Podcasts about osteoblast

When you get a stress fracture, you need the little bitty crack in the bone to heal.  How do you do that? First, you have to stop bending or torquing or twisting the bone in a way that led to the crack in the first place. Second, you have to let the healing process take place.  After the inflammation goes away, and after you get some collagen sealing up the healing crack, you start to get "ossification" of the bone where it turns into hard solid bone that you can run on.  That happens through a combination of two different types of cells in the bone called osteoblasts and osteoclasts. Osteoblast versus osteoclast, the battle that's rebuilding bone after a stress fracture.  That's what we're talking about today on the Doc On The Run Podcast. 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.10.548366v1?rss=1 Authors: Hayman, D. J., Lin, H., Prior, A., Charlesworth, G., Johnson de Sousa Brito, F. M., Hao, Y., Patel, K., Soul, J., Clark, I. M., Pirog, K. A., Barter, M. J., van 't Hof, R. J., Young, D. A. Abstract: microRNAs (miRNAs) are non-coding RNAs which modulate the expression of other RNA molecules. One miRNA can target many transcripts, allowing each miRNA to play key roles in many biological pathways. miR-324 is a miRNA previously implicated in bone and cartilage maintenance, defects of which result in common age-related diseases, such as osteoporosis or osteoarthritis (OA). In global miR-324-null mice cartilage damage was increased in both surgically and ageing-induced OA, despite minimal changes to the cartilage transcriptome, with few predicted miR-324 targets dysregulated. However, micro-computed tomography and histology demonstrated that global miR-324-null the mice had an increase in bone mineral density, trabecular thickness and cortical thickness, with many parameters increasing with age. The bone marrow of miR-324-null mice also had reduced lipid content while and in vivo TRAP staining revealed a decrease in osteoclasts, with histomorphometry demonstrating an increased rate of bone formation in miR-324-null mice. Ex vivo assays revealed that the high bone mass phenotype of the miR-324-null mice resulted from increased osteoblast activity and decreased osteoclastogenesis. RNA-seq and qRT-PCR followed by miR-324 target prediction and validation in osteoblasts, osteoclasts and bone marrow macrophages identified the osteoclast fusion regulator Pin1 as a miR-324 target in the osteoclast lineage and the master osteogenic regulator Runx2 as a target of miR-324-5p in osteoblasts, the in vitro overexpression of which recapitulated the increased osteogenesis and decreased adipogenesis phenotype observed in vivo. These data point to important roles of miR-324 in skeletal biology with altered bone homeostasis in miR-324-null mice potentially causal for the increased cartilage damage observed during OA and ageing. Elucidation of pathways regulated by miR-324 offer promise for the treatment of bone diseases such as osteoporosis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.27.514052v1?rss=1 Authors: Whitlock, J. M., de Castro, L. F., Collins, M. T., Chernomordik, L. V., Boyce, A. M. Abstract: Metabolic bone diseases are a collection of disorders resulting in diminished skeletal integrity and changes in bone mass due to perturbations in the life-long process of bone remodeling. Perturbations in the number, size and nuclear multiplicity of osteoclasts underpin the development of diverse metabolic bone diseases that impact greater than 13% of adults over age 50 world-wide. Each metabolic bone disease (e.g., osteoporosis, Pagets disease, fibrous dysplasia (FD), osteopetrosis) presents with unique phenotypes, rises from distinct etiologies and progresses with disparate severities, but all are underpinned by a breakdown in osteoclast formation/function. These perturbations of osteoclast formation/function either stem from or cause dysfunctional osteoclast-osteoblast coordination. Unfortunately, a mechanistic understanding of osteoclast-osteoblast coordination and communication is lacking and represents a major barrier to understanding the biology underpinning bone remodeling and the development of effective treatments targeting this process. Here we have developed an inducible ex vivo culture model that models osteoclast-osteoblast coordination in the bone remodeling compartment. Doxycycline addition to cultures activates GsR201C expression and RANKL release from osteoprogenitors, which elicits the differentiation and fusion of neighboring preosteoclasts. In turn, multinucleated osteoclast formation promotes the proliferation of osteoprogenitors, accompanied by the robust release of RANK+ extracellular vesicles, all within ~4 days. This system recapitulates many aspects of the complex osteoclast-osteoblast coordination required for the function of the bone remodeling compartment in both health and diseases underpinned by excessive osteoclast formation. Moreover, based on the ease of isolation, culture, reproducibility and the general adaptability of these cultures to a variety of assays, we expect that this new model will expedite the investigation of osteoclast-osteoblast coordination and osteoclast fusion in bone remodeling and offer a powerful tool for evaluating signaling cascades and novel therapeutic interventions in osteoclast-linked skeletal disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

