9. BrandIs it relevant?
Is it good?
Is it important?
provenanceinfrastructure
•What is it?
•Where can I
get it?
•What refers
to it?
•What does
it refer to?
•What has
been done
to it?
•Who
provides
stewardship
of it?
•Who funded
it?
•What can I
do with it?
•Who do we
credit it to?
•What are
their
credentials?
14. List of university and college mergers in the
United States
From Wikipedia, the free encyclopedia
This is a list of mergers of universities and/or colleges in the United States with the name of the
surviving institution, predecessors, and effective date.
This list is incomplete; you can help by expanding it (http://en.wikipedia.org/w/index.php?
title=List_of_university_and_college_mergers_in_the_United_States&action=edit) .
Contents
1 A through D
2 E through M
3 N through Z
4 See also
5 References
A through D
Alliant International University - merger of California School of Professional Psychology and
United States International University, 2001
Azusa Pacific College - absorbed Arlington College, 1968
Azusa Pacific College - merger of Azusa College and Los Angeles Pacific College, 1965
University of Baltimore - absorbed Eastern College, 1970
Benedictine College - merger of Mount Saint Scholastica College and St. Benedict's College -
1971
Boston University School of Medicine - absorbed Boston Female Medical School, 1874
Brevard College - merger of Brevard Institute, Weaverville College, and Rutherford College,
1934
University of California, Berkeley - merger of the College of California and the Agricultural,
Mining, and Mechanical Arts College, 1853
Carson-Newman College - merger of Carson College and Newman College for Women, 1889
Case Western Reserve University - merger of Case Tech and Western Reserve, 1971-72
The Catholic University of America - absorbed Columbus University, 1954
Central Nazarene College - absorbed Nazarene Bible Institute (1911)
Chicago College of Performing Arts - absorbed Roosevelt University School of Music, 1954
University of Cincinnati - absorbed Medical College of Ohio 1896; Cincinnati College of
Pharmacy, 1954
Clark Atlanta University - merger of Clark College and Atlanta University, 1988
Davenport University - merger of Davenport College, Detroit College of Business, and Great
Lakes College, 2000.
University of Delaware - merger of Newark College and Women's College of Delaware, 1921
DePaul University - absorbed Barat College, 2001
List of university and college name changes in
the United States
From Wikipedia, the free encyclopedia
Here follows a list of renamings of universities and colleges in the United States.
Contents:
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Top of Page — See also
Current Name
Former
Name(s)
Year of Change
Alabama Agricultural and
Mechanical University
Agricultural and
Mechanical
College of
Alabama
Alcorn State University
Alcorn
Agricultural and
Mechanical
College
1974
Amridge University
Southern
Christian
University
Alliant International University
California
Western
Appalachian State University
Appalachian State
Teachers College;
Appalachian
Training School
for Teachers;
Appalachian State
Normal School;
Watauga
Academy
1967 [1]
Apollo College
American
Institute of
Health
Technology
2005 [2]
Arcadia University Beaver College 2001
Arizona State University
Tempe Normal
School
1958
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Geographical renaming
From Wikipedia, the free encyclopedia
Geographical renaming is the act of changing the name of a geographical feature or area. This can
range from the uncontroversial change of a street name to a highly disputed change to the name of a
country. Some names are changed locally but are not recognised by other countries, especially when
there is a difference in language. Other names may not be officially recognised but remain in common
use.
There are many reasons to undertake renaming, with political motivation being the primary cause, such
as renaming places to honour Stalin, and reverting to the original names (see de-Stalinization). One of
the most common reasons for a country changing its name is newly acquired independence. When
borders are changed, sometimes due to a country splitting or two countries joining together, the name
of the areas can change. This, however, is more the creation of a different entity than an act of
geographical renaming.
Other more unusual reasons for renaming have included:
To stop having an unusual or embarrassing name
As part of a sponsorship deal or publicity stunt
A change might see a completely different name being adopted or may simply be just a slightly
different spelling.
In some cases established institutions preserve the old names of the renamed places in their names,
such as the Pusan National University in Busan, South Korea; the Peking University in Beijing,
People's Republic of China; Bombay Stock Exchange, IIT Bombay and the Bombay High Court in
Mumbai, Republic of India; Persian Gulf, south of Iran (formerly Persia); and the University of
Madras, Madras Stock Exchange, the Madras High Court, and IIT Madras in Chennai, Republic of
India.
U.N. Member States
U.S. State Department
List of Independent
States
Mapping.com's list of
Worldwide Country and
City Name Changes
Since 1990
Internet Domains from
the Internet Assigned
Numbers Authority (an
agency under ICANN,
the Internet Corporation
for Assigned Names
and Numbers)
All the Airport Codes
In The World (about
36,000 codes!)
ISO3166-defined
country codes 240 2-
letter codes, 3-letter
codes, and RIPE NCC
Service Region
Flags of the World, and
other information,
keyed to each country's
ISO3166 Code
Country Information
from the CIA World
Name Changes Since 1990: Countries, Cities, and More
An admittedly incomplete and imperfect list of new countries
and cities, and various name changes
Search For Cities and Countries Not Listed Here:
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Web mapping.com
1. "New" Countries Since 1990
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18. PQ7797.B635.B5213 2000
(persistent catalog #)
(current physical location)
Hayden Library, 3rd floor, shelf # 53
The Renear/Palmer article states....
http://dx.doi.org/10.1002/meet.2009.1450460141
http://www.sciencemag.org/cgi/doi/10.1126/science.1157784
(persistent URI)
(current web location)
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complete bibliographic information about the target content, with information about how the content can
be acquired and/or a hyperlink leading to the content itself.
