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1 uscle cells and endothelial cells but not in myocardial cells.
2 lpha-actin (alphaCA) transcripts and nascent myocardial cells.
3 ionally modified by other factors present in myocardial cells.
4 s that regulate transcriptional responses in myocardial cells.
5 s to cytokines and acute hypoxia in cultured myocardial cells.
6 and stage 5 cells producing endothelial and myocardial cells.
7 be involved in ischemia/reperfusion death of myocardial cells.
8 acellular calcium handling and shortening in myocardial cells.
9 can cause reversible loss of excitability in myocardial cells.
10 ing is actively repressed in differentiating myocardial cells.
11 interplay of transmembrane ionic currents in myocardial cells.
12 compensate for the absence of BMPRII in the myocardial cells.
13 d calcineurin in endothelial, epicardial and myocardial cells.
14 rdially derived smooth muscle and underlying myocardial cells.
15 role in the differentiation of ES cells into myocardial cells.
16 tivators in differentiation of ES cells into myocardial cells.
17 d away from the plasma membrane in embryonic myocardial cells.
18 ession pattern, including in all contractile myocardial cells.
19 ymphoblastic leukemia (ALL) but also injures myocardial cells.
20 I/R) is associated with an extensive loss of myocardial cells.
21 nd that these factors do not act directly on myocardial cells.
23 capillary density, a higher proliferation of myocardial cells, a lower cardiomyocyte apoptosis, and r
24 laminin receptors are likely responsible for myocardial cell adhesion to the basement membrane, DG ha
25 we conclude that in addition to its role in myocardial cell adhesion, N-cadherin is required for neu
29 Growth of the heart requires addition of myocardial cells along the endocardial-to-myocardial axi
30 We have found no mutation that deletes the myocardial cells altogether, but one, pandora, appears t
32 isruption of fibronectin assembly around the myocardial cells and consequent disorganization of the m
33 ta5 mutants exhibit a much-reduced number of myocardial cells and defects in myocardial gene expressi
35 c factor (ANF) inhibits proliferation in non-myocardial cells and is thought to be anti-hypertrophic
36 activated channels (SACs) have been found in myocardial cells and may promote AF in dilated atria.
38 nditions are thought to emanate from injured myocardial cells and, in most circumstances, have been a
39 uptions in the normal diversification of the myocardial cells, and adults exhibit severe defects in c
40 inuing elucidation of the secondarily adding myocardial cells, and how the different populations iden
41 as vascular smooth muscle, skeletal muscle, myocardial cells, and neurons also express both proteins
42 In the heart, CT-1 is primarily expressed in myocardial cells, and not in endocardial cushion or outf
51 activation, and dedifferentiation of compact myocardial cells as causative for the regenerative failu
52 but not ischemia alone, induced apoptosis in myocardial cells as demonstrated by DNA electrophoresis
53 SERCA2a also enhanced the contraction of the myocardial cells as detected by shortening measurements.
55 audally extended tube consisting entirely of myocardial cells (at both the larval and adult stages);
57 and E8.0, HGF receptor mRNA was detected in myocardial cells before fusion at the ventral midline.
58 1 (MEK1) dominant negative mutant cDNA into myocardial cells blocked the antiapoptotic effects of CT
61 tures of hypertrophy are induced in cultured myocardial cells by alpha1- adrenergic receptor agonists
62 in the initiation of apoptosis induction in myocardial cells by in vitro and in vivo ischemia and re
63 dditionally, while NF-kappaB is activated in myocardial cells by p38, this does not appear to be the
65 l for addressing how embryonic regulators of myocardial cell commitment can contribute to the establi
67 t (wingless)-mediated events may function in myocardial cell compartmentalization during early verteb
68 TNF-alpha and IL-1beta induced depression of myocardial cell contractility at substantially lower con
69 t TNF-alpha and IL-1beta cause depression of myocardial cell contraction in vitro and suggest that th
70 ve been shown to regulate iNOS expression in myocardial cells, cultured neonatal cardiac myocytes wer
72 ed for their potential in causing additional myocardial cell damage during the course of therapeutic
73 nd necrosis have been shown to contribute to myocardial cell death after myocardial ischemia and repe
74 njury, (ii) complete inhibition of apoptotic myocardial cell death as identified by terminal deoxynuc
76 ate the genetics of DCC further, we produced myocardial cell death by freeze-thaw injury to induce DC
77 GLO1-diabetic mice and corresponded to less myocardial cell death compared with the WT-diabetic grou
78 cal and interventional techniques to prevent myocardial cell death during the time of ischemia and su
80 d serum concentrations of cTnI indicate that myocardial cell death is occurring in meningococcal sept
81 ver, clinical studies have demonstrated that myocardial cell death is rare and that cardiac function
83 mechanism for mitochondrial Ca(2+) entry in myocardial cell death, and indicate that mitochondrial-t
84 I (cTnI), a sensitive and specific marker of myocardial cell death, and related this to the severity
85 Commonly used blood markers of AMI reflect myocardial cell death, but do not reflect the earlier pa
