System, Method and Software for Calculation of a Cannabis Drug Efficiency Index for the Reduction of Inflammation
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Limited Presence of IL-22 Binding Protein, a Natural IL-22 Inhibitor, Strengthens Psoriatic Skin Inflammation
Limited Presence of IL-22 Binding Protein, a Natural IL-22 Inhibitor, Strengthens Psoriatic Skin Inflammation This information is current as Jérôme C. Martin, Kerstin Wolk, Gaëlle Bériou, Ahmed of September 25, 2021. Abidi, Ellen Witte-Händel, Cédric Louvet, Georgios Kokolakis, Lucile Drujont, Laure Dumoutier, Jean-Christophe Renauld, Robert Sabat and Régis Josien J Immunol 2017; 198:3671-3678; Prepublished online 29 March 2017; Downloaded from doi: 10.4049/jimmunol.1700021 http://www.jimmunol.org/content/198/9/3671 References This article cites 47 articles, 12 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/198/9/3671.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 25, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2017 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Limited Presence of IL-22 Binding Protein, a Natural IL-22 Inhibitor, Strengthens Psoriatic Skin Inflammation Je´roˆme C. -
Mir-338-3P Is Regulated by Estrogens Through GPER in Breast Cancer Cells and Cancer-Associated Fibroblasts (Cafs)
cells Article miR-338-3p Is Regulated by Estrogens through GPER in Breast Cancer Cells and Cancer-Associated Fibroblasts (CAFs) Adele Vivacqua 1,*, Anna Sebastiani 1, Anna Maria Miglietta 2, Damiano Cosimo Rigiracciolo 1, Francesca Cirillo 1, Giulia Raffaella Galli 1, Marianna Talia 1, Maria Francesca Santolla 1, Rosamaria Lappano 1, Francesca Giordano 1, Maria Luisa Panno 1 and Marcello Maggiolini 1,* 1 Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy; [email protected] (A.S.); [email protected] (D.C.R.); [email protected] (F.C.); [email protected] (G.R.G.); [email protected] (M.T.); [email protected] (M.F.S.); [email protected] (R.L.); [email protected] (F.G.); [email protected] (M.L.P.) 2 Regional HospitalCosenza, 87100 Cosenza, Italy; [email protected] * Correspondence: [email protected] (A.V.); [email protected] (M.M.); Tel.: +39-0984-493-048 (A.V.); +39-0984-493-076 (M.M.) Received: 12 October 2018; Accepted: 7 November 2018; Published: 9 November 2018 Abstract: Estrogens acting through the classic estrogen receptors (ERs) and the G protein estrogen receptor (GPER) regulate the expression of diverse miRNAs, small sequences of non-coding RNA involved in several pathophysiological conditions, including breast cancer. In order to provide novel insights on miRNAs regulation by estrogens in breast tumor, we evaluated the expression of 754 miRNAs by TaqMan Array in ER-negative and GPER-positive SkBr3 breast cancer cells and cancer-associated fibroblasts (CAFs) upon 17β-estradiol (E2) treatment. Various miRNAs were regulated by E2 in a peculiar manner in SkBr3 cancer cells and CAFs, while miR-338-3p displayed a similar regulation in both cell types. -
Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice
Loyola University Chicago Loyola eCommons Biology: Faculty Publications and Other Works Faculty Publications 2013 Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice Mihaela Palicev Gunter P. Wagner James P. Noonan Benedikt Hallgrimsson James M. Cheverud Loyola University Chicago, [email protected] Follow this and additional works at: https://ecommons.luc.edu/biology_facpubs Part of the Biology Commons Recommended Citation Palicev, M, GP Wagner, JP Noonan, B Hallgrimsson, and JM Cheverud. "Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice." Genome Biology and Evolution 5(10), 2013. This Article is brought to you for free and open access by the Faculty Publications at Loyola eCommons. It has been accepted for inclusion in Biology: Faculty Publications and Other Works by an authorized administrator of Loyola eCommons. For more information, please contact [email protected]. This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License. © Palicev et al., 2013. GBE Genomic Correlates of Relationship QTL Involved in Fore- versus Hind Limb Divergence in Mice Mihaela Pavlicev1,2,*, Gu¨ nter P. Wagner3, James P. Noonan4, Benedikt Hallgrı´msson5,and James M. Cheverud6 1Konrad Lorenz Institute for Evolution and Cognition Research, Altenberg, Austria 2Department of Pediatrics, Cincinnati Children‘s Hospital Medical Center, Cincinnati, Ohio 3Yale Systems Biology Institute and Department of Ecology and Evolutionary Biology, Yale University 4Department of Genetics, Yale University School of Medicine 5Department of Cell Biology and Anatomy, The McCaig Institute for Bone and Joint Health and the Alberta Children’s Hospital Research Institute for Child and Maternal Health, University of Calgary, Calgary, Canada 6Department of Anatomy and Neurobiology, Washington University *Corresponding author: E-mail: [email protected]. -
Supplementary Material
