuss a recent trauma case were a young man riding his motorcycle took a beating to his premaxilla fracturing tooth numbers eight causing a maxillary dental alveolar fracture a partial lefort fracture and an avulsed tooth numbers 11 up into the maxillary vestibule lateral to the nose.

We’re back for another series – this time focussing on the sensory innervation of the face through the lens of dental anaesthesia. This is adapted from a take I gave in EuSEM 2016 in Vienna. This is part 3 The most important … Continue reading →

Basic Science Clinic by Steve Morgan & Sophie Connolly In the words of the canonical Roman poet Ovid: “Sickness seizes the body from bad ventilation”. Welcome to Basic Science Clinic Raw Science 9. Convective gas flow provides the substrate to interface with alveolar structural and functional adaptation in orchestrating gas exchange. Gas exchange is the serial interconnection of ventilation, diffusion and perfusion. Alveolar gas composition is determined by amount and type of gases delivered by ventilation, the rate and direction of gas diffusion, and the pulmonary blood flow which continuously recalibrates partial pressure gradients to direct oxygen and carbon dioxide movement. Bulk gas volume displacement is the mechanism of ventilation, but how do we conceptualise and quantify its contribution to gas exchange and its associated abnormalities? In this pod we will examine the quantification of ventilation and parse its correspondence with variance in the dead space volume and central role in carbon dioxide homeostasis. In this podcast we will cover: How do we define pulmonary ventilation? What is the relationship between alveolar minute ventilation and alveolar gas composition? What are the determinants of arterial carbon dioxide partial pressure? What are the physiological sequelae of hypercapnia? What is permissive hypercarpnia? What is dead space? How do we quantify dead space volume? What are the factors that affect dead space?   Here are your Raw Science factoids: Morphological dead space estimates give us volumes of 150mls for dogs, 380mls for cows and 150-300L for whales. In 1986 in Cameroon a paroxysmal expulsion of carbon dioxide from the volcanic lake Nyos resulted in the asphyxiation of 1700 people and 8000 animals. The highest documented PaCO2 to be measured in a subsequent survivor weighed in at 501 mmHg in a 16 year old boy swallowed, sequestered and asphyxiated by a rapidly filling grain truck. For feedback, corrections and suggestions find us on the twitter handles @falconzao and @sophmconnolly or alternatively post on ICN. Check out our new website basicscienceclinic.com where you can access the back catalogue and peruse the real brains behind our elaborate plagiarism by checking out the reference page to go direct to the source material. Thanks for listening. Next up we’ll consummate the journey of inspirate atmospheric gas into the blood phase, as we appraise gas diffusion across the alveolar-capillary membrane and dissect the pulmonary vasculature.  

Basic Science Clinic by Steve Morgan & Sophie Connolly An expert is a person who has made all the mistakes that can be made in a very narrow field. Niels Bohr   Welcome to Basic Science Clinic Raw Science 8. Convective gas flow through the tracheobronchial tree is the end-point of pulmonary mechanics but the fundamental purpose of the lung is gas exchange, comprised of three interlinked physiological processes: ventilation, diffusion and perfusion. Today we examine the incredible structural adaptation of the human lung down to the alveolus as the centrepoint of gas exchange, a process itself best conceptualized via the elegant physiological model of the alveolar gas equation.   The unraveling of the procession of pulmonary blood flow from right ventricle to lung to facilitate the mingling of blood and air involved protagonists that spanned epochs from Hippocrates to Galen and eventually in 1661 to Marcello Malpighi. He was the first person to view the pulmonary capillaries and alveoli through the augmented reality offered by the light microscope that had been invented in 1590.   The composition of gas in the alveoli determines and represents the process of pulmonary gas exchange and provides a framework for understanding the mechanisms and practical physiological limitations. Alveolar gas is practically inaccessible in vivo and hence requires an accurate and precise model to ascertain its configuration under specific conditions.   The alveolar gas equation relates the alveolar partial pressure of oxygen to inspired partial pressure of oxygen, alveolar and hence arterial partial pressure of carbon dioxide and the respiratory quotient.     How is the lung adapted to optimise gas exchange?   So how does the alveolus fit in?   What are the cell populations in the alveolar region?   How can we model pulmonary gas exchange?   Raw Science factoids:   The oxygen content of arterial blood is ~21 mls/dl, ie 21% by volume. The oxygen content of mixed venous blood is 15-16 mls/dl indicating a total body oxygen extraction of 25%.   The total alveolar surface area is approximately 80x greater than the total surface area of the skin.   Each erythrocyte contains approximately 250 million haemoglobin molecules and 400 billion erythrocytes occupy the total pulmonary capillary blood volume.   For feedback, corrections and suggestions find us on twitter @falconzao and @sophmconnolly or post on ICN.   Thanks for listening. Next up we’ll continue our examination of pulmonary gas exchange by looking in more detail at ventilation, perfusion and diffusion. Coming soon is our video series Raw Focus to delve deeper into the key concepts from each of the podcasts.    

