POPULARITY
3 episodes with Fibroblast
2 episodes with Fibroblast
3 episodes with Fibroblast
2 episodes with Fibroblast
3 episodes with Fibroblast
9 episodes with Fibroblast
3 episodes with Fibroblast
2 episodes with Fibroblast
In this podcast, Dr. Valentin Fuster discusses a groundbreaking study by Dr. Anna Barton and her team on myocardial fibroblast activation following acute myocardial infarction. Using advanced imaging techniques, the research uncovers how fibroblast activity plays a critical role in heart remodeling, revealing that fibrosis is dynamic and may offer new therapeutic opportunities for preventing heart failure and improving long-term recovery after heart attacks.
In deze podcast gaat prof. dr. Lioe-Fee de Geus-Oei, nucleair geneeskundige aan het Leids Universitair Medisch Centrum te Leiden, in gesprek met dr. Andor van den Hoven, nucleair radioloog in het St. Antonius Ziekenhuis te Nieuwegein, onderzoeker en voorzitter van de FAPI-werkgroep. Ze bespreken de ontwikkelingen rond de veelbelovende nieuwe tracer voor theranostische toepassingen: fibroblast activation protein inhibitor, oftewel FAPI. Het gesprek gaat over de moleculair-biologische eigenschappen van deze tracer, de indicaties waarbij FAPI-PET/CT mogelijk meerwaarde kunnen bieden, de lopende studies op dit gebied in Nederland, de verwachtingen met betrekking tot radionuclidentherapie, de activiteiten van de landelijke FAPI-werkgroep en de toekomstperspectieven van deze nieuwe theranostische aanpak.
BUFFALO, NY- October 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on September 18, 2024, entitled, “Fibroblast growth factor 21 inversely correlates with survival in elderly population – the results of the Polsenior2 study.” As noted in the abstract, fibroblast growth factor 21 (FGF21) is a liver-secreted hormone involved in regulating lipid, glucose, and energy metabolism. Its serum concentration increases with age and is elevated in various diseases. FGF21 is currently being investigated for its potential as a biomarker and therapeutic target. In their paper, Polish researchers Gabriela Handzlik, Aleksander J. Owczarek, Andrzej Więcek, Małgorzata Mossakowska, Tomasz Zdrojewski, Anna Chudek, Magdalena Olszanecka-Glinianowicz, and Jerzy Chudek from the Medical University of Silesia in Katowice, the International Institute of Molecular and Cell Biology in Warsaw, and the Medical University of Gdansk aimed to assess the prognostic value of FGF21 in an older, population-based cohort from the PolSenior2 study. The researchers report that in a sub-analysis of 3,512 individuals aged 60 and older, stratified into tertiles based on FGF21 levels, the survival estimate was worse in participants with middle and high FGF21 levels compared to those in the lowest tertile. These findings were supported by univariable Cox regression analysis, where participants in the middle and high FGF21 tertiles, after adjusting for age, had a 1.43-fold (HR 1.31; 95% CI, 1.05–1.62) and 2.56-fold (HR 1.94; 95% CI, 1.59–2.37) increased risk of mortality, respectively, compared to the lowest tertile. In multivariable Cox regression analysis, the highest FGF21 levels were independently associated with increased mortality (HR 1.53; 95% CI, 1.22–1.92), regardless of co-morbidities and blood parameters. "These results indicate that higher serum FGF21 concentration is an independent predictor of all-cause mortality in the general population of older adults.” DOI - https://doi.org/10.18632/aging.206114 Corresponding author - Gabriela Handzlik - ghandzlik@sum.edu.pl Video short - https://www.youtube.com/watch?v=QkPrI68nbLE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206114 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, fibroblast growth factor 21, survival, population-based study, longevity About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
From wound healing to cell growth to bone formation, fibroblast growth factors (FGF) and fibroblast growth factor receptors (FGFR) are responsible for a diverse range of biological processes. This episode begins with the basics: the functions of FGFs and FGFRs. We will then move on to an indepth dive into the structure of FGFRs and how they work with FGFs to initiate the desired cellular response. Finally, we will end the episode by exploring the three main pathways used by FGFs and their corresponding receptors. FGFR Model: https://images.app.goo.gl/FaZjvuh5H1QnTgfa8
BUFFALO, NY- July 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Modulating in vitro lung fibroblast activation via senolysis of senescent human alveolar epithelial cells.” Idiopathic pulmonary fibrosis (IPF) is an age-related disease with poor prognosis and limited therapeutic options. Activation of lung fibroblasts and differentiation to myofibroblasts are the principal effectors of disease pathology, but damage and senescence of alveolar epithelial cells, specifically type II (ATII) cells, has recently been identified as a potential trigger event for the progressive disease cycle. Targeting ATII senescence and the senescence-associated secretory phenotype (SASP) is an attractive therapeutic strategy; however, translatable primary human cell models that enable mechanistic studies and drug development are lacking. In this new study, researchers Joseph S. Spina, Tracy L. Carr, Lucy A. Phillips, Heather L. Knight, Nancy E. Crosbie, Sarah M. Lloyd, Manisha A. Jhala, Tony J. Lam, Jozsef Karman, Meghan E. Clements, Tovah A. Day, Justin D. Crane, and William J. Housley from AbbVie Bioresearch Center and Northeastern University describe a novel system of conditioned medium (CM) transfer from bleomycin-induced senescent primary alveolar epithelial cells (AEC) onto normal human lung fibroblasts (NHLF) that demonstrates an enhanced fibrotic transcriptional and secretory phenotype compared to non-senescent AEC CM treatment or direct bleomycin damage of the NHLFs. “In the current study, we confirm the presence of senescent cell populations within the human IPF lung, as well as assess primary cell reagents for sensitivity to senescent cell targeting therapies.” In this system, the bleomycin-treated AECs exhibited classical hallmarks of cellular senescence, including SASP and a gene expression profile that resembles aberrant epithelial cells of the IPF lung. Fibroblast activation by CM transfer was attenuated by pre-treatment of senescent AECs with the senolytic Navitoclax and AD80, but not with the standard of care agent Nintedanib or senomorphic JAK-targeting drugs (e.g., ABT-317, ruxolitinib). This model provided a relevant human system for profiling novel senescence-targeting therapeutics for IPF drug development. “Taken together, the model described herein provides a physiologically relevant, primary human cell system to study the effects of alveolar epithelial cell senescence on lung fibroblasts in the context of chronic fibrotic lung disease.” DOI - https://doi.org/10.18632/aging.205994 Corresponding author - Tovah A. Day - t.day@northeastern.edu Video short - https://www.youtube.com/watch?v=rpmo2PlGDKc Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205994 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Episode #76: Pete O'Heeron is one of the preeminent Biopharma inventors of his generation with over 300+ patents issued/pending in biologics, cell therapy and medical devices. As the Founder and CEO of FibroBiologics, he brings 25 years of entrepreneurial experience in developing therapeutics to treat chronic diseases and regenerative medicine using fibroblasts. In 2024, Pete took FibroBiologics public at over 1 billion dollars. In this engaging conversation we discuss fibroblasts, stem cell recovery, the cure for cancer, entrepreneurship, and more. For more info on FibroBiologic go to https://fibrobiologics.com NASDAQ: FBLG PipeDrive CRM: Free 30 Day Trial plus 20% off your first three months. https://aff.trypipedrive.com/GrantMitterlehner For business, consulting, and sales training resources from Grant Mitt. https://mittgroup.square.site/ Grant Mitt Podcast - Spotify https://open.spotify.com/show/19Z58SV... Grant Mitt Podcast - Apple Podcast https://podcasts.apple.com/us/podcast... Follow Grant on Social Media: Insta @Grantmitt YouTube @Grantmitt TikTok @Grantmitt Twitter @Grantmitt3 Learn more about your ad choices. Visit megaphone.fm/adchoices
Episode: 1131 John Hunter: idiosyncratic medical pioneer. Today, the history of medicine provides a strange hero.
Deep in a remote forest, a sick, elderly man got scratched by a stray cat — and likely died as a result.
Kenichi Nogami is the co-founder and CEO of Metcela, a clinical-stage biotechnology startup pioneering the research and development of fibroblast and stem cell-based therapy for chronic heart diseases that currently have limited therapeutic options. We talk about the current treatments for heart failure and how the fibroblast technology could help this space. We explore the founding story; setting smaller milestones and fundraising to meet those goals; the role of recruiting firms in hiring in japan; building a flat structure at the startup, as opposed to a hierarchical system that Japan is generally known for; and how Ken's investment banking experience helped with acquisition of another biotech startup; and many other stories. Shownotes https://www.metcela.com/en/ Fibroblast technology for treating Heart failure Current treatments and potential of regenerative capabilities Founding story: Investment banker meets a PhD student and launch a startup Nedo, Japan: Technology-Based Startup Support Program https://www.nedo.go.jp/english/activities/activities_ZZJP_100091.html IP: University waives its right to file a patent and the startup files the patent Co-founder chemistry Business model evolution Immune response challenges developing cell therapy for heart diseases Fundraising stories: Raising money from Japanese investors vs those outside Japan Raising from university derived VCs Cell manufacturing challenges Acquiring a startup while being a startup Evolution as a CEO Team and hiring process: Supply drove the hiring more than demand in many cases Building culture Hierarchy vs flat structure: decision making process Challenges building a biotech startup in Japan- talent, infrastructure; and need to expand globally
Pete O'Heeron, MSHA, is the CEO of FibroBiologics ( https://fibrobiologics.com/ ), a biopharmaceutical company focused on developing and commercializing fibroblast cell-based therapies for patients suffering from chronic diseases. Mr. O'Heeron has over 25 years of medical technology and biotech development experience and brings together the resources necessary to commercialize unique technologies with expertise from business start-ups and biologics, to medical devices and patient centered healthcare delivery. Prior to founding FibroBiologics, Mr. O'Heeron founded an operational investment group, Advanced Medical Technologies, LLC, that identified early-stage opportunities in the medical field with strong intellectual property potential. He also founded NeoSurg Technologies that developed the T2000 Minimally Invasive Access System. The sale of NeoSurg Technologies to Cooper Surgical occurred in 2006. Mr. O'Heeron brings decades of executive-level experience at Christus Health Care Corporation and strategic advisory to healthcare companies in the areas of biologics, advanced surgical instrumentation, and telemedicine to the company along with an academic foundation rooted in healthcare administration. He received his Bachelor's Degree in Healthcare Administration at Texas State University, his Masters in Healthcare Administration from the University of Houston Clear Lake, and his Executive Management Certification in Mergers and Acquisition from University of Chicago. Support the show
How do you get people to think about new ideas?And then, how do you move your audience from thinking - to buying? To examine how ideas go from brainstorming to industry-changing, I've invited Pete O'Heeron to join me for today's podcast. Pete is the Founder and CEO of FibroBiologics, a leading biopharmaceutical company focused on developing and commercializing fibroblast cell-based therapies. We kick the conversation off discussing how Fibroblast has gone from a few peer reviewed papers a year to dozens each week in the span of a mere eight years. Pete helps us understand exactly what fibroblast cells are and why the amount of interest and important research for them has spiked. Not only is research into fibroblast cells new but the work Pete is doing at FibroBiologics is going in directions no one else is. Pete discusses why they are doing work no one else is and how the research and science are the mechanics that steer the direction of the company. Working on such new and cutting edge ideas often means having to convert people from no, to yes. Pete shares how their scientific discovery board is made up of world leaders in stem cell research, which gives the work they do a great deal of credibility. This creates an opportunity to start conversations that spark interest in what the company is doing and allows the science to sell itself as people dig into these new ideas. Pete offers great insight into how to take new niche ideas from prototype to market and have conversations that draws your audience in. Three Key Takeaways: · Allowing research and science to dictate the direction of your company can take you in new directions. · Getting new ideas out means starting a conversation with the points that will spark interest. After that follow with research and science that can't be disputed. · Having a board within your company that is filled with respected professionals will give the new ideas you produce a level of credibility that others might not have.
