ライフサイエンスコーパス: ventricular wall

1 farction (>75% transmural extent of the left-ventricular wall).

2 as trabecular and compact components of the ventricular wall.

3 bing of field effects deep inside the intact ventricular wall.

4 ivery and stimulate angiogenesis in the left ventricular wall.

5 cal activation of myocardium vary across the ventricular wall.

6 nly distributed in some mitotic pairs at the ventricular wall.

7 their proper morphological positions in the ventricular wall.

8 of cardiomyocytes within the embryonic left ventricular wall.

9 erm effect of injecting material to the left ventricular wall.

10 strated re-entry involving the inferior left ventricular wall.

11 sing the direction of activation of the left ventricular wall.

12 sing the direction of activation of the left ventricular wall.

13 of the three standard segments in each left ventricular wall.

14 ial propagation in a one-dimensional virtual ventricular wall.

15 ion times shortened uniformly throughout the ventricular wall.

16 n depending on fiber organization within the ventricular wall.

17 ion of new neurons born close to, or in, the ventricular wall.

18 ties of Ca2+ channels across the canine left ventricular wall.

19 edominantly involved the middle third of the ventricular wall.

20 NF and GFP mRNA expression restricted to the ventricular wall.

21 RNA was expressed at equal levels across the ventricular wall.

22 lly with the remaining viable portion of the ventricular wall.

23 sion of action potential duration across the ventricular wall.

24 in neural cell migration and adhesion in the ventricular wall.

25 +/-1% of the inner circumference of the left ventricular wall.

26 ntricles and between different layers of the ventricular wall.

27 s) is heterogeneously distributed across the ventricular wall.

28 -1 was shown to promote trabeculation of the ventricular wall.

29 stiffening of the passive properties of the ventricular wall.

30 tation of layers of muscle fibers inside the ventricular wall.

31 ntact rat trabeculae isolated from the right ventricular wall.

32 lving the inner one third to one half of the ventricular wall.

33 he anterior and lateral portions of the left ventricular wall.

34 ulation located within the inner half of the ventricular wall.

35 ion was slower in the RVOT than in the right ventricular wall.

36 afety and myocardial excitability within the ventricular wall.

37 of ion channel expression across the cardiac ventricular wall.

38 hypertrabeculation with noncompaction of the ventricular wall.

39 in the ventricular septum and the atrial and ventricular walls.

40 cluded abnormal coronary patterning and thin ventricular walls.

41 e reduction in heart size, including thinner ventricular walls.

42 presence of stable rotors hidden within the ventricular walls.

43 ted cells were seen at various points in the ventricular walls.

44 ugh there was some penetration away from the ventricular walls.

45 trinsic axons also innervated the atrial and ventricular walls.

46 ventricular septum than in the right or left ventricular walls.

47 s spaced relatively uniformly throughout the ventricular walls.

48 aphe form an extensive plexus on most of the ventricular walls.

49 crucial in controlling the formation of the ventricular walls.

50 rucial for the formation and function of the ventricular walls.

51 layers were observed throughout the lateral ventricular wall: a monolayer of ependymal cells (Layer

52 ventricular noncompaction (LVNC) describes a ventricular wall anatomy characterized by prominent left

53 ibited a nonprogressive thinning of the left ventricular wall and a concomitant decrease in cardiac f

54 hat filaments are often concealed inside the ventricular wall and consequently, scroll waves do not m

55 spatial dispersion of repolarization in the ventricular wall and differences in regional recovery in

56 number of internal cardiomyocytes breach the ventricular wall and expand upon its surface.

57 ed large-scale support of the infarcted left ventricular wall and improvement of heart function.

58 rhythmogenesis involve the three-dimensional ventricular wall and its anisotropic structure.

59 hat phase 2 EAD can be generated from intact ventricular wall and produce a trigger to initiate the o

60 examination revealed a thinning of the third ventricular wall and reduction of both tanycyte and epen

61 and in discrete puncta throughout the right ventricular wall and septum, as well.

62 ng degrees was observed in the anterior left ventricular wall and septum.

