ライフサイエンスコーパス: endocardium

1 gradient (23+/-8% epicardium versus 21+/-4% endocardium).

2 nates from the sinus venosus and ventricular endocardium.

3 of the re-entry circuit was confined to the endocardium.

4 gnaling mechanisms originating in developing endocardium.

5 al iron concentration was higher than in the endocardium.

6 nd ectopic mesenchymal transformation of the endocardium.

7 has done little to clarify the origin of the endocardium.

8 tramural or epicardial with extension to the endocardium.

9 olic strains in the epicardium, midwall, and endocardium.

10 ood flow, with some cells incorporating into endocardium.

11 ires calcineurin and NFATc1 signaling in the endocardium.

12 s-mediated Notch activation localizes to the endocardium.

13 cifically inactivate Alk3 in the endothelium/endocardium.

14 tituted of a monolayered myocardium lined by endocardium.

15 d colocalize with NFATc1 in developing valve endocardium.

16 rent cell types including the epicardium and endocardium.

17 ing of two tissue layers, the myocardium and endocardium.

18 consisting of an outer myocardium and inner endocardium.

19 ater in extent on the epicardium than on the endocardium.

20 t 80% repolarization being longest at the PV endocardium.

21 novel transmembrane protein expressed in the endocardium.

22 d in the late-activated, high-stress lateral endocardium.

23 interactions between the myocardium and the endocardium.

24 ss of the AP dome in the epicardium, but not endocardium.

25 ystem develops in close association with the endocardium.

26 C current delivered to the right ventricular endocardium.

27 P<0.02), with the greatest difference in the endocardium.

28 primarily of a few large wave fronts on the endocardium.

29 g current delivered to the right ventricular endocardium.

30 bundles and trabeculas throughout the entire endocardium.

31 de <0.5 mV, to anatomic boundaries or normal endocardium.

32 ery from inactivation was >10-fold slower in endocardium.

33 ed toward the apex, and increased toward the endocardium.

34 No platelets or fibrin adhered to the endocardium.

35 nary arteries but not veins, capillaries, or endocardium.

36 C current delivered to the right ventricular endocardium.

37 and do not express markers of differentiated endocardium.

38 ation was simultaneous at the epicardium and endocardium.

39 ing notch1b transcription in the ventricular endocardium.

40 om five muscle layers between epicardium and endocardium.

41 essel populations primarily derived from the endocardium.

42 two progenitor pools, the sinus venosus and endocardium.

43 incision or atriotomy and affixed to atrial endocardium.

44 um and a previously unrecognized source, the endocardium.

45 equired for the haemogenic population of the endocardium.

46 acute AF) and similar in the epicardium and endocardium.

47 ne the haemogenic activity of the developing endocardium.

48 ant circuit near the apical left ventricular endocardium.

49 ' was lower in Scn5a(+/-) RV epicardium than endocardium.

50 ardial gene expression in the tal1-deficient endocardium.

51 on and two-dimensional reconstruction of the endocardium.

52 er, not by direct transmural spread from the endocardium.

53 ial adhesion thereby resulting in perforated endocardium.

54 (epicardium, 0.16+/-0.15 versus 0.03+/-0.06; endocardium, 0.45+/-0.40 versus 0.17+/-0.09).

55 significantly greater (P<0.01) closer to the endocardium (101%+/-62% and 41%+/-15%, respectively) com

56 area/left ventricular area: 34.0+/-17.4% at endocardium, 24.1+/-14.7% at 25%, 16.3+/-12.1% at 50%, 1

57 ixel signal intensity algorithm at 5 layers (endocardium, 25%, 50%, 75%, epicardium).

