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1 nd that these factors do not act directly on myocardial cells.
2 uscle cells and endothelial cells but not in myocardial cells.
3 lpha-actin (alphaCA) transcripts and nascent myocardial cells.
4 ionally modified by other factors present in myocardial cells.
5 s that regulate transcriptional responses in myocardial cells.
6 s to cytokines and acute hypoxia in cultured myocardial cells.
7  and stage 5 cells producing endothelial and myocardial cells.
8 be involved in ischemia/reperfusion death of myocardial cells.
9 acellular calcium handling and shortening in myocardial cells.
10 can cause reversible loss of excitability in myocardial cells.
11 regulated by molecular mediators released by myocardial cells.
12  expands via accrual of both endocardial and myocardial cells.
13 opment and intercellular communication among myocardial cells.
14 cell therapy in an attempt to regenerate new myocardial cells.
15 ing is actively repressed in differentiating myocardial cells.
16 interplay of transmembrane ionic currents in myocardial cells.
17  compensate for the absence of BMPRII in the myocardial cells.
18 d calcineurin in endothelial, epicardial and myocardial cells.
19 rdially derived smooth muscle and underlying myocardial cells.
20 role in the differentiation of ES cells into myocardial cells.
21 tivators in differentiation of ES cells into myocardial cells.
22 d away from the plasma membrane in embryonic myocardial cells.
23 cial for initiating early differentiation of myocardial cells.
24 ession pattern, including in all contractile myocardial cells.
25 ymphoblastic leukemia (ALL) but also injures myocardial cells.
26 I/R) is associated with an extensive loss of myocardial cells.
27                                       In the myocardial cell, a series of enzyme-catalyzed reactions
28 capillary density, a higher proliferation of myocardial cells, a lower cardiomyocyte apoptosis, and r
29 laminin receptors are likely responsible for myocardial cell adhesion to the basement membrane, DG ha
30  we conclude that in addition to its role in myocardial cell adhesion, N-cadherin is required for neu
31 protective effect of ERK5 in endothelial and myocardial cells after ischemia.
32                               IL-6 protected myocardial cells against apoptosis.
33 that mABC1 plays a key role in protection of myocardial cells against oxidant stress.
34     Growth of the heart requires addition of myocardial cells along the endocardial-to-myocardial axi
35   We have found no mutation that deletes the myocardial cells altogether, but one, pandora, appears t
36 n of electrical and chemical signals between myocardial cells and cells of the specialized conduction
37 rvation of connexin 40 and 43 in contracting myocardial cells and connexin 30.2 in the AV node.
38 isruption of fibronectin assembly around the myocardial cells and consequent disorganization of the m
39 ta5 mutants exhibit a much-reduced number of myocardial cells and defects in myocardial gene expressi
40                            Here we show that myocardial cells and dorsal vessels can form even though
41 c factor (ANF) inhibits proliferation in non-myocardial cells and is thought to be anti-hypertrophic
42 activated channels (SACs) have been found in myocardial cells and may promote AF in dilated atria.
43          The erbB receptors are expressed in myocardial cells and presumably mediate the neuregulin s
44 nditions are thought to emanate from injured myocardial cells and, in most circumstances, have been a
45 uptions in the normal diversification of the myocardial cells, and adults exhibit severe defects in c
46 inuing elucidation of the secondarily adding myocardial cells, and how the different populations iden
47  as vascular smooth muscle, skeletal muscle, myocardial cells, and neurons also express both proteins
48 In the heart, CT-1 is primarily expressed in myocardial cells, and not in endocardial cushion or outf
49 ed cytotoxicity on L929 cells and exert anti-myocardial cell apoptosis effects.
50 d that calcineurin signaling would stimulate myocardial cell apoptosis.
51 lear but are thought to involve p53-mediated myocardial cell apoptosis.
52 echanism of this protection is mitigation of myocardial cell apoptosis.
53 t ventricular wall preparations in which the myocardial cells are electrically well coupled.
54 nels characterized electrophysiologically in myocardial cells are explored.
55 nchymal cells at embryonic day 10.5, whereas myocardial cells are unaffected.
