In this video, we feature the MIMETAS OrganoReady® Colon Organoid! This 3D Human Colon Organoid tubule, stained for tight junction (Occludin, green) and cell nuclei (blue), is the first ready-to-use adult stem cell-derived solution offered license-free for commercial use. We offer a fully characterized gastrointestinal model delivered straight to your lab, ensuring that it captures human intestinal processes and enables more accurate predictions of drug responses. Through our fee-for-services, we also build on top of this model in house, with the incorporation of other key cellular players and disease phenotypes at scale. In this upcoming webinar, learn how we capture the complexity of inflammatory bowel disease from multiple angles, enabling more accurate predictions of drug responses. Register for our live webinar: https://lnkd.in/edQbawru Learn more about the model: https://lnkd.in/egjYn_D6
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Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover I.- An imbalance in collagen production and degradation is necessary for the characteristic collagen accumulation in pulmonary fibrosis. This article describes a new mechanism for the regulation of collagen degradation. II.- Some concepts prior to reading the article: Phagocytic cells, such as macrophages, internalize collagen into phagocytic vesicles. Non-phagocytic cells can internalize collagen through specific collagen receptors, such as the collagen I/II receptor (CD49a). Extracellular collagen is taken up by cells through several mechanisms, including: (i) Integrins are transmembrane proteins that bind to different extracellular matrix proteins, including collagen. (ii) Scavenger receptors are a family of proteins that bind to modified molecules, such as oxidized collagen. (iii) Endocytosis is a process by which cells internalize molecules from the extracellular space through vesicles. Internalized collagen is degraded in lysosomes by lysosomal proteases, such as cathepsins. In the rough endoplasmic reticulum (RER), misfolded collagen is degraded by a process known as ERAD (endoplasmic reticulum-associated degradation). III.- In notes I will refer to extracellular proteolysis and the effects of fibrosis on the ability of cells to capture extracellular collagen to degrade it. IV.- Link: https://lnkd.in/dY32gWHH
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Inflammasomes are large cytosolic multiprotein complexes that assemble in response to detection of infection- or stress-associated stimuli and lead to the activation of caspase-1-mediated inflammatory responses, including cleavage and unconventional secretion of the leaderless proinflammatory cytokines IL-1β and IL-18, and initiation of an inflammatory form of cell death referred to as pyroptosis. #inflammasomes https://lnkd.in/gytvjw3g
Inflammasome - Wikipedia
en.wikipedia.org
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Community Pharmacist 💊 | COP UNDP | Leader of the Wave Community for Hearing Disability 🦻🏻💙 | Gifted Artist 🎨
#New_Insights_Into_How_Omega3_Fatty_Acids_Improve_NASH: Omega-3 polyunsaturated fatty acids reduce hepatic dysfunction in nonalcoholic steatohepatitis (NASH) by lowering betacellulin (BTC), a protein growth factor that contributes to liver fibrosis and progression to cirrhosis and liver cancer, new data suggest. Do you know any other benefits of Omega-3? And which foods can we find it in? Soon, I'll be discussing it. 🌸 #pharmacy #communitypharmacy #health #omega3 New Insights Into How Omega-3 Fatty Acids Improve NASH https://lnkd.in/dmpqkRUG Sent using the Medscape App for Android™
New Insights Into How Omega-3 Fatty Acids Improve NASH
medscape.com
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💖 Love is in the lab this Valentine's Day! Check out this heart-shaped image of primary hepatocytes, generated using RASTRUM in our tailored matrices for an advanced liver cell model. These primary hepatocytes aren't just for one day - they can maintain viability for over 14 days while preserving innate hepatocyte function, outperforming traditional 2D cultures. Our liver 3D model using primary human hepatocytes is revolutionising drug development and disease modelling. Discover more about our groundbreaking work here: https://buff.ly/46wXYxu Image details: Primary hepatocytes stained with phalloidin (cyan) and hoechst/nuclei (magenta) #LiverResearch #3Dcellmodels #3Dcellculture
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Dr. Michael Weinstein of Capital Digestive Care interviews Dr. Andreas Muehler, chief medical officer of Immunic Therapeutics, which is developing a clinical pipeline of orally administered, small molecule therapies for chronic inflammatory and autoimmune diseases. Join Dr. Weinstein and Dr. Muehler as they explore the challenges faced by patients with #celiacdisease and new innovations that will impact the way physicians treat their patients. #independentGI #gastroenterology #endoscopy