37. Investigation of the Staphylococcus aureus GraSR
Regulon Reveals Novel Links to Virulence, Stress
Response and Cell Wall Signal Transduction Pathways
Me´lanie Falord1,2
, Ulrike Ma¨der3
, Aure´lia Hiron1,2
, Michel Dbarbouille´1,2
, Tarek Msadek1,2
*
1 Institut Pasteur, Biology of Gram-Positive Pathogens, Department of Microbiology, Paris, France, 2 CNRS, URA 2172, Paris, France, 3 Interfaculty Institute for Genetics and
Functional Genomics, Department for Functional Genomics, Ernst Moritz Arndt University, Greifswald, Germany
Abstract
The GraS/GraR two-component system has been shown to control cationic antimicrobial peptide (CAMP) resistance in the
major human pathogen Staphylococcus aureus. We demonstrated that graX, also involved in CAMP resistance and
cotranscribed with graRS, encodes a regulatory cofactor of the GraSR signaling pathway, effectively constituting a three-
component system. We identified a highly conserved ten base pair palindromic sequence (59 ACAAA TTTGT 39) located
upstream from GraR-regulated genes (mprF and the dlt and vraFG operons), which we show to be essential for
transcriptional regulation by GraR and induction in response to CAMPs, suggesting it is the likely GraR binding site.
Genome-based predictions and transcriptome analysis revealed several novel GraR target genes. We also found that the
GraSR TCS is required for growth of S. aureus at high temperatures and resistance to oxidative stress. The GraSR system has
previously been shown to play a role in S. aureus pathogenesis and we have uncovered previously unsuspected links with
the AgrCA peptide quorum-sensing system controlling virulence gene expression. We also show that the GraSR TCS controls
stress reponse and cell wall metabolism signal transduction pathways, sharing an extensive overlap with the WalKR regulon.
This is the first report showing a role for the GraSR TCS in high temperature and oxidative stress survival and linking this
system to stress response, cell wall and pathogenesis control pathways.
Citation: Falord M, Ma¨der U, Hiron A, De´barbouille´ M, Msadek T (2011) Investigation of the Staphylococcus aureus GraSR Regulon Reveals Novel Links to
Virulence, Stress Response and Cell Wall Signal Transduction Pathways. PLoS ONE 6(7): e21323. doi:10.1371/journal.pone.0021323
Editor: Malcolm James Horsburgh, University of Liverpool, United Kingdom
Received May 4, 2011; Accepted May 25, 2011; Published July 1, 2011
Copyright: ß 2011 Falord et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by research funds from the European Commission (StaphDynamics [LHSM-CT-2006-019064] and BaSysBio [LSHG-CT-2006-
037469] grants), the Centre National de la Recherche Scientifique (CNRS URA 2172), Agence Nationale de la Recherche (ANR GrabIron and NaBab), and the Institut
Pasteur (PTR Nu256 and PTR Nu336). Me´lanie Falord received a Young Scientist Fellowship from the Conseil Pasteur-Weizmann. The funders had no role in study
design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: tmsadek@pasteur.fr
Introduction
The opportunistic pathogen Staphylococcus aureus is both a
commensal and a major Gram-positive pathogen, causing a variety
of infections ranging from superficial skin abscesses to more serious
diseases such as pneumonia, meningitis, endocarditis, septicemia
and toxic shock syndrome [1]. The ubiquitous nature of this
pathogen stems mostly from its capacity to survive a large variety of
environmental conditions as well as an impressive ability to resist
host innate immune defense mechanisms and produce systemic
infections, often in healthy humans [2,3]. This unique adaptive
potential has made S. aureus one of the major causes of nosocomial
infections today, compounded by the rapid emergence of multiple
antibiotic-resistant strains over the past few decades [4], particularly
methicillin and vancomycin-intermediate resistant strains (MRSA
and VISA). Until recently, vancomycin had remained the weapon
of last resort, but the recent appearance of the enterococcal vanA
vancomycin-resistance gene cluster in S. aureus highlights the
growing threat this bacterium poses to human health and the
urgent need for developing novel therapeutic approaches [5,6].
Cationic antimicrobial peptides (CAMPs) are an important
component of host innate immunity and understanding the
molecular mechanisms involved in resistance is a key factor in
staphylococcal treatment research. CAMPs have both cationic and
amphipathic properties and are classified according to their length
and secondary structure [7]. They are produced by certain
immune, skin and epithelial cells in all living kingdoms, as defenses
against microbial proliferation, and many are known to act by
forming pores in the cell membrane, through interactions with
bacterial cell envelope components [8]. However, recent work has
shown that several CAMPs, including indolicidin and colistin, can
also kill by inhibiting intracellular processes such as protein and
DNA synthesis as well as septum formation and division [9].
To counteract CAMP antimicrobial activity during infection,
Gram-positive bacteria have developed several resistance mecha-
nisms, including degradation, sequestration or electrostatic repulsion
[10]. In Bacillus subtilis and related Gram-positive bacteria, D-
alanylation of wall teichoic acids (WTAs) and lipoteichoic acids
(LTAs), mediated by the DltABCD enzymes, as well as MprF-
dependent lysylination of phosphatidylglycerol, prevent CAMP-
binding by increasing the bacterial surface positive charge [10,11].
Two-component systems (TCSs) play an important role in these
mechanisms by coordinating the expression of resistance genes,
when CAMPs are detected at the cell surface. TCSs are typically
composed of a membrane histidine kinase (HK), acting as a signal
sensor/transducer, through phosphorylation of its cognate response
PLoS ONE | www.plosone.org 1 July 2011 | Volume 6 | Issue 7 | e21323