In today's episode we interview Leigh's friend, client and fellow business owner, Angela Strutzel, of Cottonwood Creek Boutique in Cheney, WA. We briefly discuss the science of collagen, when it was discovered and we talk about 2 of Angela's treatments she's had as a client - Fibroblast and Threads. Angela tells a ghost story about her uncle, who contacted her right before he passed away through her car radio. We all had goosebumps.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.02.551383v1?rss=1 Authors: Cohen, M. L., Brumwell, A. N., Ho, T. C., Montas, G., Golden, J. A., Jones, K. D., Wolters, P. J., Wei, Y., Chapman, H. A., Le Saux, C. J. Abstract: Reciprocal interactions between alveolar fibroblasts and epithelial cells are crucial for lung homeostasis, injury repair, and fibrogenesis, but underlying mechanisms remain unclear. To investigate this, we administered the fibroblast-selective TGF{beta}1 signaling inhibitor, epigallocatechin gallate (EGCG), to Interstitial Lung Disease (ILD) patients undergoing diagnostic lung biopsy and conducted single-cell RNA sequencing on spare tissue. Unexposed biopsy samples showed higher fibroblast TGF{beta}1 signaling compared to non-disease donor or end-stage ILD tissues. In vivo, EGCG significantly downregulated TGF{beta}1 signaling and several pro-inflammatory and stress pathways in biopsy samples. Notably, EGCG reduced fibroblast secreted Frizzle-like Receptor Protein 2 (sFRP2), an unrecognized TGF{beta}1 fibroblast target gene induced near type II alveolar epithelial cells (AEC2s). In human AEC2-fibroblast coculture organoids, sFRP2 was essential for AEC2 trans-differentiation to basal cells. Precision cut lung slices (PCLS) from normal donors demonstrated that TGF{beta}1 promoted KRT17 expression and AEC2 morphological change, while sFRP2 was necessary for KRT5 expression in AEC2-derived basaloid cells. Wnt-receptor Frizzled 5 (Fzd5) expression and downstream calcineurin-related signaling in AEC2s were required for sFRP2-induced KRT5 expression. These findings highlight stage-specific TGF{beta}1 signaling in ILD, the therapeutic potential of EGCG in reducing IPF-related transcriptional changes, and identify the TGF{beta}1-non-canonical Wnt pathway crosstalk via sFRP2 as a novel mechanism for dysfunctional epithelial signaling in Idiopathic Pulmonary Fibrosis/ILD. 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/2023.07.28.551009v1?rss=1 Authors: Azevedo, L. P., Rios-Santos, F., Branco, C. B., Pressinotti, L. N., Reis, E. d. M., Filho, S. V., Martins, D. T. d. O., de Vasconcelos, L. G., Ferraz, R. H. d. S., Mesquita, F. V., Silva, W. d. A., Junior, P. T. d. S. Abstract: In previous studies, the oil extracted from the visceral fat of Caiman yacare (Daudin, 1802) demonstrated a wound-healing effect on the skin of Wistar rats. To enhance knowledge our about the mechanism underlying this effect, we analysed the oils toxicological potential in vitro. Cytotoxicity, genotoxicity, pro-oxidant, and antioxidant activities were evaluated in a V79-4 cell line. The oil was obtained using the Soxhlet method, and the proportions of the fatty acid profile was previously identified 43.74 % saturated and 34.65 % unsaturated fatty acids. Protocol 487 of the Organisation for Economic Co-operation and Development (OECD) was employed for cell line selection and concentrations. Cytotoxicity was determined using the MTT assay and clonogenic survival. Pro-oxidant and antioxidant activities were analysed using flow cytometry. Genotoxicity was evaluated using comet and micronucleus assays. The oil did not demonstrate cytotoxicity up to a concentration of 500 g/mL. At concentrations of 250 and 500 g/mL, the oil exerted a protective effect against oxidative stress and showed genotoxic effects only at the highest concentration (2000 g/mL). Like other oils of interest for human health, the oil extracted from the visceral fat of C. yacare demonstrated low toxicological potential in vitro. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
FibroBiologics is the leading biotech company focused on developing and commercializing fibroblast cell-based therapies for patients suffering from chronic diseases. In this podcast episode, the Founder and CEO, Pete O'Heeron discusses the promise of fibroblast cell therapy to treat diseases such as multiple sclerosis, degenerative disk disease and more.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.03.535302v1?rss=1 Authors: Griffin, M., Talbott, H., Guardino, N., Guo, J., Spielman, A., Chen, K., Mascharak, S., Parker, J., Henn, D., Liang, N., King, M., Cotterell, A., Bauer-Rowe, K., Abbas, D., Deleon, N. M. D., Fahy, E., Sivaraj, D., Downer, M., Akras, D., Berry, C., Cook, J., Quarto, N., Klein, O. D., Lorenz, P., Gurtner, G., Januszyk, M., Wan, D. C., Longaker, M. T. Abstract: While past studies have suggested that plasticity exists between dermal fibroblasts and adipocytes, it remains unknown whether fat actively contributes to fibrosis in scarring. We show that adipocytes convert to scar-forming fibroblasts in response to Piezo-mediated mechanosensing to drive wound fibrosis. We establish that mechanics alone are sufficient to drive adipocyte-to-fibroblast conversion. By leveraging clonal-lineage-tracing in combination with scRNA-seq, Visium, and CODEX, we define a mechanically naive fibroblast-subpopulation that represents a transcriptionally intermediate state between adipocytes and scar-fibroblasts. Finally, we show that Piezo1 or Piezo2-inhibition yields regenerative healing by preventing adipocytes activation to fibroblasts, in both mouse-wounds and a novel human-xenograft-wound model. Importantly, Piezo1-inhibition induced wound regeneration even in pre-existing established scars, a finding that suggests a role for adipocyte-to-fibroblast transition in wound remodeling, the least-understood phase of wound healing. Adipocyte-to-fibroblast transition may thus represent a therapeutic target for minimizing fibrosis via Piezo-inhibition in organs where fat contributes to fibrosis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
If I was going to be a lab rat - I think I'd like to be these lab rats! A hormone injection that sobers up mice might offer hope for treating drunk humans according to a paper published this week in the journal Cell Metabolism. In the experiments, researchers gave mice so much alcohol that they fell unconscious and weren't able to get back up when they were pushed onto their back (known as the righting reflex). The hormone being tested is naturally produced and called Fibroblast growth factor 21 or FGF21. In the mice that were bred not to make this hormone they stayed drunk for longer than ‘normal' mice that could produce FGF21. Interestingly when the normal mice were given an injection containing FGF21 they sobered up an hour and a half faster than the other mice. The researchers think that FGF21 helps to activate nerve cells in the parts of the brain that are involved with simulating wakefulness and while FGF21 doesn't help to break down alcohol in the body, it does help to protect livers from the toxic effects of alcohol while also reducing the animals desire to continue drinking. Humans have the same FGF21 pathway as mice, which means these findings might help to create a treatment for patients with acute alcohol poisoning. These patients are at a high risk of choking by aspirating their own vomit while intoxicated, and the researchers believe that being able to increase a patients alertness could significantly reduce this risk. LISTEN ABOVESee omnystudio.com/listener for privacy information.
Dr. Hamid Khoja joins the podcast to discuss the role of fibroblasts in the process of wound healing and explain how fibroblast cell-based therapies may be an effective and accessible treatment option for diabetic wounds
Today Tanya is joined by Michelle Campbell, owner of The Pretty House in DT Gilbert. Michelle's passion for beauty started 9 years ago with lash extensions, and since then, she has pursued continuing education and gained certifications in a variety of specialties such as Microneedling, Fibroblast, Hydro Facials, and Skin Classic treatments.On this episode, Michelle shares with us how her journey began with her love for lash extensions and how it evolved into a thriving career in the beauty industry. She emphasized the importance of holding a safe space for clients and creating a welcoming environment, especially when providing services such as eyebrow shaping and eyelash extensions.At The Pretty House, Michelle offers a range of services, including laser therapy for hair removal, as well as unique experiences like the Unicorn Facial and the Red Carpet Facial. These services are designed to help women take time for themselves and feel pampered and rejuvenated.Throughout the conversation, Michelle's passion for her work and her commitment to providing her clients with high-quality beauty services is evident. Her dedication to learning and expanding her skills is a testament to her love for the beauty industry. We hope you enjoy listening to this episode and learning more about Michelle's journey as an esthetician and small business owner.A message from Michelle: "At the Pretty House we hope to be a light and an example to others! We are always striving to be more patient, charitable, empathetic, and kind. It's our hope that women smile more and stress less while looking for joy in life. Our journey has taken us from working out of our homes, to combining our skills and dreams which lead us to launching The Pretty House Studio in 2017. Come hang out with the girls at The Pretty House and let us share with you what we have learned along the way!"Follow:Instagram: @prettyhousegilbertFacebook: https://www.facebook.com/theprettyhousestudioWeb: https://theprettyhousestudio.comInstagram: @Michelle_Carlene1Follow Tanya Here:InstagramFacebookTikTokYouTubeLinkedInTwitter
Regenerative medicine is beginning to be the "next generation" in medicine and this also applies to aesthetics.We are learning how to not just treat the signs of aging, but to actually return cells back to their healthy, youthful state.We are only at the precipice of this exciting new era, but "exosomes" will begin to become an important aspect in aesthetics.Today we are going to discuss:1. What is an exosome2. How this differs from PRP and will it make PRP obsolete?3. What are senescent fibroblasts and why this is important in aging?4. How are exosomes placed on the skin?Enjoy!Thank you for your listenership!
