Sourcebook in Forensic Serology, Immunology, and Biochemistry Usually Said That Antigens Are Substances Which Elicit an One Cross-React with the Others
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Supplementary Information Changes in the Plasma Proteome At
Supplementary Information Changes in the plasma proteome at asymptomatic and symptomatic stages of autosomal dominant Alzheimer’s disease Julia Muenchhoff1, Anne Poljak1,2,3, Anbupalam Thalamuthu1, Veer B. Gupta4,5, Pratishtha Chatterjee4,5,6, Mark Raftery2, Colin L. Masters7, John C. Morris8,9,10, Randall J. Bateman8,9, Anne M. Fagan8,9, Ralph N. Martins4,5,6, Perminder S. Sachdev1,11,* Supplementary Figure S1. Ratios of proteins differentially abundant in asymptomatic carriers of PSEN1 and APP Dutch mutations. Mean ratios and standard deviations of plasma proteins from asymptomatic PSEN1 mutation carriers (PSEN1) and APP Dutch mutation carriers (APP) relative to reference masterpool as quantified by iTRAQ. Ratios that significantly differed are marked with asterisks (* p < 0.05; ** p < 0.01). C4A, complement C4-A; AZGP1, zinc-α-2-glycoprotein; HPX, hemopexin; PGLYPR2, N-acetylmuramoyl-L-alanine amidase isoform 2; α2AP, α-2-antiplasmin; APOL1, apolipoprotein L1; C1 inhibitor, plasma protease C1 inhibitor; ITIH2, inter-α-trypsin inhibitor heavy chain H2. 2 A) ADAD)CSF) ADAD)plasma) B) ADAD)CSF) ADAD)plasma) (Ringman)et)al)2015)) (current)study)) (Ringman)et)al)2015)) (current)study)) ATRN↓,%%AHSG↑% 32028% 49% %%%%%%%%HC2↑,%%ApoM↓% 24367% 31% 10083%% %%%%TBG↑,%%LUM↑% 24256% ApoC1↓↑% 16565% %%AMBP↑% 11738%%% SERPINA3↓↑% 24373% C6↓↑% ITIH2% 10574%% %%%%%%%CPN2↓%% ↓↑% %%%%%TTR↑% 11977% 10970% %SERPINF2↓↑% CFH↓% C5↑% CP↓↑% 16566% 11412%% 10127%% %%ITIH4↓↑% SerpinG1↓% 11967% %%ORM1↓↑% SerpinC1↓% 10612% %%%A1BG↑%%% %%%%FN1↓% 11461% %%%%ITIH1↑% C3↓↑% 11027% 19325% 10395%% %%%%%%HPR↓↑% HRG↓% %%% 13814%% 10338%% %%% %ApoA1 % %%%%%%%%%GSN↑% ↓↑ %%%%%%%%%%%%ApoD↓% 11385% C4BPA↓↑% 18976%% %%%%%%%%%%%%%%%%%ApoJ↓↑% 23266%%%% %%%%%%%%%%%%%%%%%%%%%%ApoA2↓↑% %%%%%%%%%%%%%%%%%%%%%%%%%%%%A2M↓↑% IGHM↑,%%GC↓↑,%%ApoB↓↑% 13769% % FGA↓↑,%%FGB↓↑,%%FGG↓↑% AFM↓↑,%%CFB↓↑,%% 19143%% ApoH↓↑,%%C4BPA↓↑% ApoA4↓↑%%% LOAD/MCI)plasma) LOAD/MCI)plasma) LOAD/MCI)plasma) LOAD/MCI)plasma) (Song)et)al)2014)) (Muenchhoff)et)al)2015)) (Song)et)al)2014)) (Muenchhoff)et)al)2015)) Supplementary Figure S2. -
書 名 等 発行年 出版社 受賞年 備考 N1 Ueber Das Zustandekommen Der
書 名 等 発行年 出版社 受賞年 備考 Ueber das Zustandekommen der Diphtherie-immunitat und der Tetanus-Immunitat bei thieren / Emil Adolf N1 1890 Georg thieme 1901 von Behring N2 Diphtherie und tetanus immunitaet / Emil Adolf von Behring und Kitasato 19-- [Akitomo Matsuki] 1901 Malarial fever its cause, prevention and treatment containing full details for the use of travellers, University press of N3 1902 1902 sportsmen, soldiers, and residents in malarious places / by Ronald Ross liverpool Ueber die Anwendung von concentrirten chemischen Lichtstrahlen in der Medicin / von Prof. Dr. Niels N4 1899 F.C.W.Vogel 1903 Ryberg Finsen Mit 4 Abbildungen und 2 Tafeln Twenty-five years of objective study of the higher nervous activity (behaviour) of animals / Ivan N5 Petrovitch Pavlov ; translated and edited by W. Horsley Gantt ; with the collaboration of G. Volborth ; and c1928 International Publishing 1904 an introduction by Walter B. Cannon Conditioned reflexes : an investigation of the physiological activity of the cerebral cortex / by Ivan Oxford University N6 1927 1904 Petrovitch Pavlov ; translated and edited by G.V. Anrep Press N7 Die Ätiologie und die Bekämpfung der Tuberkulose / Robert Koch ; eingeleitet von M. Kirchner 1912 J.A.Barth 1905 N8 Neue Darstellung vom histologischen Bau des Centralnervensystems / von Santiago Ramón y Cajal 1893 Veit 1906 Traité des fiévres palustres : avec la description des microbes du paludisme / par Charles Louis Alphonse N9 1884 Octave Doin 1907 Laveran N10 Embryologie des Scorpions / von Ilya Ilyich Mechnikov 1870 Wilhelm Engelmann 1908 Immunität bei Infektionskrankheiten / Ilya Ilyich Mechnikov ; einzig autorisierte übersetzung von Julius N11 1902 Gustav Fischer 1908 Meyer Die experimentelle Chemotherapie der Spirillosen : Syphilis, Rückfallfieber, Hühnerspirillose, Frambösie / N12 1910 J.Springer 1908 von Paul Ehrlich und S. -
