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Characterizing inflammatory response...

Pan, Jonathan Zhiyong.

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Characterizing inflammatory response after traumatic spinal cord injury and identification of protective anti-inflammatory mechanisms by microarrays.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Characterizing inflammatory response after traumatic spinal cord injury and identification of protective anti-inflammatory mechanisms by microarrays./
作者:	Pan, Jonathan Zhiyong.
面頁冊數:	175 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0102.
Contained By:	Dissertation Abstracts International65-01B.
標題:	Biology, Neuroscience. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3118351
ISBN:	049665775X

Characterizing inflammatory response after traumatic spinal cord injury and identification of protective anti-inflammatory mechanisms by microarrays.
Pan, Jonathan Zhiyong.

Characterizing inflammatory response after traumatic spinal cord injury and identification of protective anti-inflammatory mechanisms by microarrays. - 175 p.

Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0102.

Thesis (Ph.D.)--Rutgers The State University of New Jersey - Newark, 2004.

Spinal cord injury (SCI) triggers an inflammatory response, which contributes to the secondary tissue damage following primary injury. Cytokines can be produced locally in spinal cord, as well as by infiltrating peripheral leukocytes and are responsible for initiation of inflammation. After SCI, cytokines mediate the multi-directional communication between different cell types and regulate their functional activities, including effector T lymphocytes. Inflammation can be both protective and destructive, with less understood mechanisms. In the clinic, an anti-inflammatory therapy methylprednisolone (MP) is effective in reducing inflammation, diminishing tissue loss and improving functional recovery.

ISBN: 049665775XSubjects--Topical Terms:

1017680
Biology, Neuroscience.

Characterizing inflammatory response after traumatic spinal cord injury and identification of protective anti-inflammatory mechanisms by microarrays.
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245 1 0 $a Characterizing inflammatory response after traumatic spinal cord injury and identification of protective anti-inflammatory mechanisms by microarrays.
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500 $a Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0102.
500 $a Director: Ronald P. Hart.
502 $a Thesis (Ph.D.)--Rutgers The State University of New Jersey - Newark, 2004.
520 $a Spinal cord injury (SCI) triggers an inflammatory response, which contributes to the secondary tissue damage following primary injury. Cytokines can be produced locally in spinal cord, as well as by infiltrating peripheral leukocytes and are responsible for initiation of inflammation. After SCI, cytokines mediate the multi-directional communication between different cell types and regulate their functional activities, including effector T lymphocytes. Inflammation can be both protective and destructive, with less understood mechanisms. In the clinic, an anti-inflammatory therapy methylprednisolone (MP) is effective in reducing inflammation, diminishing tissue loss and improving functional recovery.
520 $a In the current study, the goal is to clarify inflammatory mechanisms following SCI. The data demonstrate that: First, cytokine protein, stored locally in spinal cord prior to injury, contributes to additional cytokine mRNA induction after SCI. Initiation of inflammation is a local tissue response and doesn't require infiltrating peripheral cells. Second, in mice over-expressing MBP reactive T lymphocytes, predominant intraspinal TH1 cytokine expression and weak neurotrophin and TH2 responses are correlated with the pathogenic effects of autoreactive T lymphocytes, which were associated with impaired neurological and behavioral deficits in the transgenic mice after spinal cord contusion. Finally, it is also the objective of this research to study the effects of different anti-inflammatory compounds using microarrays and to identify patterns of gene response for distinct neuroprotective mechanisms. It was found that a small cluster of genes was consistently up-regulated only by a cyclooxygenase-2 (COX-2) inhibitor as judged by multiple statistical analyses. In vivo testing of this drug proved its efficacy in reducing lesion volumes after SCI.
520 $a This study provides evidence that inflammatory cytokine itself is not a practical target to reduce inflammation right after SCI and may contribute to the net effect of T cell-mediated autoimmunity. Moreover, it is valuable to use microarrays to screen drugs for their biological effects, which may help us to identify protective therapeutic intervention for SCI.
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