Sentence examples for mouse heart revealed from inspiring English sources
Consistent with this, in situ hybridization of cross-sections of the adult mouse heart revealed a very strong signal for miR-143 and -145 in the walls of the aorta and coronary vessels (Fig. 1d).
Cell fate tracking of cardiomyocytes from 4-OH-Tamoxifen-treated double-transgenic MerCreMer/ZEG mouse hearts revealed that green fluorescent protein (GFP) continues to be expressed in dedifferentiated cardiomyocytes, two-thirds of which were also c-kit+.
Hystological analysis of the exercised Sgca-; Sgce-null mice heart revealed extensive alterations including large and numerous foci of necrosis (Fig. 8B), and the Masson Trichrome staining (Fig. 8C) and Evan's blue dye uptake (Fig. 8D) confirmed the presence of fibrotic and necrotic tissue and inflammatory infiltration.
Comparison with a mouse heart proteome revealed conservation at the level of molecular function, biological processes and cellular components.
Western blot analysis of mouse heart homogenates revealed a single band with molecular weight corresponding to Top2b (time 0 h, Figure 1A).
A mouse model harboring embryonic deletion of Sav1, Mst1/2 or Lats2 in the heart revealed the importance of these Hippo components for proper organ development [60].
Staining for PCM-1 on tissue sections of adult mouse hearts also revealed a good overlap with the H2B-mCh signal (Fig. 2i).
Moreover, quantitative RT-PCR analysis of gene expression in sensory ganglia and heart revealed that no gene compensation for muscarinic acetylcholines receptors and beta-adrenalin receptors were found in Asic3−/− mice.
Analyses of non-ruptured hearts revealed increased oxidative stress, reduced PAI-1 activity and enhanced VEGFα transcription in Hp−/− mice.
Histological analysis of 3 and 7 days old non-ruptured infarcted hearts revealed more frequent and more severe intramural hemorrhage and increased leukocyte infiltration in Hp−/− mice.
Our re-evaluation of Enpep expression in the developing mouse heart by in situ hybridization reveals co-expression with Pitx2 in the pulmonary veins, a region with pro-arrhythmogenic potential [ 57], and in the SAN of the right atria, a key component of the cardiac conduction system where the electrical impulse is generated.