How Macrophages Deal with Death
REVIEWS CELL DEATH AND IMMUNITY How macrophages deal with death Greg Lemke Abstract | Tissue macrophages rapidly recognize and engulf apoptotic cells. These events require the display of so- called eat-me signals on the apoptotic cell surface, the most fundamental of which is phosphatidylserine (PtdSer). Externalization of this phospholipid is catalysed by scramblase enzymes, several of which are activated by caspase cleavage. PtdSer is detected both by macrophage receptors that bind to this phospholipid directly and by receptors that bind to a soluble bridging protein that is independently bound to PtdSer. Prominent among the latter receptors are the MER and AXL receptor tyrosine kinases. Eat-me signals also trigger macrophages to engulf virus- infected or metabolically traumatized, but still living, cells, and this ‘murder by phagocytosis’ may be a common phenomenon. Finally , the localized presentation of PtdSer and other eat- me signals on delimited cell surface domains may enable the phagocytic pruning of these ‘locally dead’ domains by macrophages, most notably by microglia of the central nervous system. In long- lived organisms, abundant cell types are often process. Efferocytosis is a remarkably efficient business: short- lived. In the human body, for example, the macrophages can engulf apoptotic cells in less than lifespan of many white blood cells — including neutro- 10 minutes, and it is therefore difficult experimentally to phils, eosinophils and platelets — is less than 2 weeks. detect free apoptotic cells in vivo, even in tissues where For normal healthy humans, a direct consequence of large numbers are generated7. Many of the molecules this turnover is the routine generation of more than that macrophages and other phagocytes use to recognize 100 billion dead cells each and every day of life1,2. -
Restriction Endonucleases
Molecular Biology Problem Solver: A Laboratory Guide. Edited by Alan S. Gerstein Copyright © 2001 by Wiley-Liss, Inc. ISBNs: 0-471-37972-7 (Paper); 0-471-22390-5 (Electronic) 9 Restriction Endonucleases Derek Robinson, Paul R. Walsh, and Joseph A. Bonventre Background Information . 226 Which Restriction Enzymes Are Commercially Available? . 226 Why Are Some Enzymes More Expensive Than Others? . 227 What Can You Do to Reduce the Cost of Working with Restriction Enzymes? . 228 If You Could Select among Several Restriction Enzymes for Your Application, What Criteria Should You Consider to Make the Most Appropriate Choice? . 229 What Are the General Properties of Restriction Endonucleases? . 232 What Insight Is Provided by a Restriction Enzyme’s Quality Control Data? . 233 How Stable Are Restriction Enzymes? . 236 How Stable Are Diluted Restriction Enzymes? . 236 Simple Digests . 236 How Should You Set up a Simple Restriction Digest? . 236 Is It Wise to Modify the Suggested Reaction Conditions? . 237 Complex Restriction Digestions . 239 How Can a Substrate Affect the Restriction Digest? . 239 Should You Alter the Reaction Volume and DNA Concentration? . 241 Double Digests: Simultaneous or Sequential? . 242 225 Genomic Digests . 244 When Preparing Genomic DNA for Southern Blotting, How Can You Determine If Complete Digestion Has Been Obtained? . 244 What Are Your Options If You Must Create Additional Rare or Unique Restriction Sites? . 247 Troubleshooting . 255 What Can Cause a Simple Restriction Digest to Fail? . 255 The Volume of Enzyme in the Vial Appears Very Low. Did Leakage Occur during Shipment? . 259 The Enzyme Shipment Sat on the Shipping Dock for Two Days. -
Introduction and Historical Perspective