58 activation was significantly slowed from the endocardium (39 +/- 3 cm/s versus 49 +/- 2 cm/s in NF, P

59 The mean total force was greater on the endocardium (39+/-18 g versus 21+/-14 g for the epicardi

60 erved more frequently in ICM than in NICM in endocardium (4.1% vs. 1.3%; p = 0.0003) and epicardium (

61 tiated by mesoderm fated to give rise to the endocardium; (4) the maturation/morphogenesis of blood v

62 oanatomic maps acquired during sinus rhythm (endocardium, 509+/-291 points/map; epicardium, 716+/-323

63 r on the epicardium (97+/-78 cm(2)) than the endocardium (57+/-44 cm(2); P=0.04), with significantly

64 ificantly increased to the epicardium (71%), endocardium (93%), cerebrum (183%), brain stem (177%), r

65 riggers mesenchyme production in ventricular endocardium, a tissue that does not normally undergo EMT

66 isolated from the epicardium compared to the endocardium; a transmural difference that was also seen

67 e is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified a

68 alcineurin/NFAT signaling is required in the endocardium, adjacent to the earlier myocardial site of

69 action potential dome in epicardium but not endocardium after exposure to pinacidil (2 to 5 micromol

70 ntensifies and extends from E9.5 to E11.5 in endocardium along the atrioventricular canal and outflow

71 n endothelial cells of coronary arteries and endocardium along which Purkinje fiber recruitment from

72 tion of the Bmp type 1A receptor, Bmpr1a, in endocardium also resulted in failed cushion formation, i

73 A in 5 patients (4 from the left ventricular endocardium and 1 from the left coronary cusp); all succ

74 myocardial blood flow was reduced 84% at the endocardium and 32% at the epicardium (P<0.005, n=7), bu

75 5+/-1.5 mm) were identified, 85% between the endocardium and 50% shell and 76% present in >/=1 layer.

76 ctrode basket catheter on the left ventricle endocardium and 54 6-electrode plunge needles inserted i

77 ly 4 patients with penetrating wounds to the endocardium and all had sealed.

78 explained by a shorter path length along the endocardium and by faster circumferential and transmural

79 d preferentially in endothelial cells of the endocardium and coronary arteries where Purkinje fiber r

80 es in direct association with the developing endocardium and coronary arteries, but not with the veno

81 fiber differentiation takes place along the endocardium and coronary arteries.

82 xpression in the heart was restricted to the endocardium and coronary endothelium.

83 FGFR1 expression was detected in both endocardium and cushion mesenchyme as well as in myocard

84 Focal waves appeared equally frequent at endocardium and epicardium (11% versus 13%; P=0.18).

85 Fgf9, Fgf16, and Fgf20 are expressed in the endocardium and epicardium and that RA can induce epicar

86 demonstrate that the properties of I(to) in endocardium and epicardium are plastic and likely under

87 ly, SCFA contributions were elevated in both endocardium and epicardium despite preserved epicardial

88 Trophic factors secreted both from the endocardium and epicardium regulate appropriate growth o

89 A gradient between endocardium and epicardium was observed for radial veloc

90 ts on action potential duration (APD) in the endocardium and epicardium which may be pro-arrhythmic.

91 ession becomes activated specifically in the endocardium and epicardium, but not the myocardium.

92 and 726 +/- 483 points in the left ventricle endocardium and epicardium, respectively.

93 y, allowing gene expression in non pro-valve endocardium and extracardiac vasculature.

94 tly develop dilated chambers with compressed endocardium and fail to form identifiable cardiac valves

95 heterozygous for Gata4 in the myocardium or endocardium and heterozygous for Tbx5 (Gata4(MyoDel/wt);

96 criptional pathways upstream of Gata4 in the endocardium and its derivatives in the endocardial cushi

97 endocardium, whereas DPI was highest at the endocardium and lowest at the epicardium for the entire

98 irmed successful CD39 gene transfer into the endocardium and macrovasculature.

99 ced EMT and decreased proliferation of valve endocardium and mesenchyme.

100 c lineage and provides further evidence that endocardium and myocardium are derived from a common pre

101 e midline endoderm are incorporated into the endocardium and myocardium during closure of the foregut

102 5, in addition to apoptosis in foetal liver, endocardium and myocardium, the erythropoietin receptor

103 role in intercellular communication between endocardium and myocardium, which is crucial in controll

104 pment by targeting different pathways in the endocardium and myocardium.

105 ting reciprocal crosstalk between developing endocardium and myocardium.

