“High-multiplex proteomics at the heart of multi-omic approaches to better understand human disease”
Olink – key component for multiomic strategies
Please join us for this free webinar, at which you will learn how high-muliplex proteomics using Olink’s PEA technology can be combined with other omics approaches to provide unique insights into human disease biology, paving the way for the development of next-generation therapies.
You will learn more about the latest Olink® Explore platform for high-multiplex protein biomarker discovery with readout on Illumina® Next Generation Sequencing systems, which enables the high-throughput measurement of ~1 500 proteins from less than 3 µL of biological sample, generating up to 1.3 million protein measurements per week from one NGS instrument.
You will also hear how SciLifeLab in Stockholm have set up the Olink platform and are able to provide multiplex protein biomarker analysis to scientists in Sweden.
Finally, we are also pleased to be joined by guest speakers who will present examples of how Olink’s protein biomarker technology is being used to provide unique insights into the biology underlying important human diseases.
Please note that if you are unable to view this event live, registrants will also be able to view an on-demand recording of the presentations after the event.
Sara Sadi (Olink) – Introduction and event overview
Per Svensson (Illumina) – “Accelerate your findings with MultiOmics”
Sara Sadi (Olink) – “Reveal Protein Biomarkers on an Easily Accessible Platform”
Claudia Fredolini (SciLifeLab, Stockholm) – “Cutting edge immuno-technologies in translational proteomics”
Martin Cornillet, PhD (Karolinska Institute, Stockholm) – “Deregulated peripheral proteome reveals NASH-specific signature identifying patient subgroups with distinct liver biology”
Professor Adil Mardinoglu (KTH Royal Institute of Technology, Stockholm) – “The characterization of the patients before and after the administration of the combined metabolic activators”
Sara Sadi (Olink) – Closing remarks
About our guest speakers
Bio: Martin finished his PhD in 2014 that concerned the study of specific autoantibodies in Rheumatoid arthritis (Toulouse, France). He is now a researcher at the Center of Infectious Medicine at Karolinska Institute, focusing on the development of Mass Cytometry to analyse immune cells, and particularly NK-cell phenotype and function in different contexts relating to liver physiology/pathophysiology. He likes cooking, practicing sports (karate, tennis, football) and is interested in art and music discovering.
Abstract: Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease. The prognosis is unpredictable with some patients progressing to nonalcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma. Besides limited understanding of biological processes leading to NASH, non-invasive diagnostic tools are also lacking. The peripheral immunoproteome in biopsy-proven NAFL (n=35) and NASH patients (n=35) compared to matched, healthy controls (n=15) was studied using proximity extension assay, supplemented with spatial and single cell hepatic transcriptome analysis. We identified 13 inflammatory serum proteins that, independent of comorbidities and fibrosis stage, distinguished NASH from NAFL. Analysis of co-expression patterns and biological networks further revealed NASH-specific biological perturbations indicative of temporal deregulation of IL-4/-13, -10, -18, and non-canonical NF-kb signaling. Of the identified inflammatory serum proteins, IL-18 and EN-RAGE as well as ST1A1 mapped to hepatic macrophages and periportal hepatocytes, respectively, at the single cell level. The inflammatory serum protein signature further permitted identification of biologically distinct subgroups of NASH patients. NASH patients have a distinct inflammatory serum protein signature, which can be mapped to the liver parenchyma, disease pathogenesis, and also identifies subgroups of NASH patients with altered liver biology.
Bio: Professor Adil Mardinoglu is an expert in the field of Systems Medicine, Systems Biology, Computational Biology and Bioinformatics. He has been recruited as a Professor of Systems Biology in Center for Host-Microbiome Interactions, King’s College London, UK where he leads a computational group. He also works as group leader in Science for Life Laboratory (Scilifelab), KTH-Royal Institute of Technology in Sweden and led a team of 25 researchers working in the area of computational biology, experimental biology and drug development to develop new treatment strategies for Metabolic diseases, Neurodegenerative diseases and a certain type of cancer
Presentation title: “The characterization of the patients before and after the administration of the combined metabolic activators”
Abstract: In animal experiments and human kinetic study, we found that supplementation of combined metabolic activators (CMAs) promotes the oxidation of fat, attenuates the resulting oxidative stress, activates mitochondria and eventually removes excess fat from the liver. We tested the safety and efficacy of CMAs in NAFLD and COVID-19 patients in placebo-controlled studies. We found that CMAs significantly decreased hepatic steatosis and levels of aspartate aminotransferase, alanine aminotransferase, uric acid, and creatinine whereas found no differences on these variables in the placebo group after adjustment for weight loss. We also found that supplementation of CMAs reduced the time to complete recovery significantly in the CMA group (6.6 vs 9.3 days) in phase 2 and (5.7 vs 9.2 days) in phase 3 trials compared to placebo group in COVID-19 patients. A comprehensive analysis of the blood proteome and metabolome revealed the major metabolic changes in NAFLD and COVID-19 patients. Plasma levels of proteins and metabolites associated with inflammation and antioxidant metabolism are significantly improved in patients treated with CMAs as compared to placebo. By integrating clinical data with plasma metabolomics and inflammatory proteomics, we revealed the underlying molecular mechanisms altered in NAFLD and COVID-19 patients.
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