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1 mbryo, where they merge to assemble a linear heart tube.
2 e at the midline to give rise to the primary heart tube.
3 ction due to elastic wave propagation in the heart tube.
4 yocardial interactions within the developing heart tube.
5 ives them laterally, resulting in an unfused heart tube.
6 field by 20% before formation of the primary heart tube.
7 ses depressed Ca2+ transients in the primary heart tube.
8 a large pericardial effusion and an unlooped heart tube.
9 egions of anterior mesoderm to form a linear heart tube.
10 al wall and defects in fusion of the nascent heart tube.
11 equired for cell polarity acquisition of the heart tube.
12 orphogenesis and assembly of the contractile heart tube.
13 that migrate ventrally to fuse into a linear heart tube.
14 idline, where it fuses to form the primitive heart tube.
15 ter progenitors have fashioned the primitive heart tube.
16 tic sac immediately anterior to the existing heart tube.
17 was identified on the ventral surface of the heart tube.
18 field (FHF) progenitors assemble the linear heart tube.
19 toward the midline to form a beating linear heart tube.
20 ay (E)8.0 during morphogenesis of the linear heart tube.
21 ne to form the first segment of the straight heart tube.
22 diac induction and the formation of a linear heart tube.
23 eet of mesoderm converge to form the nascent heart tube.
24 srupted cell polarity and extrusion from the heart tube.
25 p2 during the elaboration and folding of the heart tube.
26 f Hand1 transcripts in the linear and looped heart tube.
27 -lateral pattern into the A-P pattern of the heart tube.
28 he inflow and outflow portions of the looped heart tube.
29 flow tract and right ventricle of the looped heart tube.
30 cation and throughout the linear and looping heart tube.
31 ide and eHAND on the left side of the looped heart tube.
32 e atrioventricular canal and loop the linear heart tube.
33 ecursor cells before formation of the linear heart tube.
34 orm lack of a ventral pericardial cavity and heart tube.
35 ization is disrupted, resulting in a bulbous heart tube.
36 n the heart field until they form the simple heart tube.
37 to positional information in the developing heart tube.
38 iates at the arterial pole of the developing heart tube.
39 rs towards the midline to form the primitive heart tube.
40 enerates tension to elongate the foregut and heart tube.
41 th the emergence of rhythmic activity of the heart tube.
42 tractility and altered blood flow within the heart tube.
43 bryonic midline, where they fuse to form the heart tube.
44 anterior intestinal portal (AIP) to form the heart tube.
45 se/Atp1a1 in the elongation of the zebrafish heart tube.
46 expressed predominantly in the AVC of early heart tube.
47 e they meet and fuse to create the primitive heart tube.
48 mber of cardiomyocytes and elongation of the heart tube.
49 protrudes toward and attaches to the looping heart tube.
50 soderm, resulting in aberrant looping of the heart tube.
51 1P(2) disrupt the formation of the primitive heart tube.
52 ablish the original dimensions of the linear heart tube.
53 ing the initial circumference of the nascent heart tube.
54 ardial sheets for formation of the primitive heart tube.
55 Gata6, or Gata4 and Gata5, develop defective heart tubes.
56 does not alter the Ca2+ transients of NCX-/- heart tubes.
57 ld-type heart tubes, has no effect on NCX-/- heart tubes.
58 agy and mitochondrial dynamics in Drosophila heart tubes.
59 obo2) during morphogenesis of the Drosophila heart tube, a process analogous to early heart formation
60 n or its overexpression causes disruption in heart tube alignment and assembly, and slit-deficient he
64 pressed in the precardiac mesoderm and early heart tube and control distinct developmental events dur
66 Gata4-deficient mice fail to form a ventral heart tube and die of circulatory failure at embryonic d
67 brings about a significant extension of the heart tube and extraneous looping caused by the elevated
68 tant embryos most notably lacked a primitive heart tube and foregut and developed partially outside t
70 t lateral plate mesoderm (LPM), left half of heart tube and head mesoderm, but its absence in the ext
71 rate to the ventral midline to form a linear heart tube and instead formed aberrant cardiac structure
73 dundant role with cNkx-2.5 in the coalescing heart tube and may play an important role in the transcr
75 Nkx2.5Cre is expressed in the AHF, primary heart tube and pharyngeal endoderm, while TnT-Cre is exp
76 s that regulate the formation of a patterned heart tube and provide an important framework for future
79 volved in the morphogenesis of the posterior heart tube and the development of the cardiac inflow tra
80 the cNkx-2.8 gene is expressed in the linear heart tube and the dorsal half of the vitelline vein.
81 movement of cells in the embryonic zebrafish heart tube and the flow of blood through the heart and o
83 lateral plate mesoderm, generates the linear heart tube and ultimately gives rise to the left ventric
84 embryogenesis, we found that activity in the heart tubes and its rhythmicity were greatly diminished.
