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1  as c-jun, that regulate growth of the adult cardiocyte.
2  in a computational model of the ventricular cardiocyte.
3 rea was greater in hypertrophied than normal cardiocytes.
4 es given above for pressure-hypertrophied RV cardiocytes.
5 46 +/- 1.32 dyne/cm2 in the hypertrophied RV cardiocytes.
6 87.85 +/- 6.95 poise in the hypertrophied RV cardiocytes.
7 art failure is due to ongoing loss of viable cardiocytes.
8 se metabolism in isolated skeletal muscle or cardiocytes.
9 lt cardiocytes nor at 100 nmol/L in neonatal cardiocytes.
10 sion pathways can be differentiated in adult cardiocytes.
11 ctile behavior was maintained in transfected cardiocytes.
12 sion pathways can be differentiated in adult cardiocytes.
13 fos expression was Ang II dependent in adult cardiocytes.
14  by inhibiting its expression in ventricular cardiocytes.
15 anine incorporation into protein in neonatal cardiocytes.
16 evel transcriptional activity in primary rat cardiocytes.
17 Ang II treatment of either adult or neonatal cardiocytes.
18 60-dependent impaired clearance of apoptotic cardiocytes.
19 ylation site found by mimicking it in normal cardiocytes.
20 Ro60 on the surface of apoptotic human fetal cardiocytes.
21 of betaGal mRNA in quiescent and contracting cardiocytes.
22 y regulate translational efficiency in adult cardiocytes.
23 poptotic, but not proliferating, human fetal cardiocytes.
24 y canine kidney cells (MDCK) and primary rat cardiocytes.
25 educed eIF4E promoter activity by 66+/-4% in cardiocytes.
26  matrix (ECM) and hypertrophic growth of the cardiocytes.
27 stently observed on early and late apoptotic cardiocytes.
28 pitated from apoptotic, but not nonapoptotic cardiocytes.
29 nits in model systems, which may differ from cardiocytes.
30 e normalizes contractility in these isolated cardiocytes.
31 1) is the principal Ca2+ efflux mechanism in cardiocytes.
32 cytes could damage surrounding healthy fetal cardiocytes.
33 other cardiocytes connected to an individual cardiocyte (4.60 +/- 0.10 [mean +/- SE] was significantl
34 pe calcium channel (Cav1.2) is essential for cardiocyte action potential duration (APD).
35  p70(S6K), and (iv) similar changes in adult cardiocytes after treatment with 12-O-tetradecanoylphorb
36 e fetal factors, protein/RNA on an apoptotic cardiocyte and infiltrating macrophages.
37 natants generated from cocultures of healthy cardiocytes and apo-CHB-IgG cardiocytes compared with he
38 ernatants derived from cocultures of healthy cardiocytes and apo-CHB-IgG cardiocytes promoted Smad2 p
39      Supernatants from cocultures of healthy cardiocytes and apoptotic cardiocytes bound by IgG from
40 po-CHB-IgG cardiocytes compared with healthy cardiocytes and apoptotic cardiocytes preincubated with
41 with supernatants from cocultures of healthy cardiocytes and apoptotic cardiocytes preincubated with
42                The adult heart lacks reserve cardiocytes and cannot regenerate.
43 on was determined in primary cultures of rat cardiocytes and in a murine C(2)C(12) myoblast cell line
44 cardiocytes impairs their removal by healthy cardiocytes and increases urokinase plasminogen activato
45 xin-deficient heart tissue, liver tissue and cardiocytes and observed a transcript down-regulation to
46 ocytosis of apoptotic cardiocytes by healthy cardiocytes and reverses the anti-Ro60-dependent impaire
47 c regions suggests that interactions between cardiocytes and their environment may contribute to hear
48 fflux was also found in primary hepatocytes, cardiocytes, and fibroblasts.
