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1  gradient (23+/-8% epicardium versus 21+/-4% endocardium).
2 (2) intra-ventricularly toward the activated endocardium.
3 ne the haemogenic activity of the developing endocardium.
4 ant circuit near the apical left ventricular endocardium.
5 ' was lower in Scn5a(+/-) RV epicardium than endocardium.
6 ardial gene expression in the tal1-deficient endocardium.
7 on and two-dimensional reconstruction of the endocardium.
8 er, not by direct transmural spread from the endocardium.
9 ial adhesion thereby resulting in perforated endocardium.
10  of the re-entry circuit was confined to the endocardium.
11 al iron concentration was higher than in the endocardium.
12 nd ectopic mesenchymal transformation of the endocardium.
13 has done little to clarify the origin of the endocardium.
14 tramural or epicardial with extension to the endocardium.
15 olic strains in the epicardium, midwall, and endocardium.
16 ires calcineurin and NFATc1 signaling in the endocardium.
17 cifically inactivate Alk3 in the endothelium/endocardium.
18 tituted of a monolayered myocardium lined by endocardium.
19 d colocalize with NFATc1 in developing valve endocardium.
20 h1 receptor expression in sinus venosus (SV) endocardium.
21 ing of two tissue layers, the myocardium and endocardium.
22  consisting of an outer myocardium and inner endocardium.
23 ater in extent on the epicardium than on the endocardium.
24 t 80% repolarization being longest at the PV endocardium.
25 novel transmembrane protein expressed in the endocardium.
26 d in the late-activated, high-stress lateral endocardium.
27  interactions between the myocardium and the endocardium.
28 ss of the AP dome in the epicardium, but not endocardium.
29 ystem develops in close association with the endocardium.
30 C current delivered to the right ventricular endocardium.
31 P<0.02), with the greatest difference in the endocardium.
32  primarily of a few large wave fronts on the endocardium.
33 g current delivered to the right ventricular endocardium.
34  components can usually be identified on the endocardium.
35 ate, it can bias the fate of CPCs toward the endocardium.
36  two progenitor pools, the sinus venosus and endocardium.
37 nates from the sinus venosus and ventricular endocardium.
38 gnaling mechanisms originating in developing endocardium.
39 ood flow, with some cells incorporating into endocardium.
40 s-mediated Notch activation localizes to the endocardium.
41 rent cell types including the epicardium and endocardium.
42 nary arteries but not veins, capillaries, or endocardium.
43 and do not express markers of differentiated endocardium.
44 ation was simultaneous at the epicardium and endocardium.
45 ing notch1b transcription in the ventricular endocardium.
46 om five muscle layers between epicardium and endocardium.
47 essel populations primarily derived from the endocardium.
48  incision or atriotomy and affixed to atrial endocardium.
49 um and a previously unrecognized source, the endocardium.
50 equired for the haemogenic population of the endocardium.
51  acute AF) and similar in the epicardium and endocardium.
52 (epicardium, 0.16+/-0.15 versus 0.03+/-0.06; endocardium, 0.45+/-0.40 versus 0.17+/-0.09).
53 significantly greater (P<0.01) closer to the endocardium (101%+/-62% and 41%+/-15%, respectively) com
54  area/left ventricular area: 34.0+/-17.4% at endocardium, 24.1+/-14.7% at 25%, 16.3+/-12.1% at 50%, 1
55 ixel signal intensity algorithm at 5 layers (endocardium, 25%, 50%, 75%, epicardium).
56 activation was significantly slowed from the endocardium (39 +/- 3 cm/s versus 49 +/- 2 cm/s in NF, P
57      The mean total force was greater on the endocardium (39+/-18 g versus 21+/-14 g for the epicardi
58 erved more frequently in ICM than in NICM in endocardium (4.1% vs. 1.3%; p = 0.0003) and epicardium (
59 oanatomic maps acquired during sinus rhythm (endocardium, 509+/-291 points/map; epicardium, 716+/-323
60 r on the epicardium (97+/-78 cm(2)) than the endocardium (57+/-44 cm(2); P=0.04), with significantly
61  significantly higher in the epicardium than endocardium (61.2% versus 51.6%, P<0.0001).