106 transcription factors), is expressed in the endocardium and neural crest during early mouse heart de

107 proposed, including the sinus venosus (SV), endocardium and proepicardium, but their relative contri

108 hours altered I(to) to resemble unincubated endocardium and reduced the amplitude of the phase 1 not

109 al portion of liver vessels derives from the endocardium and shares a common developmental origin wit

110 lioration of inflow cannula contact with the endocardium and suction events or ablation of specific a

111 s were well correlated spatially between the endocardium and the epicardium (dominant frequency, 0.79

112 A current delivered to the right ventricular endocardium and the perfusate flow was stopped.

113 All had ablations on the left ventricular endocardium, and 67% had ablations on the right ventricu

114 ten adjacent to a valve annulus, deep in the endocardium, and can be greater in extent on the epicard

115 y in the heart, primarily in the myocardium, endocardium, and endocardial cushion tissue.

116 ude myocardium, smooth muscle, neural crest, endocardium, and endothelium.

117 i-LAVA, low unipolar amplitude in the facing endocardium, and Epi-LAVA within a wall thinning area at

118 esis in the placental labyrinth, a collapsed endocardium, and impaired vessel network patterning.

119 tor response is reduced, particularly in the endocardium, and in proportion to the magnitude of hyper

120 EMD is longer at the epicardium than at the endocardium, and is greater near the base than at the ap

121 compartments: the epicardium, midmyocardium, endocardium, and pericardial fluid, and accounted for ca

122 ll as the cardiac neural crest cells (NCCs), endocardium, and proepicardium.

123 Injury to myocytes, endocardium, and the coronary endothelium during harvest

124 more abundant in the epicardium than in the endocardium, and this gradient paralleled the gradient i

125 ature; NTPDase1 is expressed by endothelium, endocardium, and to a lesser extent by vascular smooth m

126 elements (putative central nervous system-, endocardium-, and urogenital system-specific enhancers).

127 tely 3-fold at 60 mV) in female base but not endocardium, apex or in male base myocytes.

128 bacterial adhesion to morphologically intact endocardium are largely unknown.

129 s such as myocardium, the cardiac jelly, and endocardium are presented.

130 heart, two tissues - the myocardium and the endocardium - are closely juxtaposed throughout their de

131 Instead, these cells remain within the endocardium as a proliferative population to support val

132 sticity in the infarct zone and identify the endocardium as a site of endogenous arteriogenesis and s

133 ty was observed in RV epicardium, but not in endocardium, as a consequence of heterogeneities in the

134 cloche mutants lack endocardium, as well as head and trunk endothelium, and

135 (ALK3), BMPR-1B (ALK6) and ALK2 in chick AV endocardium at stage-14(-), the onset of epithelial to m

136 sprouting of arterial cells derived from the endocardium at the atrioventricular canal.

137 se hemo-vascular precursors give rise to the endocardium, atrioventricular cushions and coronary vasc

138 chemic border in the left ventricular apical endocardium because of mechanically induced suprathresho

139 , which is highly expressed in early cushion endocardium before becoming downregulated after EMT.

140 expression is specifically inhibited in the endocardium but not in the myocardium.

141 ignificant role in S. mitis virulence in the endocardium, but have never previously been detected in

142 comes restricted to arterial endothelium and endocardium by embryonic day 9.5 in transgenic mouse emb

143 by RT-PCR and localized BMPR-1B mRNA in the endocardium by in situ hybridization.

144 ategies: (1) distributed illumination of the endocardium by multi-optrode grids (number of optrodes,

145 nd the activation of the BMP receptor in the endocardium can promote AV EMT in the chick.

146 localized to the myocardium and absent from endocardium, cardiac cushion, outflow tract, or coronary

147 iciency in the SHF but not the myocardium or endocardium caused ASDs.

148 (e4)/lacZ expression in the developing valve endocardium colocalizes with NFATc1 and, endocardial DSC

149 argest amplitude and earliest onset near the endocardium compared with the epicardium.

150 Tmem2 is an essential mediator of myocardium-endocardium coordination during cardiac morphogenesis.

151 GFR2(+), and endoglin(-)) to the surrounding endocardium (Cx40(-), VEGFR2(-), and endoglin(+)).

152 pecific expression of a reporter gene in the endocardium, defined by the temporal and spatial express

153 The amount of endocardium demonstrating an abnormal electrogram amplit

154 er evidence for the unique susceptibility of endocardium-derived endothelial cells to undergo EndMT a

155 y vessel formation by directing migration of endocardium-derived endothelial cells.

