Characterization of the Genetic and Environmental Factors Driving Gene Expression Variability
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Abstracts Genome 10K & Genome Science 29 Aug - 1 Sept 2017 Norwich Research Park, Norwich, Uk
Genome 10K c ABSTRACTS GENOME 10K & GENOME SCIENCE 29 AUG - 1 SEPT 2017 NORWICH RESEARCH PARK, NORWICH, UK Genome 10K c 48 KEYNOTE SPEAKERS ............................................................................................................................... 1 Dr Adam Phillippy: Towards the gapless assembly of complete vertebrate genomes .................... 1 Prof Kathy Belov: Saving the Tasmanian devil from extinction ......................................................... 1 Prof Peter Holland: Homeobox genes and animal evolution: from duplication to divergence ........ 2 Dr Hilary Burton: Genomics in healthcare: the challenges of complexity .......................................... 2 INVITED SPEAKERS ................................................................................................................................. 3 Vertebrate Genomics ........................................................................................................................... 3 Alex Cagan: Comparative genomics of animal domestication .......................................................... 3 Plant Genomics .................................................................................................................................... 4 Ksenia Krasileva: Evolution of plant Immune receptors ..................................................................... 4 Andrea Harper: Using Associative Transcriptomics to predict tolerance to ash dieback disease in European ash trees ............................................................................................................ -
Chemical, Biological, and Environmental Factors Responsible for The
CHEMICAL, BIOLOGICAL, AND ENVIRONMENTAL FACTORS RESPONSIBLE FOR THE - -v - - - IN THE AUBURN CITY WATER SUPPLY AGRICULTURAL EXPERIMENT STATION/AUBURN UNIVERSITY R. DENNIS ROUSE, DIRECTOR AUBURN, ALABAMA BULLETIN 490 JULY 1977 CONTENTS Page INTRODUCTION ........ .. .. ............... 3 Background on Odors of Biological Origin in Water .......................... 3 Odor in the Auburn Water ........................... 5 PROCEDURES ............................ 5 RESULTS AND DISCUSSION ........... ...... .......... 7 Biological Factors................................ 7 Chemical Factors ............................... 22 Environmental Factors Related to the Growth and Production of Odorous Substances by Actinomycetes ....... 24 Correlation of Rainfall, Temperature, and Threshold Odor Number (TON) ................... 39 SUMMARY ... ... ...................... ........... 41 REFERENCES ................... ....... ... .......... 45 FIRST PRINTING 3M, JULY 1977 ACKNOWLEDGEMENTS The authors wish to thank the Auburn Water Board for the financial support of this project, the Auburn Water Treatment Plant for supplying TON values, Dr. John Lawrence for use of the carbon analyzer, and Sandy Williams, Frank Seesock, and Susan Brownlee for technical assistance. Information contained herein is available to all without regard to race, color, or nationalorigin. CHEMICAL, BIOLOGICAL, and ENVIRONMENTAL FACTORS RESPONSIBLE for the EARTHY ODOR in the AUBURN CITY WATER SUPPLY J. D. WEETE, W. T. BLEVINS, G. R.WILT, and D. DURHAM' INTRODUCTION Background On Odors Of Biological Origin in Water HE OCCURRENCE of objectionable odors in water used for drinking and commercial purposes is well documented in certain regions of the United States (1, 4, 12, 15) and various other parts of the world. (1, 8, 9, 11). Odors in sur- face waters may originate from industrial and municipal sewage effluents or from biological activities of algae or heterotrophic microorganisms. Odors of biological origin may be due to decomposition of organisms or to the produc- tion of microbial metabolites. -
Commentary: Facing the Challenge of Gene-Environment Interaction: the Two-By-Four Table and Beyond
American Journal of Epidemiology Vol. 153, No. 10 Copyright © 2001 by The Johns Hopkins University School of Hygiene and Public Health Printed in U.S.A. All rights reserved The Challenge of Gene-Environment Interaction Botto and Khoury PRACTICE OF EPIDEMIOLOGY Commentary: Facing the Challenge of Gene-Environment Interaction: The Two-by-Four Table and Beyond Lorenzo D. Botto1 and Muin J. Khoury2 As a result of the Human Genome Project, epidemiologists can study thousands of genes and their interaction with the environment. The challenge is how to best present and analyze such studies of multiple genetic and environmental factors. The authors suggest emphasizing the fundamental core of gene-environment interaction—the separate assessment of the effects of individual and joint risk factors. In the simple analysis of one genotype and an exposure (both dichotomous), such study can be summarized in a two-by-four table. The advantages of such a table for data presentation and analysis are many: The table displays the data efficiently and highlights sample size issues; it allows for evaluation of the independent and joint roles of genotype and exposure on disease risk; and it emphasizes effect estimation over model testing. Researchers can easily estimate relative risks and attributable fractions and test different models of interaction. The two-by-four table is a useful tool for presenting, analyzing, and synthesizing data on gene-environment interaction. To highlight the role of gene-environment interaction in disease causation, the authors propose that the two-by-four table is the fundamental unit of epidemiologic analysis. Am J Epidemiol 2001;153:1016–20. -