85 precursors, defects in the elongation of the heart tube, and a severe reduction in ECM/Fibronectin de
86 llaborate to create concentric layers of the heart tube, and communicate during formation of the atri
87 later in pharyngeal mesoderm, elongates the heart tube, and gives rise to the outflow tract and much
88 he heart fields coalesce to form the primary heart tube, and overt, morphological asymmetry first bec
90 we have demonstrated that cells in the mouse heart tube are hypoxic, while cardiac progenitor cells (
91 ll cardioblasts and pericardial cells of the heart tube as well as in associated lymph gland hematopo
92 gain insight into the genetic regulation of heart tube assembly and patterning, we examine cmlc2 and
94 rrors could originate during early stages of heart tube assembly in patients with NKX2-5 mutations.
95 nd vmhc expression throughout the process of heart tube assembly indicate the important role of an in
101 mutant embryos fail to develop a functional heart tube at E8.5 and are resorbed at approximately E10
102 is, CHAMP expression commences in the linear heart tube at embryonic day 8.0, shortly after initiatio
103 er formation of the heart tube, elongate the heart tube at the outflow pole, and give rise to three c
104 ese mesodermal progenitors then merge into a heart tube at the ventral midline (vertebrates) or the d
107 on in cardiomyocytes was found in the linear heart tube before establishment of a (pro)epicardium.
108 roughout the cardiac crescent and the linear heart tube, before becoming restricted to the right vent
109 expression throughout the myocardium of the heart tube both represses proliferation and impairs seco
110 lular Na+ induces Ca2+ overload in wild-type heart tubes but does not alter the Ca2+ transients of NC
111 developing myotome, limb bud precursors, and heart tube, but by late fetal stages of development, MNF
112 Nkx-2.8 is no longer expressed in the looped heart tube, but is expressed in the ventral pharyngeal e
113 close the neural tube, fail to form a single heart tube (cardia bifida), and show delayed migration o
114 the yolk sac, had two independent bilateral heart tubes (cardia bifida), lacked a foregut, and died
116 omitant with its expression in the primitive heart tube, cephalic mesenchyme, and yolk sac vasculatur
117 ype in the avian embryo includes an abnormal heart tube closed at the sinus venosus and the absence o
118 mitochondrial fusion in Parkin-deficient fly heart tubes completely prevented the cardiomyopathy and
120 is and causes a linear, dilated, hypoplastic heart tube, despite normal expression of Nkx2.5 and dHAN
121 homozygous for a null mutation of MEF2C, the heart tube did not undergo looping morphogenesis, the fu
122 drial morphometric heterogeneity and induces heart tube dilation with profound contractile impairment
123 e expressed in the left side of the straight heart tube during development is Pitx2, which when mutat
126 ependent enhancer is activated in the linear heart tube during mouse embryogenesis and thereafter con
128 n pharyngeal mesoderm after formation of the heart tube, elongate the heart tube at the outflow pole,
129 esent resolve this issue by showing that the heart tube elongates during looping, concomitant with ac
130 number as well as later defects in primitive heart tube elongation and atrioventricular boundary patt
131 L using morpholino oligonucleotides produced heart tube elongation defects like those found in atp1a1
136 phogenesis, Tbx5 is expressed throughout the heart tube except the anterior portion, the bulbus cordi
137 ple cardiac defects, including the primitive heart tube extension abnormality, aberrant cardiomyocyte
138 Thus, we conclude that nkx genes regulate heart tube extension and exert differential effects on v
139 ht ventricle and conus/truncus of the single heart tube fail to form and the endocardial cushions in
140 ure conus and right ventricle) of the single heart tube fails to develop normally and the endocardial
143 ashion and are restricted to segments of the heart tube fated to form the right and left ventricles,
145 is evident in the lateral mesoderm prior to heart tube formation and results from the inhibition of
146 emonstrate that MEIS2 is critical for proper heart tube formation and subsequent cardiac looping.