Eric Alvarez is the CEO and Founder of Grapefruit Health, a company that is creating a brand new workforce to help meet the significant shortage of healthcare workers today. Prior to this adventure, he has held multiple positions within the healthcare industry. Most recently Eric was the COO of a healthcare technology startup called Fibroblast, which was acquired by the EMR giant Cerner Corporation in 2020. In this role, he oversaw product, development, human resources, finance, general company operations, and was active in all major sales cycles. Before joining Fibroblast, Eric was a hospital administrator at the University of Chicago Medicine and Northwestern Medicine. In these roles, he led large clinical and nonclinical teams mostly in specialty services that included the services lines of Cardiovascular surgery, Urology, and Ophthalmology. These roles have provided Eric with a deep understanding of how health systems function as a business and what their systemic challenges are. Eric earned his Masters in Healthcare Administration from Rush University, a top 5 program, and his Bachelors in Aviation Management from Southern Illinois University, a top 10 program. Prior to college, he served in the United States Air Force during Iraqi Freedom. Most recently, Eric was named a top 100 Rising LatinX founders, Distinguished Alumni of the Year from Rush, and took a board seat at Southern Illinois University's College of Health and Human Sciences.Learn more Grapefruit Health
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.21.529458v1?rss=1 Authors: Hom, L. M., Sun, S., Campbell, J., Liu, P., Culbert, S., Murphy, I. M., Schafer, Z. T. Abstract: In normal tissue homeostasis, bidirectional communication between different cell types can shape numerous biological outcomes. Many studies have documented instances of reciprocal communication between fibroblasts and cancer cells that functionally change cancer cell behavior. However, less is known about how these heterotypic interactions shape epithelial cell function in the absence of oncogenic transformation. Furthermore, fibroblasts are prone to undergo senescence, which is typified by an irreversible cell cycle arrest. Senescent fibroblasts are also known to secrete various cytokines into the extracellular space; a phenomenon that is termed the senescence-associated secretory phenotype (SASP). While the role of fibroblast derived SASP factors on cancer cells has been well studied, the impact of these factors on normal epithelial cells remains poorly understood. We discovered that treatment of normal mammary epithelial cells with conditioned media (CM) from senescent fibroblasts (SASP CM) results in a caspase-dependent cell death. This capacity of SASP CM to cause cell death is maintained across multiple senescence-inducing stimuli. However, the activation of oncogenic signaling in mammary epithelial cells mitigates the ability of SASP CM to induce cell death. Despite the reliance of this cell death on caspase activation, we discovered that SASP CM does not cause cell death by the extrinsic or intrinsic apoptotic pathway. Instead, these cells die by an NLRP3, caspase-1, and gasdermin D (GSDMD)-dependent induction of pyroptosis. Taken together, our findings reveal that senescent fibroblasts can cause pyroptosis in neighboring mammary epithelial cells, which has implications for therapeutic strategies that perturb the behavior of senescent cells. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
On episode 409 of The Nurse Keith Show nursing and healthcare career podcast, Keith interviews Eric Alvarez, the CEO and Founder of Grapefruit Health, a company that is creating a brand new student-led workforce to help meet the significant shortage of healthcare workers today. In the course of their conversation, Keith and Eric discuss clinician shortages, lack of access to care, and other challenges within the healthcare space that led to the founding of Grapefruit Health and its unique and innovative solutions to those challenges. Prior to this adventure with Grapefruit Health, Eric has held multiple positions within the healthcare industry. Most recently Eric was the COO of a healthcare technology startup called Fibroblast, which was acquired by the EMR giant Cerner Corporation in 2020. In this role, he oversaw product, development, human resources, finance, general company operations, and was active in all major sales cycles. Before joining Fibroblast, Eric was a hospital administrator at the University of Chicago Medicine and Northwestern Medicine. In these roles, he led large clinical and nonclinical teams mostly in specialty services that included the services lines of Cardiovascular surgery, Urology, and Ophthalmology. These opportunities provided Eric with a deep understanding of how health systems function as a business and what their systemic challenges are. Eric earned his Masters in Healthcare Administration from Rush University, a top five program, and his Bachelors in Aviation Management from Southern Illinois University, a top ten program. Prior to college, he served in the United States Airforce during Iraqi Freedom. Most recently, Eric was named a top 100 Rising LatinX founder and Distinguished Alumni of the Year from his Master's program. Connect with Eric Alvarez and Grapefruit Health: Grapefruit.Health Grapefruit Health on LinkedIn Eric on LinkedIn ----------- Did you know that you can now earn CEUs from listening to podcasts? That's right — over at RNegade.pro, they're building a library of nursing podcasts offering continuing education credits, including episodes of The Nurse Keith Show! So just head over to RNegade.pro, log into the portal, select Nurse Keith (or any other Content Creator) from the Content Creator dropdown, and get CEs for any content on the platform! Nurse Keith is a holistic career coach for nurses, professional podcaster, published author, award-winning blogger, inspiring keynote speaker, and successful nurse entrepreneur. Connect with Nurse Keith at NurseKeith.com, and on Twitter, Facebook, LinkedIn, and Instagram. Nurse Keith lives in beautiful Santa Fe, New Mexico with his lovely fiancée, Shada McKenzie, a highly gifted traditional astrologer and reader of the tarot. You can find Shada at The Circle and the Dot. The Nurse Keith Show is a proud member of The Health Podcast Network, one of the largest and fastest-growing collections of authoritative, high-quality podcasts taking on the tough topics in health and care with empathy, expertise, and a commitment to excellence. The podcast is adroitly produced by Rob Johnston of 520R Podcasting, and Mark Capispisan is our stalwart social media manager and newsletter wrangler.
GUEST: Zaver Bhujwalla, BaltimoreIn this episode we discuss how targeting fibroblasts rather than tumour cells may be an effective strategy for both surgical guided resection and as an anti-cancer therapy with Tim's “academic grandmother”, Zaver Bhujwalla. We discovered Zaver's roots as a physicist and mathematician, learned about her (unpredictable) interest in cancer metabolism and how she combines tools to develop a powerful in vitro diagnostic test.Selected Publication: "Design and characterization of fibroblast activation protein targeted pan-cancer imaging agent for fluorescence-guided surgery of solid tumors" published in Journal of Materials Chemistry B, by the the authors Mukkamala R, Lindeman SD, Kragness KA, Shahriar I, Srinivasarao M, Low PS (Purdue University, West Lafayette, USA).Publication reference: Mukkamala R, Lindeman SD, Kragness KA, Shahriar I, Srinivasarao M, Low PS. Design and characterization of fibroblast activation protein targeted pan-cancer imaging agent for fluorescence-guided surgery of solid tumors. J Mater Chem B. 2022 Mar 23;10(12):2038-2046. doi: 10.1039/d1tb02651h.https://pubs.rsc.org/en/content/articlelanding/2022/TB/D1TB02651HFurther information on the European Society for Molecular Imaging:https://e-smi.eu/Contact: office@e-smi.eu
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.07.527364v1?rss=1 Authors: Mohr, M. E., Li, S., Trouten, A. M., Stairley, R. A., Roddy, P. L., Liu, C., Zhang, M., Sucov, H., TAO, G. Abstract: Neonatal mouse hearts have transient renewal capacity which is lost in juvenile and adult hearts. After myocardial infarction (MI) in neonatal hearts, an initial loss of cardiomyocytes occurs but it is unclear through which type of regulated cell death (RCD). In the current studies, we induced MI in neonatal and juvenile mouse hearts, and show that ischemic cardiomyocytes primarily undergo ferroptosis, a non-apoptotic and iron-dependent form of RCD. We demonstrate that cardiac fibroblasts (CFs) protect cardiomyocytes from ferroptosis through paracrine factors and direct cell-cell interaction. CFs show strong resistance to ferroptosis due to high ferritin expression. Meanwhile, the fibrogenic role of CFs, typically considered detrimental to heart function, is negatively regulated by paired-like homeodomain 2 (Pitx2) signaling from cardiomyocytes. In addition, Pitx2 prevents ferroptosis in cardiomyocytes by regulating ferroptotic genes. Understanding the regulatory mechanisms of cardiomyocyte survival and death can identify potentially translatable therapeutic strategies for MI. 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/2023.01.24.525311v1?rss=1 Authors: Nakazato, R., Matsuda, Y., Ikegami, K. Abstract: Various mammalian cells have autonomous cellular clocks that are produced by the transcriptional cycle of clock genes. Cellular clocks provide circadian rhythms for cellular functions via transcriptional and cytoskeletal regulation. The vast majority of mammalian cells possess a primary cilium, an organelle protruding from the cell surface. Here, we investigated the little-known relationship between circadian rhythm and primary cilia. The length and number of primary cilia showed circadian dynamics both in vitro and in vivo. The circadian rhythm of primary cilia morphology was abolished by SR9011, a clock genes suppressor. A centrosomal protein, pericentrin, transiently accumulates in centriolar satellites, the base of primary cilia at the shortest cilia phase, and induces elongation of primary cilia at the longest cilia phase in the circadian rhythm of primary cilia. In addition, rhythmic cell migration during wound healing depends on the length of primary cilia and affects the rate of wound healing. Our findings demonstrate that the circadian dynamics of primary cilia length by clock genes control fibroblast migration and could provide new insights into chronobiology. 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/2023.01.23.523684v1?rss=1 Authors: Bretherton, R. C., Reichardt, I. M., Zabrecky, K. A., Goldstein, A. J., Bailey, L. R. J., Bugg, D., McMillen, T. S., Kooiker, K. B., Flint, G., Martinson, A., Gunaje, J., Koser, F., Linke, W. A., Regnier, M., Moussavi-Harami, F., Sniadecki, N. J., DeForest, C. A., Davis, J. Abstract: Inherited mutations in contractile and structural genes, which decrease cardiomyocyte tension generation, are principal drivers of dilated cardiomyopathy (DCM)- the leading cause of heart failure1,2. Progress towards developing precision therapeutics for and defining the underlying determinants of DCM has been cardiomyocyte centric with negligible attention directed towards fibroblasts despite their role in regulating the best predictor of DCM severity, cardiac fibrosis3,4. Given that failure to reverse fibrosis is a major limitation of both standard of care and first in class precision therapeutics for DCM, this study examined whether cardiac fibroblast-mediated regulation of the hearts material properties is essential for the DCM phenotype. Here we report in a mouse model of inherited DCM that prior to the onset of fibrosis and dilated myocardial remodeling both the myocardium and extracellular matrix (ECM) stiffen from switches in titin isoform expression, enhanced collagen fiber alignment, and expansion of the cardiac fibroblast population, which we blocked by genetically suppressing p38 in cardiac fibroblasts. This fibroblast-targeted intervention unexpectedly improved the primary cardiomyocyte defect in contractile function and reversed ECM and dilated myocardial remodeling. Together these findings challenge the long-standing paradigm that ECM remodeling is a secondary complication to inherited defects in cardiomyocyte contractile function and instead demonstrate cardiac fibroblasts are essential contributors to the DCM phenotype, thus suggesting DCM-specific therapeutics will require fibroblast-specific strategies. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Clinical Journal of the American Society of Nephrology (CJASN)
Dr. Killian Donovan provides an overview of the conclusions from his study "Fibroblast Growth Factor-23 and Risk of Cardiovascular Diseases," on behalf of his colleagues.
The pancreatic cancer of Robert Baioni had returned. After his initial diagnosis in 2016, Baioni was treated near his Cincinnati home, treatment that included surgery to remove his pancreas, followed by chemotherapy. A few months later, “my oncologist told me the chemotherapy wasn't working,” Baioni said, adding his doctor also told him about a unique clinical trial at the James run by Sameek Roychowdhury, MD, PhD. “I went in there feeling kind of hopeless and by the time my wife and I left we both felt very optimistic,” Baioni said of his initial meeting with Roychowdhury. In this episode of the James Cancer-Free World podcast, Baioni and Roychowdhury describe the two clinical trials Baioni has taken part in at the James. Both trials were initiated by Roychowdhury and utilize drugs that target a specific genetic mutation that was in the cells of Baioni's cancer: Fibroblast growth factor receptors (FGFRs). This was one of the first clinical trials that focused on the specific genetic mutation causing the cancer and not the type of cancer, Roychowdhury said. “This trial was designed for any type of cancer with the FGFR mutation, the liver, the uterus, the stomach,” he said. “How could we get a therapy to patients based on the genetic mutation; how could we break the mold [of standard treatment.” Baioni and Roychowdhury describe the science behind the clinical trials, what was going on inside the patient's body, how the drugs that target FGFR work, and the side effects associated with this type of treatment. It's a fascinating look at the advances being made in cancer research and treatment, as well as an uplifting story of the bond between a patient and his James physician.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.23.521723v1?rss=1 Authors: Dill, M. N., Tabatabaei, M., Kamat, M., Basso, K. B., Simmons, C. S. Abstract: The spiny mouse (Acomys) is gaining popularity as a research organism due to its phenomenal regenerative capabilities. Acomys recovers from injuries to several organs without fibrosis. For example, Acomys heals full thickness skin injuries with rapid re-epithelialization of the wound and regeneration of hair follicles, sebaceous glands, erector pili muscles, adipocytes, and dermis without scarring. Understanding mechanisms of Acomys regeneration may uncover potential therapeutics for wound healing in humans. However, access to Acomys colonies is limited and primary fibroblasts can only be maintained in culture for a limited time. To address these obstacles, we generated immortalized Acomys dermal fibroblast cell lines using two methods: transfection with the SV40 large T antigen and spontaneous immortalization. The two cell lines (AcoSV40 and AcoSI-1) maintained the morphological and functional characteristics of primary Acomys fibroblasts, including maintenance of key fibroblast markers and ECM deposition. The availability of these cells will lower the barrier to working with Acomys as a model research organism, increasing the pace at which new discoveries to promote regeneration in humans can be made. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
FDA Drug Information Soundcast in Clinical Oncology (D.I.S.C.O.)
