Development of Non-Overlapping Multiplex ELISA Arrays for the Quantitative Measurement of 400 Human and 200 Mouse Proteins in Parallel
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Gene Expression Polarization
Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression This information is current as of September 27, 2021. Fernando O. Martinez, Siamon Gordon, Massimo Locati and Alberto Mantovani J Immunol 2006; 177:7303-7311; ; doi: 10.4049/jimmunol.177.10.7303 http://www.jimmunol.org/content/177/10/7303 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2006/11/03/177.10.7303.DC1 Material http://www.jimmunol.org/ References This article cites 61 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/177/10/7303.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 27, 2021 • No Triage! Every submission reviewed by practicing scientists • 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 © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression1 Fernando O. -
Freedom of Information Act Request – Reference Foi/13/116 New Drugs Added to Formulary
Freedom of Information Act Request – Reference FoI/13/116 New Drugs Added to Formulary Request details Please will you provide me with numbers of new drugs that your LHB has introduced over the past three years, listing the number of new drugs introduced by year in each of those years? Response 2010 = 41 2011 = 53 2012 = 71 2010 Generic Name 1. adalimumab, etanercept, infliximab, rituximab and abatacept 2. beclometasone and formoterol (Fostair®) 3. bortezomib (Velcade®) in combination with melphalan and prednisone 4. Brinzolamide/timolol (Azarga®) 5. bromocriptine 6. calcium and vitamin D3 (Calceos®) 7. calcium and vitamin D (Adcal D3 Dissolve®) 8. capecitabine 9. Carmellose eye drops (Optive®) 10. Certolizumab pegol 11. Darunavir (Prezista®▼) 12. epoetin alfa (Binocrit®) 13. epoetin theta (Eporatio®) 14. Eslicarbazepine acetate (Zebinix®) 15. Evicel 16. fentanyl buccal tablets (Effentora) 17. fentanyl intranasal spray (Instanyl®) 18. Fesoterodine (Toviaz®) 19. filgrastim (TevaGrastim®) 20. filgrastim (Zarzio®) 21. gefitinib 22. infliximab and adalimumab 23. liraglutide (Victoza®) 24. Loperamide tablets 25. losartan 26. Mepilex® Ag 27. Movicol Paediatric 28. Nebuchamber 29. paclitaxel albumin (Abraxane®) monotherapy 30. pemetrexed 31. Plerixafor (Mozobil®q) 32. pramipexole prolonged release (Mirapexin®) 33. Prontosan® wound irrigation solution and gel 34. quinagolide (Norprolac®) 35. raltegravir (Isentress®) 36. rituximab sildenafil (Revatio®) tablets 2010 Generic Name 37. sodium chloride (7%) Nebusal® 38. somatropin (NutropinAq®) 39. Topotecan 40. Trabectedin 41. Xamiol 2011 Generic Name 1. artemether and lumefantrine (Riamet®) 2. artesunate 3. atazanavir (Reyataz®) co-administered with low dose ritonavir 4. azacitidine 5. aztreonam (Azactam®) 6. bendamustine 7. Bivalirudin 8. Bortezomib 9. Calcium acetate and magnesium carbonate (Osvaren®) 10. darunavir (Prezista®) 11. -
FABP2 Ala54thr Polymorphism and Post-Training Changes of Body Composition and Biochemical Parameters in Caucasian Women
G C A T T A C G G C A T genes Article FABP2 Ala54Thr Polymorphism and Post-Training Changes of Body Composition and Biochemical Parameters in Caucasian Women Agata Leo ´nska-Duniec 1,*, Katarzyna Switała´ 1, Ildus I. Ahmetov 2,3 , Craig Pickering 4 , Myosotis Massidda 5 , Maciej Buryta 6, Andrzej Mastalerz 7 and Ewelina Maculewicz 7 1 Faculty of Physical Education, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland; [email protected] 2 Laboratory of Molecular Genetics, Kazan State Medical University, 420012 Kazan, Russia; [email protected] 3 Department of Physical Education, Plekhanov Russian University of Economics, 117997 Moscow, Russia 4 Institute of Coaching and Performance, School of Sport and Wellbeing, University of Central Lancashire, Preston PR1 2HE, UK; [email protected] 5 Department of Life and Environmental Sciences, University of Cagliari, 09124 Cagliari, Italy; [email protected] 6 Institute of Physical Culture Sciences, University of Szczecin, 70-453 Szczecin, Poland; [email protected] 7 Faculty of Physical Education, Jozef Pilsudski University of Physical Education in Warsaw, 00-968 Warsaw, Poland; [email protected] (A.M.); [email protected] (E.M.) * Correspondence: [email protected] Abstract: The functional FABP2 Ala54Thr polymorphism (rs1799883) is strongly associated with lipid Citation: Leo´nska-Duniec,A.; Switała,´ K.; Ahmetov, I.I.; Pickering, and carbohydrate metabolism, although the function of its potential modifying effect on training- C.; Massidda, M.; Buryta, M.; induced changes in obesity-related parameters is still unknown. The aim of the present study was Mastalerz, A.; Maculewicz, E. -