156 ctors that play important roles in embryonic endocardium development, Schwann and oligodendrocyte sur

157 The endocardium develops in tight association with cardiomyo

158 BZ channels, more commonly seen in the endocardium, display a 3D structure within the myocardia

159 yssynchronous failing hearts, the lateral LV endocardium displayed a 2-fold increase in phosphorylate

160 en gel assays, inactivation of Tgfbr2 in the endocardium does not prevent atrioventricular cushion me

161 lar structures, including the aortic arches, endocardium, dorsal aorta, cardinal veins, and lateral a

162 gs to record endocardial activation from the endocardium during 7 minutes of VF (controls, n=6).

163 ptional target of NFATc1 proteins within the endocardium during a critical window of heart valve form

164 mapping of the entire left ventricular (LV) endocardium during a single beat.

165 rated is expressed predominantly by valvular endocardium during cardiac valve maturation, exhibited e

166 demonstrate that Gpr126 is expressed in the endocardium during early mouse heart development.

167 es to specifically block BMP signaling in AV endocardium during EMT.

168 ted to the greater loss of blood flow at the endocardium during ischemia.

169 ere recorded from right and left ventricular endocardium during steady-state pacing, whilst subjects

170 icardium generates wavefronts that drive the endocardium early during VF.

171 eral epicardium (Epi group, N=3), and the LV endocardium (Endo group, N=3).

172 local abnormal ventricular activities in the endocardium (Endo-LAVA) and epicardium (Epi-LAVA), follo

173 ion being confined to non-myocardial layers (endocardium-endothelium-epicardium).

174 Etsrp71 was transiently expressed in the endocardium/endothelium of the developing embryo (E7.75-

175 operators were provided with 3D surfaces of endocardium, epicardium, myocardial wall thickness (rang

176 dult stages); there are no chambers, valves, endocardium, epicardium, or other differentiated feature

177 In conclusion, cells closer to the endocardium exhibit a slower decay of intracellular calc

178 rast, VEGFR2 does not exhibit robust cushion endocardium expression until after EMT is complete.

179 In addition, we find that the tal1-deficient endocardium fails to maintain its identity; over time, a

180 h signalling becomes activated in the atrial endocardium following ventricular ablation, and discover

181 in endothelial cells and endothelial-derived endocardium for cardiovascular development but is dispen

182 velopment, it is critically important in the endocardium for induction of EMT both in vitro and in vi

183 The endocardium forms the inner lining of the heart tube, wh

184 isolated preparations of rabbit ventricular endocardium from age-matched normal control female rabbi

185 s to study isolated rabbit right ventricular endocardium from control male and female and castrated m

186 To distinguish endocardium from other vasculature, we generated an NFAT

187 ngs to automatically locate and track the LV endocardium from routine grayscale digital cineloops and

188 The RV endocardium had a higher PS incidence than the epicardiu

189 The LA endocardium has complex but characteristic patterns of a

190 However, SCR events closer to the endocardium have the largest amplitude and earliest onse

191 n of ADAM15 was found in vascular cells, the endocardium, hypertrophic cells in developing bone, and

192 Epicardial VTs were targeted opposite normal endocardium in 10 patients (77%) and/or opposite ineffec

193 ession was specific to precardiac tissue and endocardium in 7.5 and 8.5 days p.c. embryos, respective

194 ic root and/or anteroseptal left ventricular endocardium in 8 patients (89%) and in the anterior card

195 rhythmias was effectively performed from the endocardium in all 5 patients.

196 ere recorded from right and left ventricular endocardium in anesthetized beagle dogs (n=11) in vivo.

197 ractions from the epicardium compared to the endocardium in both the sham and LVD groups.

198 In spite of the essential role of the endocardium in heart development and function, the trans

199 is cell-autonomous: wild-type cells can form endocardium in mutant hosts, but mutant cells never cont

200 endothelial foci were identified within the endocardium in the infarct zone.

201 rimary endothelial cells in vitro and in the endocardium in the mouse heart.

202 ts, but mutant cells never contribute to the endocardium in wild-type or mutant hosts.

203 n ZO-1 is mislocalized in the tal1-deficient endocardium, indicating a defect in intercellular juncti

204 cteristics in the ventricular myocardium and endocardium, indicating a role of frv in the regional re

205 +/-9.2 ms (P<0.01), and an S2 applied to the endocardium induced a polymorphic VT (pVT) in 9 of 12 we

206 ls to the myocardium along the axis from the endocardium (inside) to the outside of the chamber.

