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List of university and college mergers in theUnited StatesFrom Wikipedia, the free encyclopedia

This is a list of mergers of universities and/or colleges in the United States with the name of thesurviving 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) .

Contents1 A through D2 E through M3 N through Z4 See also5 References

A through DAlliant International University - merger of California School of Professional Psychology andUnited States International University, 2001Azusa Pacific College - absorbed Arlington College, 1968Azusa Pacific College - merger of Azusa College and Los Angeles Pacific College, 1965University of Baltimore - absorbed Eastern College, 1970Benedictine College - merger of Mount Saint Scholastica College and St. Benedict's College -1971Boston University School of Medicine - absorbed Boston Female Medical School, 1874Brevard College - merger of Brevard Institute, Weaverville College, and Rutherford College,1934University of California, Berkeley - merger of the College of California and the Agricultural,Mining, and Mechanical Arts College, 1853Carson-Newman College - merger of Carson College and Newman College for Women, 1889Case Western Reserve University - merger of Case Tech and Western Reserve, 1971-72The Catholic University of America - absorbed Columbus University, 1954Central Nazarene College - absorbed Nazarene Bible Institute (1911)Chicago College of Performing Arts - absorbed Roosevelt University School of Music, 1954University of Cincinnati - absorbed Medical College of Ohio 1896; Cincinnati College ofPharmacy, 1954Clark Atlanta University - merger of Clark College and Atlanta University, 1988Davenport University - merger of Davenport College, Detroit College of Business, and GreatLakes College, 2000.University of Delaware - merger of Newark College and Women's College of Delaware, 1921DePaul University - absorbed Barat College, 2001

List of university and college name changes inthe United StatesFrom 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 ZTop of Page — See also

Current Name FormerName(s) Year of Change

Alabama Agricultural andMechanical University

Agricultural andMechanicalCollege ofAlabama

Alcorn State UniversityAlcornAgricultural andMechanicalCollege

1974

Amridge UniversitySouthernChristianUniversity

Alliant International University CaliforniaWestern

Appalachian State University

Appalachian StateTeachers College;AppalachianTraining Schoolfor Teachers;Appalachian StateNormal School;WataugaAcademy

1967 [1]

Apollo CollegeAmericanInstitute ofHealthTechnology

2005 [2]

Arcadia University Beaver College 2001

Arizona State University Tempe NormalSchool 1958

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Geographical renamingFrom Wikipedia, the free encyclopedia

Geographical renaming is the act of changing the name of a geographical feature or area. This canrange from the uncontroversial change of a street name to a highly disputed change to the name of acountry. Some names are changed locally but are not recognised by other countries, especially whenthere is a difference in language. Other names may not be officially recognised but remain in commonuse.

There are many reasons to undertake renaming, with political motivation being the primary cause, suchas renaming places to honour Stalin, and reverting to the original names (see de-Stalinization). One ofthe most common reasons for a country changing its name is newly acquired independence. Whenborders are changed, sometimes due to a country splitting or two countries joining together, the nameof the areas can change. This, however, is more the creation of a different entity than an act ofgeographical renaming.

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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 inMumbai, Republic of India; Persian Gulf, south of Iran (formerly Persia); and the University ofMadras, Madras Stock Exchange, the Madras High Court, and IIT Madras in Chennai, Republic ofIndia.

Contents1 Naming disputes2 Significant name changes

2.1 Countries and territories2.2 Subnational entities2.3 Cities and towns

3 Changes resulting from splits and mergers4 Unusual name changes5 See also6 References7 External links

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Investigation of the Staphylococcus aureus GraSRRegulon Reveals Novel Links to Virulence, StressResponse and Cell Wall Signal Transduction PathwaysMelanie Falord1,2, Ulrike Mader3, Aurelia Hiron1,2, Michel Dbarbouille1,2, 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 themajor human pathogen Staphylococcus aureus. We demonstrated that graX, also involved in CAMP resistance andcotranscribed 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) locatedupstream from GraR-regulated genes (mprF and the dlt and vraFG operons), which we show to be essential fortranscriptional 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 theGraSR TCS is required for growth of S. aureus at high temperatures and resistance to oxidative stress. The GraSR system haspreviously been shown to play a role in S. aureus pathogenesis and we have uncovered previously unsuspected links withthe AgrCA peptide quorum-sensing system controlling virulence gene expression. We also show that the GraSR TCS controlsstress 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 thissystem to stress response, cell wall and pathogenesis control pathways.

Citation: Falord M, Mader U, Hiron A, Debarbouille M, Msadek T (2011) Investigation of the Staphylococcus aureus GraSR Regulon Reveals Novel Links toVirulence, 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: ! 2011 Falord et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permitsunrestricted 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 InstitutPasteur (PTR Nu256 and PTR Nu336). Melanie Falord received a Young Scientist Fellowship from the Conseil Pasteur-Weizmann. The funders had no role in studydesign, 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 acommensal and a major Gram-positive pathogen, causing a varietyof infections ranging from superficial skin abscesses to more seriousdiseases such as pneumonia, meningitis, endocarditis, septicemiaand toxic shock syndrome [1]. The ubiquitous nature of thispathogen stems mostly from its capacity to survive a large variety ofenvironmental conditions as well as an impressive ability to resisthost innate immune defense mechanisms and produce systemicinfections, often in healthy humans [2,3]. This unique adaptivepotential has made S. aureus one of the major causes of nosocomialinfections today, compounded by the rapid emergence of multipleantibiotic-resistant strains over the past few decades [4], particularlymethicillin and vancomycin-intermediate resistant strains (MRSAand VISA). Until recently, vancomycin had remained the weaponof last resort, but the recent appearance of the enterococcal vanAvancomycin-resistance gene cluster in S. aureus highlights thegrowing threat this bacterium poses to human health and theurgent need for developing novel therapeutic approaches [5,6].

Cationic antimicrobial peptides (CAMPs) are an importantcomponent of host innate immunity and understanding themolecular mechanisms involved in resistance is a key factor in

staphylococcal treatment research. CAMPs have both cationic andamphipathic properties and are classified according to their lengthand secondary structure [7]. They are produced by certainimmune, skin and epithelial cells in all living kingdoms, as defensesagainst microbial proliferation, and many are known to act byforming pores in the cell membrane, through interactions withbacterial cell envelope components [8]. However, recent work hasshown that several CAMPs, including indolicidin and colistin, canalso kill by inhibiting intracellular processes such as protein andDNA 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 thesemechanisms by coordinating the expression of resistance genes,when CAMPs are detected at the cell surface. TCSs are typicallycomposed of a membrane histidine kinase (HK), acting as a signalsensor/transducer, through phosphorylation of its cognate response

PLoS ONE | www.plosone.org 1 July 2011 | Volume 6 | Issue 7 | e21323