Chapter 1 Introduction and Historical Perspective “ Nothing in biology makes sense except in the light of evolution. ” modified by the developmental history of the organism, Theodosius Dobzhansky its physiology – from cellular to systems levels – and by the social and physical environment. Finally, behaviors are shaped through evolutionary forces of natural selection OVERVIEW that optimize survival and reproduction ( Figure 1.1 ). Truly, the study of behavior provides us with a window through Behavioral genetics aims to understand the genetic which we can view much of biology. mechanisms that enable the nervous system to direct Understanding behaviors requires a multidisciplinary appropriate interactions between organisms and their perspective, with regulation of gene expression at its core. social and physical environments. Early scientific The emerging field of behavioral genetics is still taking explorations of animal behavior defined the fields shape and its boundaries are still being defined. Behavioral of experimental psychology and classical ethology. genetics has evolved through the merger of experimental Behavioral genetics has emerged as an interdisciplin- psychology and classical ethology with evolutionary biol- ary science at the interface of experimental psychology, ogy and genetics, and also incorporates aspects of neuro- classical ethology, genetics, and neuroscience. This science ( Figure 1.2 ). To gain a perspective on the current chapter provides a brief overview of the emergence of definition of this field, it is helpful -
Barbara Mcclintock's World
Barbara McClintock’s World Timeline adapted from Dolan DNA Learning Center exhibition 1902-1908 Barbara McClintock is born in Hartford, Connecticut, the third of four children of Sarah and Thomas Henry McClintock, a physician. She spends periods of her childhood in Massachusetts with her paternal aunt and uncle. Barbara at about age five. This prim and proper picture betrays the fact that she was, in fact, a self-reliant tomboy. Barbara’s individualism and self-sufficiency was apparent even in infancy. When Barbara was four months old, her parents changed her birth name, Eleanor, which they considered too delicate and feminine for such a rugged child. In grade school, Barbara persuaded her mother to have matching bloomers (shorts) made for her dresses – so she could more easily join her brother Tom in tree climbing, baseball, volleyball, My father tells me that at the and football. age of five I asked for a set of tools. He My mother used to did not get me the tools that you get for an adult; he put a pillow on the floor and give got me tools that would fit in my hands, and I didn’t me one toy and just leave me there. think they were adequate. Though I didn’t want to tell She said I didn’t cry, didn’t call for him that, they were not the tools I wanted. I wanted anything. real tools not tools for children. 1908-1918 McClintock’s family moves to Brooklyn in 1908, where she attends elementary and secondary school. In 1918, she graduates one semester early from Erasmus Hall High School in Brooklyn. -
Complement Component 4 Genes Contribute Sex-Specific Vulnerability in Diverse Illnesses
bioRxiv preprint doi: https://doi.org/10.1101/761718; this version posted September 9, 2019. 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-ND 4.0 International license. Complement component 4 genes contribute sex-specific vulnerability in diverse illnesses Nolan Kamitaki1,2, Aswin Sekar1,2, Robert E. Handsaker1,2, Heather de Rivera1,2, Katherine Tooley1,2, David L. Morris3, Kimberly E. Taylor4, Christopher W. Whelan1,2, Philip Tombleson3, Loes M. Olde Loohuis5,6, Schizophrenia Working Group of the Psychiatric Genomics Consortium7, Michael Boehnke8, Robert P. Kimberly9, Kenneth M. Kaufman10, John B. Harley10, Carl D. Langefeld11, Christine E. Seidman1,12,13, Michele T. Pato14, Carlos N. Pato14, Roel A. Ophoff5,6, Robert R. Graham15, Lindsey A. Criswell4, Timothy J. Vyse3, Steven A. McCarroll1,2 1 Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA 2 Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA 3 Department of Medical and Molecular Genetics, King’s College London, London WC2R 2LS, UK 4 Rosalind Russell / Ephraim P Engleman Rheumatology Research Center, Division of Rheumatology, UCSF School of Medicine, San Francisco, California 94143, USA 5 Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA 6 Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, California 90095, USA 7 A full list of collaborators is in Supplementary Information. -