Listen to a soundcast of the 9/30/22 FDA approval of Lytgobi (futibatinib) for adult patients with previously treated, unresectable, locally advanced or metastatic intrahepatic cholangiocarcinoma harboring fibroblast growth factor receptor 2 gene fusions or other rearrangements.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.18.516150v1?rss=1 Authors: Ursem, S. R., Diepenbroek, C., Kool, T., Eggels, L., Heijboer, A. C., la Fleur, S. E. Abstract: Fibroblast growth factor 23 (FGF23) is a key regulator of systemic phosphate homeostasis, but also an interplay with glucose metabolism has been suggested. Several studies implicate a function of FGF23 in the brain, and indeed we have recently identified FGF23 protein in several brain areas in rats, such as the hypothalamus, third ventricle and choroid plexus. In the current study, we aimed to determine the effect of an intracerebroventricular (icv) injection of FGF23 in the third ventricle of rats on hypothalamic genes involved in glucose regulation. In addition, we assessed whether glycerol can be used safely for icv injections as glycerol is used as a stabilizing compound for FGF23 protein. Adult Wistar rats received an icv injection of recombinant rat FGF23 or vehicle. Dose dependent behavioral changes, suggestive of stress, were observed directly after infusion of FGF23. After 60 min animals were sacrificed and the arcuate nucleus, lateral hypothalamus and choroid plexus were isolated. In these brain regions gene expression was determined of the FGF23 receptor complex (FGFR1, Klotho), NPY, POMC, phosphate transporters (SLC20 and SLC34 families) and markers of cellular ER stress (ATF4 and the ratio of spliced/unspliced XBP1). We showed that glycerol is well tolerated as stabilizer for icv injections. In FGF23-treated animals, cellular ER stress markers were increased in the arcuate nucleus. FGF23 injection did not affect expression of its receptor complex, NPY, POMC, or phosphate transporters. Future studies are warranted to investigate the effect of FGF23 in the brain on the protein level and on neuronal activation. 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/2022.10.23.513410v1?rss=1 Authors: Konrad, C., Woo, E., Bredvik, K., Liu, B., Fuchs, T. J., Manfredi, G. Abstract: Objective: Amyotrophic lateral sclerosis (ALS) is a devastating neuromuscular disease with limited therapeutic options. Diagnostic and surrogate endpoint biomarkers are needed for early disease detection, clinical trial design, and personalized medicine. Methods: We tested the predictive power of a large set of primary skin fibroblast (n=443) from sporadic and familial ALS patients and healthy controls. We measured morphometric features of endoplasmic reticulum, mitochondria, and lysosomes by imaging with vital dyes. We also analysed immunofluorescence images of ALS-linked proteins, including TDP-43 and stress granule components. We studied fibroblasts under basal conditions and under metabolic (galactose medium), oxidative (arsenite), and heat stress conditions. We then employed machine learning (ML) techniques on the dataset to develop biomarkers. Results: Stress perturbations caused robust changes in the measured features, such as organellar morphology, stress granule formation, and TDP-43 mislocalization. ML approaches were able to predict the perturbation with near perfect performance (ROC-AUC greater than 0.99). However, when trying to predict disease state or disease groups (e.g., sporadic, or familial ALS), the performance of the ML algorithm was more modest (ROC-AUC Control vs ALS = 0.63). We also detected modest but significant scores when predicting clinical features, such as age of onset (ROC-AUC late vs early = 0.60). Conclusions: Our findings indicate that the ML morphometry we developed can accurately predict if human fibroblasts are under stress, but the differences between ALS and controls, while statistically significant, are small and pose a challenge for the development of biomarkers for clinical use by these approaches. 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/2022.10.20.513009v1?rss=1 Authors: Zhao, Z., Hong, L., Huang, G., He, Y., Zuo, X., Han, W. Abstract: Cells sense physical cues, such as changes in extracellular matrix (ECM) stiffness, and translate these stimuli into biochemical signals that control various aspects of cellular behavior, thereby facilitating physiological and pathological processes in various organs. Evidence from multiple studies suggests that the anterior vaginal wall stiffness is higher in POP patients than in non-POP patients. Our experiments found that the expression of -smooth muscle actin (-SMA) in the anterior vaginal wall of patients with POP was increased, and the expression of DNMT1 was decreased. We used polyacrylamide gel to simulate matrix stiffening in vitro, and substrate stiffening induced the high expression of myofibroblast markers -SMA and CTGF in L929 cells. Inhibition of DNMT1 promotes fibroblast differentiation into myofibroblasts in vitro. The results of bioinformatics analysis showed that the expression of DNMT1 was significantly correlated with microtubule polymerization-related proteins. The experiment showed that the microtubule polymerization inhibitor nocodazole could eliminate the decrease of DNMT1 expression in fibroblasts induced by high stiffness. We conclude that fibroblasts sense an increase in the stiffness of the surrounding matrix and regulate fibroblast differentiation by regulating the expression of DNA methyltransferase 1 (DNMT1) through the regulation of microtubule polymerization. This study may help to elucidate the complex crosstalk between vaginal fibroblasts and their surrounding matrix in both healthy and pathological conditions, and provide new insights into the implications of potentially targeted phenotypic regulation mechanisms in material-related therapeutic applications. 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/2022.09.09.507263v1?rss=1 Authors: PARASAR, P., Kaur, N., Poisson, L., Singh, J. Abstract: ABSTRACT Objective: The role of astrocytes largely remains to be explored in X-linked adrenoleukodystrophy (X-ALD). Due to limited study models and inaccessibility to patient-tissue samples, we differentiated astrocytes from patient fibroblast-derived induced pluripotent stem cell (iPSCs) which provided a unique system to investigate molecular and etiopathogenetic mechanisms, identify targets, and develop therapeutic agents for X-ALD. Methods: We reprogrammed fibroblasts from adrenomyeloneuropathy (AMN) and cerebral adrenoleukodystrophy (cALD) patients carrying ABCD1 with pathogenic variants and a control patient to generate iPSCs. We differentiated iPSCs into astrocytes and performed transmission electron microscopy, gene expression, immunoblotting, enzyme-linked immunosorbent assay, miRNA-Seq, and lipidomics to characterize phenotypic and molecular features of patient-derived astrocytes. Results: These differentiated astrocytes exhibit diseased phenotypes and replicate biochemical and molecular changes found in patients. We confirmed the deletion of ABCD1 gene-encoded ALD protein and identified ABCD1 variant-driven very long chain fatty acid deposition in AMN and cALD astrocytes. Especially, cALD astrocytes showed increased glycolysis, increased signal transducer and transcription activator (STAT)3 activation, higher miR-9 expression in miRNA-Seq analysis, and reduced expression of anti-inflammatory cytokines such as arginase-1 and mannose receptor C-type-1. Consequently, Toll-like receptor-signaling via myeloid differentiation primary response gene 88 (MyD88) and nuclear factor-kappa B (NF-{kappa}B; p52 and p65) induced STAT3 and an altered miR-9 expression is a potential contributor to inflammatory milieu in cALD while interleukin-6 -induced anti-inflammatory cytokine production and increased chemotactic CCL-2 (MCP-1) production in AMN potentially favors microglial recruitment protecting its further progression. Interpretation: We demonstrate for the first time that patient iPSC-derived astrocytes mimic and recapitulate neuroinflammatory and biochemical defects of X-ALD and provide an in vitro cellular system to study X-ALD. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
In this episode, we connect with Hamid Khoja, the Chief Scientific Officer of FibroBiologics. With experience as a researcher in the pharmaceutical industry, Hamid now works with FibroBiologics using fibroblast cells to cure chronic diseases. Fibroblasts are among the most abundant cells in the human body, and medical professionals are finding that they can be used effectively in regenerative medicine. Join us now to learn about: Details about fibroblast cells, and what conditions they may be able to treat. The variety of fibroblast populations that naturally occur within the body. Why reducing inflammation plays a major role in regenerative medicine. You can see the innovative research behind fibroblasts for yourself by visiting www.fibrobiologics.com. Episode also available on Apple Podcast: http://apple.co/30PvU9C
On this quick hit installment of Locked On Texans: Former NFL player Soloman Wilcots and Houston area CEO Pete O'Heeron joins the show to discuss FibroBiologics. FibroBiologics is a cell therapy for former athletes and weekend warriors. Fibroblast cell technology outperforms stem cells and is a safer, less expensive alternative, reducing barriers for patients to access treatment. Learn more about your ad choices. Visit podcastchoices.com/adchoices
On this quick hit installment of Locked On Texans: Former NFL player Soloman Wilcots and Houston area CEO Pete O'Heeron joins the show to discuss FibroBiologics. FibroBiologics is a cell therapy for former athletes and weekend warriors. Fibroblast cell technology outperforms stem cells and is a safer, less expensive alternative, reducing barriers for patients to access treatment. Learn more about your ad choices. Visit podcastchoices.com/adchoices
Thank you to our AA Mommaes for making this "Manhi Moment" release possible. We thank you, we appreciate you, and we love you. 12042020 Join us as we Fibroblast through shit. Follow Jenna: instagram.com/komodoness www.youtube.com/channel/UC-iC6X7x5_C0a3_qCjytj7Q Follow Minwoo: instagram.com/alcoholickmw/ Follow Theresa: instagram.com/enviesteari Follow Micah: instagram.com/micahillustrates Follow us: anchor.fm/makgeollimoments patreon.com/makgeollimoments instagram.com/makgeollimoments facebook.com/mamomakgeollimoments --- Send in a voice message: https://anchor.fm/makgeollimoments/message Support this podcast: https://anchor.fm/makgeollimoments/support
Professor Arun Sanyal and Stephen Harrison provide a 40-minute briefing on fibroblast growth factor (FGF) agents and why they are so important to the future of NASH and NAFLD therapy.This discussion combines a discussion of the role Fibroblast Growth Factors (FGFs) play in the liver and human body in general, followed by a discussion of what this implies for drug development in general and some of the specific agents currently in testing or market:0:15 - Opening quotes - Stephen Harrison, Arun Sanyal, Roger Green2:07 - Episode begins2:57 - Meet Professor Arun Sanyal4:47 - Quick Look at Health Systems and Policy: India, UK, future episodes - Arun, Louise Campbell, Roger8:16 - Icebreaker and episode set-up - Roger and panel13:07 - Efruxifermin trials - Stephen Harrison18:00 - How FGFs work -- Arun Sanyal21:13 - Liver pathophysiology and insulin resistance -- Stephen and Arun28:13 - Q & A comparing agents in development - Roger, Louise Campbell, Arun and Stephen42:09 - Roger offers two choices for the episode's Final Question. Arun provides an exceptionally thoughtful and thought-provoking answer.The discussion itself includes three elements: first, a discussion of recent efruxifermin trials; second, a discussion of how FGFs work in the liver and rest of the body; and third, comparing and contrasting the various FGF-21 and FGF-19 drugs that are in development (or have been discontinued).