Thu, 15 Oct 2015 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/18929/ https://edoc.ub.uni-muenchen.de/18929/1/Chen_Shanze.pdf Chen, Shanze

Phonologist’s Shanty; Traditional; From Volume CLXXIV, Number 1, of Speculative Grammarian, September 2015 — What shall we do with the velar nasal? / What shall we do with the velar nasal? / What shall we do with the velar nasal? / Early in the morning. (Performed by Pete Bleackley.)

Chronic obstructive pulmonary disease (COPD) is characterized by an irreversible loss of lung function and is one of the most prevalent and severe diseases world-wide. A major feature of COPD is emphysema- a long-term, progressive condition. The hallmark of emphysema includes the destruction of alveolar structures leading to enlarged air spaces and reduced surface area. Experimental evidence suggests that emphysema development is driven by accelerated senescence of lung cells but the underlying mechanism of senescence is yet to be fully elucidated. Protein arginine methyltransferases (PRMTs) are important for cellular processes, such as the regulation of senescence, cell proliferation, differentiation and apoptosis. The PRMT family includes 11 members classified as type I, II or III enzymes depending on their methylation pattern (asymmetric dimethylation, symmetric dimethylation or monomethylation, respectively). One member of this family is PRMT4, a type I enzyme, which is also called coactivator associated arginine methyltransferase 1 (CARM1). It was originally identified as a coactivator for steroid hormone receptors. CARM1 is known to methylate histone H3 and various non-histone proteins that play essential roles in transcriptional regulation, RNA splicing, and metabolism. Most importantly, complete loss of CARM1 leads to disrupted differentiation and maturation of alveolar epithelial type-II cells (ATII). Furthermore, CARM1 also plays a role in regulating cellular senescence via CARM1-dependent methylation. Based on these reports, we hypothesized that CARM1 regulates the development and progression of emphysema. To address this, we investigated the contribution of CARM1 to alveolar rarefication using the mouse model of elastase-induced emphysema in vivo and siRNA-mediated knockdown in ATII-like LA4 cells in vitro. We monitored emphysema progression for 161 days in mice treated with a single oropharyngeal application of elastase. The progression was manifested by the decline in lung function parameters. The mean chord length (Lm) confirmed a time dependent airspace enlargement and was directly correlated with a significant increase in dynamic lung compliance. We also observed that at later time points (day 56 and 161), emphysema progression was inflammation-independent. We demonstrated that emphysema advancement was associated with a time-dependent downregulation of CARM1, specifically in alveolar epithelial cells. Furthermore, the global CARM1 activity was also reduced as reflected by an elevated level of CARM1 phosphorylation in the lung. Most importantly, elastase-treated CARM1 haploinsufficient mice showed significantly increased airspace enlargement (52.5±9.6 µm vs. 38.8±5.5 µm, p

Background The majority of cases with severe pulmonary alveolar proteinosis (PAP) are caused by auto-antibodies against GM-CSF. A multitude of genetic and exogenous causes are responsible for few other cases. Goal of this study was to determine the prevalence of GATA2 deficiency in children and adults with PAP and hematologic disorders. Methods Of 21 patients with GM-CSF-autoantibody negative PAP, 13 had no other organ involvement and 8 had some form of hematologic disorder. The latter were sequenced for GATA2. Results Age at start of PAP ranged from 0.3 to 64 years, 4 patients were children. In half of the subjects GATA2-sequence variations were found, two of which were considered disease causing. Those two patients had the typical phenotype of GATA2 deficiency, one of whom additionally showed a previously undescribed feature – a cholesterol pneumonia. Hematologic disorders included chronic myeloic leukemia, juvenile myelo-monocytic leukemia, lymphoblastic leukemia, sideroblastic anemia and two cases of myelodysplastic syndrome (MDS). A 4 year old child with MDS and DiGeorge Syndrome Type 2 was rescued with repetitive whole lung lavages and her PAP was cured with heterologous stem cell transplant. Conclusions In children and adults with severe GM-CSF negative PAP a close cooperation between pneumologists and hemato-oncologists is needed to diagnose the underlying diseases, some of which are caused by mutations of transcription factor GATA2. Treatment with whole lung lavages as well as stem cell transplant may be successful.

Most recognize the /d/ in the pronunciation of 'little' but how about in 'out_of'? Full episode transcripts at www.pronuncian.com/podcast.

