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 elical organization of cardiomyocytes in the ventricular wall.

3 afety and myocardial excitability within the ventricular wall.

4 hypertrabeculation with noncompaction of the ventricular wall.

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

6 cal activation of myocardium vary across the ventricular wall.

7 nly distributed in some mitotic pairs at 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 is attached to the inside or outside of the ventricular wall.

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

16 ion times shortened uniformly throughout the ventricular wall.

17 n depending on fiber organization within 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 adult mice exhibit hyperplasia in the right 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 as trabecular and compact components of the ventricular wall.

34 of ion channel expression across the cardiac ventricular wall.

35 ivery and stimulate angiogenesis in the left ventricular wall.

36 their proper morphological positions in the ventricular wall.

37 images to annotate the location of each left ventricular wall.

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

39 stiffening of the passive properties of the ventricular wall.

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

41 g rapid growth and morphogenesis of the left ventricular wall.

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

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

44 crucial in controlling the formation of the ventricular walls.

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

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

47 cluded abnormal coronary patterning and thin ventricular walls.

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

49 presence of stable rotors hidden within the ventricular walls.

50 isease that causes thickening of the heart's ventricular walls.

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

52 trinsic axons also innervated the atrial and ventricular walls.

53 iliary beating on ependymal cells lining the ventricular walls.

54 s spaced relatively uniformly throughout the ventricular walls.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 isease that causes thickening of the heart's ventricular walls and is a leading cause of sudden cardi

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

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

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

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

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

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

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

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

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

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

81 R79C carriers had significantly thicker left ventricular walls compared with noncarriers while its et

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 h of ablated lesions reached 90% of the left ventricular wall in both normal and infarcted myocardium

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

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

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

115 ventricular mass, and thickening of the left ventricular wall in IAV-infected HF mice compared to bot

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

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

118 ve from embryonic day 10.5, and can traverse ventricular walls in embryonic slice cultures.

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

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

121 ne was much stronger than that of the remote ventricular wall, involving acute downregulation of mito

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

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

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

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

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

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

128 Left ventricular wall motion (WM) abnormalities have recogniz

129 Ponatinib produced segmental left ventricular wall motion abnormalities in 33% of wild-typ

130 rdiographic abnormalities that included left ventricular wall motion abnormalities, global left ventr

131 Right ventricular wall motion analysis should be routinely per

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

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

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

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

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

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

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

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

140 Left ventricular wall motion scores were similar at baseline

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

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

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

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

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

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

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

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

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

153 the width is approximately half that of the ventricular wall, or when the infarcted area is attached

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

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

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

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

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

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

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

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

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

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

164 ollowing: (1) Thinning and thickening of the ventricular wall respectively at early and late activate

165 18.5 and P0, the defects in cells lining the ventricular wall resulted in an obstructive hydrocephalu

166 Nonfailing left ventricular wall samples procured from explanted hearts

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 sodium and calcium overload and consequently ventricular wall stress.

183 n echocardiography are markers for increased ventricular wall stress.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 However, left ventricular wall thickening was not reversed.

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

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

201 , associated with concentric hypertrophy and ventricular wall thickening.

202 bnormalities and frequently have basal right ventricular wall thickening.

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

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

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

206 tion comprised patients with a baseline left ventricular wall thickness >=13 mm and no history of hyp

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

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

209 0 +/- 16 g/m(2) , P = 0.03) and maximal left ventricular wall thickness (16 +/- 1 vs. 8 +/- 1 mm, P <

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

211 ts with cardiomyopathies with increased left ventricular wall thickness (amyloidosis, septal HCM, and

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

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

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

215 tal population), patisiran reduced mean left ventricular wall thickness (least-squares mean differenc

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

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

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

219 Higher left ventricular wall thickness (odds ratio, 2.61; CI, 1.04-6

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

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

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

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

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

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

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

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

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

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

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

231 Left ventricular wall thickness and postinfarct scar thicknes

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

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

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

235 ile abnormalities are present even when left ventricular wall thickness is normal.

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

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

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

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

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

241 Cardiomyopathies with increased left ventricular wall thickness such as cardiac amyloidosis,

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

243 In the primary cohort, maximal left ventricular wall thickness was 17+/-4 mm for adults and

244 Maximum left ventricular wall thickness was 18 +/- 8 mm, and left ven

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

246 The maximum left ventricular wall thickness was 22.9 +/- 8.7 mm and left

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

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

249 icular relative wall thickness and mean left ventricular wall thickness were independent predictors o

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 ic criteria at baseline (median maximal left ventricular wall thickness, 13 mm; interquartile range,

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

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

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

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

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

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

262 Patisiran decreased mean left ventricular wall thickness, global longitudinal strain,

263 ratory cardiac end points included mean left ventricular wall thickness, global longitudinal strain,

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

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

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

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

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

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

270 contractile function and reductions in left ventricular wall thickness.

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

272 rventricular septum thickness, and mean left ventricular wall thickness.

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

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

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

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

277 Left ventricular wall thicknesses in the overall study group

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

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

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

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

282 LV left ventricular wall thinning with LV left ventricular mass

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

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

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

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

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

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

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

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 essure of carbon dioxide, and thickened left ventricular wall with prolonged professional CPR.

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.