49 SPRY2 reproduced the branching morphology in cardiocytes, and vice versa, knockdown of miR-21 using a
50 at morphological and biochemical features of cardiocyte apoptosis exist in the left ventricular myoca
51             Electron microscopic features of cardiocyte apoptosis included (1) intact sarcolemma and
52                                 Evidence for cardiocyte apoptosis was based on transmission electron
53                                  Features of cardiocyte apoptosis were observed in dogs with heart fa
54                              These opsonized cardiocytes are phagocytosed by macrophages, which secre
55  aprotinin prior to coculturing with healthy cardiocytes attenuated TGF-beta activation.
56 ultures of healthy cardiocytes and apoptotic cardiocytes bound by IgG from a mother whose child had C
57 cipate in physiologic clearance of apoptotic cardiocytes but that clearance is inhibited by opsonizat
58 crophages incubated with opsonized apoptotic cardiocytes (but not nonopsonized) dramatically increase
59 pertrophic response of cultured neonatal rat cardiocytes, but its role in the adult heart is controve
60    The cardiac promoter drives expression in cardiocytes, but not in mouse L cells.
61 tly by 3.7-fold in contracting vs. quiescent cardiocytes, but ODC/betaGal mRNA was unchanged.
62 ased threefold 1 hour after loading of adult cardiocytes, but this increased expression was not block
63 g of uPAR enhances phagocytosis of apoptotic cardiocytes by healthy cardiocytes and reverses the anti
64 and determined in nonapoptotic and apoptotic cardiocytes by indirect immunofluorescence.
65             In summary, the current model of cardiocyte Ca(2+) dynamics provides an integrated theore
66                               In this study, cardiocyte Ca(2+) dynamics were modeled using a set of s
67 tures of healthy cardiocytes and apo-CHB-IgG cardiocytes compared with healthy cardiocytes and apopto
68                           In early apoptotic cardiocytes, condensation of the PI- and Ro- or La-stain
69  tissue volume fraction, the number of other cardiocytes connected to an individual cardiocyte (4.60
70       After formalin fixation, the number of cardiocytes connected to an individual cardiocyte was co
71  constitutes primarily a viscous load on the cardiocyte contractile apparatus in pressure-overload ca
72                  Thus, the microtubule-based cardiocyte contractile dysfunction characteristic of pre
73         Increased microtubule density causes cardiocyte contractile dysfunction in right ventricular
74                                 In contrast, cardiocyte contractile function in cells from failing LV
75                                              Cardiocyte contractile function was equivalent, and unaf
76 crotubule network forms that interferes with cardiocyte contraction and microtubule-based transport.
77 , which imposes a viscous load that inhibits cardiocyte contraction.
78 pplies cyclical strain (1 Hz) to ventricular cardiocytes cultured on collagen-coated silicone elastom
79  an atrial cell-specific enhancer in primary cardiocyte cultures.
80  intrinsic to the myofilament portion of the cardiocyte cytoskeleton but rather from an increased den
81 onent of the extramyofilament portion of the cardiocyte cytoskeleton.
82 hromatin immunoprecipitation assays in adult cardiocytes demonstrate that SRF and GATA4 are associate
83                     Spontaneously contacting cardiocytes derived from the ES cells were used to evalu
84 a, the other major PKC isoform seen in adult cardiocytes, did not show a change in subcellular locali
85 aluated whether anti-Ro binding to apoptotic cardiocytes enhances plasmin-mediated activation of TGF-
86                                 Importantly, cardiocytes exposed to doxorubicin displayed reduced lev
87                               Cultured fetal cardiocytes expressed phosphatidylserine receptors (PSRs
88 acrophages cultured with opsonized apoptotic cardiocytes expressed proinflammatory markers, supported
89  and MAP4 decoration were assessed in normal cardiocytes following an equivalent level of MAP4 expres
90                                     Isolated cardiocytes from 16-24 wk abortuses were rendered apopto
91                                  Human fetal cardiocytes from 16-24-wk abortuses were cultured and in
92 ity causes decreased contractile function of cardiocytes from cats with hypertrophy produced by chron
93      Measurements were made in two groups of cardiocytes from cats with right ventricular (RV) hypert
94 m for staining of right and left ventricular cardiocytes from control cats and cats with right ventri
95                                              Cardiocytes from normal and pressure-hypertrophied cats
96 picuous in microtubules of right ventricular cardiocytes from pressure overloaded cats, i.e., the mic