BackgroundJuvenile pulmonary alveolar proteinosis (PAP) due to CSF2RA mutations is a rare disorder with only a few cases described worldwide.MethodsWe identified nine children with severe diffuse interstitial lung disease due to CSF2RA mutations. Clinical course, diagnostic findings and treatment were evaluated and correlated to the genotype. Functional impairment of the intracellular JAK/pStat5 signaling pathway was assessed using flow-cytometry of peripheral mononuclear cells (PBMC) and granulocytes.ResultsWe identified six individuals with homozygous missense/nonsense/frameshift mutations and three individuals homozygous for a deletion of the complete CSF2RA gene locus. Overall, four novel mutations (c.1125¿+¿1G¿>¿A, duplication exon 8, deletion exons 2¿13, Xp22.3/Yp11.3) were found. Reduced STAT5 phosphorylation in PBMC and granulocytes was seen in all cases examined (n =¿6). Pulmonary symptoms varied from respiratory distress to clinically silent. Early disease onset was associated with a more severe clinical phenotype (p =¿0.0092). No association was seen between severity of phenotype at presentation and future clinical course or extent of genetic damage. The clinical course was favorable in all subjects undergoing whole lung lavage (WLL) treatment.ConclusionsOur cohort broadens the spectrum of knowledge about the clinical variability and genotype-phenotype correlations of juvenile PAP, and illustrates the favorable outcome of WLL treatment in severely affected patients.

Olá ouvintes do Ortopodcast! Neste episódio falamos sobre o coquetel de abertura da Academia da Ortodontia Contemporânea, sobre um artigo de 2013 que estuda a espessura do osso cortical do alvéolo em diferentes tipos faciais e suas implicações clínicas. Falamos sobre o instrumental criado pelo Prof. Cardon, do Rio Grande do Sul-Brasil, para facilitar o trabalho com correntes elásticas. Escutem sem moderação!

Background: Pulmonary alveolar proteinosis (PAP) is a rare disorder characterised by abundant alveolar accumulation of surfactant lipoproteins. Serum levels of KL-6, high molecular weight human MUC1 mucin, are increased in the majority of patients with PAP. The prognostic significance of KL-6 in PAP is still unknown. Aim of the study was to evaluate whether serum KL-6 levels correlate with the outcome of the disease. Patients and methods: From 2006 to 2012, we prospectively studied 33 patients with primary autoimmune PAP. We measured serum KL-6 levels by ELISA (Eisai, Tokyo, Japan), and evaluated the correlation between initial KL-6 levels and clinical variables. Disease progression was defined as deterioration of symptoms, and/or lung function, and/or chest imaging. Main results: The initial serum KL-6 levels were significantly correlated with the baseline PaO2, A-aDO(2), DLCO, VC and TLC (p=0.042, 0.012, 0.012, 0.02 and 0.013, respectively). The change over time of serum KL-6 correlated with the change over time of DLCO (p=0.017). The initial serum KL-6 levels were significantly higher in patients with disease progression than in those with remission (p

After our overview episode last week, Phil and Eric look in greater detail at the full range of R consonant variation. We follow the Rhotic Consonants page on wikipedia as a means of tracking the various possible articulations. You can follow along, too! We cover: • Trills • Alveolar [r] • Uvular [ʀ] • Retroflex [ɽ] • Taps and flaps • Alveolar tap [ɾ] • Alveolar lateral flap [ɺ] • Retroflex flap [ɽ] • Labiodental flap (perceived as non-rhotic) [ⱱ] • Alveolar approximant [ɹ] • Molar approximant (aka “braced” /r/) -- see John Wells’s phonetic blog on the VASTA discussion and Erik Singer’s “anchor” [] • Retroflex approximant [ɻ] • Uvular fricative [ʁ]

Background: Clinical presentation, diagnosis, management and outcome of molecularly defined congenital pulmonary alveolar proteinosis (PAP) due to mutations in the GM-CSF receptor are not well known. Case presentation: A 2 1/2 years old girl was diagnosed as having alveolar proteinosis. Whole lung lavages were performed with a new catheter balloon technique, feasible in small sized airways. Because of some interstitial inflammation in the lung biopsy and to further improve the condition, empirical therapy with systemic steroids and azathioprin, and inhaled and subcutaneous GMCSF, were used. Based on clinical measures, total protein and lipid recovered by whole lung lavages, all these treatments were without benefit. Conversely, severe respiratory viral infections and an invasive aspergillosis with aspergilloma formation occurred. Recently the novel homozygous stop mutation p.Ser25X of the GMCSF receptor alpha chain was identified in the patient. This mutation leads to a lack of functional GMCSF receptor and a reduced response to GMCSF stimulation of CD11b expression of mononuclear cells of the patient. Subsequently a very intense treatment with monthly lavages was initiated, resulting for the first time in complete resolution of partial respiratory insufficiency and a significant improvement of the overall somato-psychosocial condition of the child. Conclusions: The long term management from early childhood into young adolescence of severe alveolar proteinosis due to GMCSF receptor deficiency requires a dedicated specialized team to perform technically demanding whole lung lavages and cope with complications.

