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Type I Interferons and the Development of Impaired Vascular Function and Repair in Human and Murine Lupus
Type I Interferons and the Development of Impaired Vascular Function and Repair in Human and Murine Lupus by Seth G Thacker A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Immunology) in The University of Michigan 2011 Doctoral Committee: Associate Professor Mariana J. Kaplan, Chair Professor David A. Fox Professor Alisa E. Koch Professor Matthias Kretzler Professor Nicholas W. Lukacs Associate Professor Daniel T. Eitzman © Seth G Thacker 2011 Sharon, this work is dedicated to you. This achievement is as much yours as it is mine. Your support through all six years of this Ph.D. process has been incredible. You put up with my countless miscalculations on when I would finish experiments, and still managed to make me and our kids feel loved and special. Without you this would have no meaning. Sharon, you are the safe harbor in my life. ii Acknowledgments I have been exceptionally fortunate in my time here at the University of Michigan. I have been able to interact with so many supportive people over the years. I would like to express my thanks and admiration for my mentor. Mariana has taught me so much about writing, experimental design and being a successful scientist in general. I could never have made it here without her help. I would also like to thank Mike Denny. He had a hand in the beginning of all of my projects in one way or another, and was always quick and eager to help in whatever way he could. He really made my first year in the lab successful. -
WHU Otto Beisheim School of Management Handbook
International Student Handbook Welcome to WHU Message from the Dean Welcome to WHU – Otto Beisheim School of Management. WHU is a private, state-accredited business school of university rank located in the center of Germany – in Vallendar, just outside of Koblenz. The school has frequently been ranked top in international rankings, such as the renowned Financial Times rankings and the Wall Street Jour- nal ranking and is accredited by AACSB, EQUIS and FIBAA. The school’s main mission is to provide first-class education in management at all levels. We are known for the international orientation of our programs, our international joint ventures we have had for a number of years and our extensive student exchange programs. Our students have access to a network of partner universities which has grown to more than 180 first-class institutions world- wide. Student exchanges are a very important element in our programs, because studying abroad deepens a student’s knowledge of other cultures and increases both flexibility and mobility. Just as WHU students spend considerable time abroad (one term at the undergraduate level and another term at the graduate level), we are happy to welcome many students from our partner in- stitutions at our school and to offer them a unique learning environment. Currently, about 25% of the students on our campus come from abroad and we are proud that their number is growing con- tinuously. We appreciate very much the contributions of our exchange students both in the class- room and outside, because they enrich the discussion and give our campus life an international flair. -
Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7 -
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 -
Supplementary Material
Supplementary Material Table S1: Significant downregulated KEGGs pathways identified by DAVID following exposure to five cinnamon- based phenylpropanoids (p < 0.05). p-value Term: Genes (Benjamini) Cytokine-cytokine receptor interaction: FASLG, TNFSF14, CXCL11, IL11, FLT3LG, CCL3L1, CCL3L3, CXCR6, XCR1, 2.43 × 105 RTEL1, CSF2RA, TNFRSF17, TNFRSF14, CCNL2, VEGFB, AMH, TNFRSF10B, INHBE, IFNB1, CCR3, VEGFA, CCR2, IL12A, CCL1, CCL3, CXCL5, TNFRSF25, CCR1, CSF1, CX3CL1, CCL7, CCL24, TNFRSF1B, IL12RB1, CCL21, FIGF, EPO, IL4, IL18R1, FLT1, TGFBR1, EDA2R, HGF, TNFSF8, KDR, LEP, GH2, CCL13, EPOR, XCL1, IFNA16, XCL2 Neuroactive ligand-receptor interaction: OPRM1, THRA, GRIK1, DRD2, GRIK2, TACR2, TACR1, GABRB1, LPAR4, 9.68 × 105 GRIK5, FPR1, PRSS1, GNRHR, FPR2, EDNRA, AGTR2, LTB4R, PRSS2, CNR1, S1PR4, CALCRL, TAAR5, GABRE, PTGER1, GABRG3, C5AR1, PTGER3, PTGER4, GABRA6, GABRA5, GRM1, PLG, LEP, CRHR1, GH2, GRM3, SSTR2, Chlorogenic acid Chlorogenic CHRM3, GRIA1, MC2R, P2RX2, TBXA2R, GHSR, HTR2C, TSHR, LHB, GLP1R, OPRD1 Hematopoietic cell lineage: IL4, CR1, CD8B, CSF1, FCER2, GYPA, ITGA2, IL11, GP9, FLT3LG, CD38, CD19, DNTT, 9.29 × 104 GP1BB, CD22, EPOR, CSF2RA, CD14, THPO, EPO, HLA-DRA, ITGA2B Cytokine-cytokine receptor interaction: IL6ST, IL21R, IL19, TNFSF15, CXCR3, IL15, CXCL11, TGFB1, IL11, FLT3LG, CXCL10, CCR10, XCR1, RTEL1, CSF2RA, IL21, CCNL2, VEGFB, CCR8, AMH, TNFRSF10C, IFNB1, PDGFRA, EDA, CXCL5, TNFRSF25, CSF1, IFNW1, CNTFR, CX3CL1, CCL5, TNFRSF4, CCL4, CCL27, CCL24, CCL25, CCL23, IFNA6, IFNA5, FIGF, EPO, AMHR2, IL2RA, FLT4, TGFBR2, EDA2R, -