New research unveils an autoimmune mechanism for Osteopenia and Osteoporosis driven by gut dysbiosis. Calcium is the the answer for bone loss.

Welcome To The MedFlashGo Podcast. This Is Your Daily 4 Minutes Or Less Rapid Review for medical students. Topics are based on medical board examinations including USMLE, COMLEX, And Shelf Exams. We release a new episode every weekday! In this question of the day, Percy asks students to identify the enzyme that would be elevated in the pathology presented. These questions are powered by MedFlashGo The First Voice-based interactive medical question bank currently available on Alexa. This tool allows medical students to study medical topics and be interactively tested without the use of a screen. You can study on your couch, in your car, and on the move without the use of a screen. To get access to the free audio-interactive question bank, click here or go to your Alexa application and search medflashgo In the skills section. To learn more details go to medflashgo.com and check out our frequently asked questions section. Please know that these questions were creatively designed by medical students and physicians for the purpose of education and do not replace health information given from your health professionals. We have tried our best to make sure the information is accurate please, so please let us know if you find any errors and we will be sure to correct them. --- Send in a voice message: https://anchor.fm/medflashgo/message

We have an exciting episode today as Justin, and Yanagida Fitness' Head Coach, Tyler Hultquist, catch up with their coach and mentor, Chris Williams, the Director of Education of the National Personal Training Institute. Enjoy today's fun and inspiring episode, as they talk about Chris' life, personal experiences, and the REAL talk about becoming a personal trainer. If you'd like to contact Chris Williams, visit www.nptiflorida.edu/npti-orlando/ or visit the facebook page @Osteoblast training, LLC. --- Support this podcast: https://anchor.fm/justinyanagida/support

Bones. Far from static objects. In this podcast, Anne discusses aspects of bone physiology that made their way into THE SILVER SKULL.

Just like the old saying always says: it's time to fight a giant skeleton. Chuck faces Schizm. Frankie goes for a ride. Jack makes a bomb. A breakdown occurs.CAST & CREW:Aaron J. Amendola/GM: @ImAaronJLiz Brodzinski/Jack: @PaperbackLizardMatt Peters/Chuck: @MightyInkMattCaitlin Rosberg/Frankie: @crosbergSam Begich/Music: @TravelingSamSamChris Chapin/QA: @ChapoliUniCURSEity uses the School Spirits RPG system. Get a copy of School Spirits by becoming a Patron at www.Patreon.com/VStheUNIVERSEHang out with us on Discord! Here's your invite link: http://bit.ly/VtUDiscordLeave us a 5-star review on iTunes (or your favorite podcatcher) and we'll send you a special UniCURSEity sticker pack through the ol' snail mail! Just screenshot your review and e-mail it to VTUCrew@gmail.com or tweet it at the twitter handle @ImAaronJ.Support us on Patreon at www.patreon.com/VStheUNIVERSEFacebook: facebook.com/VStheUNIVERSEInstagram: instagram.com/VStheUNIVERSEWebsite: www.VStheUNIVERSE.comEmail: VTUCrew@gmail.comYouTube: youtube.com//VStheUNIVERSEtube

A Vibration Plate is used during whole-body vibration therapy to stimulate bone growth and bone density by increasing osteoblast production. It can also increase metabolism, flexibility, mobility, range of motion, and balance.

