1 edition of Endocardial endothelium found in the catalog.
Includes bibliographical references (p. -139) and index.
|The Physical Object|
|Pagination||xvi, 137 p. :|
|Number of Pages||83|
|2||Medical intelligence unit (Unnumbered)|
|3||Medical intelligence unit|
nodata File Size: 2MB.
When the valve formation is initiated, valve endothelial cells, a subpopulation of endocardium expressing JB3 and lining the AVC and OFT, exhibit activated Dll4-Notch signaling.
We observed significant differences between base and apex for time-averaged magnitude, axial and circumferential WSS. Background Myocardial function is regulated by endocardial endothelium EE.
With cellular trajectory analysis from single-cell RNA-seq of aortic valve leaflets in calcific aortic valve disease CAVD patients, it has been reported that valve endothelial cells may participate in the calcification and thickening of aortic valve disease though more active EndoMT, demonstrated by greater expressions of secreted protein acidic and rich in cysteine and mesenchymal markers Col1A1 and Cnn1 in transformed valve endothelial cells of CAVD patients than healthy controls.
As a consequence, this surprisingly large contact surface area of the EE offers an astonishingly high ratio of cavitary surface area to ventricular volume more so in the right than in the left ventriclesuggesting an important sensor function for the EE. What evidence do we Endocardial endothelium at present that the EE would, by analogy with the capillary endothelium of the blood—brain barrier, function as a blood—heart barrier?
In our study, we further evaluated a possible involvement of the nitric oxide pathway in the observed EE-dependent effects of thiopental.
Huang Endocardial endothelium W, Sherman BT, Lempicki RA. Muscles were allowed to stabilize for 30 min at each concentration before measurements were recorded for analysis. FFR was measured in intact trabeculae controlendocardial endothelium-denuded trabeculae EEDand EED trabeculae treated with a low concentration of ISO 0. As our results show, it also results in strong precocious induction of endocardial nfatc1 expression, as analyzed at the 20-somite stage.
Expression of MFng is promoted in endocardial during trabeculation, but is required to be down-regulated during compaction to activate myocardial Jag1 and Jag2 signaling to Notch1. Etv2 directly binds to Fox:Ets consensus sequence within the nfatc1 promoter Our results show that Etsrp function is both necessary and sufficient for early endocardial nfatc1 expression.
7 Departments of Radiology, Northwestern University, Chicago, IL, USA.
Single cell analysis of a mouse model of ventricular non-compaction and in vitro assays of cardiomyocyte growth demonstrated that coronary endothelial cells ECs normally promote myocardial compaction through secreted factors, but that endocardial and ECs can contribute to noncompaction under pathological conditions.