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

Perfusion studies of trabecular outflow.

Wan, Zhou.

FindBook

Google Book

Amazon

博客來

Perfusion studies of trabecular outflow.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Perfusion studies of trabecular outflow./
作者:	Wan, Zhou.
面頁冊數:	169 p.
附註:	Adviser: William D. Stamer.
Contained By:	Dissertation Abstracts International68-03B.
標題:	Health Sciences, Ophthalmology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3257917

Perfusion studies of trabecular outflow.
Wan, Zhou.

Perfusion studies of trabecular outflow. - 169 p.

Adviser: William D. Stamer.

Thesis (Ph.D.)--The University of Arizona, 2007.

Glaucoma is the second leading cause of irreversible blindness in the United States. It is characterized by progressive loss of retinal ganglion cells with associated loss of vision that is often coupled with elevated intraocular pressure (IOP). Primary open-angle glaucoma (POAG) is the most common form of glaucoma that is caused by increased resistance in the conventional outflow pathway. Unfortunately, the biology and physiology of the human outflow tract and its role in ocular hypertension remains poorly understood. The purpose of our study is to investigate the pharmacological regulation of aqueous outflow in human conventional outflow pathway using anterior segment perfusion model.Subjects--Topical Terms:

1019445
Health Sciences, Ophthalmology.

Perfusion studies of trabecular outflow.
LDR:03308nam 2200289 a 45 001 855178
005 20100708
008 100708s2007 ||||||||||||||||| ||eng d
035 $a (UMI)AAI3257917
035 $a AAI3257917
040 $a UMI $c UMI
100 1 $a Wan, Zhou. $3 1021709
245 1 0 $a Perfusion studies of trabecular outflow.
300 $a 169 p.
500 $a Adviser: William D. Stamer.
500 $a Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1571.
502 $a Thesis (Ph.D.)--The University of Arizona, 2007.
520 $a Glaucoma is the second leading cause of irreversible blindness in the United States. It is characterized by progressive loss of retinal ganglion cells with associated loss of vision that is often coupled with elevated intraocular pressure (IOP). Primary open-angle glaucoma (POAG) is the most common form of glaucoma that is caused by increased resistance in the conventional outflow pathway. Unfortunately, the biology and physiology of the human outflow tract and its role in ocular hypertension remains poorly understood. The purpose of our study is to investigate the pharmacological regulation of aqueous outflow in human conventional outflow pathway using anterior segment perfusion model.
520 $a Human anterior segments were perfusion cultured for one or two weeks while the functional response of cells in the conventional outflow pathway was measured by recording the pressure change in the anterior chamber and the outflow facility was calculated. In addition, the central corneal thickness was recorded every 24 hours during the perfusion and the relationship between functional corneal endothelial cells and viable trabecular meshwork cells were examined. After perfusion-fixation, drainage tissues of each anterior segment were histologically graded. At last, an effective anti-glaucoma agent---bimatoprost and a prostamide specific antagonist were introduced to the anterior segment perfusion model and their pharmacological function in regulating outflow facility in human conventional outflow pathway was investigated. We attained stable outflow facility from the perfusion culture of anterior segment and found that the outflow pathway tissues were viable after dissection and weeks of incubation in the perfusion system. In addition, we found that there was a recovery in central corneal thickness over time of perfusion and this recovery correlated with the viability of the trabecular meshwork tissues. Finally, we observed that bimatoprost increased outflow facility and a prostamide specific antagonist significantly attenuated this effect.
520 $a In conclusion, these studies demonstrate that the tissues of conventional outflow pathway are viable after weeks of perfusion and the function of corneal endothelial cells reflects the viability of the trabecular meshwork cells in conventional outflow pathway. Finally, our data supports that bimatoprost increases outflow facility by targeting a novel receptor in the conventional outflow pathway.
590 $a School code: 0009.
650 4 $a Health Sciences, Ophthalmology. $3 1019445
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0381
690 $a 0419
710 2 $a The University of Arizona. $3 1017508
773 0 $t Dissertation Abstracts International $g 68-03B.
790 $a 0009
790 1 0 $a Stamer, William D., $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3257917