Endothelial Cells and the IGF System
L A Bach Endothelial cells as IGF targets 54:1 R1–R13 Review Endothelial cells and the IGF system Correspondence 1,2 Leon A Bach should be addressed to L A Bach 1Department of Medicine (Alfred), Monash University, Prahran 3181, Australia Email 2Department of Endocrinology and Diabetes, Alfred Hospital, Commercial Road, Melbourne 3004, Australia [email protected] Abstract Endothelial cells line blood vessels and modulate vascular tone, thrombosis, inflammatory Key Words responses and new vessel formation. They are implicated in many disease processes including " insulin-like growth factor atherosclerosis and cancer. IGFs play a significant role in the physiology of endothelial cells " binding protein by promoting migration, tube formation and production of the vasodilator nitric oxide. " receptor These actions are mediated by the IGF1 and IGF2/mannose 6-phosphate receptors and are " endothelial cell modulated by a family of high-affinity IGF binding proteins. IGFs also increase the number " angiogenesis and function of endothelial progenitor cells, which may contribute to protection from atherosclerosis. IGFs promote angiogenesis, and dysregulation of the IGF system may contribute to this process in cancer and eye diseases including retinopathy of prematurity and diabetic retinopathy. In some situations, IGF deficiency appears to contribute to endothelial dysfunction, whereas IGF may be deleterious in others. These differences may be due to tissue-specific endothelial cell phenotypes or IGFs having distinct roles in different phases of vascular disease. Further studies are therefore required to delineate the Journal of Molecular therapeutic potential of IGF system modulation in pathogenic processes. Endocrinology (2015) 54, R1–R13 Journal of Molecular Endocrinology Introduction Insulin-like growth factor 1 (IGF1) and IGF2 are essential metabolically active and regulate vascular tone, thrombosis, for normal pre- and postnatal growth and development inflammatory responses and new vessel formation. -
Complementary DNA Microarray Analysis of Chemokines and Their Receptors in Allergic Rhinitis RX Zhang,1 SQ Yu,2 JZ Jiang,3 GJ Liu3
RX Zhang, et al ORIGINAL ARTICLE Complementary DNA Microarray Analysis of Chemokines and Their Receptors in Allergic Rhinitis RX Zhang,1 SQ Yu,2 JZ Jiang,3 GJ Liu3 1 Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China 2 Department of Otolaryngology , Jinan General Hospital of PLA, Shandong, China 3 Department of Otolaryngology, Changhai Hospital, Second Military Medical University, Shanghai, China ■ Abstract Objective: To analyze the roles of chemokines and their receptors in the pathogenesis of allergic rhinitis by observing the complementary DNA (cDNA) expression of the chemokines and their receptors in the nasal mucosa of patients with and without allergic rhinitis, using gene chips. Methods: The total RNAs were isolated from the nasal mucosa of 20 allergic rhinitis patients and purifi ed to messenger RNAs, and then reversely transcribed to cDNAs and incorporated with samples of fl uorescence-labeled with Cy5-dUPT (rhinitis patient samples) or Cy3- dUTP (control samples of nonallergic nasal mucosa). Thirty-nine cDNAs of chemokines and their receptors were latticed into expression profi le chips, which were hybridized with probes and then scanned with the computer to study gene expression according to the different fl uorescence intensities. Results: The cDNAs of the following chemokines were upregulated: CCL1, CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL17, CCL18, CCL19, CCL24, and CX3CL1 in most of the allergic rhinitis sample chips. CCR2, CCR3, CCR4, CCR5, CCR8 and CX3CR1 were the highly expressed receptor genes. Low expression of CXCL4 was found in these tissues. Conclusion: The T helper cell (TH) immune system is not well regulated in allergic rhinitis. -
ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are The