WO 2018/067991 Al 12 April 2018 (12.04.2018) W !P O PCT
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2018/067991 Al 12 April 2018 (12.04.2018) W !P O PCT (51) International Patent Classification: achusetts 021 15 (US). THE BROAD INSTITUTE, A61K 51/10 (2006.01) G01N 33/574 (2006.01) INC. [US/US]; 415 Main Street, Cambridge, Massachu C07K 14/705 (2006.01) A61K 47/68 (2017.01) setts 02142 (US). MASSACHUSETTS INSTITUTE OF G01N 33/53 (2006.01) TECHNOLOGY [US/US]; 77 Massachusetts Avenue, Cambridge, Massachusetts 02139 (US). (21) International Application Number: PCT/US2017/055625 (72) Inventors; and (71) Applicants: KUCHROO, Vijay K. [IN/US]; 30 Fairhaven (22) International Filing Date: Road, Newton, Massachusetts 02149 (US). ANDERSON, 06 October 2017 (06.10.2017) Ana Carrizosa [US/US]; 110 Cypress Street, Brookline, (25) Filing Language: English Massachusetts 02445 (US). MADI, Asaf [US/US]; c/o The Brigham and Women's Hospital, Inc., 75 Francis (26) Publication Language: English Street, Boston, Massachusetts 021 15 (US). CHIHARA, (30) Priority Data: Norio [US/US]; c/o The Brigham and Women's Hospital, 62/405,835 07 October 2016 (07.10.2016) US Inc., 75 Francis Street, Boston, Massachusetts 021 15 (US). REGEV, Aviv [US/US]; 15a Ellsworth Ave, Cambridge, (71) Applicants: THE BRIGHAM AND WOMEN'S HOSPI¬ Massachusetts 02139 (US). SINGER, Meromit [US/US]; TAL, INC. [US/US]; 75 Francis Street, Boston, Mass c/o The Broad Institute, Inc., 415 Main Street, Cambridge, (54) Title: MODULATION OF NOVEL IMMUNE CHECKPOINT TARGETS CD4 FIG. -
Case No COMP/M.4942 - NOKIA / NAVTEQ
EN This text is made available for information purposes only. A summary of this decision is published in all Community languages in the Official Journal of the European Union. Case No COMP/M.4942 - NOKIA / NAVTEQ Only the English text is authentic. REGULATION (EC) No 139/2004 MERGER PROCEDURE Article 8 (1) Date: 02/VII/2008 COMMISSION OF THE EUROPEAN COMMUNITIES Brussels, 02/VII/2008 C (2008) 3328 PUBLIC VERSION COMMISSION DECISION of 02/VII/2008 declaring a concentration to be compatible with the common market and the EEA Agreement (Case No COMP/M.4942 - NOKIA/ NAVTEQ) COMMISSION DECISION of 02/VII/2008 declaring a concentration to be compatible with the common market and the EEA Agreement (Case No COMP/M.4942 - NOKIA/ NAVTEQ) (Only the English text is authentic) (Text with EEA relevance) THE COMMISSION OF THE EUROPEAN COMMUNITIES, Having regard to the Treaty establishing the European Community, Having regard to the Agreement on the European Economic Area, and in particular Article 57 thereof, Having regard to Council Regulation (EC) No 139/2004 of 20 January 2004 on the control of concentrations between undertakings1, and in particular Article 8(1) thereof, Having regard to the Commission's decision of 28 March 2008 to initiate proceedings in this case, After consulting the Advisory Committee on Concentrations, Having regard to the final report of the Hearing Officer in this case, Whereas: I. INTRODUCTION (1) On 19 February 2008, the Commission received a notification of a proposed concentration pursuant to Article 4 and following a referral pursuant to Article 4(5) of Council Regulation (EC) No 139/2004 ("the Merger Regulation") by which the undertaking Nokia Inc. -
Prevalent Homozygous Deletions of Type I Interferon and Defensin Genes in Human Cancers Associate with Immunotherapy Resistance