88 he cells can thrive, enabling an insult-free myocardial cell delivery to normalize myocardial biomech
91 irst is driven by an asymmetric migration of myocardial cells during cardiac jogging, resulting in th
93 f-beta signaling via Alk5 is not required in myocardial cells during mammalian cardiac development, b
99 genitors of asymmetric cell lineages adopt a myocardial cell fate as opposed to a pericardial fate wh
100 Reprogramming of mouse fibroblasts toward a myocardial cell fate by forced expression of cardiac tra
104 ad-induced HF mice and isolated hypertrophic myocardial cells, fatty acid beta-oxidation and heart fu
105 n of fibroblast proliferation in cultures of myocardial cells from 8-day embryonic chicks was achieve
108 ression of V12Ras in transgenic mice induces myocardial cell growth and expression of genes that are
109 ase other than Ras is involved in regulating myocardial cell growth and gene expression in response t
110 etion of calcineurin in either epicardial or myocardial cells had no effect on coronary vasculature d
112 te that CT-1 can activate a distinct form of myocardial cell hypertrophy, characterized by the promot
114 only of one cell type, either endocardial or myocardial cells; i.e., 95.1% of the mesoderm-derived cl
115 protein (BMP)-2 is known to be expressed in myocardial cells in a manner consistent with the segment
118 yos have large aggregates of N-cadherin(-/-) myocardial cells in the heart lumen, indicating that the
120 olved, and in the young woman, there were no myocardial cells in which these pathways normally exist.
121 revascularization causes the least amount of myocardial cell injury and is associated with superior l
125 activation contributes to the progression of myocardial cell injury, cardiac fibrosis, and left ventr
126 I (cTnI), a sensitive and specific marker of myocardial cell injury, is useful in diagnosing and asse
133 As a result, the number of differentiating myocardial cells is severely reduced whereas pericardial
135 these functions have now been identified in myocardial cells isolated from different species, as wel
136 We find that while sox9b is expressed in myocardial cells, it is not normally expressed in the af
137 viability and induced apoptosis in the H9c2 myocardial cell line measured by flow cytometry and fluo
138 rsist in pig myocardium and can infect human myocardial cells make it an important infectious agent t
139 rmal convergence affected all three modes of myocardial cell migration, probably due to the disruptio
140 urthermore, metformin significantly improved myocardial cell mitochondrial respiration and ATP synthe
143 ish ctr9 mutant with a dramatic reduction in myocardial cell number as well as later defects in primi
145 , the Noggin gene is mainly expressed in the myocardial cells of the outflow tract, atrioventricular
147 ns form electrical conduits between adjacent myocardial cells, permitting rapid spatial passage of th
151 he Gax protein was detected in the nuclei of myocardial cells relatively late in chicken heart develo
155 conduction system is a specialized tract of myocardial cells responsible for maintaining normal card
156 rtrophic response characterized by increased myocardial cell size and activation of fetal cardiac gen
157 fects valve development due to its effect on myocardial cell size and shape, which changes the morpho
161 gly show a critical role for this pathway in myocardial cell specification and heart development.
163 Explantation studies provided evidence that myocardial cell specification is underway by stage 3, in
164 ct roles of Wg, particularly with respect to myocardial cell specification, have not been well define
166 a was relatively ineffective, IL-6 activated myocardial cell STAT3 by about 8-fold, indicating a prob
167 utocrine and/or paracrine fashion to augment myocardial cell survival during stresses that activate p
168 ern is novel and appears to mark specialized myocardial cells that induce underlying endocardial cell
169 conclude that tin has a crucial role within myocardial cells that is required for the proper diversi
170 t tube is an endocardial tube, ensheathed by myocardial cells, that develops from bilateral primary h
171 porter was expressed in neural crest but not myocardial cells to document the pattern of cardiac neur
172 ryos, the secondary heart field fails to add myocardial cells to the outflow tract and elongation of
173 nchnic mesenchyme, which provides additional myocardial cells to the outflow tract as the heart tube
174 lling that directs the spatial allocation of myocardial cells to their proper morphological positions
178 ly shown that shortly after this activation, myocardial cells undergo epithelial maturation [1], sugg
179 t-elevation myocardial infarction found that myocardial cell uptake is determined by infarct size rat
180 s normal when the BMPRII gene was deleted in myocardial cells using Mox2-Cre, alphaMHC-Cre, or SM22al
183 er-stained fibres coursing amongst ventricle myocardial cells were most likely cardiac parasympatheti
184 idazole-treated myl7:nitroreductase embryos, myocardial cells were targeted for apoptosis, which resu
186 s and centers it on the microvasculature and myocardial cell where the ischemia is taking place.
187 LIX expression was localized to resident myocardial cells, whereas KC and MIP-2 were expressed on
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