This week we discuss BET inhibitors and fibroblast activation with Michael Alexanian @m_alexanian a Postdoctoral researcher at Gladstone Institutes @Gladstoneinst. Michael explains how BET inhibitors have emerged as a potent tool to reversibly interfere with enhancers to promoter signalling. This has been shown to ameliorate heart failure in mouse models and is a highly translatable method of preventing heart failure in humans. We discuss two powerful tools, scRNASeq and scATAC-seq, and how they were used to investigate transcription and epigenetic changes of activated fibroblasts. We then discuss the impact of downstream targets and the impact on drug discovery and the limitation of BET inhibitors. Like every week we also highlight the benefits of preprinting, and increasing the accessibility of data within them to scientists around the world. Read the full preprint - https://www.biorxiv.org/content/10.1101/2020.07.21.214874v1.full Other links https://www.nature.com/articles/s41586-021-03674-1 This episode was produced by Emma Wilson and edited by John D Howard. If you enjoyed this show then hit that subscribe button and leave a review. If you love what we are trying to do then support us on Patreon https://www.patreon.com/preprintsinmotion where tiers start at as little as £1 a month! For the latest podcast news and updates follow us on Twitter @MotionPod or visit our website; www.preprintsinmotion.com. Produced by JEmJ Productions (find us on Twitter: Jonny @JACoates, Emma @ELWilson92, John @JohnDHoward8) and generously supported by ASAPbio (https://asapbio.org | @asapbio_).
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.31.363416v1?rss=1 Authors: Martinez-Espinosa, P. L., Yang, C., Xia, X., Lingle, C. J. Abstract: Adrenal chromaffin cells (CCs) in rodents express a rapidly inactivating, TTX-sensitive sodium current. The current has generally been attributed to Nav1.7, although a possible role for Nav1.3 has also been suggested. Nav channels in rat CCs rapidly inactivate into two separable pathways, which differ in their time course of recovery from inactivation. One population recovers with time constants similar to traditional fast inactivation and the other about 10-fold slower. Inactivation properties suggest that the two pathways result from a single homogeneous population of channels. Here we probe the properties and molecular components of the Nav current present in mouse CCs. We first confirm that functional properties of Nav current in rat and mouse cells are generally similar in terms of activation range, steady-state inactivation, and dual pathway fast inactivation. The results then show that all inward Nav current is absent in CCs from Nav1.3 KO mice. Subsequently, in a mouse with KO of fibroblast growth factor homology factor 14 (FGF14), we find that the slow component of recovery from fast inactivation is completely absent in most CCs, with no change in the time constant of fast recovery. Experiments probing the use-dependence of Nav current diminution between WT and FGF14 KO mice directly demonstrate a role of slow recovery from inactivation in determination of Nav current availability. Overall, the results indicate that the FGF14-mediated inactivation is the major determinant in defining use-dependent changes in Nav availability in CCs. We also consider the potential impact that inactivating FGFs with different recovery kinetics can exert on differential use-dependent changes in Nav availability. Copy rights belong to original authors. Visit the link for more info
Want to understand why IASTM, or soft tissue work using a tool, feels so good and is SO common? Join Dr. Jen and Dr. Dom as they explain some of the tools commonly used in IASTM and what they are really meant to do. Listen in to be empowered with the right questions to ask your clinician so you can better understand what is happening within your body during massage or tissue work. If you love hands on treatment from your clinician, great! This podcast will help you understand what you can add into your soft tissue work routine to achieve tissue recovery long term. Dr. Jen and Dr. Dom wants you to have the power to incorporate what feels great to you in a healthy, sustainable, and up to date way. What You Will Learn in this PT Pearl: 00:39 – Why it's empowering to ask questions to your clinician 02:35 – What IASTM, instrument assisted soft tissue mobilization, means and tool examples 06:49 – Popular sayings associated with IASTM which might not necessarily be true and why 07:25 – What the terms tendon repair and fibroblast really mean in relation to IASTM 12:24 – What soft tissue work really does 15:15 – Why understanding why your body has tension is a step closer to a long term solution 18:28 – Why IASTM needs to be coupled with movement 19:20 – What the goal of IASTM is and what does not achieve that goal To Watch the PT Pearl on YouTube, click here: https://youtu.be/kaGXux-W3Gg Research Citations: Gehlsen, G. M., Ganion, L. R., & Helfst, R. (1999). Fibroblast responses to variation in soft tissue mobilization pressure. Medicine & Science in Sports & Exercise, 31(4), 531-535. doi:10.1097/00005768-199904000-00006 Hussey, M. J., Boron-Magulick, A. E., Mcleod, T. C., & Bacon, C. E. (2018). The Comparison of Instrument-Assisted Soft Tissue Mobilization and Self-Stretch Measures to Increase Shoulder Range of Motion in Overhead Athletes: A Critically Appraised Topic. Journal of Sport Rehabilitation, 27(4), 385-389. doi:10.1123/jsr.2016-0213 Ikeda, N., Otsuka, S., Kawanishi, Y., & Kawakami, Y. (2020). Effects of Instrument-assisted Soft Tissue Mobilization on Musculoskeletal Properties—Corrigendum. Medicine & Science in Sports & Exercise, 52(2), 524. doi:10.1249/mss.0000000000002230 Seffrin, C. B., Cattano, N. M., Reed, M. A., & Gardiner-Shires, A. M. (2019). Instrument-Assisted Soft Tissue Mobilization: A Systematic Review and Effect-Size Analysis. Journal of Athletic Training, 54(7), 808-821. doi:10.4085/1062-6050-481-17 We Think You’ll Love: FREE QuaranTeam Challenge The Free 7 Day Mobility Challenge Jen’s Instagram Dom’s Instagram YouTube Channel Thank you so much for checking out this episode of The Optimal Body Podcast. If you haven’t done so already, please take a minute to subscribe and leave a quick rating and review of the show! To check out the rest of Doc Jen’s website, click here: www.docjenfit.com/podcast/episode40 --- Send in a voice message: https://anchor.fm/TOBpodcast/message
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.20.228056v1?rss=1 Authors: Govind Kumar, V., Agrawal, S., Suresh Kumar, T. K., Moradi, M. Abstract: Human fibroblast growth factor (FGF) 1 or hFGF1 is a member of the FGF family that isare involved in various vital processes such as cell proliferation, cell differentiation, angiogenesis and wound healing. hFGF1, which is associated with low stability in vivo, is known to be stabilized by binding heparin sulfate, a glycosaminoglycan that aids the protein in the activation of its cell surface receptor. The poor thermal and proteolytic stability of hFGF1 and the stabilizing role of heparin have long been observed experimentally; however, the mechanistic details of these phenomena either phenomenon are still not well understood. Here, we have used a combination of microsecond-level equilibrium molecular dynamics (MD) simulations, and state-of-the-art enhanced sampling MD simulations to quantitatively characterize the structural dynamics of monomeric hFGF1 in the presence and absence of heparin hexasaccharide. We have observed a local conformational changeconformational change in the heparin-binding pocketregion of hFGF1 that only occurs only in the absence of heparin. Several intramolecular hydrogen bonds were also identified within the heparin-binding pocket region, that form only when hFGF1 interacts with heparin. The loss of both intermolecular and intramolecular electrostatic interactions in the absence of heparin plausibly leads to the observed conformational change. This conformational transition results in increased flexibility of the heparin-binding pocket region and provides an explanation for the susceptibility of apo hFGF1 to proteolytic degradation and thermal instability . The hFGF1-heparin interactions) has also been quantified using absolute binding free energy calculations. Binding affinity (Kd) estimates determined computationally using our novel MD approach are in a good quantitative agreement with experimental Kd values from isothermal titration calorimetry experiments. The successful application of a combination of rigorous physics-based simulation techniques microsecond-level MD and accurate free energy calculations and its ability to accurately explain the biomolecular phenomena such as the heparin-mediated stabilization of hFGF1 at a quantitative level, provides open new opportunitiesrepresents a promising approach for studying complex towards understanding biological processesbiomolecular interactions between proteins and their binding partners at a detailed molecular level. using rigorous physics-based simulation techniques. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.17.207837v1?rss=1 Authors: Yusuf, I. O., Chen, H.-M., Cheng, P.-H., Chang, C.-Y., Tsai, S.-J., Chuang, J.-I., Wu, C.-C., Huang, B.-M., Sun, H. S., Chen, C.-M., Yang, S.-H. Abstract: Proper development of neuronal cells is important for brain functions, and impairment of neuronal development may lead to neuronal disorders, implying that improvement in neuronal development may be a therapeutic direction for these diseases. Huntington's disease (HD) is a neurodegenerative disease characterized by impairment of neuronal structures, ultimately leading to neuronal death and dysfunctions of the central nervous system. Based on previous studies, fibroblast growth factor 9 (FGF9) may provide neuroprotective functions in HD, and FGFs may enhance neuronal development and neurite outgrowth. However, whether FGF9 can provide neuronal protective functions through improvement of neuronal morphology in HD is still unclear. Here, we study the effects of FGF9 on neuronal morphology in HD and attempt to understand the related working mechanisms. Taking advantage of striatal cell lines from HD knock-in mice, we found that FGF9 increases neurite outgrowth and upregulates several structural and synaptic proteins under HD conditions. In addition, activation of nuclear factor kappa B (NF-kB) signaling by FGF9 was observed to be significant in HD cells, and blockage of NF-kB leads to suppression of these structural and synaptic proteins induced by FGF9, suggesting the involvement of NF-kB signaling in these effects of FGF9. Taken these results together, FGF9 may enhance neurite outgrowth through upregulation of NF-kB signaling, and this mechanism could serve as an important mechanism for neuroprotective functions of FGF9 in HD. Copy rights belong to original authors. Visit the link for more info
Fibroblast growth factors are a group cell signaling proteins that play a critical role in growth and development. They have been implicated in achondroplasia, the most common genetic form of dwarfism, but these growth factors are also involved in a number of rare cancers. QED Therapeutics, a BridgeBio company, is developing infigratinib, an experimental tyrosine kinase inhibitor that targets multiple fibroblast growth factors, for both achondroplasia and certain forms of bile duct and bladder cancers. We spoke to Susan Moran, CEO of QED Therapeutics, about the company’s experimental tyrosine kinase inhibitor, the role fibroblast growth factors play in seemingly disparate rare diseases, and the challenges of learning to work with very different types of patient communities.