63 al transsection, outward displacement of the ventricular wall and transverse shearing deformation wer

64 patients with echocardiographic evidence of ventricular wall and valve thickening before transplanta

65 KO-2a) died in the embryonic stage with thin ventricular wall and ventricular septal defects.

66 te the timing of force generation across the ventricular wall and work production during systole.

67 cular disease characterized by thickening of ventricular walls and decreased left ventricular chamber

68 e dilated cardiomyopathy with thickened left ventricular walls and profound impairment of systolic fu

69 , especially in the interventricular septum, ventricular wall, and outflow tract, which correlated we

70 mines the repolarization sequence across the ventricular wall, and plays an important role in the dev

71 or leaflet was displaced and adherent to the ventricular wall, and the annulus fibrosus was disrupted

72 bres that in rare events breach the juvenile ventricular wall, and then expand over the surface.

73 l stress and strain distribution through the ventricular wall are also computed.

74 circulation, and drug deposition across the ventricular wall, around the circumference and down the

75 sic differences in APD of cells spanning the ventricular wall as well as a heterogeneous distribution

76 d end-systolic chamber volumes and a thinned ventricular wall, associated with heterogeneous myocyte

77 arge dispersion of repolarization across the ventricular wall at slow stimulation rates.

78 Dispersion of APD90 across the left ventricular wall averaged 51+/-19 and 64+/-25 ms at basi

79 500 ms, there was no ARI gradient across the ventricular wall before and during quinidine infusion.

80 lic cardiac impairment with septal and right ventricular wall being predominantly affected.

81 ophic factor accumulates not only around the ventricular walls, but also in specific brain regions in

82 l stress and strain distribution in the left ventricular wall considering it to be made of homogeneou

83 tion among different cell types spanning the ventricular wall creates the substrate for the genesis o

84 ild-to-moderate thickening in left and right ventricular walls, decreased left ventricular dimensions

85 Tissue samples isolated from the left ventricular wall demonstrate that sarcoplasmic reticulum

86 ice had fewer coronary microvessels, thinned ventricular walls, depressed basal contractile function,

87 Later in development, the bulk of the ventricular wall derives from the compaction process, ye

88 nt in utero, we understand little of how the ventricular walls develop.

89 P10-Tbx20 signaling cascade is important for ventricular wall development and maturation.

90 ls and impaired myocardial trabeculation and ventricular wall development.

91 unction, progenitors accumulate in the third ventricular wall, die or are inappropriately specified,

92 ss systolic and diastolic function, and left ventricular wall dimensions.

93 Surgical restoration of the left ventricular wall (Dor procedure) has been advocated as a

94 tricular septal defect, noncompaction of the ventricular wall, double-outlet right ventricle, and dil

95 le and the deformation parameters of the rat ventricular wall during adaptation of the passive left v

96 f a signaling pathway in the control of left ventricular wall edema during sepsis.

97 Interestingly, exaggerated left ventricular wall edema was not coupled with aggravated s

98 The mPDK1(-/-) animals had thinner ventricular walls, enlarged atria and right ventricles.

99 e, are essential for normal formation of the ventricular walls.Fetal trabecular muscles in the heart

100 contrast of 0.25 were simulated in the left ventricular wall for 6 locations.

101 Ablation of BMP10 leads to hypoplastic ventricular wall formation, and elevated levels of BMP10

102 During ventricular wall formation, the compact myocardium proli

103 atial gradients of repolarization across the ventricular wall from 4.3+/-2.1 (control) to 12.4+/-3.5

104 endent upon the concentric thickening of the ventricular wall generated by the addition of cells to t

105 dial glia-derived cells in the adult lateral ventricular wall generated self-renewing, multipotent ne

106 of noncontractile material to a damaged left ventricular wall has important effects on cardiac mechan

107 f repolarization that exists across the left ventricular wall, how this dispersion of repolarization

108 ase in ventricular wall proliferation and in ventricular wall hypoplasia.

109 ating microelectrode from the anterior right ventricular wall in 6 pigs during up to 60 seconds of VF

110 hocks (2 to 50 V/cm) were applied across the ventricular wall in an epicardial-to-endocardial directi

111 ere implanted into the anterior-lateral left ventricular wall in C57BL/6J (allogeneic model, n = 17)

112 differentiation, is the reason for the thin ventricular wall in CFKO-2a mice.