Investigation of Candidate Genes and Mechanisms Underlying Obesity
Prashanth et al. BMC Endocrine Disorders (2021) 21:80 https://doi.org/10.1186/s12902-021-00718-5 RESEARCH ARTICLE Open Access Investigation of candidate genes and mechanisms underlying obesity associated type 2 diabetes mellitus using bioinformatics analysis and screening of small drug molecules G. Prashanth1 , Basavaraj Vastrad2 , Anandkumar Tengli3 , Chanabasayya Vastrad4* and Iranna Kotturshetti5 Abstract Background: Obesity associated type 2 diabetes mellitus is a metabolic disorder ; however, the etiology of obesity associated type 2 diabetes mellitus remains largely unknown. There is an urgent need to further broaden the understanding of the molecular mechanism associated in obesity associated type 2 diabetes mellitus. Methods: To screen the differentially expressed genes (DEGs) that might play essential roles in obesity associated type 2 diabetes mellitus, the publicly available expression profiling by high throughput sequencing data (GSE143319) was downloaded and screened for DEGs. Then, Gene Ontology (GO) and REACTOME pathway enrichment analysis were performed. The protein - protein interaction network, miRNA - target genes regulatory network and TF-target gene regulatory network were constructed and analyzed for identification of hub and target genes. The hub genes were validated by receiver operating characteristic (ROC) curve analysis and RT- PCR analysis. Finally, a molecular docking study was performed on over expressed proteins to predict the target small drug molecules. Results: A total of 820 DEGs were identified between -
DNA Replication
Introduction to genome biology Sandrine Dudoit and Robert Gentleman Bioconductor short course Summer 2002 © Copyright 2002, all rights reserved Outline • Cells and cell division • DNA structure and replication •Proteins • Central dogma: transcription, translation • Pathways A brief history Gregor Mendel (1823(1823---1884)1884) Thomas Hunt Morgan (1866(1866---1945)1945) Francis Crick (1916(1916---)))) James D. Watson (1928(1928---)))) From chromosomes to proteins Cells Cells • Cells: the fundamental working units of every living organism. • Metazoa: multicellular organisms. E.g. Humans: trillions of cells. • Protozoa: unicellular organisms. E.g. yeast, bacteria. Cells • Each cell contains a complete copy of an organism’s genome, or blueprint for all cellular structures and activities. • Cells are of many different types (e.g. blood, skin, nerve cells), but all can be traced back to a single cell, the fertilized egg. Cell composition • 90% water. • Of the remaining molecules, dry weight – 50% protein – 15% carbohydrate – 15% nucleic acid – 10% lipid – 10% miscellaneous. • By element: 60% H, 25% O, 12%C, 5%N. The genome • The genome is distributed along chromosomes, which are made of compressed and entwined DNA. • A (protein-coding) gene is a segment of chromosomal DNA that directs the synthesis of a protein. Eukaryotes vs. prokaryotes Eukaryotes vs. prokaryotes • Prokaryotic cells: lack a distinct, membrane-bound nucleus. E.g. bacteria. • Eukaryotic cells: distinct, membrane- bound nucleus. Larger and more complex in structure than prokaryotic cells. E.g. mammals, yeast. The eukaryotic cell The eukaryotic cell • Nucleus: membrane enclosed structure which contains chromosomes, i.e., DNA molecules carrying genes essential to cellular function. • Cytoplasm: the material between the nuclear and cell membranes; includes fluid (cytosol), organelles, and various membranes. -
Appendix Table A.2.3.1 Full Table of All Chicken Proteins and Human Orthologs Pool Accession Human Human Protein Human Product Cell Angios Log2( Endo Gene Comp