I've recently become a huge fan of something called "Hyperbaric Oxygen Therapy" treatment. After getting an softshell unit for my home (the ), I've been in it every day for 40-60 minutes for reading or napping, and it's become a complete game changer in my personal recovery and health protocol. You can read more in my guest's new book "", but the benefits include: Hyperoxygenation: The delivery of 100% oxygen under pressure (1.5 to 3 ATA) within the hyperbaric chamber provides up to 20 times normal oxygen to all tissues within the body. This oxygen supersaturation is in marked contrast to breathing room air (21% oxygen at 1 ATA). Direct Pressure to Oxygen Molecules: Inside the hyperbaric chamber, oxygen molecules are compressed and become more soluble, obeying the scientific principles of Boyle’s Universal Gas Law. This phenomenon allows oxygen to effortlessly cross cell membranes and enter all of the body’s fluid systems, including plasma, synovial, lymphatic, interstitial (between cells) and cerebrospinal fluids. Normally, only the red blood cells are capable of transporting oxygen throughout the body. Now, all body fluids combine to provide alternate transport routes for extra oxygen and cumulatively can provide up to 20 times normal O2. Bactericidal Ammunition – Aids in Killing Bacteria: Conditions created within the hyperbaric oxygen chamber are not favorable for the viability of bacteria, fungi and viruses – organisms that cannot survive in an oxygen rich environment. Extra oxygen is provided to the white blood cells (leukocytes) which become supercharged in the battle against bacteria responsible for causing infection and illness. Angiogenesis – The Formation of New Blood Vessels: Hyperbaric Oxygen stimulates the body to grow new capillaries (angiogenesis), essentially building a new collateral circulatory system to serve injured and healthy tissues alike. The resulting neovascularization is extremely helpful for reaching tissues and organs that have restricted blood flow (ischemic areas) as well as areas of the body that are lacking or compromised in available oxygen (hypoxic areas). Superoxide Dismutase (SOD) Stimulation – A Surge of Antioxidant Capabilities: Superoxide Dismutase (SOD) is an important enzyme found in human cells that inactivates superoxides, the most common free radicals in the body, responsible for destruction of cells. Hyperbaric Oxygen stimulates SOD production thereby helping the body to rid itself of the byproducts of inflammation and damaging free radicals. Synergy With Antibiotics: Hyperbaric Oxygen has been proven to create a synergistic effect when administered in conjunction with certain antibiotics. Synergy can be understood as two or more agents working together to produce a result not obtainable by any of the agents independently. Administration of HBOT biomechanically potentiates the effectiveness of antibiotic therapy. The capabilities of sulfanomides are increased up to ten fold when HBOT is added. Increased oxygen levels from HBOT alone also act as antibiotics by impairing bacterial metabolism. Improves Osteoblast and Osteoclast Production: Faster regeneration of bone is derived by hyperbaric oxygen’s ability to stimulate and increase production of specialized cells (osteoblasts and osteoclasts) responsible for bone repair and formation. Increases Fibroblast and Collagen Production: These essential building blocks of connective-tissue, tendon and skin matrix (fibroblasts and collagen) provide the structural framework throughout the body and play a critical role in wound healing. Fibroblast and collagen reproduction and growth are aided by the added availability of increased oxygen provided during hyperbaric conditions. Decreases Inflammation Inflammation, one of the most common mechanisms of disease and injury, is caused by biochemical byproducts that are manufactured by the body’s natural immune response. Hyperbaric oxygen markedly decreases inflammation by stimulating the body’s own anti-inflammatory defenses. This may be the single most important function of HBOT. This podcast is all about . Jason Sonners DC, DIBAK, DCBCN is owner and Clinic Director of , , and Corp. As the owner and one of the doctors at , Dr. Sonners primarily practices functional medicine taking on complex cases including autoimmune conditions, chronic inflammation and neurologic dysfunction and using treatment methods to help improve function and tap into the body’s innate ability to heal. He uses nutrition, detoxification, hyperbaric oxygen and herbal therapies to improve the health and quality of life for his patients. Dr. Sonners works with families all over the country helping them find answers to their toughest health questions. As the clinical director of and , Dr. Jason Sonners utilizes Hyperbaric Oxygen Therapy (HBOT) for many of his chronic patients and helps get Hyperbaric Oxygen both into the homes of patients in need as well into the offices of doctors who want to build hyperbaric therapy clinics. Dr. Sonners is on the faculty for the Medical Academy of Pediatric and Special Needs (MedMAPS) as well as the International Hyperbaric Association (IHA) educating other doctors on alternative and complementary treatment methods. He also guest lectures for various functional medicine conferences around the country talking about the use of nutrition, fasting, red light therapy and hyperbaric oxygen in helping the chronic illnesses plaguing our country. During our discussion, you'll discover: -What HBOT is, and how Jason began using it...10:22 Herniated disk and injured foot; suffered drop foot for 18 months as a result Several months of led to full recovery Jason's father had amazing improvements in his MS after HBOT Eventually implemented it in his clinic What is HBOT? Hyperbaric = increased pressure Air is 21% oxygen Add varying amounts of pressure and oxygen to create different "doses" Used traditionally in hospitals for more severe conditions: gangrene, radiation burns, diabetic neuropathy, etc. How assists w/ wound care: Trauma, infection damages micro-circulation (in the capillaries) Hyperbaric oxygen can get into areas of the body that are oxygen starved HBOT is able to bypass the red blood cells and inject oxygen into the plasma; much more expedient delivery mechanism -Various delivery mechanisms and how much oxygen one needs using HBOT...18:20 All gases move in gradient (high to low pressure) A pressurized environment causes the pressure in your body to increase The more pressure you're exposed to, and higher percentages of oxygen, the larger the gradient of pressure Oxygen concentrator increases the amount of oxygen you're breathing in (and that's pressurized in a HBOT chamber) HBOT chambers in hospitals can have 100% oxygen inside 3 types of chambers: Hospital grade (~$200k + cost of oxygen) Hard chamber ($90-100k) Home model ($15-22k) -Actual use frequency and volume of a HBOT chamber...22:42 Match the right tool to your goals Short-term benefits: Increase in oxygenation More ATP production Some immune activation Long-term benefits: Super oxide dismutase increase Body begins replicating mitochondrial content Increase in stem cells Rebuilding blood vessels Antimicrobial benefits Front load the therapy for the most efficacy in therapy (first 3-5 months), then space it out Sessions range from 60-120 minutes There is a point of diminishing returns Extra oxygen stimulates parasympathetic nervous system (increased relaxation) -The effects of HBOT on aerobic or endurance activity...35:23 Performance enhancing effects do not come from red blood cell changes Red blood cell adaptation has to do w/ hypoxia, not hyperoxia -How HBOT promotes angiogenesis when cancer cells are present...38:04 The understanding of the metabolism of cancer has changed in recent years Cancer cells don't use oxygen to make ATP Drive blood glucose levels down, oxygen levels high Starve cancer cells, while nourishing healthy cells Bottom line: Angiogenesis isn't the concern -Antioxidant mechanisms affected by HBOT...42:35 Superoxide dismutase (SODS) upregulation is stimulated by HBOT Hormesis: induce stress to the body, produce an adaptation -The effect of HBOT on bacteria growth in the microbiome...47:11 Upregulation in your own immune system: will affect neutrophils and macrophages Used on anaerobic pathogens (serious infections) Environment of high oxygen is conducive for healthy bacteria to thrive Watch out for a new BGF podcast w/ Dr. Matt Cook! -How HBOT works with bone repair and formation...51:25 It's all about cell signaling Growth factors are the signals for healing and recovery Regenerator cells Platelet derived growth factors Vascular endothelial growth factor (VEGF) promotes angiogenesis is one of many modalities used for healing -Treatments that work well in conjunction w/ HBOT...57:07 High-dose red light right before lights Synergy between red light and oxygen Ben uses holotropic breath work The course of Dr. Nick's "Inspire" Oil Do not hold your breath while transitioning between pressure -Safety concerns w/ HBOT chambers...1:01:05 The risk is when there's 100% oxygen, not a home chamber Oxygen is not flammable, it's an accelerant Pneumothorax (collapsed lung) will be problematic in a chamber Don't do w/ ear pain The pressure you're in is equivalent to being 10 feet under water -How HBOT affects mental performance...1:06:10 Article: -HBOT vs. exercise w/ oxygen therapy (EWOT)...1:07:31 for EWOT of -And much more... Resources from this episode: - - - - Book: by Jason Sonners - Dr. Nick's "Inspire" Oil - - Red Light Therapy - for EWOT - - BGF podcasts mentioned: Episode sponsors: -: Use Kion Serum anywhere you’d like for more vibrant, youthful skin and hair. BGF listeners, receive a 20% discount off your order when you use discount code: BGF20 -: After using the Joovv for close to 2 years, it's the only light therapy device I'd ever recommend. Give it a try: you won't be disappointed. Order using and receive my brand new book, Boundless absolutely free! (While supplies last) -: A wellness company specializing in innovative nutraceuticals made from healing hive compounds and plant-based ingredients. Get 15% off your order when you use discount code: BEN -: Delivers healthy 100% grass-fed and finished beef, free-range organic chicken, and heritage breed pork directly to your door on a monthly basis. All their products are humanely raised and NEVER given antibiotics or hormones. 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Asia and Samantha her fellow Esthetician friend explains the Plasma Fibroblast Pen. Then nothing is off limits when Sam reveals her CONFESSION OF AN ESTHETICIAN, this one may gross you out! Then the girls cut up over THE BACHELOR. Show her some love by subscribing and giving her a 5 stars. Take a minute to write a review, it helps us know if we are doing something right. Asia doesn't promote brands so if you have specific questions follow and DM her on instagram at BEAUTASIA2.0 she loves friends. --- Send in a voice message: https://anchor.fm/asia-demarcos/message
The new craze right now to reverse and repair again is fibroblast treatments! But for most of us who are dying to invest in anti-aging treatments, there is also a lot of skepticism and questions swirling around on whether or not it's worth it. Skincare expert, Jennifer Carrasco, is answering all of your fibroblast treatment questions. Is it worth? How long does it last? Why is fibroblast the biggest craze right now? What does it actually do to your skin cells? Are there any risks or side effects? Don't miss this episode that will help you decide whether or not Fibroblast treatments are something you are ready for! Book your next appointment one on one with Jennifer Carrasco here: https://virago.studio/book-spa-appointments
Commentary by Dr. Valentin Fuster
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Education] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Education] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Education] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Education] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Professional Medical Education] [Show ID: 35063]
Marius Wernig, MD, PhD, discusses how his lab has worked to convert non-neuronal cell types (lymphocytes, pluripotent stem cells, fibroblasts, hepatocytes, lymphocytes) to neurons. The lab is now working on identifying the molecular mechanisms underlying induced lineage fate changes, the phenotypic consequences of disease-causing mutations in human neurons and other neural lineages. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Professional Medical Education] [Show ID: 35063]
Learn about why your wounds heal faster in the daytime; the Peter Principle, which explains why so much goes wrong; and why there’s one tame population of foxes on Earth, and what they’ve taught us about evolution. In this podcast, Cody Gough and Ashley Hamer discuss the following stories from Curiosity.com to help you get smarter and learn something new in just a few minutes: Here's Why Wounds Heal Faster in the Daytime — https://curiosity.im/2rMVzgo The Peter Principle Explains Why So Much Goes Wrong — https://curiosity.im/2rNmw3E There Is One Tame Population Of Foxes On Earth, All Thanks To A Russian Geneticist — https://curiosity.im/2rO3cmN If you love our show and you're interested in hearing full-length interviews, then please consider supporting us on Patreon. You'll get exclusive episodes and access to our archives as soon as you become a Patron! https://www.patreon.com/curiositydotcom Download the FREE 5-star Curiosity app for Android and iOS at https://curiosity.im/podcast-app. And Amazon smart speaker users: you can listen to our podcast as part of your Amazon Alexa Flash Briefing — just click “enable” here: https://curiosity.im/podcast-flash-briefing.
