語系:
繁體中文
English
說明(常見問題)
回圖書館首頁
手機版館藏查詢
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
Neuroimmune mediators in rheumatoid ...
~
Alex, Philip Jacob.
FindBook
Google Book
Amazon
博客來
Neuroimmune mediators in rheumatoid arthritis.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Neuroimmune mediators in rheumatoid arthritis./
作者:
Alex, Philip Jacob.
面頁冊數:
178 p.
附註:
Chair: Michael B. Centola.
Contained By:
Dissertation Abstracts International66-09B.
標題:
Biology, Molecular. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3188535
ISBN:
9780542342004
Neuroimmune mediators in rheumatoid arthritis.
Alex, Philip Jacob.
Neuroimmune mediators in rheumatoid arthritis.
- 178 p.
Chair: Michael B. Centola.
Thesis (Ph.D.)--The University of Oklahoma Health Sciences Center, 2005.
The mystery of rheumatoid arthritis is plagued by its intricacy. Characterized as a prevalent autoimmune, chronic and progressive systemic disease, rheumatoid arthritis (RA) owes its complexity to its multifactorial etiopathogenesis and clinical heterogeneity. The immune system has the ability to 'sense' pathological influences and relays it to the central nervous system, either directly by crossing the blood brain barrier or indirectly through sensory receptors or the afferent vagus nerve. These afferent signals are synchronized and processed at the central nervous system following which efferent signals are relayed through the efferent vagus nerve and the hypothalamo-pituitary-adrenal axis to influence anti-inflammatory signals back into the immune system. Neuropeptides and cytokines therefore serve as the molecular basis of a neuro-immune axis that, through the autonomic nervous system, provides antiinflammatory feedback to the immune system. Dysregulation of this pathway through the disruption of the synapse between the cholinergic nervous system and the immune system may be an early primary event in the overproduction of cytokines and the pathophysiology of RA, perhaps during the optimal window for aggressive therapeutic strategy in RA. Introducing appropriate therapy early in the course of RA before permanent damage to the joints has occurred can minimize disease severity and may limit pathologic immune system changes later in the course of the disease. This dissertation explored the above hypothesis using clinical, genomic, proteomic and bioinformatic approaches in patients with early RA. This approach has expounded plausible annotations into pathogenic neuroimmune mechanisms and has enabled the identification of novel molecular neuroimmune mediators as potential therapeutic targets in RA.
ISBN: 9780542342004Subjects--Topical Terms:
1017719
Biology, Molecular.
Neuroimmune mediators in rheumatoid arthritis.
LDR
:02750nam 2200301 a 45
001
965561
005
20110906
008
110906s2005 eng d
020
$a
9780542342004
035
$a
(UnM)AAI3188535
035
$a
AAI3188535
040
$a
UnM
$c
UnM
100
1
$a
Alex, Philip Jacob.
$3
1288333
245
1 0
$a
Neuroimmune mediators in rheumatoid arthritis.
300
$a
178 p.
500
$a
Chair: Michael B. Centola.
500
$a
Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4651.
502
$a
Thesis (Ph.D.)--The University of Oklahoma Health Sciences Center, 2005.
520
$a
The mystery of rheumatoid arthritis is plagued by its intricacy. Characterized as a prevalent autoimmune, chronic and progressive systemic disease, rheumatoid arthritis (RA) owes its complexity to its multifactorial etiopathogenesis and clinical heterogeneity. The immune system has the ability to 'sense' pathological influences and relays it to the central nervous system, either directly by crossing the blood brain barrier or indirectly through sensory receptors or the afferent vagus nerve. These afferent signals are synchronized and processed at the central nervous system following which efferent signals are relayed through the efferent vagus nerve and the hypothalamo-pituitary-adrenal axis to influence anti-inflammatory signals back into the immune system. Neuropeptides and cytokines therefore serve as the molecular basis of a neuro-immune axis that, through the autonomic nervous system, provides antiinflammatory feedback to the immune system. Dysregulation of this pathway through the disruption of the synapse between the cholinergic nervous system and the immune system may be an early primary event in the overproduction of cytokines and the pathophysiology of RA, perhaps during the optimal window for aggressive therapeutic strategy in RA. Introducing appropriate therapy early in the course of RA before permanent damage to the joints has occurred can minimize disease severity and may limit pathologic immune system changes later in the course of the disease. This dissertation explored the above hypothesis using clinical, genomic, proteomic and bioinformatic approaches in patients with early RA. This approach has expounded plausible annotations into pathogenic neuroimmune mechanisms and has enabled the identification of novel molecular neuroimmune mediators as potential therapeutic targets in RA.
590
$a
School code: 0361.
650
4
$a
Biology, Molecular.
$3
1017719
650
4
$a
Biology, Neuroscience.
$3
1017680
650
4
$a
Health Sciences, Immunology.
$3
1017716
650
4
$a
Health Sciences, Pathology.
$3
1017854
690
$a
0307
690
$a
0317
690
$a
0571
690
$a
0982
710
2 0
$a
The University of Oklahoma Health Sciences Center.
$3
1023966
773
0
$t
Dissertation Abstracts International
$g
66-09B.
790
$a
0361
790
1 0
$a
Centola, Michael B.,
$e
advisor
791
$a
Ph.D.
792
$a
2005
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3188535
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9125162
電子資源
11.線上閱覽_V
電子書
EB W9125162
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入