Environmental Factors Affecting the Composition and Diversity of The
Imai et al. Journal of Ecology and Environment (2017) 41:8 Journal of Ecology DOI 10.1186/s41610-017-0027-2 and Environment RESEARCH Open Access Environmental factors affecting the composition and diversity of the avian community in igune, a traditional agricultural landscape in northern Japan Haruka Imai1*, Tohru Nakashizuka1,2 and Michio Oguro1,3 Abstract Background: “Igune,” a traditional agricultural landscape in the Tohoku region of Japan, is characterized by small-scale artificial woodlots surrounding a farmer’s house that are interspersed with paddy fields. During the rapid economic growth of Japan over recent decades, some igune woodlots have been abandoned or logged. Biodiversity conservation is an important issue worldwide, and traditional agricultural landscapes are of particular interest. To elucidate the role of igune landscapes in conserving biodiversity, we examined the effects of environmental factors on avian communities. Results: The study was conducted in the suburban areas of Oshu and Hanamaki cities, Iwate Prefecture, Japan, at eight sites that varied in the density and area of igune woodlots within the landscape. Bird surveys were conducted from the middle to late breeding season, and several environmental factors of the igune landscape were also measured. The results of canonical correspondence analysis indicated that the characteristics of avian communities were mainly determined by the total forested area in the landscape. Increased total forested area and shrubs layer of igune woodlots did not cause a reduction in number of bird species of any habitat and foraging types, while increased both in species number and abundance of insectivores and forest species. The number of raptor species increased in igune sites without shrubs. -
How Much Global Ill Health Is Attributable to Environmental Factors?
ORIGINAL ARTICLES How Much Global Ill Health Is Attributable to Environmental Factors? Kirk R. Smith,1 Carlos F. Corvalán2, and Tord Kjellström3 Over the years, estimates have been made of the portions of attributed to environmental risk factors. Children under 5 human mortality and morbidity that can be attributed to years of age seem to bear the largest environmental burden, environmental factors. Frustratingly, however, even for a and the portion of disease due to environmental risks seems single category of disease such as cancer, these estimates to decrease with economic development. A summary of have often varied widely. Here we attempt to explain why these estimates first appeared in the 1997 report, "Health such efforts have come to such different results in the past and Environment in Sustainable Development," which was and to provide guidance for doing such estimates more the World Health Organization's contribution to the 5-year consistently in the future to avoid the most important pitfalls. anniversary of the Rio Earth Summit. A full explanation of We do so by carefully defining what we mean by the terms how these estimates were made is first presented here. We "environmental," "ill health," and "attributable." Finally, end with a call for a program of "strategic epidemiology," based on these recommendations, we attempt our own which would be designed to fill important gaps in the estimate, appropriately qualified according to the many understanding of major environmental health risks in remaining uncertainties. Our estimate is that 25-33% of the important population groups worldwide. (Epidemiology global burden of disease can be 1999;10:573-584) Keywords: environmental exposures, morbidity, mortality, children, environmental health risks, populations, global factors, public health. -
Exploiting High Throughput DNA Sequencing Data for Genomic Analysis
Exploiting high throughput DNA sequencing data for genomic analysis Markus Hsi-Yang Fritz Darwin College A dissertation submitted to the University of Cambridge for the degree of Doctor of Philosophy 14th October 2011 Markus Hsi-Yang Fritz EMBL-European Bioinformatics Institute Wellcome Trust Genome Campus Hinxton, Cambridge, CB10 1SD United Kingdom email: [email protected] This dissertation is the result of my own work and includes nothing which is the outcome of work done in collaboration except where specifically indicated in the text. No part of this work has been submitted or is currently being submitted for any other qualification. This document does not exceed the word limit of 60,000 words1 as defined by the Biology Degree Committee. Markus Hsi-Yang Fritz 14th October 2011 1 excluding bibliography, figures, appendices etc. To an exceptional scientist — my Dad. Exploiting high throughput