Appendix table A.2.3.1 Full table of all chicken proteins and human orthologs Pool Accession Human Human Protein Human Product Cell AngioS log2( Endo Gene comp. core FC) Specific CIKL F1NWM6 KDR NP_002244 kinase insert domain receptor (a type III receptor tyrosine M 94 4 kinase) CWT Q8AYD0 CDH5 NP_001786 cadherin 5, type 2 (vascular endothelium) M 90 8.45 specific CWT Q8AYD0 CDH5 NP_001786 cadherin 5, type 2 (vascular endothelium) M 90 8.45 specific CIKL F1P1Y9 CDH5 NP_001786 cadherin 5, type 2 (vascular endothelium) M 90 8.45 specific CIKL F1P1Y9 CDH5 NP_001786 cadherin 5, type 2 (vascular endothelium) M 90 8.45 specific CIKL F1N871 FLT4 NP_891555 fms-related tyrosine kinase 4 M 86 -1.71 CWT O73739 EDNRA NP_001948 endothelin receptor type A M 81 -8 CIKL O73739 EDNRA NP_001948 endothelin receptor type A M 81 -8 CWT Q4ADW2 PROCR NP_006395 protein C receptor, endothelial M 80 -0.36 CIKL Q4ADW2 PROCR NP_006395 protein C receptor, endothelial M 80 -0.36 CIKL F1NFQ9 TEK NP_000450 TEK tyrosine kinase, endothelial M 77 7.3 specific CWT Q9DGN6 ECE1 NP_001106819 endothelin converting enzyme 1 M 74 -0.31 CIKL Q9DGN6 ECE1 NP_001106819 endothelin converting enzyme 1 M 74 -0.31 CWT F1NIF0 CA9 NP_001207 carbonic anhydrase IX I 74 CIKL F1NIF0 CA9 NP_001207 carbonic anhydrase IX I 74 CWT E1BZU7 AOC3 NP_003725 amine oxidase, copper containing 3 (vascular adhesion protein M 70 1) CIKL E1BZU7 AOC3 NP_003725 amine oxidase, copper containing 3 (vascular adhesion protein M 70 1) CWT O93419 COL18A1 NP_569712 collagen, type XVIII, alpha 1 E 70 -2.13 CIKL O93419 -
Alpha-Agarases Define a New Family of Glycoside Hydrolases, Distinct from Beta-Agarase Families
Alpha-agarases define a new family of glycoside hydrolases, distinct from beta-agarase families Didier Flament, Tristan Barbeyron, Murielle Jam, Philippe Potin, Mirjam Czjzek, Bernard Kloareg, Gurvan Michel To cite this version: Didier Flament, Tristan Barbeyron, Murielle Jam, Philippe Potin, Mirjam Czjzek, et al.. Alpha- agarases define a new family of glycoside hydrolases, distinct from beta-agarase families. Applied and Environmental Microbiology, American Society for Microbiology, 2007, 73 (14), pp.4691-4694. 10.1128/AEM.00496-07. hal-00616725 HAL Id: hal-00616725 https://hal.univ-brest.fr/hal-00616725 Submitted on 5 Sep 2011 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. 1 Short communication 2 3 Alpha-agarases define a new family of glycoside hydrolases, distinct from 4 beta-agarase families 5 6 Didier FLAMENT §, Tristan BARBEYRON, Murielle JAM, Philippe POTIN, Mirjam 7 CZJZEK, Bernard KLOAREG and Gurvan MICHEL* 8 9 Centre National de la Recherche Scientifique; Université Pierre et Marie Curie-Paris6, Unité 10 Mixte de Recherche 7139 "Marine -
Tests for the Evaluation of Preterm Labor and Premature Rupture of Membranes
Medical Coverage Policy Effective Date ............................................. 7/15/2021 Next Review Date ....................................... 7/15/2022 Coverage Policy Number .................................. 0099 Tests for the Evaluation of Preterm Labor and Premature Rupture of Membranes Table of Contents Related Coverage Resources Overview .............................................................. 1 Recurrent Pregnancy Loss: Diagnosis and Treatment Coverage Policy ................................................... 1 Ultrasound in Pregnancy (including 3D, 4D and 5D General Background ............................................ 2 Ultrasound) Medicare Coverage Determinations .................. 13 Coding/Billing Information .................................. 13 References ........................................................ 15 INSTRUCTIONS FOR USE The following Coverage Policy applies to health benefit plans administered by Cigna Companies. Certain Cigna Companies and/or lines of business only provide utilization review services to clients and do not make coverage determinations. References to standard benefit plan language and coverage determinations do not apply to those clients. Coverage Policies are intended to provide guidance in interpreting certain standard benefit plans administered by Cigna Companies. Please note, the terms of a customer’s particular benefit plan document [Group Service Agreement, Evidence of Coverage, Certificate of Coverage, Summary Plan Description (SPD) or similar plan document] may differ