62 myocardium is tightly coupled to that of the endocardium, a specialized endothelial tissue that lines
63 riggers mesenchyme production in ventricular endocardium, a tissue that does not normally undergo EMT
64 isolated from the epicardium compared to the endocardium; a transmural difference that was also seen
65 e is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified a
66 alcineurin/NFAT signaling is required in the endocardium, adjacent to the earlier myocardial site of
67 ntensifies and extends from E9.5 to E11.5 in endocardium along the atrioventricular canal and outflow
68 n endothelial cells of coronary arteries and endocardium along which Purkinje fiber recruitment from
69 tion of the Bmp type 1A receptor, Bmpr1a, in endocardium also resulted in failed cushion formation, i
70 A in 5 patients (4 from the left ventricular endocardium and 1 from the left coronary cusp); all succ
71 5+/-1.5 mm) were identified, 85% between the endocardium and 50% shell and 76% present in >/=1 layer.
72 ctrode basket catheter on the left ventricle endocardium and 54 6-electrode plunge needles inserted i
73 ly 4 patients with penetrating wounds to the endocardium and all had sealed.
74 explained by a shorter path length along the endocardium and by faster circumferential and transmural
75  fiber differentiation takes place along the endocardium and coronary arteries.
76 xpression in the heart was restricted to the endocardium and coronary endothelium.
77        FGFR1 expression was detected in both endocardium and cushion mesenchyme as well as in myocard
78     Focal waves appeared equally frequent at endocardium and epicardium (11% versus 13%; P=0.18).
79  Fgf9, Fgf16, and Fgf20 are expressed in the endocardium and epicardium and that RA can induce epicar
80 ly, SCFA contributions were elevated in both endocardium and epicardium despite preserved epicardial
81       Trophic factors secreted both from the endocardium and epicardium regulate appropriate growth o
82 olution activation mapping (Rhythmia) of the endocardium and epicardium via the coronary sinus.
83                           A gradient between endocardium and epicardium was observed for radial veloc
84 ts on action potential duration (APD) in the endocardium and epicardium which may be pro-arrhythmic.
85 ession becomes activated specifically in the endocardium and epicardium, but not the myocardium.
86 and 726 +/- 483 points in the left ventricle endocardium and epicardium, respectively.
87 y, allowing gene expression in non pro-valve endocardium and extracardiac vasculature.
88 tly develop dilated chambers with compressed endocardium and fail to form identifiable cardiac valves
89  heterozygous for Gata4 in the myocardium or endocardium and heterozygous for Tbx5 (Gata4(MyoDel/wt);
90 h single-cell RNA profiling of hiPSC-derived endocardium and human fetal heart tissue with an underde
91 diffuse fibrosis that is more predominant in endocardium and is accompanied by papillary fibrosis.
92 criptional pathways upstream of Gata4 in the endocardium and its derivatives in the endocardial cushi
93  provide insight into differentiation of the endocardium and its role in heart development.
94  endocardium, whereas DPI was highest at the endocardium and lowest at the epicardium for the entire
95 ced EMT and decreased proliferation of valve endocardium and mesenchyme.
96 c lineage and provides further evidence that endocardium and myocardium are derived from a common pre
97 e midline endoderm are incorporated into the endocardium and myocardium during closure of the foregut
98 5, in addition to apoptosis in foetal liver, endocardium and myocardium, the erythropoietin receptor
99  role in intercellular communication between endocardium and myocardium, which is crucial in controll
100 pment by targeting different pathways in the endocardium and myocardium.
101 ting reciprocal crosstalk between developing endocardium and myocardium.
102  transcription factors), is expressed in the endocardium and neural crest during early mouse heart de
103  proposed, including the sinus venosus (SV), endocardium and proepicardium, but their relative contri
104 al portion of liver vessels derives from the endocardium and shares a common developmental origin wit
105 lioration of inflow cannula contact with the endocardium and suction events or ablation of specific a
106 s were well correlated spatially between the endocardium and the epicardium (dominant frequency, 0.79
107    All had ablations on the left ventricular endocardium, and 67% had ablations on the right ventricu
108 ten adjacent to a valve annulus, deep in the endocardium, and can be greater in extent on the epicard
109 ude myocardium, smooth muscle, neural crest, endocardium, and endothelium.
110 i-LAVA, low unipolar amplitude in the facing endocardium, and Epi-LAVA within a wall thinning area at
111 esis in the placental labyrinth, a collapsed endocardium, and impaired vessel network patterning.
112 tor response is reduced, particularly in the endocardium, and in proportion to the magnitude of hyper
113  EMD is longer at the epicardium than at the endocardium, and is greater near the base than at the ap
114 compartments: the epicardium, midmyocardium, endocardium, and pericardial fluid, and accounted for ca
115 ll as the cardiac neural crest cells (NCCs), endocardium, and proepicardium.
