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The role of inducible nitric oxide synthase in macrophage activation following acute lung injury

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TitleInfo
Title
The role of inducible nitric oxide synthase in macrophage activation following acute lung injury
Name (type = personal)
NamePart (type = family)
Golden
NamePart (type = given)
Thea Noreen
NamePart (type = date)
1986-
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Thea Noreen Golden
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RoleTerm (authority = RULIB)
author
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ANDREW
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ANDREW GOW
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Advisory Committee
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chair
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Laskin
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Debra
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Debra Laskin
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Advisory Committee
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internal member
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Guo
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Grace
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Grace Guo
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Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Laumbach
NamePart (type = given)
Robert
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Robert Laumbach
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Advisory Committee
Role
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internal member
Name (type = personal)
NamePart (type = family)
Ischiropoulos
NamePart (type = given)
Harry
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Harry Ischiropoulos
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School - New Brunswick
Role
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school
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Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2016
DateOther (qualifier = exact); (type = degree)
2016-10
CopyrightDate (encoding = w3cdtf); (qualifier = exact)
2016
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Macrophage origin and activity is complex in response to acute lung injury. Inducible nitric oxide synthase (iNOS) has a divergent role in the stages following intratracheal bleomycin mediated lung injury (ITB). We hypothesize iNOS is necessary for macrophage activation during the inflammatory and resolution phases that follow ITB. Further, recruited macrophages classically activate during inflammation and resident macrophages alternatively activate during resolution. To test these hypotheses, iNOS was manipulated via scavenge of products, systemic selective iNOS inhibition and chimeric mice in which particular populations were NOS2-/-. C57/BL6 mice were intratracheally instilled with bleomycin and samples collected 8 and 15 days following instillation. This work identified oxidants to promote inflammation during the early stages following ITB. Systemic iNOS inhibition reduced classical activation of recruited macrophages during inflammation and alternative activation of recruited macrophages during resolution. Resident macrophage alternative activation was not dependent on iNOS activity. Chimeric mice demonstrated iNOS of a particular cell population is necessary for macrophage activation. Classical activation of recruited cells is dependent on recruited cell iNOS. Early alternative activation is promoted when recruited macrophages were iNOS incompetent. A pulmonary source of iNOS plays a role in alternative activation during resolution. This work has demonstrated iNOS is important to classical and alternative activation of macrophages. The cell population expressing iNOS determines the effect on activation. The complexity of macrophage populations and effect of iNOS activity on macrophage activation furthers our understanding of the response to ITB and adapted therapeutic approaches have potential for clinical improvement.
Subject (authority = RUETD)
Topic
Toxicology
Subject (authority = ETD-LCSH)
Topic
Lungs--Wounds and injuries
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
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ETD
Identifier
ETD_7590
PhysicalDescription
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electronic resource
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application/pdf
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text/xml
Extent
1 online resource (xii, 137 p. : ill.)
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Thea Noreen Golden
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3HM5BRV
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Golden
GivenName
Thea
MiddleName
Noreen
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2016-09-19 12:02:45
AssociatedEntity
Name
Thea Golden
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
AssociatedObject
Type
License
Name
Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
RightsEvent
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2016-10-31
DateTime (encoding = w3cdtf); (qualifier = exact); (point = end)
2017-10-31
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after October 31st, 2017.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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