0031-3998/07/6103-0267 PEDIATRIC RESEARCH Vol. 61, No. 3, 2007 Copyright © 2007 International Pediatric Research Foundation, Inc. Printed in U.S.A. ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are the Predominant FGF Ligands Expressed in Human Fetal Growth Plate Cartilage PAVEL KREJCI, DEBORAH KRAKOW, PERTCHOUI B. MEKIKIAN, AND WILLIAM R. WILCOX Medical Genetics Institute [P.K., D.K., P.B.M., W.R.W.], Cedars-Sinai Medical Center, Los Angeles, California 90048; Department of Obstetrics and Gynecology [D.K.] and Department of Pediatrics [W.R.W.], UCLA School of Medicine, Los Angeles, California 90095 ABSTRACT: Fibroblast growth factors (FGF) regulate bone growth, (G380R) or TD (K650E) mutations (4–6). When expressed at but their expression in human cartilage is unclear. Here, we deter- physiologic levels, FGFR3-G380R required, like its wild-type mined the expression of entire FGF family in human fetal growth counterpart, ligand for activation (7). Similarly, in vitro cul- plate cartilage. Using reverse transcriptase PCR, the transcripts for tivated human TD chondrocytes as well as chondrocytes FGF1, 2, 5, 8–14, 16–19, and 21 were found. However, only FGF1, isolated from Fgfr3-K644M mice had an identical time course 2, 17, and 19 were detectable at the protein level. By immunohisto- of Fgfr3 activation compared with wild-type chondrocytes and chemistry, FGF17 and 19 were uniformly expressed within the showed no receptor activation in the absence of ligand (8,9). growth plate. In contrast, FGF1 was found only in proliferating and hypertrophic chondrocytes whereas FGF2 localized predominantly to Despite the importance of the FGF ligand for activation of the resting and proliferating cartilage. -
ALCAM Regulates Mediolateral Retinotopic Mapping in the Superior Colliculus
15630 • The Journal of Neuroscience, December 16, 2009 • 29(50):15630–15641 Development/Plasticity/Repair ALCAM Regulates Mediolateral Retinotopic Mapping in the Superior Colliculus Mona Buhusi,1 Galina P. Demyanenko,1 Karry M. Jannie,2 Jasbir Dalal,1 Eli P. B. Darnell,1 Joshua A. Weiner,2 and Patricia F. Maness1 1Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, and 2Department of Biology, University of Iowa, Iowa City, Iowa 52242 ALCAM [activated leukocyte cell adhesion molecule (BEN/SC-1/DM-GRASP)] is a transmembrane recognition molecule of the Ig superfamily (IgSF) containing five Ig domains (two V-type, three C2-type). Although broadly expressed in the nervous and immune systems, few of its developmental functions have been elucidated. Because ALCAM has been suggested to interact with the IgSF adhesion molecule L1, a determi- nant of retinocollicular mapping, we hypothesized that ALCAM might direct topographic targeting to the superior colliculus (SC) by serving as a substrate within the SC for L1 on incoming retinal ganglion cell (RGC) axons. ALCAM was expressed in the SC during RGC axon targeting and on RGC axons as they formed the optic nerve; however, it was downregulated distally on RGC axons as they entered the SC. Axon tracing with DiI revealedpronouncedmistargetingofRGCaxonsfromthetemporalretinahalfofALCAMnullmicetoabnormallylateralsitesinthecontralateral SC, in which these axons formed multiple ectopic termination zones. ALCAM null mutant axons were -
Disruption of Fibroblast Growth Factor Signal
Cancer Therapy: Preclinical Disruption of Fibroblast Growth Factor Signal Pathway Inhibits the Growth of Synovial Sarcomas: Potential Application of Signal Inhibitors to MolecularTarget Therapy Ta t s u y a I s hi b e , 1, 2 Tomitaka Nakayama,2 Ta k e s h i O k a m o t o, 1, 2 Tomoki Aoyama,1Koichi Nishijo,1, 2 Kotaro Roberts Shibata,1, 2 Ya s u ko Shim a ,1, 2 Satoshi Nagayama,3 Toyomasa Katagiri,4 Yusuke Nakamura, 4 Takashi Nakamura,2 andJunya Toguchida 1 Abstract Purpose: Synovial sarcoma is a soft tissue sarcoma, the growth regulatory mechanisms of which are unknown.We investigatedthe involvement of fibroblast growth factor (FGF) signals in synovial sarcoma andevaluatedthe therapeutic effect of inhibiting the FGF signal. Experimental Design:The expression of 22 FGF and4 FGF receptor (FGFR) genes in18prima- ry tumors andfive cell lines of synovial sarcoma were analyzedby reverse transcription-PCR. Effects of recombinant FGF2, FGF8, andFGF18 for the activation of mitogen-activatedprotein kinase (MAPK) andthe growth of synovial sarcoma cell lines were analyzed.Growth inhibitory effects of FGFR inhibitors on synovial sarcoma cell lines were investigated in vitro and in vivo. Results: Synovial sarcoma cell lines expressedmultiple FGF genes especially those expressed in neural tissues, among