113 eased this epicardial supplementation of the ventricular wall in growing zebrafish, and led to sponta

114 construct subepicardially in the canine left ventricular wall in situ.

115 d a transmural incision was made through the ventricular wall in the middle of the mapped region and

116 ats, surviving cells were observed along the ventricular wall, in the SVZ, and in the posterior rostr

117 cardium recurrently contributes cells to the ventricular wall, indicating an active homeostatic proce

118 Electric excitability in the ventricular wall is influenced by cellular electrophysio

119 closed-chest dogs with acute posterior left ventricular wall ischemia either with (MR) or without (n

120 ow embryonic cardiomyocytes assemble to form ventricular wall layers of appropriate spatial dimension

121 versal of repolarization sequence across the ventricular wall, leading to alternation in the polarity

122 nous progenitor cells in the adult forebrain ventricular wall may be induced by the local viral overe

123 orderline increases in thickness of the left ventricular wall, mild morphologic expression of hypertr

124 tern that involves the proximal lateral left ventricular wall most severely, with relative sparing of

125 Left ventricular wall motion (WM) abnormalities have recogniz

126 Right ventricular wall motion analysis should be routinely per

127 Patients (n = 119) with abnormal left ventricular wall motion and a left ventricular ejection

128 perative TEE for assessment of regional left ventricular wall motion and measurement of hemodynamic v

129 for the echocardiographic assessment of left ventricular wall motion based on acoustic quantification

130 ography or positron emission tomography, and ventricular wall motion imaging by stress echocardiograp

131 disease or hypertension, Killip class, left ventricular wall motion index, and sex.

132 o estimated glomerular filtration rate, left ventricular wall motion index, sex, blood pressure, and

133 y can be a cost-effective method to quantify ventricular wall motion objectively, but few studies hav

134 MPI and two supplementary codes (add-on left ventricular wall motion or left ventricular ejection fra

135 Left ventricular wall motion score (LVWMS) increased signific

136 ery disease (P < .0001), global resting left ventricular wall motion score index (P < .0001), infarct

137 chocardiography underwent DCMR in which left ventricular wall motion score index (WMSI), defined as t

138 Large MIs (based on echocardiographic left ventricular wall motion score index) were created by lef

139 Left ventricular wall motion scores were similar at baseline

140 In 78 women (85%), left ventricular wall motion was normal at baseline and durin

141 Ventricular wall motion was noted in two patients with s

142 ith experience in analysis of volumes, right ventricular wall motion, and delayed-enhancement imaging

143 ed to reconstruct the three-dimensional left ventricular wall motion.

144 small-angle x-ray diffraction of mouse left ventricular wall muscle.

145 farcts greater than at least 35% of the left ventricular wall (n = 8).

146 ern blot analysis of whole extracts from the ventricular wall of adult chicken hearts revealed that t

147 cardiac-enriched hESC progeny into the left ventricular wall of athymic rats.

148 nt of KChIP2 expression was found across the ventricular wall of human heart, but not rat heart.

149 a retroviral promoter were implanted in the ventricular wall of immunodeficient mice (n=11) via a su

150 planar wavefronts on the surface of the left ventricular wall of Langendorff-perfused isolated rabbit

151 d miRNAs were injected in vivo into the left ventricular wall of mice, and, 48 hours later, the heart

152 ach 0.15 mL, 5 mg.mL-1 saline) into the left ventricular wall of rat hearts before a 60-minute occlus

153 ion in the subepicardial layer of the dorsal ventricular wall of the developing mouse heart.

154 the presence of tanycyte barriers along the ventricular walls of other brain CVOs.

155 proximal flow constraint induced by the left ventricular wall on the accuracy of calculated flow rate

156 heart failure in juveniles by fortifying the ventricular wall, one that is reiterated in adults to pr

157 ptake allowing clear delineation of the left ventricular wall over 60 min after tracer administration

158 gical properties of myocytes across the left ventricular wall play an important role in both the norm

159 the endocardial and epicardial zones of the ventricular wall postnatally.