Author Manuscript Published OnlineFirst on April 4, 2018; DOI: 10.1158/1078-0432.CCR-17-3008 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Prevalent Homozygous Deletions of Type I Interferon and Defensin Genes in Human Cancers Associate with Immunotherapy Resistance Zhenqing Ye1; Haidong Dong2,3; Ying Li1; Tao Ma1,4; Haojie Huang4; Hon-Sing Leong4; Jeanette Eckel-Passow1; Jean-Pierre A. Kocher1; Han Liang5; LiguoWang1,4,* 1Division of Biomedical Statistics and Informatics, Department of Health Sciences, Mayo Clinic, Rochester, Minnesota 55905, United States of America 2Department of Immunology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, United States of America 3Department of Urology, Mayo Clinic, Rochester, Minnesota 55905, United States of America 4Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, United States of America 5Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, United States of America Running title: Pervasive Deletion of Interferon/Defensin in Human Cancers Keywords: Homozygous deletion, Type-I interferon, Defensin, immunotherapy resistance, cancer * Correspondence to: Liguo Wang, Ph.D. Associate Professor Division of Biomedical Statistics and Informatics, Mayo Clinic 200 1st St SW Rochester, MN 55905, USA Phone: +1-507-284-8728 Fax: +1-507-284-0745 Email: [email protected] The authors declare no potential conflicts of interest. 1 Downloaded from clincancerres.aacrjournals.org on September 29, 2021. © 2018 American Association for Cancer Research. Author Manuscript Published OnlineFirst on April 4, 2018; DOI: 10.1158/1078-0432.CCR-17-3008 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. -
David Thesis 2007
The Role of Nuclear Factor-B in -Cell Survival and Function David Liuwantara A submission to the University of New South Wales in candidature for the degree of Doctor of Philosophy Gene Therapy and Autoimmunity Research Program Department of Inflammation and Immunology Garvan Institute of Medical Research Darlinghurst, Sydney, Australia November 2007 Statement of Originality ‘I hereby declare that this submission is my own work and to the best of my knowledge it contains no materials previously published or written by another person, or substantial proportions of material which have been accepted for the award of any other degree or diploma at UNSW or any other educational institution, except where due acknowledgement is made in the thesis. Any contribution made to the research by others, with whom I have worked at UNSW or elsewhere, is explicitly acknowledged in the thesis. I also declare that the intellectual content of this thesis is the product of my own work, except to the extent that assistance from others in the project’s design and conception or in style, presentation and linguistic expression is acknowleged.’ Signed …………………………………………………………… In Christ alone will I glory Though I could pride myself in battles won For I've been blessed beyond measure And by His strength alone I overcome Oh I could stop and count successes Like diamonds in my hands But those trophies could not equal To the grace by which I stand In Christ alone will I glory For only by His grace I am redeemed And only His tender mercy Could reach beyond my weakness to my need And now I seek no greater honor Than just to know Him more And to count my gains But losses to the glory of my Lord In Christ alone I place my trust And find my glory in the power of the cross In every victory let it be said of me My source of strength, my source of hope is Christ alone In Christ Alone by: Don Koch and Shawn Craig Paragon Music Corp © 1990 BMG Music Pty. -
GEP Analysis Validates High Risk MDS and Acute Myeloid Leukemia Post
Guerenne et al. Journal of Hematology & Oncology (2016) 9:5 DOI 10.1186/s13045-016-0235-8 RESEARCH Open Access GEP analysis validates high risk MDS and acute myeloid leukemia post MDS mice models and highlights novel dysregulated pathways Laura Guerenne1,2, Stéphanie Beurlet1,2, Mohamed Said3, Petra Gorombei1,2, Carole Le Pogam1,2, Fabien Guidez1,2, Pierre de la Grange4, Nader Omidvar5, Valérie Vanneaux6, Ken Mills7, Ghulam J Mufti3, Laure Sarda-Mantel8,9, Maria Elena Noguera10, Marika Pla1,2,11, Pierre Fenaux1,2,10, Rose Ann Padua1,2,10†, Christine Chomienne1,2,10† and Patricia Krief1,2* Abstract Background: In spite of the recent discovery of genetic mutations in most myelodysplasic (MDS) patients, the pathophysiology of these disorders still remains poorly understood, and only few in vivo models are available to help unravel the disease. Methods: We performed global specific gene expression profiling and functional pathway analysis in purified Sca1+ cells of two MDS transgenic mouse models that mimic human high-risk MDS (HR-MDS) and acute myeloid leukemia (AML) post MDS, with NRASD12 and BCL2 transgenes under the control of different promoters MRP8NRASD12/tethBCL-2 or MRP8[NRASD12/hBCL-2], respectively. Results: Analysis of dysregulated genes that were unique to the diseased HR-MDS and AML post MDS mice and not their founder mice pointed first to pathways that had previously been reported in MDS patients, including DNA replication/damage/repair, cell cycle, apoptosis, immune responses, and canonical Wnt pathways, further validating these models at the gene expression level. Interestingly, pathways not previously reported in MDS were discovered. -