56                           Using the ischemic myocardial cell as a paradigm, competitive coronary reva
57 activation, and dedifferentiation of compact myocardial cells as causative for the regenerative failu
58 but not ischemia alone, induced apoptosis in myocardial cells as demonstrated by DNA electrophoresis
59 SERCA2a also enhanced the contraction of the myocardial cells as detected by shortening measurements.
60       The present study utilized an in vitro myocardial cell assay to examine the role of various hum
61 audally extended tube consisting entirely of myocardial cells (at both the larval and adult stages);
62          These findings reveal a ventricular myocardial cell-autonomous function for Hrt2 in the supp
63  and E8.0, HGF receptor mRNA was detected in myocardial cells before fusion at the ventral midline.
64 teins of gap junctions, can adversely impact myocardial cell behavior, thus leading to the developmen
65  1 (MEK1) dominant negative mutant cDNA into myocardial cells blocked the antiapoptotic effects of CT
66                                   Before any myocardial cell bodies have entered the trabecular layer
67 intermediate mesoderm, and in differentiated myocardial cells, but not in the streak.
68 tures of hypertrophy are induced in cultured myocardial cells by alpha1- adrenergic receptor agonists
69  in the initiation of apoptosis induction in myocardial cells by in vitro and in vivo ischemia and re
70 dditionally, while NF-kappaB is activated in myocardial cells by p38, this does not appear to be the
71                  We showed that apoptosis of myocardial cells can occur after ischemic myocardial cel
72 his review focuses on endocardial (EdCs) and myocardial cells (cardiomyocytes, CMs), key cell types i
73 l for addressing how embryonic regulators of myocardial cell commitment can contribute to the establi
74                   We propose a model whereby myocardial cell compartmentalization also defines the en
75 t (wingless)-mediated events may function in myocardial cell compartmentalization during early verteb
76 TNF-alpha and IL-1beta induced depression of myocardial cell contractility at substantially lower con
77 t TNF-alpha and IL-1beta cause depression of myocardial cell contraction in vitro and suggest that th
78 ve been shown to regulate iNOS expression in myocardial cells, cultured neonatal cardiac myocytes wer
79 gap junction content along with induction of myocardial cell cycle activity.
80 -dependent regenerative circuit that invokes myocardial cell cycle re-entry, proteolysis, and mitocho
81 ed for their potential in causing additional myocardial cell damage during the course of therapeutic
82 nd necrosis have been shown to contribute to myocardial cell death after myocardial ischemia and repe
83 njury, (ii) complete inhibition of apoptotic myocardial cell death as identified by terminal deoxynuc
84  time of coronary occlusion suppressed acute myocardial cell death by >50%.
85 ate the genetics of DCC further, we produced myocardial cell death by freeze-thaw injury to induce DC
86  GLO1-diabetic mice and corresponded to less myocardial cell death compared with the WT-diabetic grou
87 cal and interventional techniques to prevent myocardial cell death during the time of ischemia and su
88   Although acute inflammation in response to myocardial cell death has been extensively studied, subs
89                                              Myocardial cell death is initiated by excessive mitochon
90 d serum concentrations of cTnI indicate that myocardial cell death is occurring in meningococcal sept
91 ver, clinical studies have demonstrated that myocardial cell death is rare and that cardiac function
92  addition to oxidative stress, inflammation, myocardial cell death pathways, and neurohumoral mechani
93 infarction (MI) is defined pathologically as myocardial cell death resulting from prolonged ischaemia
94      We were interested to determine whether myocardial cell death was occurring in the presence of m
95  mechanism for mitochondrial Ca(2+) entry in myocardial cell death, and indicate that mitochondrial-t
96 I (cTnI), a sensitive and specific marker of myocardial cell death, and related this to the severity
97   Commonly used blood markers of AMI reflect myocardial cell death, but do not reflect the earlier pa
98 XCR2-mediated chemotaxis may be important in myocardial cell death.
99 ocardial ischaemia and biomarker evidence of myocardial cell death.
100 fferent cAMP-Epac1 microdomains that control myocardial cell death.
101 he cells can thrive, enabling an insult-free myocardial cell delivery to normalize myocardial biomech
102            Second, SHH mediates signaling to myocardial cells derived from the AHF to complete septat
103 myocardin in Xenopus embryos interferes with myocardial cell differentiation.
104 irst is driven by an asymmetric migration of myocardial cells during cardiac jogging, resulting in th
105                 LIX is expressed by resident myocardial cells during ischemia-reperfusion and is indu
106 f-beta signaling via Alk5 is not required in myocardial cells during mammalian cardiac development, b
107  effects of antibody action, thus preventing myocardial cell dysfunction and death.
