東華大學圖書館 |

語系: 繁體中文

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

Lipoprotein interactions with the ar...

Mullick, Adam Emile.

FindBook

Google Book

Amazon

博客來

Lipoprotein interactions with the arterial wall: Pro- vs. anti-atherogenic effects.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Lipoprotein interactions with the arterial wall: Pro- vs. anti-atherogenic effects./
作者:	Mullick, Adam Emile.
面頁冊數:	103 p.
附註:	Source: Dissertation Abstracts International, Volume: 64-07, Section: B, page: 3028.
Contained By:	Dissertation Abstracts International64-07B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3097979

Lipoprotein interactions with the arterial wall: Pro- vs. anti-atherogenic effects.
Mullick, Adam Emile.

Lipoprotein interactions with the arterial wall: Pro- vs. anti-atherogenic effects. - 103 p.

Source: Dissertation Abstracts International, Volume: 64-07, Section: B, page: 3028.

Thesis (Ph.D.)--University of California, Davis, 2003.

Complications from atherosclerosis represent a major cause of morbidity and mortality in western society. This disease process is characterized as a chronic inflammatory process that occurs within the vascular wall. There remain questions as to what factors initiate and advance the injury, but it is widely held that the process requires both the deposition of lipids within the vascular wall and an inappropriate inflammatory response. The hypotheses of this dissertation revolve around the putative pro- and anti-atherogenic effects of plasma lipoproteins and their components. Specifically, this dissertation addresses the following: (1) Are triglyceride-rich lipoproteins such as very low density lipoprotein (VLDL) atherogenic? (2) Can plasma lipoprotein apolipoprotein E3 (apoE3) directly protect against vascular lipid accumulation? and (3) Does apoE directly modulate vascular inflammation? With this work, we hope to clarify the role of some of the important factors that contribute to, or impede, the initiation and progression of atherosclerotic vascular disease.Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Lipoprotein interactions with the arterial wall: Pro- vs. anti-atherogenic effects.
LDR:03362nmm 2200301 4500 001 1860785
005 20041108070324.5
008 130614s2003 eng d
035 $a (UnM)AAI3097979
035 $a AAI3097979
040 $a UnM $c UnM
100 1 $a Mullick, Adam Emile. $3 1948413
245 1 0 $a Lipoprotein interactions with the arterial wall: Pro- vs. anti-atherogenic effects.
300 $a 103 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-07, Section: B, page: 3028.
500 $a Adviser: J. C. Rutledge.
502 $a Thesis (Ph.D.)--University of California, Davis, 2003.
520 $a Complications from atherosclerosis represent a major cause of morbidity and mortality in western society. This disease process is characterized as a chronic inflammatory process that occurs within the vascular wall. There remain questions as to what factors initiate and advance the injury, but it is widely held that the process requires both the deposition of lipids within the vascular wall and an inappropriate inflammatory response. The hypotheses of this dissertation revolve around the putative pro- and anti-atherogenic effects of plasma lipoproteins and their components. Specifically, this dissertation addresses the following: (1) Are triglyceride-rich lipoproteins such as very low density lipoprotein (VLDL) atherogenic? (2) Can plasma lipoprotein apolipoprotein E3 (apoE3) directly protect against vascular lipid accumulation? and (3) Does apoE directly modulate vascular inflammation? With this work, we hope to clarify the role of some of the important factors that contribute to, or impede, the initiation and progression of atherosclerotic vascular disease.
520 $a In our first two studies we utilized a novel vessel perfusion apparatus to demonstrate that VLDL is capable of contributing to vascular lipid accumulation only if undergoing lipolysis. Furthermore, this study is the first to directly demonstrate HDL-dependent reverse lipid transport from the vascular wall. Next, we demonstrate a previously unknown function of apoE3; it can prevent the penetration of lipid into the arterial wall. Furthermore, we establish a key role of lipoprotein lipase and heparan sulfate proteoglycans in mediating this effect. In the last study, we used cultured endothelial cells to demonstrate that apoE3 can attenuate TNF-induced cell activation, partly via a nitric oxide(NO)-dependent pathway. Finally, with dose response experiments of NO, we reveal a biphasic effect of NO on cell activation; low to moderate levels of NO augment TNF-induced cellular activation, whereas high levels of NO attenuate inflammation.
520 $a Considering the evidence for the atheroprotective effects of HDL, apoE3, and NO, a better understanding of their vascular wall effects could help in developing a therapeutic agent effective in thwarting premature atherosclerosis. A clarification of the pathogenesis and pathophysiology of atherosclerosis will be important in a disease that is responsible for enormous morbidity and mortality in western societies.
590 $a School code: 0029.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Chemistry, Biochemistry. $3 1017722
690 $a 0433
690 $a 0307
690 $a 0487
710 2 0 $a University of California, Davis. $3 1018682
773 0 $t Dissertation Abstracts International $g 64-07B.
790 1 0 $a Rutledge, J. C., $e advisor
790 $a 0029
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3097979