Coagulation & Its Disorders SUPPLEMENTARY APPENDIX Dexamethasone promotes durable factor VIII-specific tolerance in hemophilia A mice via thymic mechanisms Maria T. Georgescu, 1 Paul C. Moorehead, 2,3 Alice S. van Velzen, 4 Kate Nesbitt, 1 Birgit M. Reipert, 5 Katharina N. Steinitz, 5 Maria Schuster, 5 Christine Hough 1 and David Lillicrap 1 1Department of Pathology and Molecular Medicine, Queen’s University, Kingston, ON, Canada; 2Janeway Children’s Health and Reha - bilitation Centre, St. John’s, NL, Canada; 3Faculty of Medicine, Memorial University, St. John’s, NL, Canada; 4Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children’s Hospital, Amsterdam, the Netherlands and 5Baxalta Innovations GmbH, Vienna, Austria ©2018 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2018.189852 Received: January 30, 2018. Accepted: April 19, 2018. Pre-published: April 19, 2018. Correspondence: [email protected] Supplementary Material 100 80 60 40 20 Anti-VWF IgG Positive IgG Mice (%)Anti-VWF 0 FVIII/FVIII FVIII+Dex/FVIII FVIII+Dex/intFVIII+FVIII n=4 n=13 n=12 Figure S1. Administration of Dex during initial FVIII exposure does not impair the immune response to VWF. Anti-VWF IgG incidence at week 22, following exposure to VWF (Week 18-21) in mice initially treated with FVIII or FVIII+Dex and with no evidence of anti-FVIII IgG at week 4. Table S1. Genes down-regulated following FVIII+Dex treatment. Transcript Count Ratio Gene Name FVIII+Dex vs FVIII Dex vs HBSS Ccr4 -5.82 -14.45 Rag1 -4.18 -16.00 Cd69 -3.51 -4.40 Ccr9 -3.46 -9.90 Slamf1 -3.20 -6.50 Cd8b1 -3.18 -7.77 Cd40lg -2.99 -2.56 Cxcl1 -2.90 -2.37 Rag2 -2.84 -9.21 Rorc -2.78 -5.65 Cd8a -2.67 -7.74 Cd4 -2.66 -5.06 Il9 -2.64 -2.26 Il12b -2.60 -2.49 Bcl6 -2.59 -3.30 Il27 -2.54 -3.06 Mr1 -2.48 -3.26 Sh2d1a -2.39 -6.68 Il13 -2.23 -2.38 Ccl22 -2.22 -2.51 Il16 -2.22 -3.05 Socs1 -2.20 -4.55 Card9 -2.12 -3.32 Cxcr4 -2.12 -3.98 Tcf7 -2.12 -5.16 Lck -2.06 -4.47 Icam2 -2.02 -3.09 Table S2. -
KLF2 Induced
UvA-DARE (Digital Academic Repository) The transcription factor KLF2 in vascular biology Boon, R.A. Publication date 2008 Link to publication Citation for published version (APA): Boon, R. A. (2008). The transcription factor KLF2 in vascular biology. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:23 Sep 2021 Supplementary data: Genes induced by KLF2 Dekker et al. LocusLink Accession Gene Sequence Description Fold p-value ID number symbol change (FDR) 6654 AK022099 SOS1 cDNA FLJ12037 fis, clone HEMBB1001921. 100.00 5.9E-09 56999 AF086069 ADAMTS9 full length insert cDNA clone YZ35C05. 100.00 1.2E-09 6672 AF085934 SP100 full length insert cDNA clone YR57D07. 100.00 6.7E-13 9031 AF132602 BAZ1B Williams Syndrome critical region WS25 mRNA, partial sequence. -
IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis Hannes Lindahl, André O
IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis Hannes Lindahl, André O. Guerreiro-Cacais, Sahl Khalid Bedri, Mathias Linnerbauer, Magdalena Lindén, Nada This information is current as Abdelmagid, Karolina Tandre, Claire Hollins, Lorraine of September 24, 2021. Irving, Colin Glover, Clare Jones, Lars Alfredsson, Lars Rönnblom, Ingrid Kockum, Mohsen Khademi, Maja Jagodic and Tomas Olsson J Immunol published online 10 July 2019 Downloaded from http://www.jimmunol.org/content/early/2019/07/09/jimmun ol.1900400 Supplementary http://www.jimmunol.org/content/suppl/2019/07/10/jimmunol.190040 http://www.jimmunol.org/ Material 0.DCSupplemental Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 24, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2019 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published -
Chemical Tools for Studying Lipid-Binding Class a G Protein–Coupled Receptors
1521-0081/69/3/316–353$25.00 https://doi.org/10.1124/pr.116.013243 PHARMACOLOGICAL REVIEWS Pharmacol Rev 69:316–353, July 2017 Copyright © 2017 by The American Society for Pharmacology and Experimental Therapeutics ASSOCIATE EDITOR: STEPHEN P. H. ALEXANDER Chemical Tools for Studying Lipid-Binding Class A G Protein–Coupled Receptors Anna Cooper, Sameek Singh, Sarah Hook, Joel D. A. Tyndall, and Andrea J. Vernall School of Pharmacy, University of Otago, Dunedin, New Zealand Abstract. ....................................................................................317 I. Introduction. ..............................................................................317 A. Cannabinoid Receptor . ..................................................................317 1. Ligand Classes. ......................................................................318 B. Free Fatty Acid Receptor ................................................................320 1. Ligand Classes. ......................................................................320 C. Lysophospholipid Receptors. ............................................................321 1. Ligand Classes. ......................................................................321 D. Prostanoid Receptor . ..................................................................321 Downloaded from 1. Ligand Classes. ......................................................................322 E. Leukotriene Receptor . ..................................................................322 1. Ligand Classes. ......................................................................322 -
