ライフサイエンスコーパス: coronary vessel

1 unohistochemistry in the EC lining the human coronary vessel.

2 50% stenosis in at least 1 major epicardial coronary vessel.

3 lls capable of generating cardiomyocytes and coronary vessels.

4 scle lineages including smooth muscle of the coronary vessels.

5 irement for Tgfbr3 during development of the coronary vessels.

6 um composed of integrated cardiomyocytes and coronary vessels.

7 ssociated with revascularization of occluded coronary vessels.

8 issue boundary and create cardiomyocytes and coronary vessels.

9 MDCT allow for noninvasive assessment of the coronary vessels.

10 the carotid bifurcation, and in the proximal coronary vessels.

11 widely used in practice, especially in large coronary vessels.

12 d a high-fat diet combined with injury to 22 coronary vessels.

13 e method to identify plaque apoptosis in the coronary vessels.

14 ls (BMCs) to differentiate into myocytes and coronary vessels.

15 images were interpreted for tracer uptake in coronary vessels.

16 yocytes and absent in interstitial cells and coronary vessels.

17 opmental mechanisms underlying generation of coronary vessels.

18 olocalized with endothelial cells from small coronary vessels.

19 rst seen in the endothelial cells from small coronary vessels.

20 ed amyloid deposition in the intramyocardial coronary vessels.

21 er balloon angioplasty of stenoses of native coronary vessels.

22 al amounts of class II MHC antigens to human coronary vessels.

23 e, ejection fraction, and number of diseased coronary vessels.

24 genic potential and do not contribute to new coronary vessels.

25 vulnerability of both culprit and nonculprit coronary vessels.

26 nd vessel features, and so plaque burden, in coronary vessels.

27 orming linear structures along and preceding coronary vessels.

28 curring at cathodal tissue surfaces or large coronary vessels.

29 rct caused by obstruction of major and minor coronary vessels.

30 hallenging and often limited by the adjacent coronary vessels.

31 cells (EPDCs) contribute to the formation of coronary vessels.

32 smooth muscle (SM) cells, which support the coronary vessels.

33 cells that are required for the formation of coronary vessels.

34 er number of newly formed cardiomyocytes and coronary vessels.

35 art with immunocompatible cardiomyocytes and coronary vessels.

36 ive VPCs were identified within the walls of coronary vessels.

37 ferential use of BMS for patients with large coronary vessels.

38 and smooth muscle cells within them to form coronary vessels.

39 ion of stromal-derived factor 1 from hypoxic coronary vessels.

40 Histology was performed on 55 stents in 35 coronary vessels (32 native arteries and 3 vein grafts)

41 nonsmokers, P=0.02) and fatty streaks in the coronary vessels (8.27 percent vs. 2.89 percent, P=0.04)

42 verriding aorta, ventricular septal defects, coronary vessel abnormalities and valve defects.

43 causes embryonic death by E18.5 with reduced coronary vessel and fibrous matrix penetration into myoc

44 ries assessed by both the number of diseased coronary vessels and also by the Gnesini score.

45 Endocardial flowers are contiguous with coronary vessels and associated with subendocardial smoo

46 Three-dimensional coronary vessels and CTA slices were extracted and fused

47 c cells (HCs), which are located proximal to coronary vessels and encased by extracellular matrix (EC

48 r summit is limited by the presence of major coronary vessels and epicardial fat.

49 The coronary vessels and epicardium arise from an extracardi

50 ved cells (EPDCs) contribute to formation of coronary vessels and fibrous matrix of the mature heart.

51 ed clinically to form functionally competent coronary vessels and improve CBF in patients with ischem

52 relationship between the number of diseased coronary vessels and mean calcium score, i.e. the mean c

53 ciated with bleeding, extra-cardiac damages, coronary vessels and phrenic nerve injury.

54 Analysis of the distribution of coronary vessels and stenoses provided a measure of myoc

55 istinct sites (either in the target or other coronary vessels) and further classified as procedural,

56 ssion, cardiovascular risk factors, multiple coronary vessel, and left main stem disease were more fr

57 FFR was measured in 64 of 159 coronary vessels, and 39 had an FFR <0.75.

58 on with respect to the myocardial substrate, coronary vessels, and phrenic nerve.

59 tudies also show that the atria, epicardium, coronary vessels, and the majority of outflow tract smoo

60 d spatial requirements of NFAT signaling for coronary vessel angiogenesis.