160 d cells are maintained in intact canine left ventricular wall preparations in which the myocardial ce

161 performed in isolated coronary perfused pig ventricular wall preparations stained with near-infrared

162 ain regionalized neural stem cells along the ventricular walls produce olfactory bulb (OB) interneuro

163 rhPDGF-BB are the result of proliferation of ventricular wall progenitor cells and reversed by blocki

164 , each resulted in a significant decrease in ventricular wall proliferation and in ventricular wall h

165 attach to the trabeculae carneae lining the ventricular wall rather than directly to the solid porti

166 eventually repaired: SVZ reconstitution and ventricular wall remodeling were mediated by progenitors

167 atal period of progenitor cell expansion and ventricular wall remodeling, loss of Wrp results in the

168 18.5 and P0, the defects in cells lining the ventricular wall resulted in an obstructive hydrocephalu

169 Nonfailing left ventricular wall samples procured from explanted hearts

170 etermine whether mechanical behavior of left ventricular wall segments that contain different degrees

171 nent dispersion of repolarization across the ventricular wall, setting the stage for induction of TdP

172 nstrated a prominent trabecular layer in the ventricular wall, so called noncompaction, along with di

173 n perfused (8 mm thick) slabs of sheep right ventricular wall stained with the voltage-sensitive dye

174 Compared with baseline, mean left ventricular wall stress and stroke work were not changed

175 esenting symptoms, PVC burden, and increased ventricular wall stress in patients with frequent PVCs a

176 End-systolic left ventricular wall stress was calculated by finite element

177 End-systolic left ventricular wall stress was significantly higher when MM

178 njury and NT-proBNP levels as marker of left ventricular wall stress were determined.

179 We tested the hypothesis that reducing left ventricular wall stress with a percutaneous left atrial-

180 eperfusion in the MI+unload group (mean left ventricular wall stress, 44 658 versus 22 963 dynes/cm(2

181 eriole density, while reducing infarct size, ventricular wall stress, and apoptosis without inducing

182 in left ventricular loading conditions, left ventricular wall stress, desensitization of proinflammat

183 nk between fatigue and PVC-induced increased ventricular wall stress, despite preserved LV function.

184 nt was change in NT-proBNP, a marker of left ventricular wall stress, from baseline to 12 weeks; anal

185 otentially related to chronic increased left ventricular wall stress, including age, hypertension, pr

186 sodium and calcium overload and consequently ventricular wall stress.

187 n echocardiography are markers for increased ventricular wall stress.

188 obrain natriuretic peptide, a marker of left ventricular wall stress.

189 absence of a gradient of protein across the ventricular wall suggest that KChIP2 is either not a req

190 f the papillary muscles and inferobasal left ventricular wall, suggesting a myocardial stretch by the

191 crometric crystals in the region of the left ventricular wall supplied by the occluded left anterior

192 In response to increased ventricular wall tension or neurohumoral stimuli, the my

193 o augment cardiac pump function and decrease ventricular wall tension.

194 al factors or when faced with an increase in ventricular-wall tension, individual cardiomyocytes unde

195 s of the HC were defined by reference to the ventricular wall, the brain surface, or differences in n

196 ynamic function, myocardial blood flow, left ventricular wall thickening and pulmonary gas exchange w

197 gesting a model by which FOG-2/NuRD promotes ventricular wall thickening by repression of this cell c

198 With LAD constriction, left ventricular wall thickening fell 45+/-8% (P<0.01).

199 The mean percentages of left ventricular wall thickening in infarcted, stunned, and r

200 identification of otherwise unexplained left ventricular wall thickening in the presence of a nondila

201 substantiated by localized patterns of left ventricular wall thickening occurring more commonly than

202 ynamic function, myocardial blood flow, left ventricular wall thickening or pulmonary gas exchange wh

203 easured regional myocardial blood flow, left ventricular wall thickening or pulmonary gas exchange.

204 Ventricular wall thickening was measured on spin-echo (S

205 However, left ventricular wall thickening was not reversed.

206 on, five patients showed progression of left ventricular wall thickening with increased left ventricu

207 Young female transgenic mice exhibited left ventricular wall thickening without dilatation, whereas

208 cterize microstructural dynamics during left ventricular wall thickening, and apply the technique in

209 , associated with concentric hypertrophy and ventricular wall thickening.