Episode 6 sees Eric and Phil dissecting the final pair of stop/plosive sounds in English: /k/ and /ɡ/. As always, we work our way around the task of describing the sounds, their history, and usage in the course of about an hour and 10 minutes.Show Notes:Correction: Phil referred to "Findlay" as derived from Finn's Lea, but it turns out that it's from Gaelic, and that means Fionnlagh – "fair warrior." Bradley would have been a much better example: Brad=broad and Lea=meadow.voiceless/voiced velar plosive: co-articulation, double action of closing the mouth with the back of the tongue at the soft palate, and closing off the nasal passage by lifting the soft palate at the velo-pharyngeal port.Let’s take a tour of the anatomy. This will help us to deal with the idea that /t/ is apico alveolar but /k/ is dorsovelarThe Roof of the MouthTectal: an adjective derived from the anatomical term "tectum," a roof-like structure. Labia/labial: the lips; bilabial with both lips, labio-dental with lower lip and upper teeth, as in /f/ and /v/. (For people with an extreme overbite, one might make a dento-labial sound (upper lip and lower teeth.)Dental: the teeth (as heard in the “th” sounds, /θ/ & /ð/ )Alveolar ridge/alveolar: the gum ridge, behind the upper front teethPalate/palatal: the hard palate, rising up behind the alveolar ridge. Phil describes a small hole in his palate; Eric, in searching the net for information on this, could only find stuff about "Jacobsen's Organ" aka Vomeronasal organ http://en.wikipedia.org/wiki/Vomeronasal_organ, an auxiliary olfactory sense organ; it's thoroughly debatable whether it exists in humans at all. Who knows what Phil has? (apparently, he hasn't had any of this since college days...)Velum/velar: the soft palate, behind the hard palateUvula/uvular: the "small grape"-like structure that hangs down from the arch of the soft palatePharynx/pharyngeal: the column or space behind the tongue, the "chimney" that goes from the larynx up to the noseEpiglottis/epiglottal: the flap-like value that protects the larynx during swallowingGlottis/glottal: the vocal folds (technically the SPACE between the vocal folds, which disappears every time the vocal folds vibrateAri-Epiglottal/ False Vocal Folds: [there was some debate between Phil and Eric how Dudley Do-Right sounded, and whether it was ari-epiglottal tension or velar tension...The Parts of the TongueTip or Apex/apical: front edge of the tongue, the 'rim' of the tongueBlade or Lamina/laminal: the front part of the tongue, the top surfaceBack or Dorsum/dorsal: the back of the tongue, which is subdivided into: Front, Middle, Back, or, Front and Back —antero-dorsal or postero-dorsalRoot or Radix/radical: the root of the tongue/k/ and /ɡ/ are different from other plosives because it is made on the back of the tongue, which works in a more gross mannercan be made further forward /ki/ or further back /kɑ/. Challenge of learning /k/ and /ɡ/ for children because they are made further back in the mouthThe McGurk Effect Experiment: Can you identify Phil's 3 sounds? World Atlas of Language Structures: http://wals.info/ WALS shows 2,650 languages and notes 32 missing / ɡ /Languages that are missing /ɡ/ but not /k/From Wikipedia [http://en.wikipedia.org/wiki/Voiced_velar_plosive ] "Of the six plosives that would be expected from the most common pattern world-wide—that is, three places of articulation plus voicing ([p b, t d, k ɡ])—[p] and [ɡ] are the most frequently missing, being absent in about 10% of languages that otherwise have this pattern.[...] It seems that [ɡ] is somewhat more difficult to articulate than the other basic plosives. "Ian Maddieson speculates that this may be due to a physical difficulty in voicing velars: Voicing requires that air flow into the mouth cavity, and the relatively small space allowed by the position of velar consonants means that it will fill up with air quickly, making voicing difficult to maintain in [ɡ] for as long as it is in [d] or [b]."HISTORY OF THE LETTERS:In Greek the symbol of the K (Kappa) turned the "right way" (the way it is in our writing), prior to this it was facing the other direction. Gamma was brought into Latin to represent the C. C had a line added to it to indicate the voiced version, G.SPELLINGS:k “key, keep, koala, kangaroo” “mask, make, pink, walk”c “cat, cost, cut” (contrast “cease, ace, ,macerate ”) Hard/softcc “accuse, stucco” ck “pick, stock”ch “charisma, Christ, choir, ache”Shakespeare's "Petruchio" probably should be [pəʼtɹu.tʃo] not [pəʼtɹu.ki.oʊ]g “game, gate, bag, agony” (contrast “gem, badge,magical ”) Hard/softgg “egg, dagger”gh “ghost, ghetto” (contrast “night, ought”)gu “guide, guest, guerrilla” foreign originckg blackguardx “examine, exhaust”Note that "x" can be /ks/ or /gz/ depending on the word, e.g. /ks/ "excellent" , /gz/ "exist".Soft G is the affricate /dʒ/, while Soft C is /s/.PHONETIC NOTATION: represented by lower case k and ɡIPA symbol for /ɡ/ is the "single-story" version of the g lowercase with an open tail, rather than a looptail. VARIATIONS:Not a lot of variations: mostly to do with voice onset timeVariation: final /k/ becoming fricative in Liverpool week [wiç], like [laiç], back [bax], dock [dɒχ]John Maidment, commenting on JC Wells' blog post on "VOT is more":"One might also like to add that VOT is sensitive to place of articulation. Other things being equal, the VOT of posterior articulations, velar and uvular, are considerably longer, at least for native English speakers, than articulations further forward in the vocal tract. A typical VOT for stressed syllable initial [k] in English is in the region of 120ms, while that for an equivalent [p]is only 60-70ms. I am pretty sure that this difference is an important secondary cue for the perception of place in voiceless plosives and one which, as far as I know, has not been properly investigated."Non-English Stop plosivesPalatalized stops (often heard in Russian, [tʲ] [dʲ] vs. Palatal stop [c] or [ɟ]Uvular stop, as in Arabic pronunciation of Qatar or Iraq [q].Though it's unlikely that a character will do a sound substitution on stop-plosives, however, characters might speak foreign language work, or say words within the text, such as place names or character names.Original Pronunciation: David Crystal is the leading proponent of this type of pronunciation, especially at the Globe Shakespeare Company in London. http://www.davidcrystal.com/DC_articles/Shakespeare11.pdf