61 e the strong colocalization of HS with major coronary vessels anticipated from theory.

62 New coronary vessels are added to the heart around birth to

63 With time, a large number of myocytes and coronary vessels are generated.

64 igin and developmental mechanisms underlying coronary vessels are not fully elucidated.

65 ion (EMT) and endothelial differentiation of coronary vessels are relatively unaffected.

66 Structurally, women's coronary vessels are smaller in size and appear to conta

67 ound that a substantial portion of postnatal coronary vessels arise de novo in the neonatal mouse hea

68 Cells of the coronary vessels arise from a unique extracardiac mesoth

69 ysis in mice and cardiac organ culture, that coronary vessels arise from angiogenic sprouts of the si

70 Coronary vessels as defined by CT were assigned to each

71 Fog2MC adult hearts displayed a paucity of coronary vessels, associated with myocardial hypoxia, in

72 pable of obtaining cross-sectional images of coronary vessels at a resolution of approximately 10 mic

73 However, in null mice nascent coronary vessels attach to the aorta, form 2 coronary os

74 coronary endothelium and targeting sprouting coronary vessels (but not ventricular endocardium) durin

75 tification method in subjects and individual coronary vessels by using t tests and analysis of varian

76 ing may permit robust discrimination between coronary vessels causing ischemia versus not causing isc

77 plasty treatment of de novo lesions in large coronary vessels could be a safe and effective strategy

78 , as HH agonists have been shown to increase coronary vessel density and improve coronary function af

79 g in the adult heart leads to an increase in coronary vessel density.

80 V-derived) and ventral (endocardial-derived) coronary vessels developed in response to different grow

81 suggest that HEXIM1 plays critical roles in coronary vessel development and myocardial growth.

82 ta4 (Tbeta4) as essential for all aspects of coronary vessel development in mice, and demonstrate tha

83 iferation and invasion contributes to failed coronary vessel development in Tgfbr3(-/-) mice.

84 Here we provide a detailed analysis of coronary vessel development in zebrafish.

85 demonstrate a requirement for Tgfbr3 during coronary vessel development that is essential for embryo

86 n remodeller gene Ino80 results in defective coronary vessel development that leads to ventricular no

87 Furthermore, in coronary vessel development we show exclusive cytoplasmi

88 for embryonic viability, heart development, coronary vessel development, and adult myocardial functi

89 regeneration likely recapitulates embryonic coronary vessel development, which involves the activati

90 e cellular distribution of Bves/Pop1A during coronary vessel development.

91 e answered for a meaningful understanding of coronary vessel development.

92 a dynamic subcellular redistribution during coronary vessel development.

93 in myocardium is required and sufficient for coronary vessel development.

94 severe defects in mural cell recruitment and coronary vessel development.

95 profound cardiac defects, including impaired coronary vessel development.

96 nticular compact layer outgrowth and altered coronary vessel development.

97 lls within specific time windows to regulate coronary vessel development.

98 imilar in morphology, conduit and resistance coronary vessels differ importantly in size, function an

99 with angioplasty regardless of the number of coronary vessels diseased.

100 r weight PLLA were well tolerated within the coronary vessel during the 28-day experiment.

101 ee independent regulatory pathways active in coronary vessels during development through analysis of

102 , there was significant monocyte adhesion to coronary vessel endothelium at 2 hours post-reperfusion

103 Results There were 92 coronary vessels evaluated in 53 patients (mean age, 65

104 dose-response relationship to the number of coronary vessels exhibiting obstructive CAD, with increa

105 le starts to envelop the myocardium and that coronary vessels form by ingrowth of these migratory pre

106 We observe that coronary vessels form in zebrafish by angiogenic sprouti

107 chemokine signaling has an essential role in coronary vessel formation by directing migration of endo

108 s important roles in epicardial function and coronary vessel formation during heart regeneration in z

109 lecular mechanism by which TGFbetaR3 signals coronary vessel formation is unknown.

110 e ability of grafted cells to participate in coronary vessel formation was monitored by staining with

111 al EMT is required for myocardial growth and coronary vessel formation, and it generates cardiac fibr

112 r understanding of the processes involved in coronary vessel formation, with mechanistic insights tak

113 ly expressed in a mouse model with deficient coronary vessel formation.

114 ectopic expression of Cxcl12b ligand induces coronary vessel formation.

115 ot result in defects in cardiac structure or coronary vessel formation.

