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

Feedback Regulation of Human Hematop...

Qiao, Wenlian.

FindBook

Google Book

Amazon

博客來

Feedback Regulation of Human Hematopoietic Stem Cell Fate.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Feedback Regulation of Human Hematopoietic Stem Cell Fate./
作者:	Qiao, Wenlian.
面頁冊數:	216 p.
附註:	Source: Dissertation Abstracts International, Volume: 77-07(E), Section: B.
Contained By:	Dissertation Abstracts International77-07B(E).
標題:	Biomedical engineering. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10014499
ISBN:	9781339485317

Feedback Regulation of Human Hematopoietic Stem Cell Fate.
Qiao, Wenlian.

Feedback Regulation of Human Hematopoietic Stem Cell Fate. - 216 p.

Source: Dissertation Abstracts International, Volume: 77-07(E), Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2015.

Hematopoietic stem cell (HSC) fate decisions at least in part determine cellular composition of the hematopoietic system. It is known that differentiated blood cells produce ligands that act on HSCs to influence HSC fate. However, fundamentals underlying the feedback regulation of HSC fate are poorly understood. Here, we explored the fundamentals of the feedback regulation of HSC fate at the microenvironmental, intercellular (between cells), and intracellular (inside a cell) levels. First, we developed a machine learning algorithm to decompose heterogeneous blood cell samples isolated from cell culture. The results suggest the microenvironmental condition in which HSCs reside affects their transcriptional program. Further, we explicitly mapped feedback signals from 11 differentiated blood cells to HSCs by integrating microarray data, bioinformatics databases, and high content in vitro screening data. The results demonstrate the existence of blood cell type-specific feedback effect on HSC fate decisions. Intriguingly, we found that HSC self-renewal inducing ligands and proliferation inducing ligands were enriched in the NF-kappaB pathway and the STAT3 pathway, respectively. We constructed a kinetic model of the NF-kappaB -- STAT3 pathway. The model serves a foundation for future development and optimization, and the final model could generate hypotheses of extracellular and intracellular intervention for controlling in vitro HSC expansion. Overall, this work has laid a conceptual and technical foundation for investigating cell-cell communication in other multicellular dynamic systems; one important application is in the use of cell-cell communication as a therapeutic avenue to treat various diseases.

ISBN: 9781339485317Subjects--Topical Terms:

535387
Biomedical engineering.

Feedback Regulation of Human Hematopoietic Stem Cell Fate.
LDR:02595nmm a2200277 4500 001 2077116
005 20161114130225.5
008 170521s2015 ||||||||||||||||| ||eng d
020 $a 9781339485317
035 $a (MiAaPQ)AAI10014499
035 $a AAI10014499
040 $a MiAaPQ $c MiAaPQ
100 1 $a Qiao, Wenlian. $3 3192607
245 1 0 $a Feedback Regulation of Human Hematopoietic Stem Cell Fate.
300 $a 216 p.
500 $a Source: Dissertation Abstracts International, Volume: 77-07(E), Section: B.
500 $a Adviser: Peter W. Zandstra.
502 $a Thesis (Ph.D.)--University of Toronto (Canada), 2015.
520 $a Hematopoietic stem cell (HSC) fate decisions at least in part determine cellular composition of the hematopoietic system. It is known that differentiated blood cells produce ligands that act on HSCs to influence HSC fate. However, fundamentals underlying the feedback regulation of HSC fate are poorly understood. Here, we explored the fundamentals of the feedback regulation of HSC fate at the microenvironmental, intercellular (between cells), and intracellular (inside a cell) levels. First, we developed a machine learning algorithm to decompose heterogeneous blood cell samples isolated from cell culture. The results suggest the microenvironmental condition in which HSCs reside affects their transcriptional program. Further, we explicitly mapped feedback signals from 11 differentiated blood cells to HSCs by integrating microarray data, bioinformatics databases, and high content in vitro screening data. The results demonstrate the existence of blood cell type-specific feedback effect on HSC fate decisions. Intriguingly, we found that HSC self-renewal inducing ligands and proliferation inducing ligands were enriched in the NF-kappaB pathway and the STAT3 pathway, respectively. We constructed a kinetic model of the NF-kappaB -- STAT3 pathway. The model serves a foundation for future development and optimization, and the final model could generate hypotheses of extracellular and intracellular intervention for controlling in vitro HSC expansion. Overall, this work has laid a conceptual and technical foundation for investigating cell-cell communication in other multicellular dynamic systems; one important application is in the use of cell-cell communication as a therapeutic avenue to treat various diseases.
590 $a School code: 0779.
650 4 $a Biomedical engineering. $3 535387
650 4 $a Cellular biology. $3 3172791
690 $a 0541
690 $a 0379
710 2 $a University of Toronto (Canada). $b Biomedical Engineering. $3 2101094
773 0 $t Dissertation Abstracts International $g 77-07B(E).
790 $a 0779
791 $a Ph.D.
792 $a 2015
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10014499