東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Using a gene transfer technique to s...

Smith, Robert Stephen, Jr.

Linked to FindBook

Google Book

Amazon

博客來

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction./
Author:	Smith, Robert Stephen, Jr.
Description:	156 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1702.
Contained By:	Dissertation Abstracts International65-04B.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3129378
ISBN:	0496766388

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.
Smith, Robert Stephen, Jr.

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction. - 156 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1702.

Thesis (Ph.D.)--Medical University of South Carolina, 2004.

Endothelial nitric oxide synthase (eNOS) plays a vital role in cardiovascular homeostasis. Nitric oxide (NO), generated from eNOS, is involved in various processes including blood pressure regulation, endothelial function, vessel growth, and cardiac function. Cardiovascular ischemic disease results in decreased blood flow and prevents tissues from obtaining vital nutrients, leading to adaptive responses which are in part mediated by NO. In order to elucidate the role of NO in cardiovascular ischemic disease, gene transfer of eNOS using an adenovirus vector was used in models of rat hindlimb ischemia and myocardial infarction.

ISBN: 0496766388Subjects--Topical Terms:

1017719
Biology, Molecular.

Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.
LDR:03071nmm 2200313 4500 001 1840335
005 20050721102959.5
008 130614s2004 eng d
020 $a 0496766388
035 $a (UnM)AAI3129378
035 $a AAI3129378
040 $a UnM $c UnM
100 1 $a Smith, Robert Stephen, Jr. $3 1928675
245 1 0 $a Using a gene transfer technique to study the role of endothelial nitric oxide synthase in neovascularization and myocardial infarction.
300 $a 156 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1702.
500 $a Director: Julie Chao.
502 $a Thesis (Ph.D.)--Medical University of South Carolina, 2004.
520 $a Endothelial nitric oxide synthase (eNOS) plays a vital role in cardiovascular homeostasis. Nitric oxide (NO), generated from eNOS, is involved in various processes including blood pressure regulation, endothelial function, vessel growth, and cardiac function. Cardiovascular ischemic disease results in decreased blood flow and prevents tissues from obtaining vital nutrients, leading to adaptive responses which are in part mediated by NO. In order to elucidate the role of NO in cardiovascular ischemic disease, gene transfer of eNOS using an adenovirus vector was used in models of rat hindlimb ischemia and myocardial infarction.
520 $a After induction of hindlimb ischemia and eNOS gene delivery, rats showed increased blood perfusion as evidenced by laser Doppler perfusion imaging and a fluorescent microsphere assay compared to rats injected with control virus. Capillary density also significantly increased in eNOS-injected rats. The effects of eNOS gene transfer were abolished by concomitant delivery of adenovirus encoding a dominant negative form of phosphatidylinosiltol-3 kinase (PI3K). In addition, eNOS gene transfer resulted in increased phosphorylation of Akt/PKB in a context of hindlimb ischemia, suggesting that the effects of NO on neovascularization were mediated in part through the PI3K-Akt pathway.
520 $a The effects of eNOS genie delivery were also evaluated in a rat model of myocardial infarction. Six weeks after gene transfer, rats receiving eNOS adenovirus via tail vein injection had improved cardiac performance, attenuation of cardiac hypertrophy and fibrosis, as well as decreased levels of apoptosis compared to rats with MI receiving a control virus. eNOS gene delivery resulted in suppression of oxidative stress induced by MI which led to decreases in TGF-beta1 and p27 expression, JNK activation, and nuclear translocation of NF-kappaB, proteins known to be induced by reactive oxygen species. Taken together, these results suggest that NO protects the heart against left ventricle remodeling by inhibiting oxidative stress induced by MI.
590 $a School code: 0122.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0307
690 $a 0433
690 $a 0571
710 2 0 $a Medical University of South Carolina. $3 700119
773 0 $t Dissertation Abstracts International $g 65-04B.
790 1 0 $a Chao, Julie, $e advisor
790 $a 0122
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3129378