Inhalational anthrax is an acute infectious disease caused by exposure of the lungs to B. anthracis spores. Alveolar macrophages engulf spores causing them to germinate to the vegetative form of B. anthracis, which secretes edema toxin (ET)and lethal toxin (LT). The pathogenesis of inhalational anthrax is characterized by flu-like symptoms, respiratory distress, meningitis and shock, which is fatal in almost all cases. The mechanism behind the respiratory distress is not well understood. Therefore, our goal was to determine the effects of lethal toxin in the human lung epithelium. To study alterations in a more physiological setting, we developed a differentiated, polarized lung epithelial system. Lethal toxin exposure disrupted the lung barrier function and wound healing. Assembly defects of junction proteins and additional multicellular junction sites resulted in a higher permeability. Pretreatment with keratinocyte growth factor (KGF) and dexamethasone increased the viability, resulting in the rescue of the permeability changes. Upon LT treatment, a more rigid cytoskeleton was observed, evidenced by enhanced actin stress fiber formations and tubulin stabilization. Cytoskeleton and adhesion alterations prevented the epithelial cells from polarization, directed migration, and wound healing. The MAPK pathway and Cdc42 activity might be partially responsible for these motility defects. Lethal toxin is known to induce rapid cell death in murine macrophages. In contrast, human epithelial cells are more resistant to the cytotoxic effect of LT. By following the growth of epithelial cells after LT treatment, we observed inhibited cell proliferation due to a cell cycle arrest in the G1 phase. Surprisingly, biotinylated lethal factor did not induce cytotoxicity in murine macrophages. This is not due to an internalization or proteolytic activity defect; instead changes in the mitochondrial potential and proteasome activity were observed. Biotinylated LT did not reduce proteasome activity as seen in LT treated cells and caused hypopolarization of the mitochondria. However, it is possible that biotinylation of lethal toxin could prevent interaction of LT with proteins that induce cell death. The major challenge for anthrax treatment is to find a treatment, which can act faster, is easy to use and can bring patient out of the dangerous physiological state in late pathogenesis. Our study has implications in saving the viability and barrier function of lung epithelial cells. One can devise better dosage and delivery of KGF and dexamethasone as treatment modality for post anthrax exposure to reduce respiratory distress. Furthermore, overcoming the cell cycle arrest by the development of a drug would reduce the damage of lung epithelial cells and induce proliferation. The discovery that biotinylated LT is non-toxic to murine macrophages could revolutionize treatment of anthrax infection. Exploring the types of posttranslational modifications of LT that decrease toxicity and finding the mechanism behind it might, lead to therapies that directly counteract the effects of the lethal toxin in vivo.