207 ransformation of atrioventricular (AV) canal endocardium into invasive mesenchyme correlates spatiall

208 Notch patterns the embryonic endocardium into prospective territories for valve and c

209 Our findings reveal that the endocardium is a dynamic, injury-responsive source of RA

210 n together, these studies emphasize that the endocardium is a unique cardiac lineage and provides fur

211 seen in Ccbe1 knockouts, indicating that the endocardium is activated in multiple cases where sinus v

212 paracrine signaling from the epicardium and endocardium is critical for proper development of the he

213 DSCR1(e4) expression in the developing valve endocardium is dependent on NFATc1 and support a role fo

214 e evidence that BMP signaling through the AV endocardium is required for the EMT and the activation o

215 repression of Bmp10 by Irx3 and Irx5 in the endocardium is required for ventricular septation.

216 Endocardium is specified as a cardiac cell lineage, inde

217 m the epicardium, but not the trabeculae and endocardium, is required in embryonic day 10 (E10) chick

218 head, reduced branching morphogenesis in the endocardium, lack of hierarchical order of large and sma

219 ed from the RV, LV epicardium (LVepi) and LV endocardium (LVendo) of adult mice were evaluated.

220 y, endothelial cells that originate from the endocardium maintain increased susceptibility to undergo

221 ential (AP) notch in the epicardium, but not endocardium, manifests as a J-wave on the ECG.

222 We hypothesized that activity on the endocardium may be driving these activation patterns in

223 f VF, which suggests that focal sites on the endocardium may represent foci and not breakthrough.

224 R, which was more marked in left ventricular endocardium/midmyocardium compared with epicardium, resu

225 t, migrates into the heart and gives rise to endocardium, myocardium, and smooth muscle.

226 When PM was trimmed to the level of endocardium (n = 4), sustained VT was no longer inducibl

227 ty Pentaray mapping catheter was used in the endocardium (n=35) and epicardially.

228 NS result from mutant Shp2 expression in the endocardium, not in the myocardium or neural crest.

229 Fifteen lesions were created in the endocardium of 13 pigs.

230 tion of ventricular fibrillation (VF) on the endocardium of humans.

231 arts or administered percutaneously into the endocardium of infarcted pigs.

232 ed large cells with pale cytoplasm along the endocardium of PV muscle sleeves.

233 ment in the heart, DSCR1 is expressed in the endocardium of the developing atrioventricular and semil

234 erfamily are expressed in the myocardium and endocardium of the developing heart, including the atrio

235 s expressed in the myocardium as well as the endocardium of the developing heart.

236 (DSCR1(e4)/lacZ) show gene activation in the endocardium of the developing valves and aorticopulmonar

237 specifically deleted in the endothelium and endocardium of the developing vasculature and heart.

238 rior ventral blood island (aVBI), and to the endocardium of the heart.

239 ed fatty infiltration from epicardium toward endocardium of the RV free wall.

240 rsectional genetics, we demonstrate that the endocardium of the sinus venosus is a source for the hep

241 lation sites were correctly mapped to either endocardium or epicardium.

242 e ablated from the right or left ventricular endocardium or from the aortic sinus of Valsalva (ASOV).

243 n can be rescued by expression of 3-OST-7 in endocardium, or by genetic loss of bmp4.

244 p < 0.01), and higher in the epicardium than endocardium (p < 0.01).

245 id of CF information, from 78% to 98% on the endocardium (P<0.001) and from 90% to 100% on the epicar

246 pre-QRS (versus 16+/-5 ms pre-QRS in the LV endocardium; P=0.068).

247 Thus, the endocardium plays a crucial early role in cardiac morpho

248 d in Scl(-/-) hearts, where the disorganized endocardium precociously differentiated into cardiomyocy

249 ulting in activation of almost the entire LV endocardium prior to septal breakout, thereby limiting a

250 xhibits less estimated block than the slower endocardium, raising the possibility that faster activat

251 riate modeling, fractional shortening at the endocardium (relative risk [RR] 1.85 per 10-unit decreas

252 ibute to the early sinus venosus and cardiac endocardium, respectively, two tissues linked to vascula

253 Alterations in NOTCH signaling in the endocardium result in congenital structural malformation

254 Arterial endothelial foci within the endocardium reveal extensive endothelial cell plasticity

255 relationship observed between myocardium and endocardium seen in vivo.