116 r the first time that BAF180 is critical for coronary vessel formation.

117 rating scRNA-seq data of endocardial-derived coronary vessels from mid- and late-gestation identified

118 We found that coronary vessels from patients with coronary artery dise

119 dent region, preserves endothelium-dependent coronary vessel function, and upregulates markers of ang

120 However, the mechanism of interventions in coronary vessel geometry over time is less well characte

121 icient and the regulatory pathways directing coronary vessel growth are not well understood.

122 amental divergence between the regulation of coronary vessel growth in healthy and ischemic adult hea

123 view or >/=50% in 2 orthogonal views in all coronary vessels >/=2.5 mm diameter) within 12 months.

124 rid angioplasty for de novo lesions in large coronary vessel (> 2.75 mm).

125 e that subtle variation in the patterning of coronary vessels has significant but uncharacterized eff

126 Multiple sources of coronary vessels have been proposed, including the sinus

127 The postnatal coronary vessels have been viewed as developing through

128 nts with normal flow at rest and supplied by coronary vessels having </=50% diameter stenosis were st

129 scarred myocardium and generate myocytes and coronary vessels improving the hemodynamics of the infar

130 immediately after reperfusion of the culprit coronary vessel in STEMI patients to determine whether t

131 The direct role of coronary vessels in defibrillation, although hypothesize

132 previous model in which the formation of new coronary vessels in neonates from ventricular endocardia

133 ng factors VEGFR3 and DLL4 and generates new coronary vessels in neonates.

134 maintained the epicardium and contributed to coronary vessels in newborn and adult mice.

135 ted between October 2019 and September 2020, coronary vessels in patients with stable chest pain and

136 s a critical regulator for the remodeling of coronary vessels in the developing heart.

137 of morphological and biochemical features of coronary vessels in vivo.

138 Finally, scRNAseq of developing human coronary vessels indicated that the human heart followed

139 MC) differentiation and in stent-induced pig coronary vessel injury.

140 staining also reveal that there are very few coronary vessels inside the myocardium of mutant hearts.

141 ailed to reconstitute healthy myocardium and coronary vessels integrated structurally and functionall

142 Thrombus formation within a coronary vessel is the acute precipitating event in most

143 m an atherosclerotic plaque in an epicardial coronary vessel is the cause of STEMI in the majority of

144 Formation of the coronary vessels is a fundamental event in heart develop

145 wever, the formation and maturation of these coronary vessels is not fully understood.

146 rat and regenerated human cardiomyocytes and coronary vessels, leading to a remarkable restoration of

147 c heart disease following the obstruction of coronary vessels leads to the death of cardiac tissue an

148 e (FFR)-guided PCI in the treatment of small coronary vessel lesions as compared with an angio-guided

149 In stented pig coronary vessels, LPP was expressed in the neointima of

150 ncluded 758 patients with de novo lesions in coronary vessels <3 mm and an indication for percutaneou

151 ng the 3D volume along the major axis of the coronary vessels may help to overcome such limitations.

152 stolic compression of sections of epicardial coronary vessels (myocardial bridging) with myocardial p

153 mediate and maintain collateral formation in coronary vessel occlusion are yet to be identified.

154 In coronary vessels of patients with near-normal or minimal

155 Coronary vessels of the mouse heart derive from at least

156 DGFRbeta(-/-) hearts failed to form dominant coronary vessels on the ventral heart surface, had a thi

157 the left main stem, >70% stenosis in a major coronary vessel, or 30% to 70% stenosis with fractional

158 2-5 mutant embryonic hearts showed defective coronary vessel organization, which was improved by inte

159 Coronary vessels originate from multiple cellular source

160 the current view of a common source for the coronary vessels, our findings indicate that the coronar

161 ere associated with the number of obstructed coronary vessels (p = 4.8 x 10(-12)).

162 nts to interrogate cellular contributions to coronary vessel patterning and maturation.

163 that are essential for fetal cardiac growth, coronary vessel patterning, and regenerative heart repai

164 nd, therefore, FGF may act as a template for coronary vessel patterning.

165 Endocardial cells lining the heart lumen are coronary vessel progenitors during embryogenesis.

166 events by making atherosclerotic plaques in coronary vessels prone to rupture.