DNA sequencing data for genomic analysis Summary Markus Hsi-Yang Fritz Darwin College The last few years have witnessed a drastic increase in genomic data. This has been facilitated by the shift away from the Sanger sequencing tech- nique to an array of high-throughput methods — so-called next-generation sequencing technologies. This enormous growth of available DNA data has been a tremendous boon to large-scale genomics studies and has rapidly advanced fields such as environmental genomics, ancient DNA research, population genomics and disease association. On the other hand, however, researchers and sequence archives are now facing an enormous data deluge. Critically, the rate of sequencing data accumulation is now outstripping advances in hard drive capacity, network bandwidth and processing power. -
Strategic Plan 2011-2016
Strategic Plan 2011-2016 Wellcome Trust Sanger Institute Strategic Plan 2011-2016 Mission The Wellcome Trust Sanger Institute uses genome sequences to advance understanding of the biology of humans and pathogens in order to improve human health. -i- Wellcome Trust Sanger Institute Strategic Plan 2011-2016 - ii - Wellcome Trust Sanger Institute Strategic Plan 2011-2016 CONTENTS Foreword ....................................................................................................................................1 Overview .....................................................................................................................................2 1. History and philosophy ............................................................................................................ 5 2. Organisation of the science ..................................................................................................... 5 3. Developments in the scientific portfolio ................................................................................... 7 4. Summary of the Scientific Programmes 2011 – 2016 .............................................................. 8 4.1 Cancer Genetics and Genomics ................................................................................ 8 4.2 Human Genetics ...................................................................................................... 10 4.3 Pathogen Variation .................................................................................................. 13 4.4 Malaria -
2011 Gairdner Foundation Annual Report
2011 GAIRDNER FOUNDATION ANNUAL REPORT May 30, 2012 TABLE OF CONTENTS TABLE OF CONTENTS ...................................................................................................................................... 2 HISTORY OF THE GAIRDNER FOUNDATION .............................................................................................. 3 MISSION,VISION ................................................................................................................................................ 4 GOALS .................................................................................................................................................................. 5 MESSAGE FROM THE CHAIR .......................................................................................................................... 6 MESSAGE FROM THE PRESIDENT/SCIENTIFIC DIRECTOR ..................................................................... 7 2011 YEAR IN REVIEW ..................................................................................................................................... 8 REPORT ON 2011 OBJECTIVES ..................................................................................................................... 12 THE YEAR AHEAD: OBJECTIVES FOR 2012 ............................................................................................... 13 2011 SPONSORS ................................................................................................................................................ 14 GOVERNANCE -
Queensland Brain Institute 2014 Annual Report
Queensland Brain Institute 2014 Annual Report Queensland Brain Institute 2014 Annual Report Cover Image: Garden of Neurons by Gonzalo Almarza We are studying different populations of neurons in the cortex. In this image, subplate neurons (green) extend their processes towards the pial surface during early cortical development. These neurons project through the emerging cortical plate (in red), arborising in the marginal zone (in blue). Queensland Brain Institute Annual Report 2014 UQ Vice-Chancellor and President’s Report ........................1 QBI Director’s Report ...........................................2 Discovery 4 Genome analysis reveals schizophrenia’s secrets ...................6 Halting the damaging effects of stroke ............................8 Revealing the complexity of wiring the brain. .10 Redefining how we plan movement in the brain ....................12 Controlling fear may be possible by controlling DNA ................14 Research 16 Anggono Laboratory ........17 Goodhill Laboratory .........27 Mowry Laboratory ..........37 Srinivasan Laboratory .......43 Bartlett Laboratory ..........18 Götz Laboratory ............28 Osborne Laboratory .........38 van Swinderen Laboratory ...44 Bredy Laboratory ...........19 Hilliard Laboratory ..........29 Piper Laboratory ............39 Visscher Laboratory .........45 Burne Laboratory ...........20 Jiang Laboratory ............30 Reinhard Laboratory ........40 Williams Laboratory .........46 Cheung Laboratory .........21 Lynch Laboratory ...........31 Richards Laboratory .........41 -