97 Ro60 bound and inhibited uptake of apoptotic cardiocytes from wild-type but not Ro60-knockout mice.
98 increased IK+Ach activity in ES cell-derived cardiocytes from wild-type cells, in cells lacking alpha
99          We developed methods for culture of cardiocytes from zebrafish embryos and found that, even
100           Thus, the PKC signaling pathway in cardiocytes has different effects depending on the timin
101 hanced Na+-Ca2+ exchanger gene expression in cardiocytes; however, load induced c-fos expression is A
102  maternal anti-SSA/Ro Abs to fetal apoptotic cardiocytes impairs their removal by healthy cardiocytes
103                The increase in junctions per cardiocyte in concentrically hypertrophied hearts sugges
104      Cell membrane lesion sealing of hypoxic cardiocytes in culture with CSIL has been reported.
105           There was no evidence of apoptotic cardiocytes in normal dogs.
106                                  The role of cardiocytes in physiologic removal of apoptotic cells an
107 eases during growth of cardiac muscle cells (cardiocytes) in vitro.
108 cally stimulated contraction of adult feline cardiocytes increased eIF-4E phosphorylation to 34% afte
109 d with nonapoptotic cardiocytes or apoptotic cardiocytes incubated with normal sera, apoptotic cardio
110              One hour after loading of adult cardiocytes, induction of c-fos expression was increased
111     These data show that a nuclear factor in cardiocytes interacts with an enhancer element (+25 and
112 ajor PKC isoforms seen in the adult heart in cardiocytes isolated from diabetic rats and determined p
113  TnI phosphorylation was increased 5-fold in cardiocytes isolated from the hearts of diabetic animals
114                  The contractile function of cardiocytes isolated from the ventricles at the end of t
115 ogenitor cells that can give rise to beating cardiocyte-like cells and vascular components, and the a
116 this study, we examined the possibility that cardiocyte loss in heart failure may be due, in part, to
117           We sought to determine whether the cardiocyte microtubule network densification characteris
118 ional corroborative data show that increased cardiocyte microtubule network density is an important m
119 lly, apparent viscosity in the two groups of cardiocytes, microtubule depolymerization by colchicine
120 ase protein synthesis after 4 hours in adult cardiocytes nor at 100 nmol/L in neonatal cardiocytes.
121                                              Cardiocytes obtained by biopsy before and after in vivo
122 ning was equal in right and left ventricular cardiocytes of control cats, but Glu-tubulin and Delta2-
123 e results suggest that direct stimulation of cardiocyte opioid delta(1) receptors leads to activation
124 ate and direct effect of load input into the cardiocyte or instead a concomitant of hypertrophic grow
125 protein synthesis in both adult and neonatal cardiocytes or 24-hour [3H]phenylalanine incorporation i
126                   Compared with nonapoptotic cardiocytes or apoptotic cardiocytes incubated with norm
127 uclear DNA fragments showed that 11% were of cardiocyte origin confirmed by positive labeling with st
128            Our results suggest that resident cardiocytes participate in physiologic clearance of apop
129 n of SSA/Ro and SSB/La antigens to the fetal cardiocyte plasma membrane were common downstream events
130 ocytes incubated with normal sera, apoptotic cardiocytes preincubated with affinity-purified Abs to S
131 pared with healthy cardiocytes and apoptotic cardiocytes preincubated with IgG from a healthy donor,
132 ultures of healthy cardiocytes and apoptotic cardiocytes preincubated with IgG from a healthy donor.
133 ulated that in vivo such opsonized apoptotic cardiocytes promote an inflammatory response by resident
134      To evaluate whether opsonized apoptotic cardiocytes promote inflammation, cells were cocultured
135 tures of healthy cardiocytes and apo-CHB-IgG cardiocytes promoted Smad2 phosphorylation and fibroblas
136 3H]phenylalanine incorporation into neonatal cardiocyte protein over a 24-hour period by 10%, whereas
137  by anti-Ro60 binding to the apoptotic fetal cardiocyte provide a molecular basis by which these anti
138 opy, coculturing of healthy cardiocytes with cardiocytes rendered apoptotic via extrinsic pathways re
139  of the sarcolemmal surface in myofibers and cardiocytes, respectively.