Laurein ist eines der vier Dörfer in der sogenannten Deutschgegend am Nonsberg im Südwesten der heutigen Autonomen Provinz Bozen (Südtirol). Die Mundart ist südbairisch mit tirolischem Einschlag und die Muttersprache des Verfassers. Daher wurden, um die Mundart synchron zu untersuchen, keine klassische Erhebung mit Fragekatalog oder gezielt Audioaufnahmen gemacht. Als Referenz diente im ersten Anlauf stets die eigene muttersprachliche Kenntnis. Wenn diese nicht ausreichte, was recht oft der Fall war, wurden kompetentere Sprecher zu Rate gezogen. Über Textkorpora verfügt die Mundart von Laurein so gut wie keine. Auf diachroner Ebene ist insbesondere in der Lautlehre der Bezugspunkt in der Regel das Mittelhochdeutsche bairischer Prägung, und bei jüngeren Lehnwörtern aus dem Romanischen das Westromanische bzw. die welsche (halbladinische) Nachbarmundart des Nonsbergs als dessen unmittelbarer Nachfolger. In manchen Fällen muss, wenn es gilt, die Geschichte eines Lautes in einem ganz bestimmten Einzelwort zu beleuchten, über das Mittelhochdeutsche hinaus ins Altgermanische und über das Westromanische hinaus ins Lateinische, mitunter auch ins Indogermanische zurückgegriffen werden. Dabei begibt man sich zwangsläufig in den Bereich der Etymologie, die mitunter problematisch ist. Letzteres gilt auch für den Namen Laurein, der in der Mundart Lafreng lautet. Der Vokalismus der Mundart von Laurein kennt Kürzen und Längen, Oralität und Nasalität und fallende Diphthonge. Nasalvokale oder -diphthonge sind nicht zwangsläufig kombinatorische Varianten der entsprechenden Oralvokale oder -diphthonge, zumal erstere auch in nicht-nasaler Umgebung vorkommen können. Zu den Diphthongen gehören auch so genannte „einmorige Diphthonge“, die positionsbedingt sind. Auch bestimmte zweimorige Diphthonge können über kombinatorische Varianten verfügen. Die Vokale bzw. Diphthonge haben, je nachdem in welchem Wort sie erscheinen, unterschiedliche Entsprechungen in der Bezugsprache (sei sie historisch, sei sie synchron wie die nhd. Standardsprache oder das jüngere Romanische bzw. Italienische). Wie in der nhd. Standardsprache konnten Vokale in offener Tonsilbe in Zweisilbern und analog dazu auch in Ein- und Dreisilbern gedehnt werden. Es gibt aber auch Fälle, in denen in Dreisilbern keine analoge Dehnung stattgefunden hat. Daneben gibt es rezentere Dehnungserscheinungen, wie z. B. vor ehemaligem rr oder vor r + stimmhaftem Alveolar. Besonders hervorzuheben in der diachronen Betrachtung der Vokale sind zwei Aspekte: Die Datierung und Qualität des Primär- und Sekundärumlauts; die Behandlung der romanischen Qualitäten (von e und o) und der Quantitäten. Die wichtigsten Merkmale des Konsonantismus der Mundart von Laurein sind: Der w-Laut wird als [b] gesprochen. Unterschiede im Stimmton gibt es nur bei den Okklusiven. Die Mundart kennt bei den Okklusiven keine Auslautverhärtung (außer bei d nach r), keine Geminierung, keinen Unterschied zwischen einem ich- und ach-Laut. Das System der Okklusive und Affrikaten ist auch in der alveolaren Reihe dreigliedrig. Die Mundart von Laurein ist die einzige am gesamten Nonsberg, in der der r-Laut uvular gesprochen wird, und dieser ist in jeder Position hörbar. Auch erwähnenswert ist, dass [k], also der nicht affrizierte Velar, relativ häufig vorkommt – nicht zuletzt dank zahlreicher Lehnwörter aus dem Romanischen. Andererseits haben wir in der Mundart [g] für rom. [k]; und aus diesem Grund wurde vorsichtig die Überlegung angestellt, ob dieses [g] mit jenem ahd. *[k] zusammenfiel, das interimsmäßig aus *[g] verhärtet war. In diesem Zusammenhang wurde auch die Frage gestellt, ob es bei [k] eine zweite Welle der Zweiten Lautverschiebung geben konnte. In Einzelfällen kann ein stimmloser Okklusiv [p] für germ. *b auch im In- und Auslaut erscheinen, was wahrscheinlich für Kontinuität seit ahd. Zeit spricht. Bei der Deklination sind folgende Aspekte zu nennen: Das Substantiv kennt keine Kasusflexion mehr; diese gilt nur mehr bei den Adjektiven und Indefinitpronomina. Bei einzelnen Substantiven zeigt die Pluralbildung eine noch schwächere Kontinuität des mhd. Musters als die nhd. Standardsprache. Bei den Maskulina und Neutra ist das Pluralmorphem -er am stärksten verallgemeinert worden und hat ferner vielfach analogen Umlaut bewirkt. Bei den Feminina zeigt wie in der nhd. Standardsprache das Pluralmorphem -en die stärkste Verallgemeinerung. Je nach ihrem Verhalten bei der Pluralbildung auf synchroner Ebene können die Substantive unterschiedlichen Typen zugeordnet werden. Bei der starken Adjektivdeklination kennt die Mundart von Laurein im Gegensatz zur nhd. Standardsprache nur einen Typ (Typ 1), während die starke Deklination der Standardsprache zwei Typen unterscheidet, von denen sich der so genannte Mischtyp (Typ 3) erst in nhd. Zeit herausgebildet hat, und zwar aus Typ 1 und Typ 2. Letzterer gilt bei der schwachen Deklination und kommt in der Mundart von Laurein seltener zur Anwendung als in der nhd. Standardsprache. Die Steigerung der Adjektive (und Adverbien) zeigt zudem häufig analogen Umlaut. Bei den Personalpronomen sind je nach syntaktischem Umfeld drei Typen zu unterscheiden. Beim Reflexivpronomen wird wie im Mhd. zwischen indirekter und direkter Reflexivität unterschieden. Das Pronomen der 2. Person Plural lautet in „unbairischer“ Weise im Nominativ „ihr“, dagegen im Dativ und Akkusativ durchaus „enk“. Die wichtigste Besonderheit des Possessivpronomens ist, dass „sein“ sich auch auf das Femininum Singular und den Plural beziehen kann. Der bestimmte Artikel zeigt dagegen weitgehend dieselben Abweichungen vom Mhd. wie in der nhd. Standardsprache. Das nahdeiktische Demonstrativpronomen reflektiert meist nur mittelbar den bestimmten Artikel des Mittelhochdeutschen in betonter Stellung. Das ferndeiktische Demonstrativpronomen wird auf der Grundlage von mhd. sëlp, -bes gebildet. Beim neutralen Interrogativpronomen wird nach Präpositionen ein Dativ gebraucht, der formal historischer Instrumental ist. Der unbestimmte Artikel kommt in gemeinbairischer Weise nur schwachtonig vor und lautet im Nominativ für alle drei Genera gleich. In Bezug auf die Zahlwörter ist u. a. zu erwähnen, dass es je nachdem, ob die Uhrzeit oder ein allgemeiner Zahlwert gemeint ist, zwei Formen für ‘drei’ gibt. In der Konjugation finden wir besonders viele Auffälligkeiten: Wie allgemein im Bairischen fehlt das Präteritum; eine Ausnahme speziell in der Mundart von Laurein bilden das Verb für ‘sein’ und für ‘haben’. Im Unterschied zur nhd. Standardsprache gilt die so genannte „e-Erweiterung“ auch bei Verbalstämmen auf [k] und [p]. Die Verben mit „e-Erweiterung“ sind gleichzeitig auch jene Verben, die, auch wenn sie schwach konjugiert werden, das Partizip Präteritum auf /ən/ bilden – es sei denn, es handelt sich um Proparoxytona. Eine Reihe von starken Verben setzt die mhd. Tradition fort, das Partizip Präteritum ohne das Präfix ge- zu gebrauchen. Auf synchroner Ebene können die Verben in regelmäßige und unregelmäßige Verben und innerhalb dieser in unterschiedliche Typen unterteilt werden. Von der 3. Ablautstufe des Mittelhochdeutschen gibt es in der Mundart von Laurein nur mehr einen Reflex, und zwar im Konjunktiv II des Verbs für ‘werden’, der [bu:ʀət] lautet. Das Morphem [ət] wurde von den starken Verben auf die schwachen Verben (bis auf wenige Ausnahmen, die positionsbedingt sind) übertragen. Verben mit so genanntem „Rückumlaut“ sind der Mundart von Laurein fremd. Dieser ist immer zugunsten des Stammvokals des Infinitivs beseitigt worden. Der grammatische Wechsel ist in weniger Fällen ausgeglichen worden als in der nhd. Standardsprache. Recht archaisch ist der Stammvokal (eigentlich Stammdiphthong) im Singular Präsens der ehemaligen Klassen IIa, IIb, zumal dieser nicht zugunsten des Vokalismus des Infinitivs und der Pluralformen ausgeglichen wurde. Kein Ausgleich hat ferner in der 1. Person Singular Präsens der ehemaligen Klassen IIIb, IV und V stattgefunden, sehr wohl dagegen in der 2. und 3. Person Singular Präsens der ehemaligen Klasse VI. Besonders erwähnenswert ist, dass der Umlaut üe zur 3. Ablautstufe des Konjunktivs II der ehemaligen Klasse VI auf einige „schwache“ Verben übertragen werden konnte. Freilich gibt es auch in der Mundart von Laurein einige Verben, die als Mischtypen zu bezeichnen sind, weil sie je nach Tempus oder finiter Form „schwach“ oder „stark“ flektieren. Als Sondertypen werden schließlich jene Verben bezeichnet, die aus synchroner Sicht ein äußerst unsystematisch und unlogisch erscheinendes Bild zeigen. Hierher gehören die Hilfsverben, die Verben für ‘gehen’ und ‘stehen’ und die Modalverben. Insbesondere bei den Modalverben kam es in hohem Ausmaß zu regelrecht kettenreaktionsartigen Analogien.