210 bnormalities and frequently have basal right ventricular wall thickening.

211 d before and after training and defined by a ventricular wall thickness >/=13.0 mm that was >1.5x the

212 Risk factors for SCD were left ventricular wall thickness >/=30 mm (20%), family histor

213 HCM patients and compared with ATH with left ventricular wall thickness >13 mm.

214 prehypertensive participants had higher left ventricular wall thickness (0.83 and 0.78 versus 0.72 cm

215 us 0.85+/-0.13 cm, P:<0.005), posterior left ventricular wall thickness (1.00+/-0.24 versus 0.88+/-0.

216 ents in the DE group (n=35) had greater left ventricular wall thickness (2.09+/-0.44 versus 1.78+/-0.

217 xane, relative to doxorubicin alone, on left ventricular wall thickness (difference between groups: 0

218 elated to NYHA class as well as age and left ventricular wall thickness (each with a value of P=0.000

219 At 4 weeks after MI, left ventricular wall thickness (echocardiography; 0.89+/-0.0

220 es, but their contribution to increased left ventricular wall thickness (LVWT) in the community is un

221 mily history of sudden death (FHSD) and left ventricular wall thickness (LVWT).

222 Left ventricular wall thickness (mean 16+/-6 mm) and disease

223 ed or had infarction comprising <25% of left ventricular wall thickness (P<0.005 for ejection fractio

224 ated to LV mass (r = 0.42), LVID (r = 0.45), ventricular wall thickness (r = 0.20 to 0.29) and caroti

225 end-diastolic diameter (r2=.32, P<.05), left ventricular wall thickness (r2=.38, P<.01), left atrial

226 M; n=36), mutation carriers with normal left ventricular wall thickness (subclinical HCM; n=28), and

227 ity as well as confounding variables of left ventricular wall thickness and age.

228 rse cardiac remodeling after MI, maintaining ventricular wall thickness and contractile function.

229 graphy showed a significantly increased left ventricular wall thickness and decreased fractional shor

230 analyses of 24 subjects with increased left ventricular wall thickness and electrocardiograms sugges

231 t ventricular hypertrophy, with reduced left ventricular wall thickness and heart weight/body weight

232 As expected, ventricular wall thickness and heart weights were simila

233 rate that LHFS of the MI region altered left ventricular wall thickness and material properties, like

234 ventricular tachycardia (nsVT), maximum left ventricular wall thickness and obstruction were signific

235 Left ventricular wall thickness and postinfarct scar thicknes

236 cular magnetic resonance to investigate left ventricular wall thickness and the presence of asymmetri

237 s T2-weighted imaging and assessment of left ventricular wall thickness in detecting patients with ac

238 nth-old mice and may account for the greater ventricular wall thickness in young 1vDelta5-14 mice com

239 Left ventricular wall thickness increased from 10 to 14 mm (p

240 ing features from normal pregnancy were left ventricular wall thickness of >/=1.0 cm, exaggerated red

241 Echocardiography demonstrated maximal left ventricular wall thickness of 19.9+/-3.8 mm, systolic an

242 ars, p = 0.0002), had more hypertrophy (left ventricular wall thickness of 24.2 vs. 21.1 mm, p = 0.00

243 uction of at least 30 mm Hg, and marked left ventricular wall thickness of more than 25 mm-were clini

244 If left ventricular wall thickness seemed nonuniform, the size a

245 diac disorder, is characterized by increased ventricular wall thickness that cannot be explained by u

246 The mean maximal left ventricular wall thickness was 21 mm.

247 Left ventricular wall thickness was also measured.

248 cardiovascular magnetic resonance, the left ventricular wall thickness was measured in all 17 segmen

249 ood (90%), although CMR measurements of left ventricular wall thickness were approximately 19% lower

250 d left ventricular dimension and normal left ventricular wall thickness) and dilated cardiomyopathy.

251 l (with the addition of T2-weighted and left ventricular wall thickness) increased the specificity, p

252 ning [FS]), end-diastolic diameter, and left ventricular wall thickness).

253 phenotype (by virtue of showing normal left ventricular wall thickness).

