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 curring at cathodal tissue surfaces or large coronary vessels.

3 ssociated with revascularization of occluded coronary vessels.

4 issue boundary and create cardiomyocytes and coronary vessels.

5 MDCT allow for noninvasive assessment of the coronary vessels.

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

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

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

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

10 images were interpreted for tracer uptake in coronary vessels.

11 yocytes and absent in interstitial cells and coronary vessels.

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

13 opmental mechanisms underlying generation of coronary vessels.

14 olocalized with endothelial cells from small coronary vessels.

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

16 ed amyloid deposition in the intramyocardial coronary vessels.

17 er balloon angioplasty of stenoses of native coronary vessels.

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

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

20 hallenging and often limited by the adjacent coronary vessels.

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

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

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

24 er number of newly formed cardiomyocytes and coronary vessels.

25 vulnerability of both culprit and nonculprit coronary vessels.

26 art with immunocompatible cardiomyocytes and coronary vessels.

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

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

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

30 lls capable of generating cardiomyocytes and coronary vessels.

31 scle lineages including smooth muscle of the coronary vessels.

32 irement for Tgfbr3 during development of the coronary vessels.

33 um composed of integrated cardiomyocytes and coronary vessels.

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

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

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

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

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

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

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

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

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

43 The coronary vessels and epicardium arise from an extracardi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Coronary vessels as defined by CT were assigned to each

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Furthermore, in coronary vessel development we show exclusive cytoplasmi

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

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

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

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

82 a dynamic subcellular redistribution during coronary vessel development.

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

84 profound cardiac defects, including impaired coronary vessel development.

85 nticular compact layer outgrowth and altered coronary vessel development.

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

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

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

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

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

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

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

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

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

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

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

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

98 ectopic expression of Cxcl12b ligand induces coronary vessel formation.

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

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

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

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

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

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

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

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

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

108 The postnatal coronary vessels have been viewed as developing through

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Coronary vessels of the mouse heart derive from at least

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

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

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

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

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

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

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

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

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

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

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

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

139 Small coronary vessels supply small myocardial territories.

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

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

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

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

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

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

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

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

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

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

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

151 Coronary vessel wall images were readily acquired in all

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

153 The TRAPD coronary vessel wall imaging sequence was developed and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 15 patients had total obstruction of a major coronary vessel without actual infarction.