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Fetal mouse heart in organ structure: ultrastructure.
The fetal mouse heart in organ culture: maintenance of the differentiated state.
A low dose of A61603 (10 ng/kg/d) activated ERK in the mouse heart in vivo, but did not change blood pressure.
This study directly compares morphological features of the mouse heart in its end-relaxed state based on constructed morphometric maps and atlases using principal component analysis in C57BL/6J (n=8) and DBA (n=5) mice.
The effects of heart rate (HR) on myocardial contractility in the mouse heart in situ were first investigated in open-chest mice (n = 7) by left ventricular (LV) catheter-tip micromanometry.
To find that gene, developmental biologist Deepak Srivastava of the University of Texas Southwestern Medical Center at Dallas and colleagues studied development of the mouse heart, in which a transcription factor called dHAND was known to turn on an array of crucial genes.
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Ingwall JS, Wildential K. Fetal mouse hearts in organ culture.
Perfusion of mouse hearts in the absence of ApoE and ApoCII yielded LPL-dependent uptake of intralipid emulsions [54].
Like miR-1, miR-25 has also been reported to repress the postnatal expression of Hand2 in cultured cardiomyocytes and in mouse hearts in vivo.
More than 100 lncRNAs were shown to be differentially expressed in hypertrophic mouse hearts in a recent RNA-seq analysis (Lee et al., 2011).
For these experiments, myocytes isolated from Na/Ca exchanger 1 (NCX1) knockout mouse hearts, in which ouabain induces hypertrophy but no increase in contractility, were used.
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