116                          Injury to myocytes, endocardium, and the coronary endothelium during harvest
117  more abundant in the epicardium than in the endocardium, and this gradient paralleled the gradient i
118 ature; NTPDase1 is expressed by endothelium, endocardium, and to a lesser extent by vascular smooth m
119 tely 3-fold at 60 mV) in female base but not endocardium, apex or in male base myocytes.
120 bacterial adhesion to morphologically intact endocardium are largely unknown.
121 s such as myocardium, the cardiac jelly, and endocardium are presented.
122  heart, two tissues - the myocardium and the endocardium - are closely juxtaposed throughout their de
123       Instead, these cells remain within the endocardium as a proliferative population to support val
124 sticity in the infarct zone and identify the endocardium as a site of endogenous arteriogenesis and s
125 ty was observed in RV epicardium, but not in endocardium, as a consequence of heterogeneities in the
126  (ALK3), BMPR-1B (ALK6) and ALK2 in chick AV endocardium at stage-14(-), the onset of epithelial to m
127 sprouting of arterial cells derived from the endocardium at the atrioventricular canal.
128 se hemo-vascular precursors give rise to the endocardium, atrioventricular cushions and coronary vasc
129 chemic border in the left ventricular apical endocardium because of mechanically induced suprathresho
130 , which is highly expressed in early cushion endocardium before becoming downregulated after EMT.
131  expression is specifically inhibited in the endocardium but not in the myocardium.
132 ignificant role in S. mitis virulence in the endocardium, but have never previously been detected in
133 comes restricted to arterial endothelium and endocardium by embryonic day 9.5 in transgenic mouse emb
134  by RT-PCR and localized BMPR-1B mRNA in the endocardium by in situ hybridization.
135 ategies: (1) distributed illumination of the endocardium by multi-optrode grids (number of optrodes,
136 nd the activation of the BMP receptor in the endocardium can promote AV EMT in the chick.
137  localized to the myocardium and absent from endocardium, cardiac cushion, outflow tract, or coronary
138 iciency in the SHF but not the myocardium or endocardium caused ASDs.
139  homologous mutation bmpr1aa(p.R438H) within endocardium causes a reduced AV valve area, a downregula
140 (e4)/lacZ expression in the developing valve endocardium colocalizes with NFATc1 and, endocardial DSC
141 argest amplitude and earliest onset near the endocardium compared with the epicardium.
142 Tmem2 is an essential mediator of myocardium-endocardium coordination during cardiac morphogenesis.
143 GFR2(+), and endoglin(-)) to the surrounding endocardium (Cx40(-), VEGFR2(-), and endoglin(+)).
144 pecific expression of a reporter gene in the endocardium, defined by the temporal and spatial express
145 er evidence for the unique susceptibility of endocardium-derived endothelial cells to undergo EndMT a
146 y vessel formation by directing migration of endocardium-derived endothelial cells.
147 ecifically in the mesoderm markedly impaired endocardium development with regard to cell proliferatio
148 ctors that play important roles in embryonic endocardium development, Schwann and oligodendrocyte sur
149                                          The endocardium develops in tight association with cardiomyo
150       BZ channels, more commonly seen in the endocardium, display a 3D structure within the myocardia
151 yssynchronous failing hearts, the lateral LV endocardium displayed a 2-fold increase in phosphorylate
152 en gel assays, inactivation of Tgfbr2 in the endocardium does not prevent atrioventricular cushion me
153 gs to record endocardial activation from the endocardium during 7 minutes of VF (controls, n=6).
154 ptional target of NFATc1 proteins within the endocardium during a critical window of heart valve form
155 rated is expressed predominantly by valvular endocardium during cardiac valve maturation, exhibited e
156  demonstrate that Gpr126 is expressed in the endocardium during early mouse heart development.
157 es to specifically block BMP signaling in AV endocardium during EMT.
158 ted to the greater loss of blood flow at the endocardium during ischemia.
159 ere recorded from right and left ventricular endocardium during steady-state pacing, whilst subjects
160 outing coronary vessels (but not ventricular endocardium) during development.
161 icardium generates wavefronts that drive the endocardium early during VF.
162 eral epicardium (Epi group, N=3), and the LV endocardium (Endo group, N=3).
163 local abnormal ventricular activities in the endocardium (Endo-LAVA) and epicardium (Epi-LAVA), follo
164 ion being confined to non-myocardial layers (endocardium-endothelium-epicardium).
165     Etsrp71 was transiently expressed in the endocardium/endothelium of the developing embryo (E7.75-
166  operators were provided with 3D surfaces of endocardium, epicardium, myocardial wall thickness (rang
167 dult stages); there are no chambers, valves, endocardium, epicardium, or other differentiated feature
168  RV showed increased cell death close to the endocardium especially at 8 hours.
169           In conclusion, cells closer to the endocardium exhibit a slower decay of intracellular calc
170 rast, VEGFR2 does not exhibit robust cushion endocardium expression until after EMT is complete.