108                    During these periods, the myocardial cells exhibited different stage-dependent mig
109                                              Myocardial cells express the specific marker MF-20 and a
110 e, but not in LPL-/--->C57BL/6 mice, whereas myocardial cells expressed LPL in all groups.
111 s to cardia bifida, a phenotype in which the myocardial cells fail to migrate to the midline.
112 genitors of asymmetric cell lineages adopt a myocardial cell fate as opposed to a pericardial fate wh
113  Reprogramming of mouse fibroblasts toward a myocardial cell fate by forced expression of cardiac tra
114 cus here upon regulation by the notochord of myocardial cell fate in zebrafish.
115 injury through phenotypic reprogramming to a myocardial cell fate.
116  correct specification of myocardial and non-myocardial cell fates.
117 ad-induced HF mice and isolated hypertrophic myocardial cells, fatty acid beta-oxidation and heart fu
118 n of fibroblast proliferation in cultures of myocardial cells from 8-day embryonic chicks was achieve
119                                              Myocardial cells from failing human hearts are character
120 outflow tract to lengthen by the addition of myocardial cells from the secondary heart field.
121 ression of V12Ras in transgenic mice induces myocardial cell growth and expression of genes that are
122 ase other than Ras is involved in regulating myocardial cell growth and gene expression in response t
123 etion of calcineurin in either epicardial or myocardial cells had no effect on coronary vasculature d
124 used by an increase in the overall number of myocardial cells (hyperplasia).
125 te that CT-1 can activate a distinct form of myocardial cell hypertrophy, characterized by the promot
126  roles for MKK6 and p38 in the regulation of myocardial cell hypertrophy.
127 only of one cell type, either endocardial or myocardial cells; i.e., 95.1% of the mesoderm-derived cl
128 eflex is a crucial mechanism in adapting the myocardial cell in response to altered loading due to ao
129 eflex is a crucial mechanism in adapting the myocardial cell in response to altered ventricular loadi
130  protein (BMP)-2 is known to be expressed in myocardial cells in a manner consistent with the segment
131                                              Myocardial cells in newborn SAN tissue exhibited clear h
132 ion of cardiac neural crest, endothelial and myocardial cells in the conotruncal cushions.
133 yos have large aggregates of N-cadherin(-/-) myocardial cells in the heart lumen, indicating that the
134 on expression of the inducible NOS (iNOS) in myocardial cells in vivo and in vitro.
135 olved, and in the young woman, there were no myocardial cells in which these pathways normally exist.
136 revascularization causes the least amount of myocardial cell injury and is associated with superior l
137                                      Whereas myocardial cell injury can occur during electrical defib
138          Immunologic mechanisms that mediate myocardial cell injury during rejection are not fully un
139                         Although substantial myocardial cell injury has been reported after high-ener
140 activation contributes to the progression of myocardial cell injury, cardiac fibrosis, and left ventr
141 I (cTnI), a sensitive and specific marker of myocardial cell injury, is useful in diagnosing and asse
142 nts have been used to identify perioperative myocardial cell injury.
143 been identified as an important mechanism of myocardial cell injury.
144 of myocardial cells can occur after ischemic myocardial cell injury.
145 w tract and in the maintenance of epicardial-myocardial cell interactions.
146              FGF signaling also promoted OFT myocardial cell invasion to the cushion.
147                                       If the myocardial cell is placed at the center of the model, al
148   As a result, the number of differentiating myocardial cells is severely reduced whereas pericardial
149                                              Myocardial cells isolated from 9 patients with end-stage
150  these functions have now been identified in myocardial cells isolated from different species, as wel
151     We find that while sox9b is expressed in myocardial cells, it is not normally expressed in the af
152  viability and induced apoptosis in the H9c2 myocardial cell line measured by flow cytometry and fluo
153 rsist in pig myocardium and can infect human myocardial cells make it an important infectious agent t
154 d CaMKII promotes sequestration of KATP from myocardial cell membranes.
155 rmal convergence affected all three modes of myocardial cell migration, probably due to the disruptio
156 urthermore, metformin significantly improved myocardial cell mitochondrial respiration and ATP synthe
157 on and function through active adjustment of myocardial cell morphology.
158 ing fibroblast cells (3T3), or proliferating myocardial cells (MOT).