Objective: To evaluate maxillary growth following in utero repair of surgically created cleft lip and alveolar (CLA)-like defects by means of three-dimensional (3D) computer tomographic (CT) cephalometric analysis in the mid-gestational sheep model. Methods: In 12 sheep fetuses a unilateral CLA-like defect was created in utero (untreated control group: 4 fetuses). Four different bone grafts were used for the alveolar defect closure. After euthanasia, CT scans of the skulls of the fetuses, 3D re-constructions, and a 3D-CT cephalometric analysis were performed. Results: The comparisons between the operated and nonoperated skull sides as well as of the maxillary asymmetry among the experimental groups revealed no statistically significant differences of the 12 variables used. Conclusions: None of the surgical approaches used for the in utero correction of CLA-like defects seem to affect significantly postsurgical maxillary growth; however, when bone graft healing takes place, a tendency for almost normal maxillary growth can be observed. Copyright (c) 2006 S. Karger AG, Basel.

Tue, 1 Jan 2002 12:00:00 +0100 https://epub.ub.uni-muenchen.de/16774/1/10_1159_000048887.pdf Krombach, Fritz; Dörger, Martina ddc:610, Medizin

The pulmonary capillary microvasculature harbors a large pool of intravascularly marginated leukocytes. In this study, we investigated the interrelationship of leukocyte margination with characteristics of functional capillary geometry and microhemodynamics in alveolar capillary networks. In 22 anesthetized rabbits we assessed functional capillary density, average capillary length, red blood cell velocity and leukocyte kinetics in alveolar capillary networks in vivo by intravital fluorescence microscopy. In alveolar wall areas of 12,800 +/- 1,800 mu m(2), we detected 3.6 +/- 0.5 sticking leukocytes and 21.0 +/- 1.9 functional capillary segments with an average capillary length of 35.7 +/- 2.1 mu m. We calculated that approximately 15% of functional capillary segments are blocked by marginated leukocytes. Leukocyte margination was predominantly observed in capillary networks characterized by a high functional capillary density, short capillary segments and low red blood cell velocities. The multitude of interconnected capillary channels in these networks may allow alveolar blood flow to bypass marginated leukocytes. Hence, this interrelationship may be relevant for maintenance of adequate alveolar perfusion and low capillary network resistance despite excessive leukocyte margination in the pulmonary microvasculature. Local microhemodynamic factors may play a regulatory role in the spatial distribution of leukocyte margination.

In the present study, we examined the number of alveolar macrophages in lung tissue from 17 cases of fresh water drowning, 22 cases of acute death and 6 cases of lung emphysema. When counting only the number of alveolar macrophages per alveolus without consideration of the alveolar size we found no relevant differences between the groups investigated. To exclude any influence of the alveolar size on the results the surface density of the alveolar macrophages and interstitial tissue was estimated and compared in the different groups. In cases of drowning, the lungs showed significantly lower values in both categories. The ratio of ‘alveolar macrophages/interstitial tissue’ was also reduced in cases of drowning in comparison to the other groups, however, without significant differences. These morphometrical results characterizing the ‘emphysema aquosum’ with almost ‘empty’ and dilated alveoli could be explained by a wash-out effect of the drowning fluid leading to a partial removal of the macrophages from the alveoli. This hypothesis was confirmed by the detection of alveolar macrophages in the drowning froth by immunohistochemical analysis. Even though alveolar macrophages were unambiguously identified in advanced putrefied lungs in HE-stained sections as well as by immunohistochemical staining, an estimation of the number of these cells cannot provide further information for the diagnosis of drowning in putrefied corpses due to the autolytic destruction of the lung architecture providing no reliable values.

Tue, 1 Jan 1991 12:00:00 +0100 https://epub.ub.uni-muenchen.de/9378/1/9378.pdf Jochum, Marianne

Thu, 1 Jan 1987 12:00:00 +0100 https://epub.ub.uni-muenchen.de/9305/1/9305.pdf Zilow, G.; Jochum, Marianne; Kreutzfelder, E.; Pison, V.; Oberste-Beulmann, S.; Schönfeld, W.; Obertacke, U.; Joka, T. ddc:610, Medizin