Episode #51: Treating Celiac Disease by Restoring a Healthy Gut Wall (clinical trial on an innovative treatment shows promise)
http://gastrobroadcast.com
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#cellmorphology #apoptosis #TBI 🔬 HoloMonitor M4 was used to study the cell morphology, including the cell area and thickness of the injured cells. #mondayread "GSK’872 Improves Prognosis of Traumatic Brain Injury by Switching Receptor-Interacting Serine/Threonine-Protein Kinase 3-dependent Necroptosis to Cysteinyl Aspartate Specific Proteinase-8-Dependent Apoptosis" ABOUT this #publication 🔍📄 https://bit.ly/3wRQWGS The paper presents a significant breakthrough in the understanding and treatment of Traumatic Brain Injury (TBI). The study explores the role of receptor-interacting serine/threonine-protein kinase 3 (RIP3)-mediated necroptosis in TBI. Necroptosis, a form of programmed cell death, has been observed in TBI, but its underlying mechanisms and roles were not well understood. The researchers established a cell-stretching injury and mouse TBI model to evaluate the relationships among necroptosis, apoptosis, inflammation, and TBI. They found that necroptosis mediated by RIP1, RIP3, and mixed lineage kinase domain-like protein (MLKL) was involved in secondary TBI. Interestingly, the inhibition of RIP3 by GSK’872, a specific inhibitor, blocked necroptosis and reduced the activity of Akt/mTOR, leading to the alleviation of inflammation by reducing the levels of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3). Moreover, the inhibition of RIP3 by GSK’872 promoted the activity of cysteinyl aspartate-specific proteinase-8 (Caspase-8), an enzyme involved in apoptosis and inflammation1. The results suggest that RIP3 inhibition could improve the prognosis of TBI by attenuating inflammation by switching RIP3-dependent necroptosis to Caspase-8-dependent apoptosis. #holomonitor #QPI
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Clonal hematopoiesis driven by mutated DNMT3A promotes inflammatory bone loss https://lnkd.in/e32kNzuj
Clonal hematopoiesis driven by mutated DNMT3A promotes inflammatory bone loss
cell.com
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#ScientificSaturday 🔬Diosmin ― is a flavonoid compound primarily derived from the citrus family plants, notably present in the pericarp of various citrus fruits. It is extensively used in the medical field for its vascular-protective properties, including treating chronic venous insufficiency, hemorrhoids, lymphedema, and varicose veins. Diosmin's therapeutic effects stem from its ability to improve venous tone, enhance lymphatic drainage, reduce capillary fragility, and inhibit inflammatory responses. Furthermore, it has been shown to exert antioxidant, anti-inflammatory, and anti-apoptotic activities, making it beneficial in a wider range of disorders beyond vascular issues. ❗This study investigates the neuroprotective effects of #Diosmin (DIOS) against #Doxorubicin (DOX)-induced chemobrain in male rats. Doxorubicin, a potent chemotherapy agent, commonly causes cognitive impairments known as chemobrain. To explore potential remedies, researchers administered DIOS to rats subjected to DOX, monitoring cognitive performance and brain neurochemical statuses. The findings revealed that DIOS significantly improved cognitive functions in DOX-treated rats by enhancing exploration of novel objects and ameliorating DOX-induced oxidative stress, inflammation, and apoptosis in the brain. DIOS treatment resulted in decreased expression of inflammatory and apoptotic markers, restoration of brain metabolic enzyme activities, increased levels of neurotransmitters, and reduced α-synuclein and PON1 enzyme activity. The study concludes that DIOS effectively shields the brain from the adverse effects of DOX, offering a promising approach to mitigating chemobrain through oxidative stress inhibition, autophagy modulation, and down-regulation of inflammatory and apoptotic pathways. BioPharma Services Inc. has previously completed multiple clinical trials on Diosmin. Trust our world-class Pharmacokinetic team with your next #Phase1, BA/BE or Human Abuse Liability (#HAL) drug development project. Read the full blog here: 👇 https://hubs.li/Q02r5vM90 Discover our Services: 👇 https://hubs.li/Q02r55Mq0 #clinicalresearch #biopharma #drugdevelopment #drugresearch #cro #clinicaltrials
NEAT1_1 confers gefitinib resistance in lung adenocarcinoma through promoting AKR1C1-mediated ferroptosis defence - Cell Death Discovery
sciencedirect.com
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