148 t/Robo signaling components are required for heart tube formation in zebrafish and that this network
149 rmore, instead of interfering with primitive heart tube formation or cardiac chamber differentiation,
150 ld, and contributes myocardium after initial heart tube formation, giving rise to both smooth muscle
151 genesis achieves gut internalization, linear heart tube formation, ventral body wall closure, and enc
158 Several mutations that result in abnormal heart-tube formation have been studied; however, an unde
160 definitive endocardial lining of the primary heart tube formed directly from the ventral plexus of en
161 7 that the outflow tract was added after the heart tube formed, the source of these secondarily added
162 so required in the second heart field as the heart tube forms, reflecting the temporal delay in diffe
165 d within the myogenic cells of the primitive heart tube from stages 9 to 18 and is not detected in th
166 drugs are applied to electrically stimulated heart tubes from control mouse embryos or embryos with t
168 38 is not activated by KB-R7943 treatment in heart tubes from Ncx1(-/-) mice at 9.5 days postcoitum b
170 as a dual role during assembly of the linear heart tube, functioning to regulate both cell positionin
171 and gridlock mutants, which have failure of heart tube fusion and aortic atresia, respectively, are
175 nesis, the myocardial layer of the primitive heart tube grows outward from the endocardial-lined lume
180 ent that occurs during assembly of a midline heart tube (HH Stage 9) is NOT due to "migration" (auton
182 d circuit in the adult, but selection of the heart tube (HT) as a definitive target by heart excitor
183 ntribute to longitudinal subdivisions of the heart tube (HT), with the FHF contributing the left vent
184 e Drosophila dorsal vessel and the primitive heart tube in early vertebrate embryos, these data sugge
186 bidirectional WSS across the AV canal in the heart tube in response to peristaltic motion of the wall
188 activity in the heart tube while disrupting heart tube innervation by some HE neurons still resulted
189 ocess that transforms the initially straight heart tube into a curved tube normally directed toward t
190 Valvuloseptal morphogenesis of the primitive heart tube into a four-chambered organ requires the form
193 le on how the anterior/posterior axis of the heart tube is determined and whether the left and right
195 t that postsynaptic rhythmic activity of the heart tube is necessary and sufficient for the developme
196 hile the initial patterning of the primitive heart tube is not affected in leo1(LA1186) mutant embryo
197 dentified genes suggests that the Drosophila heart tube is segmentally patterned, like axial patterni
198 ft-right symmetry of the primitive zebrafish heart tube is the shift in pattern of BMP4 expression fr
200 numbers on the maturation of the myocardial heart tube, its contractility, and acquisition of a norm
202 nman was previously shown to be required for heart tube looping morphogenesis and ventricular chamber
205 ssion is maintained throughout the period of heart tube morphogenesis and differentiation of myocardi
210 s normally GATA-4, and develops a nonlooping heart tube morphogenetic defect that is a model for cong
213 c alpha-actin in the myotomes and developing heart tube of the tadpole requires distinct enhancers wi
215 k most of these redundant genes, we examined heart tubes of parkin knockout flies and observed accumu
217 es of epicardial-like tissue surrounding the heart tube on the structural and functional integrity of
218 This complex repressed Isl1 in the hypoxic heart tube or following induction of ectopic hypoxic res
219 ventral pharynx, we cultured stage 12 chick heart tube or myocardial strips in the presence or absen
220 ocytes that are accreted to the poles of the heart tube over a well-defined developmental window.
221 enables rapid cross-sectional imaging of the heart tube over various cardiac cycles for the measureme
222 we examined 12 zebrafish mutants for initial heart tube position and later heart looping direction (c
223 Peristaltic contraction of the embryonic heart tube produces time- and spatial-varying wall shear
224 ion of a secondary myocardium to the primary heart tube provides a new framework for understanding se
226 the morphogenetic assembly of the primitive heart tube requires the medial migration and midline fus
228 es, it remains unknown whether the mammalian heart tube serves as a haemogenic organ akin to the dors
229 igrate to the arterial pole of the zebrafish heart tube soon after their specification in the nkx2.5(
232 form and function normally through the early heart tube stage, manifesting only a slight bradycardia
233 velopment of the heart arrests at the looped heart tube stage, with cardiovascular defects indicated
240 mained lateral and generated two independent heart tubes that contained differentiated cardiomyocytes
241 we propose here that, in the early embryonic heart tube, the signaling mechanism coordinating beats i
244 cent, throughout the myocardium of the early heart tube, then in the outflow tract and right ventricl
245 nt proceeds from the formation of the linear heart tube, through complex looping and septation, all t
248 nopus laevis, from the formation of a linear heart tube to the appearance of morphologically distinct
251 ence, the process during which the primitive heart tube transforms into morphologically distinct cham
254 rticipation in formation of a single midline heart tube, we propose that the ventral midline endoderm
256 both associated with segments of the primary heart tube where endothelial cells "re-transform" back t
257 on in the diencephalon and in the developing heart tube where Pax6 is not normally expressed, while C
258 he endocardium forms the inner lining of the heart tube, where it enables blood flow and also interac
259 e involved in development of segments of the heart tube which give rise to specific chambers of the h
260 ions that preserved rhythmic activity in the heart tube while disrupting heart tube innervation by so
261 were observed in mutant embryos: hypoplastic heart tubes with misaligned cardioblasts and the absence
262 al fusion defects in Drosophila melanogaster heart tubes with tincDelta4Gal4-directed expression of R
263 is an alteration in the configuration of the heart tube, with inadequate remodeling of the inner hear
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