Renate Pilz discusses an alternative form of the thyroid hormone receptor that mediates nongenomic signaling at the plasma membrane.

Leptin secreted by adipose tissue decreases insulin production through both direct and indirect mechanisms.

Mit zunehmendem Wissen über die Komplexität der Osteogenese wurde die Aussagekraft einzelner osteoblasten-assoziierter Marker in den letzten Jahren immer mehr in Frage gestellt. Denn der Nachweis einzelner Marker erlaubt weder eine eindeutige Identifikation undifferenzierter hMSC noch eine Abgrenzung von hMSC zu anderen Reifungsstufen der osteoblastären Kaskade. Das Ziel dieser Untersuchung war es daher, über die Erstellung eines immunzytochemischen Färbeprofils mehrerer Marker gleichzeitig, undifferenzierte hMSC eindeutig zu identifizieren und sie gegenüber hOB und evtl. weiteren Differenzierungsstufen der osteoblastären Kaskade abzugrenzen. Durch die Erstellung eines immunzytochemischen Färbeprofils ist es möglich, heterogene Zellpopulationen auf Einzelzellniveau zu charakterisieren und sie voneinander zu unterscheiden. Diese Untersuchung stellt einen sehr erfolgversprechenden Ansatz dar, undifferenzierte humane mesenchymale Stammzellen (hMSC) zu identifizieren und sie von Zellen der osteoblastären Differenzierungskaskade sowie anderen Zelltypen abgrenzen zu können. Insgesamt konnte in dieser Arbeit gezeigt werden, dass humane MSC und humane Osteoblasten jeweils spezifische Färbeprofile aufweisen, die eine eindeutige Diskriminierung der beiden Zellpopulationen erlauben. Für eine spezifische Unterscheidung auf Einzelzellnineau ist eine intensive Suche nach spezifischen Markern oder die Kombination mehrerer Marker notwendig. Von den in dieser Arbeit ausgewählten Proteinen ergaben Bone Sialoprotein, Osteocalcin, Decorin sowie Kollagen-IV und Kollagen-X unterschiedliche Färbemuster. Kollagen-IV und –X waren besonders in hMSC positiv, weswegen sie sich für eine Erkennung unreifer osteoblastärer Zellen anbieten. Bone Sialoprotein, Osteocalcin und Decorin eignen sich dagegen für einen Nachweis reifer osteoblastärer Zellen, denn sie waren nur in hOB positiv. Osteocalcin und Decorin erlaubten außerdem eine Abgrenzung differenzierter hOB. Die Proteine Versican und Matrixmetalloproteinase-2 erscheinen darüber hinaus für eine Unterscheidung von osteoblastären und fibroblastären Zellen nützlich zu sein. Die klassischen osteoblastären Marker alkalische Phosphatase, Kollagen-I, Osteopontin oder Osteonectin waren für eine Unterscheidung von hMSC und hOB nicht geeignet, da sie in beiden Zellpopulationen gleiche Ergebnisse lieferten. Insbesondere der Wert der alkalische Phosphatase als immunzytochemischer Marker der osteoblastären Kaskade wird in dieser Untersuchung in Frage gestellt. Eine osteogene Stimulation von hMSC mit Dexamethason, b-Glyzerophosphat und Askorbinsäure bewirkte eine deutliche Veränderung der Morphologie, der Wachstumseigenschaften und des Färbeprofils. Allerdings konnte durch eine osteogene Stimulation kein immunzytochemischer Phänotyp von hMSC induziert werden, welcher identisch mit dem der hOB war. Daher ist es unwahrscheinlich, dass eine Stimulation in vitro mit den oben aufgeführten Zusätzen die komplizierten Verhältnisse der Osteogenese in vivo nachahmen kann.