256 yocardial development coincident with normal endocardium suggest that the presence of cardiac neural

257 pproximately 25% faster when pacing from the endocardium than from the epicardium.

258 n the left ventricular and right ventricular endocardium than in the epicardium (15 [8-25] and 13 [7-

259 ned tissue were significantly thinner at the endocardium than the epicardium at end systole (24+/-5%

260 usually thought to be more depressed in the endocardium than the epicardium.

261 rotein, to repress ADAMTS1 expression in the endocardium that overlies the developing trabeculae.

262 le in induction of EMT in the avian epi- and endocardium, the function of Tgf-betas in corresponding

263 genesis, ADAMTS1 expression initiates in the endocardium to degrade the cardiac jelly and prevent exc

264 Scar area decreased progressively from endocardium to epicardium (scar area/left ventricular ar

265 s (n=12; P<0.001) as pacing was shifted from endocardium to epicardium.

266 m(3)) with a fiber twist of 120 degrees from endocardium to epicardium.

267 hod to detect and track such features on the endocardium to extract a metric that reflects local myoc

268 extracellular space abutting myocardium and endocardium to form endocardial cushions (EC) in a proce

269 hat Bmp2 signals directly to cushion-forming endocardium to induce EMT.

270 b2a (efnb2a) and neuregulin 1 (nrg1) in the endocardium to promote trabeculation and that forced Not

271 Irx3 and Irx5 have redundant function in the endocardium to regulate atrioventricular canal morphogen

272 mem2, we find that Tmem2 can function in the endocardium to repress atrioventricular differentiation

273 led myocardial infarction decreases from the endocardium to the epicardium.

274 e opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular d

275 dogs indicate activation propagates from the endocardium toward the epicardium after 1 minute of VF,

276 Atrioventricular (AV) endocardium transforms into the cushion mesenchyme, the

277 ithin 3 hr of ventricular injury, the entire endocardium undergoes morphological changes and induces

278 ng oxidation in both ischemic epicardium and endocardium versus only 38+/-4% and 40+/-6% in respectiv

279 ent and significantly more pronounced at the endocardium versus the epicardium, with thresholds of 22

280 Deleting endocardium via the clochesk4 mutants downregulated Notc

281 e of valve-forming activity: Smad4-deficient endocardium was associated with acellular endocardial cu

282 For the magnetic mapping, normal endocardium was defined by an amplitude >1.5 mV; this me

283 The extent and location of abnormal endocardium was estimated by measuring areas of abnormal

284 ames/sec) of the posterior left atrial (PLA) endocardium was performed during sustained AF (burst pac

285 pacing, cytoplasmic calcium elevation at the endocardium was significantly increased (15+/-4%) compar

286 area (<1.0 mV for epicardium and <1.5 mV for endocardium) was more extensive on the epicardium (95+/-

287 g current delivered to the right ventricular endocardium, was untreated for 3 mins.

288 MP signal transduction in the myocardium and endocardium, we show that the cardiac defects of Noggin

289 Video snapshots of the endocardium were acquired at sites distributed throughou

290 tentials from epicardium, midmyocardium, and endocardium were recorded simultaneously, together with

291 Cartesian coordinates of points on a virtual endocardium were used to calculate the length and thus t

292 in cardiac development but restricts to the endocardium where it remains active through cardiogenesi

293 highest at the epicardium and lowest at the endocardium, whereas DPI was highest at the endocardium

294 aortic root or anteroseptal left ventricular endocardium, whereas inferolateral scars frequently requ

295 erplay of signals between the myocardium and endocardium whereby secreted cues induce the endothelial

296 ner tube of specialized endothelium known as endocardium, which performs multiple essential functions

297 The amount of endocardium with an abnormal electrogram amplitude was e

298 ed (activation that spreads rapidly over the endocardium with diastolic periods between activations).

299 ly more in the epicardium as compared to the endocardium, with subsequent application E-4031 increasi

300 ng functions sequentially from myocardium to endocardium within a valvular morphogenetic field to ini