The Molecular Basis of Mecp2 Function in the Brain
Edinburgh Research Explorer The molecular basis of MeCP2 function in the brain Citation for published version: Tillotson, R & Bird, A 2020, 'The molecular basis of MeCP2 function in the brain', Journal of Molecular Biology, vol. 432, no. 6. https://doi.org/10.1016/j.jmb.2019.10.004 Digital Object Identifier (DOI): 10.1016/j.jmb.2019.10.004 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Journal of Molecular Biology General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Review The Molecular Basis of MeCP2 Function in the Brain Rebekah Tillotson 1,2 and Adrian Bird 3 1 - Genetics and Genome Biology Program, The Hospital for Sick Children, The Peter Gilgan Centre for Research and Learning, Toronto, ON M5G 0A4, Canada 2 - Medical Research Council (MRC) Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Headington, Oxford, OX3 9DS, UK 3 - Wellcome Centre for Cell Biology, University of Edinburgh, The Michael Swann Building, King's Buildings, Max Born Crescent, Edinburgh, EH9 3BF, UK Correspondence to Adrian Bird: [email protected] https://doi.org/10.1016/j.jmb.2019.10.004 Edited by Tuncay Baubec Abstract MeCP2 is a reader of the DNA methylome that occupies a large proportion of the genome due to its high abundance and the frequency of its target sites. -
Acknowledgment of Reviewers, 2015
Acknowledgment of Reviewers, 2015 The PNAS editors would like to thank all the individuals who dedicated their considerable time and expertise to the journal by serving as reviewers in 2015. Their generous contribution is deeply appreciated. A Peter B. Adler Colin J. Akerman Eric E. Allen James Ammerman Duur K. Aanen Ralph Adolphs Joshua M. Akey Heather C. Allen David M. Amodio Adam R. Abate Ruedi Aebersold Anna Akhmanova Jim Allen Valentin Amrhein John T. Abatzoglou Hugo Aerts Hajime Akimoto Karen N. Allen Esther Amstad Jonathan Abbatt Hagit P. Affek Akin Akinc Michael F. Allen Ronald Amundson Allison Abbott Arash Afraz Shizuo Akira Paul M. Allen Weihua An Jeffrey Abbott Theodor Agapie Ozan Akkus Rosalind J. Allen Zhiqiang An Larry F. Abbott David A. Agard Ivona Aksentijevich Morten Erik Allentoft Laura Diaz Anadon Nicholas L. Abbott Sapan Agarwal Serap Aksoy Stefano Allesina Ganesh Srinivasan Anand Chaouki T. Abdallah Joel W. Ager III Yousef Al-Abed David B. Allison Cort Anastasio Omar Abdel-Wahab Ingi Agnarsson Ashraf Al-Amoudi Steven D. Allison Lefteris Jason Ikuro Abe Anurag A. Agrawal Eric E. Alani Julian M. Allwood Anastasopoulos Stephen Tobias Abedon Ashutosh Agrawal Balbino Alarcón Eric J. Alm Hossain Anawar Moshe Abeles Rakesh Agrawal Qais Al-Awqati Benjamin A. Alman Elissar Andari Asa Abeliovich Jon Ågren Joseph Albanesi Ingvild Almas William R. L. Anderegg John Aber Alan Agresti Francis Albarede Steven C. Almo John M. Anderies Clara Abraham Jeremy J. Agresti Umberto Albarella Douglas Almond Mark L. Andermann John Abraham Jay J. Ague Silas D. Alben Uri Alon Bogi Andersen Daniel A. Abrams Fernan Agüero Frank Alber José M. -
DNA Methylation Patterns and Cancer
restriction/modification system, which brought Werner Arber, Daniel Nathans and Hamilton Smith the 1978 Nobel Prize in Physiology or Medicine, and made restriction enzymes the primary tools of Charles Rodolphe Brupbacher Foundation molecular biology. Four decades have passed since then, but the role of 5-methylcytosine in eukaryotic DNA metabolism is still shrouded in mystery. We know that the sperm methylation pattern is largely The erased after fertilization and that methylation is gradually reintroduced Charles Rodolphe Brupbacher Prize during embryogenesis and differentiation, but the processes that for Cancer Research 2017 regulate the cell type- and tissue-specific methylation patterns remain is awarded to to be elucidated. We have also learned that DNA can be not only methylated, but also demethylated, and that aberrant methylation can lead to disease - including cancer. Again, how these processes are regulated remains to be discovered. However, we have learnt a great Sir Adrian Peter Bird, deal about 5-methylcytosine metabolism during the past three decades and much of our knowledge came from the laboratory of Adrian Bird. PhD Adrian spent his doctoral and postdoctoral time in Max Birnstiel’s for his contributions to our understanding laboratory, first in Edinburgh and then in Zurich, studying the amplification of ribosomal DNA in Xenopus laevis. In this organism, of the role of DNA methylation in genomic rDNA in somatic tissues is highly methylated, while the development and disease extrachromosomal amplicons are unmethylated. When he returned to Edinburgh to establish his own group, Adrian set out to study The President The President of the Foundation of the Scientific Advisory Board the methylation pattern of these loci using the newly-available methylation-sensitive restriction enzymes.