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 到查詢結果 [ null ]

切換: 標籤 | MARC模式 | ISBD

Mechanisms of calcium alternans in c...

Lee, Young-Seon.

FindBook

Google Book

Amazon

博客來

Mechanisms of calcium alternans in cardiac cells.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mechanisms of calcium alternans in cardiac cells./
作者:	Lee, Young-Seon.
面頁冊數:	103 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0303.
Contained By:	Dissertation Abstracts International67-01B.
標題:	Mathematics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3200182
ISBN:	9780542472275

Mechanisms of calcium alternans in cardiac cells.
Lee, Young-Seon.

Mechanisms of calcium alternans in cardiac cells. - 103 p.

Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0303.

Thesis (Ph.D.)--The University of Utah, 2006.

Life-threatening cardiac arrhythmia is the most common cause of sudden cardiac death, killing more than 400,000 people each year. Abnormal calcium (Ca2+) handling has recently been suggested as a potential initiator of arrhythmia. One example of abnormal Ca2+ handling in cardiac cells is Ca2+ alternans; characterized by a beat-to-beat alternation in the amplitude of the intracellular Ca2+ transient at a constant rate of electrical stimulus. In this dissertation we, use mathematical model to explore possible underlying mechanisms of Ca2+ alternans.

ISBN: 9780542472275Subjects--Topical Terms:

515831
Mathematics.

Mechanisms of calcium alternans in cardiac cells.
LDR:03346nmm 2200337 4500 001 1827546
005 20070104081201.5
008 130610s2006 eng d
020 $a 9780542472275
035 $a (UnM)AAI3200182
035 $a AAI3200182
040 $a UnM $c UnM
100 1 $a Lee, Young-Seon. $3 1916472
245 1 0 $a Mechanisms of calcium alternans in cardiac cells.
300 $a 103 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0303.
500 $a Adviser: James P. Keener.
502 $a Thesis (Ph.D.)--The University of Utah, 2006.
520 $a Life-threatening cardiac arrhythmia is the most common cause of sudden cardiac death, killing more than 400,000 people each year. Abnormal calcium (Ca2+) handling has recently been suggested as a potential initiator of arrhythmia. One example of abnormal Ca2+ handling in cardiac cells is Ca2+ alternans; characterized by a beat-to-beat alternation in the amplitude of the intracellular Ca2+ transient at a constant rate of electrical stimulus. In this dissertation we, use mathematical model to explore possible underlying mechanisms of Ca2+ alternans.
520 $a Mathematical models and experimental data suggest that a steep and nonlinear dependence of sarcoplasmic reticulum (SR) Ca2+ release on SR Ca2+ content is a mechanism of Ca2+ alternans. Here, we build a time discrete model of Ca2+ movement that uses a nonlinear function of SR release with steep slope. The model shows that reduced effectiveness of SR Ca2+ release leads to a build up of the SR content above a threshold value, causing alternation of the SR content and the Ca2+ transient. The discrete time model prompts further investigation to find what determines the steeply nonlinear function.
520 $a To explore the basis for this steep nonlinear SR Ca2+ dependence, we use a temporal model of Ca2+ cycling to show that reopening of ryanodine receptor (RyR) channel under Ca2+ overload produces spontaneous SR Ca2+ release and yields a nonlinear relationship between SR Ca2+ release and SR content.
520 $a A new RyR kinetic model is built based on the hypothesis that calsequestrin (CSQ), a SR lumenal Ca2+ buffer, inhibits and activates RyR channel activity by sensing the SR lumenal Ca2+ concentration. The RvR, kinetic model is derived systematically by assuming two Ca 2+ binding sites on the cytosolic side and one CSQ binding site within the SR membrane of the RyR channel. A local control model using the RyR kinetic model produces a nonlinear relationship between fractional SR Ca2+ release and SR content similar to experimental data.
520 $a Finally, we use a spatial-temporal model to show that an alternating pattern of Ca2+ wave propagation occurs under Ca2+ overload condition with high rate of Ca2+ stimulation. This model suggests that delayed recovery of refractoriness of the RyR channel is a mechanism of alternans without an alternation of SR content. This mechanism of alternans is different from the steeply nonlinear Ca2+ release function.
590 $a School code: 0240.
650 4 $a Mathematics. $3 515831
650 4 $a Engineering, Biomedical. $3 1017684
650 4 $a Biology, Animal Physiology. $3 1017835
690 $a 0405
690 $a 0541
690 $a 0433
710 2 0 $a The University of Utah. $3 1017410
773 0 $t Dissertation Abstracts International $g 67-01B.
790 1 0 $a Keener, James P., $e advisor
790 $a 0240
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3200182