140 Binding of anti-Ro60 antibodies to apoptotic cardiocytes results in increased uPAR expression, as wel
141  summary, induction of apoptosis in cultured cardiocytes results in surface translocation of Ro/La an
142 ocal microscopy analyses at the level of the cardiocyte revealed that p70(S6K) is present predominant
143 nostaining of nonpermeabilized myofibers and cardiocytes revealed that some obscurin kinase isoforms
144                In permeabilized nonapoptotic cardiocytes, Ro and La were predominantly nuclear, and p
145 ransfection of reporter gene constructs into cardiocytes showed that deletion of the region between -
146 ects were assessed in protocol C by defining cardiocyte sigma versus epsilon during an increase in si
147 in protocol B from the loop area between the cardiocyte sigma-versus-epsilon relationship during an i
148                           In protocol A, the cardiocyte sigma-versus-epsilon relationship was similar
149 agarose gel at a constant rate to define the cardiocyte sigma-versus-epsilon relationship.
150 mice and in in vitro systems of neonatal rat cardiocytes stimulated with peptide growth factors.
151  a pathologic cascade involving apoptosis of cardiocytes, surface translocation of Ro and La antigens
152 ve shown the levels of the sarcomere and the cardiocyte that a persistent increase in microtubule den
153 protein synthesis in both adult and neonatal cardiocytes; this response was unaltered by 1 mumol/L [S
154 ures enclose sarcomeres and connect adjacent cardiocytes through functional gap junctions.
155                  The genetic response of the cardiocyte to load was examined by assessing c-fos and N
156  +/- 0.77 dyne/cm2 in the normally loaded LV cardiocytes to 16.46 +/- 1.32 dyne/cm2 in the hypertroph
157 .97 +/- 1.92 poise in the normally loaded LV cardiocytes to 87.85 +/- 6.95 poise in the hypertrophied
158 introduced an improved model of loaded adult cardiocytes to address a proposed requirement for angiot
159 r has been isolated and characterized in rat cardiocytes to investigate the role of MMP-13 in cardiac
160 combination may cause pressure-hypertrophied cardiocytes to resist changes in shape during diastole a
161 arent viscosity values of normally loaded LV cardiocytes to the abnormal values given above for press
162 ted that binding of anti-Ro Abs to apoptotic cardiocytes triggers TGF-beta activation, by virtue of i
163                                      Whereas cardiocytes under both conditions showed RGD-stimulated
164 stiffness and apparent viscosity in isolated cardiocytes via magnetic twisting cytometry, a technique
165 er of cardiocytes connected to an individual cardiocyte was counted in tissues from the middle portio
166 gma-versus-epsilon relation in hypertrophied cardiocytes was shifted to the left compared with normal
167                                Subsequently, cardiocytes were electrically stimulated to contract at
168                                    Apoptotic cardiocytes were incubated with affinity-purified Abs to
169                                 The isolated cardiocytes were subjected to passive load by step incre
170                        Isolated adult feline cardiocytes were treated with a 14-mer phosphorothioate
171  understand its role, we overexpressed it in cardiocytes where it revealed a unique type of cell-to-c
172 immunofluorescent staining of chicken embryo cardiocytes with anti-C-RZF antibodies demonstrated that
173                     Treatment of apo-CHB-IgG cardiocytes with anti-uPAR or anti-uPA Abs or plasmin in
174  confocal microscopy, coculturing of healthy cardiocytes with cardiocytes rendered apoptotic via extr
175 hibited following preincubation of apoptotic cardiocytes with chicken and murine anti-SSA/Ro and -SSB
176                           Treatment of adult cardiocytes with either 0.1 microM insulin or 0.1 microM
177  by the treatment of transfected primary rat cardiocytes with interleukin-1 (IL-1) and basic fibrobla
178 e used embryonic stem cell (ES cell)-derived cardiocytes with targeted inactivations of specific PT-s
179 w intercellular junctions developing between cardiocytes within developed myocardium.

 
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