167 Patients with a greater number of diseased coronary vessels received an IMA more often (one, 78%; t

168 or stable or unstable angina in small native coronary vessels (reference vessel diameter and stent si

169 uggest that correct transmural patterning of coronary vessels requires the correct transmural express

170 Sox17 causes deficient cardiac remodeling of coronary vessels, resulting in improper coronary artery

171 We identified Col15a1 as a coronary vessel-secreted angiocrine factor, downregulate

172 At 90 days postoperative, 23.8% of all coronary vessels showed evidence of GVD in group I, 18.4

173 Overall, coronary vessel size increased 25.9 mm2 per millimeter i

174 The aim of our study was to analyze coronary vessel status in AIS patients with elevated cTn

175 Small coronary vessels supply small myocardial territories.

176 The formation of the coronary vessel system is vital for heart development, a

177 current was compared in cells isolated from coronary vessels taken from different points along the v

178 to develop the fine and continuous plexus of coronary vessels that cover the entire ventricle around

179 h muscle and endothelial cell lineage of the coronary vessels, the expression of WT1 and RALDH2 becom

180 ositive EPDCs, and provoked anomalies in the coronary vessels, the ventricular myocardium, and the AV

181 endothelium-derived peptide that constricts coronary vessels through stimulation of the ET-A and ET-

182 of subjects with stenosis of all three major coronary vessels to be distinguished from subjects with

183 etion of KCNJ8 blunted the responsiveness of coronary vessels to cytokine- or metabolic-mediated vaso

184 n as radio-opaque dye is flushed through the coronary vessels to visualize the severity of vessel nar

185 The capacity of leukotrienes to affect coronary vessel tone and the influence of atherosclerosi

186 , SE-RegUNet, designed to accurately segment coronary vessels using 100 labeled angiographies from an

187 lated during the sprouting and remodeling of coronary vessels, visualized by a specific neural enhanc

188 In vivo free-breathing coronary vessel wall and plaque imaging with MR has been

189 RI) late gadolinium enhancement (LGE) of the coronary vessel wall can detect and grade coronary allog

190 Coronary vessel wall images were readily acquired in all

191 The use of DE-CMR coronary vessel wall imaging may provide a noninvasive m

192 The TRAPD coronary vessel wall imaging sequence was developed and

193 Free-breathing 3D coronary vessel wall imaging was performed along the maj

194 noninvasive free-breathing MR technique for coronary vessel wall imaging.

195 approach may be useful for the assessment of coronary vessel wall in patients with suspected coronary

196 Direct noninvasive visualization of the coronary vessel wall may enhance risk stratification by

197 We evaluated coronary vessel wall thickening, coronary plaque, and ep

198 Both coronary vessel wall thickness (1.5+/-0.2 versus 1.0+/-0

199 isotropic resolution identified an increased coronary vessel wall thickness with preservation of lume

200 Keywords: Coronary Vessel Wall Thickness, Diastolic Function, HIV,

201 anced MR imaging of the aortic, carotid, and coronary vessel wall will be discussed.

202 Recent research indicates that the coronary vessel wall, especially the vasa vasorum, as we

203 presence of the metallic stent frame in the coronary-vessel wall.

204 vide a noninvasive method to assess diseased coronary vessel walls.

205 Restoration of the dilatory capacity of coronary vessels was required to rescue the Kir6.1 knock

206 ctors of >/=70% stenosis in at least 1 major coronary vessel were identified from >200 candidate vari

207 ODS AND A large number of cardiomyocytes and coronary vessels were created in a rather short period o

208 The coronary vessels were removed, and the stented vessels w

209 In 215 patients, 512 coronary vessels were successfully treated with the rand

210 ays after balloon angioplasty, and uninjured coronary vessels were used as controls.

211 e due to a widespread process throughout the coronary vessels, which may have implications for the ma

212 ctivation of Nestin's enhancer in developing coronary vessels while its genetic deletion leads to ina

213 on of Slit2 ligand in the endothelium of the coronary vessels, while Slit3 was highly present in the

214 model were leptin (p = 0.004) and number of coronary vessels with >50% stenosis (p < 0.001).

215 ive protein (CRP), fibrinogen, and number of coronary vessels with >50% stenosis.

216 defined as at least 1 graft to all diseased coronary vessels with >50% stenosis.

217 AC 1000 (n=257) had a greater mean number of coronary vessels with CAC (3.4 0.5), greater total area

218 efficiently differentiate into myocytes and coronary vessels with no detectable differentiation into

219 vention led to the formation of myocytes and coronary vessels within the infarct.

220 15 patients had total obstruction of a major coronary vessel without actual infarction.