Oncostatin M Exhibit Elevated Responsiveness to IL-31 Receptor
IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M This information is current as Janine Bilsborough, Sherri Mudri, Eric Chadwick, Brandon of September 28, 2021. Harder and Stacey R. Dillon J Immunol 2010; 185:6023-6030; Prepublished online 18 October 2010; doi: 10.4049/jimmunol.0902769 http://www.jimmunol.org/content/185/10/6023 Downloaded from References This article cites 29 articles, 6 of which you can access for free at: http://www.jimmunol.org/content/185/10/6023.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 28, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M Janine Bilsborough,1 Sherri Mudri,1 Eric Chadwick,2 Brandon Harder,3 and Stacey R. Dillon IL-31 signals through the heterodimeric receptor IL-31RA and oncostatin M receptor (OSMR), and has been linked with the development of atopic dermatitis, a Th2 cytokine-associated disease in humans. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Profiling G Protein-Coupled Receptors of Fasciola Hepatica Identifies Orphan Rhodopsins Unique to Phylum Platyhelminthes
bioRxiv preprint doi: https://doi.org/10.1101/207316; this version posted October 23, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Profiling G protein-coupled receptors of Fasciola hepatica 2 identifies orphan rhodopsins unique to phylum 3 Platyhelminthes 4 5 Short title: Profiling G protein-coupled receptors (GPCRs) in Fasciola hepatica 6 7 Paul McVeigh1*, Erin McCammick1, Paul McCusker1, Duncan Wells1, Jane 8 Hodgkinson2, Steve Paterson3, Angela Mousley1, Nikki J. Marks1, Aaron G. Maule1 9 10 11 1Parasitology & Pathogen Biology, The Institute for Global Food Security, School of 12 Biological Sciences, Queen’s University Belfast, Medical Biology Centre, 97 Lisburn 13 Road, Belfast, BT9 7BL, UK 14 15 2 Institute of Infection and Global Health, University of Liverpool, Liverpool, UK 16 17 3 Institute of Integrative Biology, University of Liverpool, Liverpool, UK 18 19 * Corresponding author 20 Email: [email protected] 21 1 bioRxiv preprint doi: https://doi.org/10.1101/207316; this version posted October 23, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 22 Abstract 23 G protein-coupled receptors (GPCRs) are established drug targets. Despite their 24 considerable appeal as targets for next-generation anthelmintics, poor understanding 25 of their diversity and function in parasitic helminths has thwarted progress towards 26 GPCR-targeted anti-parasite drugs. -
The Role of High Density Lipoprotein Compositional and Functional Heterogeneity in Metabolic Disease
The role of high density lipoprotein compositional and functional heterogeneity in metabolic disease By Scott M. Gordon B.S. State University of New York College at Brockport October, 2012 A Dissertation Presented to the Faculty of The University of Cincinnati College of Medicine in partial fulfillment of the requirements for the Degree of Doctor of Philosophy from the Pathobiology and Molecular Medicine graduate program W. Sean Davidson Ph.D. (Chair) David Askew Ph.D. Professor and Thesis Chair Professor Department of Pathology Department of Pathology University of Cincinnati University of Cincinnati Francis McCormack M.D. Gangani Silva Ph.D. Professor Assistant Professor Department of Pathology Department of Pathology University of Cincinnati University of Cincinnati Jason Lu Ph.D. Assistant Professor Division of Bioinformatics Cincinnati Children’s Hospital i Abstract High density lipoproteins (HDL) are complexes of phospholipid, cholesterol and protein that circulate in the blood. Epidemiological studies have demonstrated a strong inverse correlation between plasma levels of HDL associated cholesterol (HDL-C) and the incidence of cardiovascular disease (CVD). Clinically, HDL-C is often measured and used in combination with low density lipoprotein cholesterol (LDL-C) to assess overall cardiovascular health. HDL have been shown to possess a wide variety of functional attributes which likely contribute to this protection including anti-inflammatory and anti- oxidative properties and the ability to remove excess cholesterol from peripheral tissues and deliver it to the liver for excretion, a process known as reverse cholesterol transport. This functional diversity might be explained by the complexity of HDL composition. Recent studies have taken advantage of advances in mass spectrometry technologies to characterize the proteome of total HDL finding that over 50 different proteins can associate with these particles. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of