Vegetation of Andean Wetlands (Bofedales) in Huascarán National Park, Peru
Vegetation of Andean wetlands (bofedales) in Huascarán National Park, Peru M.H. Polk1, K.R. Young1, A. Cano2 and B. León1,2 1Department of Geography & the Environment, The University of Texas at Austin, USA 2Museo de Historia Natural, Universidad Nacional Mayor de San Marcos, Lima, Perú _______________________________________________________________________________________ SUMMARY Hybrid terrestrial-aquatic ecosystems in the Andes, commonly known as bofedales, consist of both peatlands and wet meadows and line valley floors at elevations > 3800 m. Compared with similar ecosystems at lower altitudes and higher latitudes, the ecosystem processes and spatial patterns of bofedales are only just beginning to be understood. The research presented here provides the first exploratory and descriptive analysis of the biodiversity and place-to-place variation of vegetation in bofedales in three valleys inside Peru’s Huascarán National Park. Through vegetation surveys, we recorded 112 plant species in 29 families. Over a short geographical distance, a valley-to-valley comparison showed high dissimilarity in terms of species composition. Based on dominant life form and species composition, vegetation in bofedales can be grouped into five assemblages. Our preliminary analysis suggests that several abiotic factors could influence the floristic composition of bofedales: elevation, bulk density, percent organic matter, and cation exchange capacity. The findings of high valley-to-valley variation in species, soil and elevation influences may be useful to land managers of high mountain landscapes that are undergoing transformation related to glacier recession. While our findings advance research on tropical Andean bofedales, they also highlight the need for additional comprehensive investigations to fill gaps in knowledge about the tropical mountains of Latin America. -
Interferonsource.Com What's Inside New Products Research Tools Protocols & Tips Product Citations What's Your IFN-Α
Interferon Matters A quarterly newsletter by PBL InterferonSource interferonsource.com May 2007, Issue 2 u What’s Inside What’s Your IFN-a Type? New Products Are all Type I IFNs created equal? Of Mice and Men page 4 & 5 Type I Interferons were the first cytokines to be The biological significance of the expression of discovered. They are a family of homologous cytokines so many different IFN-a subtypes has yet to be Rhesus/Cynomolgus originally identified for their antiviral activity but have determined. However, reports suggest that they show IFN-a2 Subtype also been shown to have both anti-proliferative and quantitatively distinct anti-viral, anti-proliferative, immunomodulatory activities. In humans and mice and killer cell-stimulatory activities. It is therefore Mouse IFN-a4 Subtype they are encoded by an intronless multigene family of importance for researchers to characterize and clustered on human chromosome 9 and murine study these IFN-a subtypes and their possible post- chromosome 4 respectively. translational modifications. Research Tools Also in both species there are multiple Interferon- The common models for IFN-a subtypes study are page 6 & 7 Alpha (IFN-a) genes and one Interferon-Beta (IFN-b) human and mouse. In 1998, Lawson et al showed that Human IFN-a gene. Other Type I Interferon genes described include there are in vivo differences in the antiviral activity of the Interferon-Omega (IFN-w) gene, murine limitin the mouse IFN-a subtypes.1 Using an experimental Multi-Subtype ELISA Kit gene, as well as the human/murine Interferon-Epilson, mouse model of IFN transgene expression in vivo, TM Interferon-Kappa, and Interferon-Tau (IFN-e, IFN-k, and the authors showed that mouse IFN-a1 has a greater iLite Human IFN-a Kit IFN-t).