11 March 2014: In this Skinpod episode Dr. John McGrath, from King's College London, discusses fibroblast cell therapy for patients with recessive dystrophic epidermolysis bullosa (RDEB).
In this episode Mairi McLean, Associate Editor of Gut journal, talks to Matias Avila and Carmen Berasai, University of Navarra, Pamplona, Spain. They discuss their published paper "Fibroblast growth factor 15/19 (FGF15/19) protects from diet-induced hepatic steatosis: development of an FGF19-based chimeric molecule to promote fatty liver regeneration". Full article >> http://gut.bmj.com/content/66/10/1818.info
Commentary by Dr. Valentin Fuster
Tumor cells feel the pressure after protease inhibition Primary fibroblasts use a high pressure, “nuclear piston” mode of migration to move through highly cross-linked 3D extracellular matrices. Petrie et al. reveal that tumor cells with high levels of matrix metalloproteinase activity generally migrate by forming lamellipodia but, when their protease activity is inhibited, they can switch to the nuclear piston mechanism to force their nuclei through small gaps in the extracellular matrix. This biosights episode presents the paper by Petrie et al. from the January 2nd, 2017, issue of The Journal of Cell Biology and includes an interview with the paper's senior author, Ryan Petrie (Drexel University, Philadelphia, PA). Produced by Caitlin Sedwick and Ben Short. See the associated paper in JCB for details on the funding provided to support this original research. Subscribe to biosights via iTunes or RSS View biosights archive The Rockefeller University Press biosights@rockefeller.edu
Fakultät für Biologie - Digitale Hochschulschriften der LMU - Teil 06/06
Super-resolution fluorescence microscopy performed via 3D structured illumination microscopy (3D-SIM) features an 8-fold volumetric resolution improvement over conventional microscopy and is well established on flat, adherent cells. However, blastomeres in mammalian embryos are non-adherent, round and large. Scanning whole mount mammalian embryos with 3D-SIM is prone to failure due to non-adherent embryos moving during scanning and a large distance to the cover glass. The biggest challenge and achievement of this doctorate thesis was the development of a novel method to perform 3D-SIM on mammalian embryos (“3D structured illumination microscopy of mammalian embryos and spermatozoa” published in BMC Developmental Biology). The development and fine-tuning of this method took over two years due to the time-intense generation of embryos and the subsequent two day long embryo staining, embedding and scanning with steps that required novel techniques such as micromanipulation which was not associated with sample preparation prior to this protocol. Problem identification was time-intensive since each of the numerous steps necessary could negatively affect the image quality. This method was fine-tuned during three studies. The first study “Reprogramming of fibroblast nuclei in cloned bovine embryos involves major structural remodeling with both striking similarities and differences to nuclear phenotypes of in vitro fertilized embryos” (published in Nucleus) investigates the profound changes of nuclear architecture during cattle preimplantation development of embryos generated by somatic cell nuclear transfer (SCNT) and in vitro fertilization (IVF). Fibroblast nuclei in embryos generated by SCNT go through similar changes in nuclear architecture as embryos generated by IVF. In both embryo types the occurrence of a large, chromatin-free lacuna in the center of nuclei around major embryonic genome activation (EGA) was noted. Similarly, the chromosome territory-interchromatin compartment (CT-IC) model applied to both types of embryos, featuring a lacuna or not, with an enrichment of RNA polymerase II and H3K4me3, a histone modification for transcriptionally competent chromatin, in less concentrated chromatin and an enrichment of H3K9me3, a transcriptionally restrictive histone modification, in more concentrated chromatin. However, large, highly concentrated H3K4me3 and H3K9me3 clusters were noted in both embryo types at chromatin concentrations that did not fit to the model. The chromatin-free lacunas were highly enriched in newly synthesized mRNA. The second study “Remodeling of the Nuclear Envelope and Lamina during Bovine Preimplantation Development and Its Functional Implications” (published in PLOS ONE) presents the changes of the nuclear envelope and lamina during bovine preimplantation development. Before major EGA, chromatin-free areas of the nuclear periphery were also free of nuclear pore complexes (NPCs), whereas after major EGA, the entire nuclear periphery was equipped with at least a fine layer of chromatin and associated NPCs. Three types of nuclear invaginations were predominant at different stages. The most common invagination was lamin B and NUP153 positive and was most prominent between the 2-cell and 8-cell stages until the onset of major EGA. Lamin B positive, but NUP153 negative invaginations were most prominent during stages with large nuclear volume and surface reductions. The least common invagination was lamin B negative but NUP153 positive and occurred almost exclusively at the morula stage. RNA-Seq and 3D-SIM data showed large deposits of spliced NUP153 mRNA and cytoplasmic NUP153 protein clusters until shortly after major EGA. NUP153 association with chromatin was initiated at metaphase. The third study “Stage-dependent remodeling of the nuclear envelope and lamina during rabbit early embryonic development” (published in the Journal of Reproduction and Development) demonstrated that rabbit embryonic nuclei feature a nuclear invagination type containing a large volume of cytoplasm that provides cytoplasmic proximity to nucleoli in addition to the small volume invaginations that were previously observed in bovine nuclei. The underlying mechanism for these two invaginations must differ from each other since small volume invaginations were frequently emanating from large volume invaginations emanating from the nuclear border but large volume invaginations were never emanating from small volume invaginations emanating from the nuclear border. Abundance of import/export competent invaginations featuring NPCs peaked at the 4-cell stage, which is the last stage before a drastic nuclear volume decline and also the last stage before major EGA is initiated at the 8- to 16-cell stage. Import/export incompetent invaginations positive for lamin B but not NUP153 peaked at the 2-cell stage. This was the stage with the largest variability in nuclear volumes. This may hint at an interphase nuclear surface reduction mechanism. Additionally, previously generated but unpublished 3D-FISH data about the localization changes of a stably inserted reporter gene upon activation in cloned bovine embryos was analyzed and documented in the study “Positional changes of a pluripotency marker gene during structural reorganization of fibroblast nuclei in cloned early bovine embryos” (published in Nucleus). This study showed that the stably inserted OCT-4 reporter gene “GOF” in bovine fetal fibroblasts was initially moved towards the nuclear interior in day 2 bovine embryos generated by SCNT of bovine fetal fibroblasts. However, in day 4 SCNT embryos the localization of GOF had moved towards the periphery while it was still activated. Its carrier chromosome territory did not significantly move differently compared with the non-carrier homolog. Constant proximity of GOF to its carrier chromosome territory ruled out a movement by giant loops. In cooperation with the Department of Histology and Embryology of the Ege University (Izmir, Turkey) the destructive effects of cryopreservation on blastomere integrity were analyzed in the study “Ultra-Structural Alterations in In Vitro Produced Four-Cell Bovine Embryos Following Controlled Slow Freezing or Vitrification” (published in Anatomia, Histologia, Embryologia). The cryopreservation method slow freezing caused more damage to blastomeres and to the zona pellucida than its fast freezing alternative vitrification. This was most likely caused by ice crystal formation and the longer exposure to the toxic side effects of cryoprotectants before freezing was complete.
Dr. Ross Camidge discusses a clinical trial studying patients with advanced stage lung cancer to identify those who may respond to a drug called ponatinib. Both small cell and non small cell lung cancer patients may be eligible. http://bit.ly/UCponatinib
Dr. Ross Camidge discusses a clinical trial studying patients with advanced stage lung cancer to identify those who may respond to a drug called ponatinib. Both small cell and non small cell lung cancer patients may be eligible. http://bit.ly/UCponatinib
Dr. Ross Camidge discusses a clinical trial studying patients with advanced stage lung cancer to identify those who may respond to a drug called ponatinib. Both small cell and non small cell lung cancer patients may be eligible. http://bit.ly/UCponatinib
Commentary by Dr. Valentin Fuster
The effect of platelet-rich plasma (PRP) on chondrocytes has been studied in cell and tissue culture, but considerably less attention has been given to the effect of PRP on synoviocytes. Fibroblast-like synoviocytes (FLS) compose 80% of the normal human synovium and produce cytokines and matrix metalloproteinases that can mediate cartilage catabolism. Treatment of synovial cells with LR-PRP and RBCs resulted in significant cell death and proinflammatory mediator production. Click here to read the article.
Fibroblast growth factor receptor (FGFR) mutations may play a role in the growth of squamous cell lung cancer. Dr. Jonathan Riess talks about what they are learning in this area.
Fibroblast growth factor receptor (FGFR) mutations may play a role in the growth of squamous cell lung cancer. Dr. Jonathan Riess talks about what they are learning in this area.
Fibroblast growth factor receptor (FGFR) mutations may play a role in the growth of squamous cell lung cancer. Dr. Jonathan Riess talks about what they are learning in this area.
Yong Ho Bae and Richard Assoian discuss a signaling pathway that causes cells to stiffen their cytoskeletons and proliferate when placed on stiff substrates.
Dr. Joel Neal of Stanford University Medical Center talks about FGFR - fibroblast growth factor receptor - and how it can impact non-small cell lung cancer growth.
Dr. Joel Neal of Stanford University Medical Center talks about FGFR - fibroblast growth factor receptor - and how it can impact non-small cell lung cancer growth.
Dr. Joel Neal of Stanford University Medical Center talks about FGFR - fibroblast growth factor receptor - and how it can impact non-small cell lung cancer growth.
1) Fibroblast growth factor-21 being a sensitive biomarker of mitochondrial disease and 2) Topic of the month: Area of functional symptoms and conversion disorder. This podcast for the Neurology Journal begins and closes with Dr. Robert Gross, Editor-in-Chief, briefly discussing highlighted articles from the print issue of Neurology. In the second segment Dr. James Addington interviews Dr. Carolyn Sue about her paper on fibroblast growth factor-21 being a sensitive biomarker of mitochondrial disease. Dr. Roy Strowd is reading our e-Pearl of the week about MAD for seizures. In the next part of the podcast Dr. Shanna Patterson interviews Dr. Jon Stone about functional neurologic symptoms and how to discuss this diagnosis with patients. The participants had nothing to disclose except Drs. Sue, Strowd and Stone.Dr. Sue receives research support from the National Health and Medical Research Council of Australia.Dr. Strowd serves on the editorial team for the Neurology® Resident and Fellow Section. Dr. Stone receives speaker honoraria from the Movement Disorders Society, Norwegian Neuropsychiatric Association, British Medical Association, Royal College of Psychiatrists, UCB, Tribunals Judiciary (UK) and St Louis Dept of Neurology; does expert witness work and runs a free patient information website.