159 ish ctr9 mutant with a dramatic reduction in myocardial cell number as well as later defects in primi
160                                 Apoptosis of myocardial cells occurs during cardiac allograft rejecti
161 , the Noggin gene is mainly expressed in the myocardial cells of the outflow tract, atrioventricular
162  a promiscuous BirA2 localized to the entire myocardial cell or membrane compartment were generated,
163  through its earlier activity in neighboring myocardial cells or their progenitors.
164 ns form electrical conduits between adjacent myocardial cells, permitting rapid spatial passage of th
165 smission of electrical signals from adjacent myocardial cells, primarily via specialized channels cal
166                                              Myocardial cell proliferation, which has been shown prev
167  and epo signals work in parallel to support myocardial cell proliferation.
168                                      For the myocardial cells, PSpc averaged 3.7 +/- 3.1 ml min-1 g-1
169 he Gax protein was detected in the nuclei of myocardial cells relatively late in chicken heart develo
170                                           In myocardial cells, relaxation is governed primarily by th
171                                       Direct myocardial cell repopulation has been proposed as a pote
172                                   Developing myocardial cells respond to signals from the endocardial
173  conduction system is a specialized tract of myocardial cells responsible for maintaining normal card
174 rtrophic response characterized by increased myocardial cell size and activation of fetal cardiac gen
175 fects valve development due to its effect on myocardial cell size and shape, which changes the morpho
176 process characterized by regional changes in myocardial cell size and shape.
177 tion of cardiac-specific genes and increased myocardial cell size.
178  myocardium and explore reasons why multiple myocardial cell sources exist.
179 gly show a critical role for this pathway in myocardial cell specification and heart development.
180 o investigate tissue interactions regulating myocardial cell specification in birds.
181  Explantation studies provided evidence that myocardial cell specification is underway by stage 3, in
182 ct roles of Wg, particularly with respect to myocardial cell specification, have not been well define
183  establishes these developmental events upon myocardial cell specification.
184 a was relatively ineffective, IL-6 activated myocardial cell STAT3 by about 8-fold, indicating a prob
185 utocrine and/or paracrine fashion to augment myocardial cell survival during stresses that activate p
186                      The AVC contains unique myocardial cells that are essential for valvuloseptal de
187 ern is novel and appears to mark specialized myocardial cells that induce underlying endocardial cell
188  conclude that tin has a crucial role within myocardial cells that is required for the proper diversi
189 t tube is an endocardial tube, ensheathed by myocardial cells, that develops from bilateral primary h
190 al cell-cell interactions of endocardial and myocardial cells throughout heart development, we hypoth
191 porter was expressed in neural crest but not myocardial cells to document the pattern of cardiac neur
192 ryos, the secondary heart field fails to add myocardial cells to the outflow tract and elongation of
193 nchnic mesenchyme, which provides additional myocardial cells to the outflow tract as the heart tube
194 lling that directs the spatial allocation of myocardial cells to their proper morphological positions
195              The current method of analyzing myocardial cell transplantation relies on postmortem his
196  K+ currents/channels expressed in different myocardial cell types are the focus of this review.
197  natural epicardial fates are limited to non-myocardial cell types in zebrafish.
198 m and modulate phenotype and function of all myocardial cell types through activation of intracellula
199 ly shown that shortly after this activation, myocardial cells undergo epithelial maturation [1], sugg
200 t-elevation myocardial infarction found that myocardial cell uptake is determined by infarct size rat
201 chnique to directly convert nonmyocytes into myocardial cells using genes or small molecules.
202 s normal when the BMPRII gene was deleted in myocardial cells using Mox2-Cre, alphaMHC-Cre, or SM22al
203 e the mechanism whereby calcineurin affected myocardial cell viability.
204 1), 8 mL/m(2) absolute reduction in the mean myocardial cell volume (P = 0.04), and 61% relative redu
205                                          Rat myocardial cells were incubated with pioglitazone plus a
206 er-stained fibres coursing amongst ventricle myocardial cells were most likely cardiac parasympatheti
207 idazole-treated myl7:nitroreductase embryos, myocardial cells were targeted for apoptosis, which resu
208                                              Myocardial cells, when plated at 80 cells/mm2 in Gln- me
209 s and centers it on the microvasculature and myocardial cell where the ischemia is taking place.
210     LIX expression was localized to resident myocardial cells, whereas KC and MIP-2 were expressed on

 
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