which FGF8 showedgrowth stimulatory effects in all synovial sarcoma cell lines. FGF signals in synovial sarcoma induced the phosphorylation of extracellular signal ^ regulatedkinase (ERK1/2) andp38MAPK but not c-Jun NH 2-terminal kinase. Disruption of the FGF signaling pathway in synovial sarcoma by specific inhibitors of FGFR causedcell cycle ar- rest leading to significant growth inhibition both in vitro and in vivo.Growthinhibitionbythe FGFR inhibitor was associatedwith a down-regulation of phosphorylatedERK1/2 but not p38MAPK, andan ERK kinase inhibitor also showedgrowth inhibitory effects for synovial sar- coma, indicating that the growth stimulatory effect of FGF was transmitted through the ERK1/2. -
(Epoetin and Darbepoetin) for Treating Cancer Treatment-Induced Anaemia (Including Review of Technology Appraisal No
HEALTH TECHNOLOGY ASSESSMENT VOLUME 20 ISSUE 13 FEBRUARY 2016 ISSN 1366-5278 The effectiveness and cost-effectiveness of erythropoiesis-stimulating agents (epoetin and darbepoetin) for treating cancer treatment-induced anaemia (including review of technology appraisal no. 142): a systematic review and economic model Louise Crathorne, Nicola Huxley, Marcela Haasova, Tristan Snowsill, Tracey Jones-Hughes, Martin Hoyle, Simon Briscoe, Helen Coelho, Linda Long, Antonieta Medina-Lara, Ruben Mujica-Mota, Mark Napier and Chris Hyde DOI 10.3310/hta20130 The effectiveness and cost-effectiveness of erythropoiesis-stimulating agents (epoetin and darbepoetin) for treating cancer treatment-induced anaemia (including review of technology appraisal no. 142): a systematic review and economic model Louise Crathorne,1* Nicola Huxley,1 Marcela Haasova,1 Tristan Snowsill,1 Tracey Jones-Hughes,1 Martin Hoyle,1 Simon Briscoe,1 Helen Coelho,1 Linda Long,1 Antonieta Medina-Lara,2 Ruben Mujica-Mota,1 Mark Napier3 and Chris Hyde1 1Peninsula Technology Assessment Group (PenTAG), University of Exeter Medical School, Exeter, UK 2University of Exeter Medical School, Exeter, UK 3Royal Devon and Exeter Hospital, Exeter, UK *Corresponding author Declared competing interests of authors: none Published February 2016 DOI: 10.3310/hta20130 This report should be referenced as follows: Crathorne L, Huxley N, Haasova M, Snowsill T, Jones-Hughes T, Hoyle M, et al. The effectiveness and cost-effectiveness of erythropoiesis-stimulating agents (epoetin and darbepoetin) for treating cancer treatment-induced anaemia (including review of technology appraisal no. 142): a systematic review and economic model. Health Technol Assess 2016;20(13). Health Technology Assessment is indexed and abstracted in Index Medicus/MEDLINE, Excerpta Medica/EMBASE, Science Citation Index Expanded (SciSearch®) and Current Contents®/ Clinical Medicine. -
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. -
United States Patent (19) 11 Patent Number: 5,766,866 Center Et Al
USOO5766866A United States Patent (19) 11 Patent Number: 5,766,866 Center et al. 45) Date of Patent: Jun. 16, 1998 54 LYMPHOCYTE CHEMOATTRACTANT Center, et al. The Journal of Immunology. 128:2563-2568 FACTOR AND USES THEREOF (1982). 75 Inventors: David M. Center. Wellesley Hills; Cruikshank, et al. The Journal of Immunology, William W. Cruikshank. Westford; 138:3817-3823 (1987). Hardy Kornfeld, Brighton, all of Mass. Cruikshank, et al., The Journal of Immunology, 73) Assignee: Research Corporation Technologies, 146:2928-2934 (1991). Inc., Tucson, Ariz. Cruikshank, et al., EMBL Database. Accession No. M90301 (21) Appl. No.: 580,680 (1992). 22 Filed: Dec. 29, 1995 Cruikshank. et al. The Journal of Immunology, 128:2569-2574 (1982). Related U.S. Application Data Rand, et al., J. Exp. Med., 173:1521-1528 (1991). 60 Division of Ser. No. 480,156, Jun. 7, 1995, which is a continuation-in-part of Ser. No. 354,961, Dec. 13, 1994, Harlow (1988) Antibodies, a laboratory manual. Cold Spring which is a continuation of Ser. No. 68,949, May 21, 1993, Harbor Laboratory, 285, 287. abandoned. Waldman (1991) Science. vol. 252, 1657-1662. (51) Int. Cl. ....................... G01N 33/53; CO7K 1700; CO7K 16/00: A61K 45/05 Hams et al. (1993) TIBTECH Feb. 1993 vol. 111, 42-44. 52 U.S. Cl. ......................... 424/7.24; 435/7.1; 435/7.92: 435/975; 530/350:530/351; 530/387.1: Center, et al. (Feb. 1995) "The Lymphocyte Chemoattractant 530/388.23: 530/389.2: 424/85.1: 424/130.1 Factor”. J. Lab. Clin. Med. 125(2):167-172. -
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