Geçen defa değişik kök hücresi türlerinden, embriyonun kök hücrelerinin vücudunuzdaki tüm hücreleri nasıl oluşturduğundan ve 2012 yılı Nobel Ödülü'nün bu alanda araştırma yapan iki bilim adamına verildiğinden bahsetmiştim. 1960’lardan önce zannediyorduk ki, bir kök hücresi mesela bir deri hücresine bir kere dönüştü mü artık hep deri hücresi olarak kalır. Erişkin bir hücreyi pluripotent bir kök hücresine dönüştürmenin bir yöntemini bulsak, araştırmalar için embriyo bulmaya gerek kalmayacaktı. Şinya Yamanaka (Fotoğraf: Jun Sella / Flickr) John B. Gurdon, daha öğrenciyken, bunu yaptı. Döllenmiş bir kurbağa yumurta hücresinden çekirdiğini camdan bir pipet ile çıkardı. Daha sonra bir iribaşın bağırsaklarından birkaç hücre aldı, yine camdan bir pipet ile çekirdeğini çıkartıp bunu önceden boşalttığı yumurta hücresine aktardı. O çekirdek gelişkin bir iribaşınki olmakla birlikte, nasıl olduysa hücrenin saati başa sardı ve bağısaktan gelen DNA, normal bir iribaşın gelişme ve büyümesini sağladı. (Bu arada buna “klonlama” deniyor.) Gurdon, elindeki artık özelleşmiş olan erişkin bağırsak hücresini, bir şekilde bir iribaşın ihtiyaç duyacağı her tür hücreye geri dönüştürmüştü. Doktorasını 1960’ta aldıysa da araştırmasını ancak 1962’de, bağısaktaki DNA’nın normal kurbağaların oluşmasına yol açtığından emin olduktan sonra yayınladı. Dolly adlı koyunu duymuşsunuzdur, 1996 doğumlu, ilk klonlanan hayvan. Burada da bilim insanları benzeri bir iş yaptılar, özelleşmiş bir hücrenin DNA’sını, döllendikten sonra DNA’sı atılmış bir embriyoya aktardılar. Bu sefer bağırsak hücrelerini değil, meme bezi hücrelerini kullandılar - Koyunun adı da buradan geliyordu, Country şarkıcısı Dolly Parton’ın adından. Bu teknik kurbağalar ve amfibiler için zaten zorken memeli hayvanlar için daha da zorluydu: Bu yüzden Dolly’nin doğması 35 yıl aldı - Unutmadan, Dolly, 277 deneme içindeki tek başarıydı. 2012 Nobel Tıp veya Fizyoloji Ödülü'nü kazanan diğer bilim insanı ise Dr. Şinya Yamanaka. Yamanaka, erişkin hücreleri pluripotent kök hücrelerine dönüşecek şekilde programlamayı başardı. Ama bunun için camdan pipet değil, genler kullandı. Öyle genler var ki, embriyonik kök hücrelerinin diğer hücrelere dönüşmesini önlüyor. Bu genleri önce ehlileştirilmiş virüslere yerleştirip sonra o virüsleri yaşayan hücrelere musallat ederek canlı hücrelere aktarabiliyoruz. Dr Yamanaka 2006’da farklılaşmış deri hücrelerine bu genlerden 24 tanesini bulaştırdı, ve bir baktı ki bu farklılaşmış deri hücreleri artık aynı embriyonik kök hücrelerine benziyor. Ama Dr. Yamanaka bu genlerin pluripotent kök hücrelerini meydana getiren özgül dörtlü bileşenini bulana kadar çok çalıştı. Bu genlerin, memelilerin döllenmiş yumurtalarının zamanında henüz özelleşmeden, farklılaşmamış olarak kalmak için kullandıkları genler olduğu neredeyse muhakkak. Canlı hücrelere virüs bulaştırmanın bazı muhtemel sakıncaları var, o yüzden şimdilerde DNA’yı değiştirmeden bunu becerecek yöntemler üzerinde çalışılıyor. Bu pluripotent kök hücreleri, düzinelerce değişik türünün bir hücre bankasında saklanmasıyla yüzlerce değişik hastalığın tedavisinde kullanılabilir. Her seferinde kişiye özel hücreleri sıfırdan hazırlamaktansa, kullanıma hazır hücreleri depoda hazır bulundurmak hem para hem de zaman tasarrufu sağlayacak. Japonların kalıtım bilgisi birbirine çok benzediğinden, 75 tür hücrenin toplumun yüzde 80’inin tedavisine yeteceği tahmin ediliyor. Bunun için Yamanaka’nın hedefi 2020 yılı. O vakte kadar, bu hücreleri laboratuvarda tabaklara koyup gözleyeceğiz. Böylece artık sinir, kalp ve karaciğer hücrelerini etkileyen hastalıkların nasıl meydana geldiğini anlamaya başlayabileceğiz. Fibroblast adlı hücreleri sinir ve kalp hücrelerine çevirdik bile. Belki de Parkinson hastalığı ya da tip 1 şeker hastalığındaki gibi hasarlı veya kayıp hücreleri yenileyebileceğiz. Yani çevrecilerin değidiği gibi, çözüm "geri dönüşüm"de... Çeviren: Çağrı Yalgın; Seslendiren: Tevfik Uyar; Müzi...
Soft Active Materials: From Granular Rods to Flocks, Cells and Tissues
This presentation discusses tissue stiffness and how cells react to this type of stress. In addition, the effects of gels on cell signaling are also examined.
Tierärztliche Fakultät - Digitale Hochschulschriften der LMU - Teil 03/07
Fibroblast growth factor-23 (FGF-23), a molecule that is mutated in patients with autosomal dominant hypophosphatemic rickets (ADHR), appears to be involved in the regulation of phosphate homeostasis. Although increased levels of circulating FGF-23 were detected in patients with different phosphate-wasting disorders, it is not yet clear whether FGF-23 is directly responsible for the abnormal regulation of mineral ion homeostasis and consequently bone development. To explore these questions further, we generated a mouse model in which the entire Fgf-23 gene was replaced with the lacZ gene. Fgf-23 null (Fgf-23-/-) mice showed signs of growth retardation, developed severe hyperphosphatemia with elevated serum 1,25(OH)2D3 levels, and died by 13 weeks of age. Hyperphosphatemia in Fgf-23-/- mice was accompanied by skeletal abnormalities, as demonstrated by histological, molecular, and morphometric analyses. Fgf-23-/- mice had decreased bone mineral density of the limbs due to an accumulation of unmineralized osteoid leading to marked limb deformities. Moreover, Fgf-23-/- mice showed excessive mineralization in soft tissues. To further expand our understanding regarding the role of Fgf-23 in phosphate homeostasis and skeletal mineralization, we crossed Fgf-23-/- animals with Hyp mice, the murine equivalent of XLH. Interestingly, Hyp males lacking both Fgf-23 alleles were indistinguishable from Fgf-23-/- mice, both in terms of serum phosphate levels and skeletal changes, suggesting that Fgf-23 is downstream of the phosphate regulating gene with homologies to endopeptidases on the X chromosome (Phex). To explore further the role of the vitamin D axis for FGF-23 signaling, we mated Fgf-23 deficient mice and vitamin D receptor (VDR) mutant mice with a non-functioning VDR. To prevent secondary hyperparathyroidism in VDR and compound mutant mice, all mice were kept on a rescue diet enriched with calcium, phosphorus, and lactose. In analogy to previous findings, Fgf-23-/- animals showed hypercalcemia, hyperphosphatemia, growth retardation, ectopic calcifications, severe osteoidosis, skin atrophy, and renal dysfunction. In addition, here we describe that Fgf-23-/- mice are hypoglycemic, and have profoundly increased peripheral insulin sensitivity and improved subcutaneous glucose tolerance, but normal renal expression of the aging suppressor gene Klotho. Although VDR and double mutants on the rescue diet still had moderately elevated parathyroid hormone serum levels and lower bone mineral 76 density compared to wild-type mice, double mutant mice had normal body weight, were normocalcemic and normophosphatemic, and ectopic calcifications as well as renal dysfunction were absent. Ablation of vitamin D signaling in compound mutants also normalized subcutaneous glucose tolerance tests and insulin secretory response. In conclusion, our results indicate that the alterations in mineral and carbohydrate metabolism present in Fgf-23-/- mice require an intact vitamin D signaling pathway.
To date, mesenchymal cells have only been associated with bone resorption indirectly, and it has been hypothesized that the degradation of bone is associated exclusively with specific functions of osteoclasts. Here we show, in aseptic prosthesis loosening, that aggressive fibroblasts at the bone surface actively contribute to bone resorption and that this is independent of osteoclasts. In two separate models ( a severe combined immunodeficient mouse coimplantation model and a dentin pit formation assay), these cells produce signs of bone resorption that are similar to those in early osteoclastic resorption. In an animal model of aseptic prosthesis loosening (i.e. intracranially self-stimulated rats), it is shown that these fibroblasts acquire their ability to degrade bone early on in their differentiation. Upon stimulation, such fibroblasts readily release acidic components that lower the pH of their pericellular milieu. Through the use of specific inhibitors, pericellular acidification is shown to involve the action of vacuolar type ATPases. Although fibroblasts, as mesenchymal derived cells, are thought to be incapable of resorbing bone, the present study provides the first evidence to challenge this widely held belief. It is demonstrated that fibroblast-like cells, under pathological conditions, may not only enhance but also actively contribute to bone resorption. These cells should therefore be considered novel therapeutic targets in the treatment of bone destructive disorders.
We have previously described a 30 kDa basic fibroblast growth factor (bFGF)-like protein in rodent testicular homogenates and have shown that pachytene spermatocytes are the sites of predominant immunoreactivity for this bFGF-like protein (Mayerhofer, A., Russell, L.D., Grothe, C., Rudolf, M. and Gratzl, M. (1991) Endocrinology 129, 921–924). We have now addressed the question whether this 30 kDa bFGF-like protein is a large bFGF form and whether it is produced by pachytene spermatocytes. We detected bFGF mRNA in homogenates of isolated mouse spermatocytes (which consisted mainly of pachytene spermatocytes) using S1 nuclease protection assays. As shown by Western blot analyses, the bFGF mRNA in mouse spermatocytes is translated into bFGF of an approximate molecular weight of 30 kDa. Neither bFGF mRNA, nor bFGF itself, was observed in isolated mouse Leydig cells. These results indicate that the immunoreactive bFGF-like protein observed previously in germ cells of the murine testis is identical to bFGF. Thus, germ cells of the testis produce bFGF, which may exert regulatory function in the process of spermatogenesis.
We have used a recently characterized rabbit antiserum against basic fibroblast growth factor (bFGF), which recognizes various forms of bFGF, to examine the presence and localization of bFGF in the testes of adult rats and mice and the 5-day-old rat. In Western blots of testicular homogenates of adult rats and mice and immature rats, immunoreactive single bands at approximately 30 kDa were detected. Immunocytochemistry revealed specific staining restricted to the tubular compartment. In 5-day-old rat testes, prespermatogonia were immunoreactive. The cytoplasm of pachytene spermatocytes was heavily stained in the adult testes of both species. Staining of these cells became evident around stage IV/V, was prominent in stage VII through IX and declined about stage XII/XIII (rat) or X-XI (mouse). Staining was seen in type A spermatogonia and in elongating spermatids in their cytoplasmatic lobes and along their flagellae. Sertoli cells were unstained. We propose that the pluripotential growth factor bFGF could be involved in the regulation of germ cell proliferation and differentiation in the adult and immature testis.
The influence of ionising radiations on ageing is still controversial. Since Hayflick established the concept that diploid cells have finite lifespan in vitro, human diploid fibroblast (HDF) cultures have been recognised as a potent experimental model for cytogerontological investigations. In this study HDF cultures in phase II were exposed to acute irradiation with either X-rays on fast neutrons. The replicative potentials and labelling indices with [3H]thymidine were measured post irradiation until the cultures ceased growth in phase III. Cell mortality was measured by cloning. The apparent loss in replicative potential of irradiated mass cultures was wholly attributable to the loss of viable clonogenic cells. The current concept of precocious clonal senescence in vitro as a late effect of irradiation in clonogenic survivors is not supported by the present experiments. Instead, our results suggest that exposure to a single dose of ionising radiations either causes total replicative incapacitation (killing) of HDF cells and their progeny early after irradiation or leaves their replicative potentials unperturbed.
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