171 In addition, we find that the tal1-deficient endocardium fails to maintain its identity; over time, a
172 ugh Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward th
173 h signalling becomes activated in the atrial endocardium following ventricular ablation, and discover
174 in endothelial cells and endothelial-derived endocardium for cardiovascular development but is dispen
175 velopment, it is critically important in the endocardium for induction of EMT both in vitro and in vi
176                                          The endocardium forms the inner lining of the heart tube, wh
177  isolated preparations of rabbit ventricular endocardium from age-matched normal control female rabbi
178                               To distinguish endocardium from other vasculature, we generated an NFAT
179 ngs to automatically locate and track the LV endocardium from routine grayscale digital cineloops and
180                                       The RV endocardium had a higher PS incidence than the epicardiu
181                                       The LA endocardium has complex but characteristic patterns of a
182            However, SCR events closer to the endocardium have the largest amplitude and earliest onse
183 n of ADAM15 was found in vascular cells, the endocardium, hypertrophic cells in developing bone, and
184 Epicardial VTs were targeted opposite normal endocardium in 10 patients (77%) and/or opposite ineffec
185 ic root and/or anteroseptal left ventricular endocardium in 8 patients (89%) and in the anterior card
186 rhythmias was effectively performed from the endocardium in all 5 patients.
187 ere recorded from right and left ventricular endocardium in anesthetized beagle dogs (n=11) in vivo.
188 ractions from the epicardium compared to the endocardium in both the sham and LVD groups.
189                     However, the role of the endocardium in early cardiac ontogeny remains under-expl
190        In spite of the essential role of the endocardium in heart development and function, the trans
191 er, these results reveal a critical role for endocardium in HLHS etiology and provide a rationale for
192  to E8.5 specifically differentiate into the endocardium in mouse embryos.
193  endothelial foci were identified within the endocardium in the infarct zone.
194 rimary endothelial cells in vitro and in the endocardium in the mouse heart.
195 lation that displays many characteristics of endocardium, including expression of the cohort of genes
196 n ZO-1 is mislocalized in the tal1-deficient endocardium, indicating a defect in intercellular juncti
197 cteristics in the ventricular myocardium and endocardium, indicating a role of frv in the regional re
198 +/-9.2 ms (P<0.01), and an S2 applied to the endocardium induced a polymorphic VT (pVT) in 9 of 12 we
199 ls to the myocardium along the axis from the endocardium (inside) to the outside of the chamber.
200                                          The endocardium interacts with the myocardium to promote pro
201 ransformation of atrioventricular (AV) canal endocardium into invasive mesenchyme correlates spatiall
202                 Notch patterns the embryonic endocardium into prospective territories for valve and c
203 fic Nfatc1-Cre mouse revealed that hemogenic endocardium is a de novo source of tissue macrophages in
204                 Our findings reveal that the endocardium is a dynamic, injury-responsive source of RA
205 n together, these studies emphasize that the endocardium is a unique cardiac lineage and provides fur
206 seen in Ccbe1 knockouts, indicating that the endocardium is activated in multiple cases where sinus v
207     Yet, it is unknown how the growth of the endocardium is coordinated with that of the myocardium.
208  paracrine signaling from the epicardium and endocardium is critical for proper development of the he
209 DSCR1(e4) expression in the developing valve endocardium is dependent on NFATc1 and support a role fo
210                                The embryonic endocardium is essential for early heart development as
211 est that transient hemogenic activity in the endocardium is indispensable for the valvular tissue rem
212   On the other hand, Sox17 expression in the endocardium is required for heart development.
213 e evidence that BMP signaling through the AV endocardium is required for the EMT and the activation o
214  repression of Bmp10 by Irx3 and Irx5 in the endocardium is required for ventricular septation.
215                                              Endocardium is specified as a cardiac cell lineage, inde
216                                          The endocardium is the endothelial component of the vertebra
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 ty Pentaray mapping catheter was used in the endocardium (n=35) and epicardially.
227 NS result from mutant Shp2 expression in the endocardium, not in the myocardium or neural crest.
228          Fifteen lesions were created in the endocardium of 13 pigs.
229 tion of ventricular fibrillation (VF) on the endocardium of humans.
230 arts or administered percutaneously into the endocardium of infarcted pigs.
231 ibrosis with ageing, which was higher in the endocardium of OVX and OVF groups.