254 f 20 subjects with massive hypertrophy (left ventricular wall thickness, > or =30 mm) but without ele

255 ed 465 patients with hypertension, increased ventricular wall thickness, and body mass index >25 kg/m

256 ght, enlarged cardiomyocytes, increased left ventricular wall thickness, and decreased fractional sho

257 stored postischemic contractile performance, ventricular wall thickness, and electric stability while

258 raphy was performed to verify an increase in ventricular wall thickness, and mice were given rapamyci

259 livery system in improving cardiac function, ventricular wall thickness, angiogenesis, cardiac muscle

260 imaging reveals a dramatic increase in left ventricular wall thickness, as compared with Cav-1-KO, C

261 r increases in systolic blood pressure, left ventricular wall thickness, left ventricular mass, ratio

262 rest of the cohort in age at diagnosis, left ventricular wall thickness, left ventricular outflow tra

263 , an inherited human disorder with increased ventricular wall thickness, myocyte hypertrophy, and dis

264 revealed significant associations among left ventricular wall thickness, postinfarct scar thickness,

265 Some infiltrative cardiac diseases increase ventricular wall thickness, while others cause chamber e

266 ic resonance imaging, and assessment of left ventricular wall thickness.

267 art weight (296 versus 140 mg in TG(WT)) and ventricular wall thickness.

268 by confounding due to changes in BSA or left ventricular wall thickness.

269 icular function and a partial rescue of left ventricular wall thickness.

270 Rs regardless of BP, mainly by reducing left ventricular wall thickness.

271 contractile function and reductions in left ventricular wall thickness.

272 nt cardiac hypertrophy (average maximal left-ventricular-wall thickness, 8.5 mm) nor histopathologica

273 Left ventricular wall thicknesses in the overall study group

274 d atrial and ventricular chambers, and their ventricular wall thicknesses were only 1/2 to 1/3 the th

275 These mice develop left ventricular wall thinning and chamber dilation, with con

276 myocardial infarct (MI) contributes to left ventricular wall thinning and changes in regional stiffn

277 e are deficient in Fbln1 and exhibit cardiac ventricular wall thinning and ventricular septal defects

278 LV left ventricular wall thinning with LV left ventricular mass

279 rct border zone, reduced cardiac dilatation, ventricular wall thinning, and fibrosis when compared wi

280 chamber dilatation, atrial enlargement, and ventricular wall thinning.

281 At 60 min, the uptake ratios of left ventricular wall to blood, lung, and liver (mean of 7 do

282 sition of abnormal substances that cause the ventricular walls to become progressively rigid, thereby

283 e found that some radial glia in the lateral ventricular wall transform to give rise to mature ependy

284 orphology of the action potential across the ventricular wall underlies the manifestation of the elec

285 papillary muscle still attached to the left ventricular wall was also noted but was less sensitive i

286 linical heart disease, thinning of the right ventricular wall was noted in only 1 patient (patients v

287 hortening in the basal segment of the septal ventricular wall was observed in 57% of the FGR cases an

288 Reduction of the akinetic left ventricular wall was observed in BMCeP-treated hearts at

289 Myocardial blood flow of the anterior left ventricular wall was reduced from 1.00 +/- 0.18 to 0.66

290 The left ventricular wall was segmented and characterized using a

291 These changes in the ventricular wall were associated with reduced diffusion

292 istributions for anterior and inferior right ventricular walls were 3.4% and 4.5%, respectively.

293 farction (<50% transmural extent of the left-ventricular wall), whereas SPECT identified only 31 (28%

294 cytes make biased contributions to build the ventricular wall, whereas gata4(+) cardiomyocytes have l

295 cal I(P) is approximately uniform across the ventricular wall, whereas transporters that utilize the

296 EPCM was sutured to the anterolateral left ventricular wall, which included the region of ischemia.

297 by advancing the fiberoptic through the left ventricular wall with the laser inactivated.

298 eal, pial layer, vasculature) and around the ventricular walls (with some cellular labelling and labe

299 on in this region is heterogeneous along the ventricular wall, with GFAP-positive cells aligned to th

300 and morphological improvement of the injured ventricular wall without loss of scar tissue.