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 tch pathway and Kmt2d during endothelium and endocardium patterning and shows that pharmacological in
248 y unknown vasculogenesis defect that affects endocardium patterning and, consequently, heart ventricl
249                                    Thus, the endocardium plays a crucial early role in cardiac morpho
250 d in Scl(-/-) hearts, where the disorganized endocardium precociously differentiated into cardiomyocy
251 ulting in activation of almost the entire LV endocardium prior to septal breakout, thereby limiting a
252 xhibits less estimated block than the slower endocardium, raising the possibility that faster activat
253 ibute to the early sinus venosus and cardiac endocardium, respectively, two tissues linked to vascula
254        Alterations in NOTCH signaling in the endocardium result in congenital structural malformation
255 tivator inhibitor serpine1 in myocardium and endocardium, resulting in increased levels of plasminoge
256     Our work suggests that the growth of the endocardium results from myocardial chamber volume expan
257         Arterial endothelial foci within the endocardium reveal extensive endothelial cell plasticity
258 relationship observed between myocardium and endocardium seen in vivo.
259                     Where, when, and how the endocardium segregates during embryogenesis have remaine
260 the E9.0 mouse atrio-ventricular canal (AVC) endocardium signature.
261 ate that the injury-activated epicardium and endocardium support cardiomyocyte replenishment initiall
262 pproximately 25% faster when pacing from the endocardium than from the epicardium.
263 n the left ventricular and right ventricular endocardium than in the epicardium (15 [8-25] and 13 [7-
264 rotein, to repress ADAMTS1 expression in the endocardium that overlies the developing trabeculae.
265 le in induction of EMT in the avian epi- and endocardium, the function of Tgf-betas in corresponding
266 genesis, ADAMTS1 expression initiates in the endocardium to degrade the cardiac jelly and prevent exc
267       Scar area decreased progressively from endocardium to epicardium (scar area/left ventricular ar
268 s (n=12; P<0.001) as pacing was shifted from endocardium to epicardium.
269 hod to detect and track such features on the endocardium to extract a metric that reflects local myoc
270  extracellular space abutting myocardium and endocardium to form endocardial cushions (EC) in a proce
271 hat Bmp2 signals directly to cushion-forming endocardium to induce EMT.
272  b2a (efnb2a) and neuregulin 1 (nrg1) in the endocardium to promote trabeculation and that forced Not
273 Irx3 and Irx5 have redundant function in the endocardium to regulate atrioventricular canal morphogen
274 mem2, we find that Tmem2 can function in the endocardium to repress atrioventricular differentiation
275 led myocardial infarction decreases from the endocardium to the epicardium.
276 pothesized that paracrine signaling from the endocardium to the myocardium is crucial for initiating
277 e opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular d
278 dogs indicate activation propagates from the endocardium toward the epicardium after 1 minute of VF,
279                        Atrioventricular (AV) endocardium transforms into the cushion mesenchyme, the
280 ithin 3 hr of ventricular injury, the entire endocardium undergoes morphological changes and induces
281 ng oxidation in both ischemic epicardium and endocardium versus only 38+/-4% and 40+/-6% in respectiv
282                                     Deleting endocardium via the clochesk4 mutants downregulated Notc
283 e of valve-forming activity: Smad4-deficient endocardium was associated with acellular endocardial cu
284          The extent and location of abnormal endocardium was estimated by measuring areas of abnormal
285 ames/sec) of the posterior left atrial (PLA) endocardium was performed during sustained AF (burst pac
286 ional activations (n=6) from the epi- to the endocardium was seen in 2 patients.
287 pacing, cytoplasmic calcium elevation at the endocardium was significantly increased (15+/-4%) compar
288 area (<1.0 mV for epicardium and <1.5 mV for endocardium) was more extensive on the epicardium (95+/-
289 g current delivered to the right ventricular endocardium, was untreated for 3 mins.
290 MP signal transduction in the myocardium and endocardium, we show that the cardiac defects of Noggin
291                       Video snapshots of the endocardium were acquired at sites distributed throughou
292 Cartesian coordinates of points on a virtual endocardium were used to calculate the length and thus t
293  in cardiac development but restricts to the endocardium where it remains active through cardiogenesi
294  highest at the epicardium and lowest at the endocardium, whereas DPI was highest at the endocardium
295 aortic root or anteroseptal left ventricular endocardium, whereas inferolateral scars frequently requ
296 erplay of signals between the myocardium and endocardium whereby secreted cues induce the endothelial
297 ner tube of specialized endothelium known as endocardium, which performs multiple essential functions
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

 
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