ライフサイエンスコーパス: vascular bed

1 ace area in tight apposition to an extensive vascular bed.

2 ved blood flow patterns throughout the islet vascular bed.

3 yx in angiogenic sprouting in the developing vascular bed.

4 dependent on the resistance of the pulmonary vascular bed.

5 s but not survival of mature vessels in this vascular bed.

6 mal selectivity and efficacy in the intended vascular bed.

7 elopment and is strictly associated with the vascular bed.

8 embrane potential within the skeletal muscle vascular bed.

9 frames as the heart pushes blood through the vascular bed.

10 th observed alterations in the primary tumor vascular bed.

11 changes in various portions of the pulmonary vascular bed.

12 uring acute hypoxemia, such as the umbilical vascular bed.

13 ed vasodilatation and desensitization in the vascular bed.

14 trk B by capillaries and arterioles in this vascular bed.

15 ent in different tissues and within the same vascular bed.

16 There was no net release of PAI-1 across the vascular bed.

17 event injecting atheromatous debris into the vascular bed.

18 ow to the skeletal muscle and the splanchnic vascular bed.

19 vitro when perfused through their intrinsic vascular bed.

20 accumulate particularly within the placental vascular bed.

21 urces during embryogenesis, depending on the vascular bed.

22 pression can result in a more stable retinal vascular bed.

23 t not the coronary, abdominal, or peripheral vascular beds.

24 ompetition between respiratory and locomotor vascular beds.

25 thelial expression of ANTXR2/CMG2 in several vascular beds.

26 this mechanism may not equally apply to all vascular beds.

27 tly reduced promoter activity in a subset of vascular beds.

28 ulted in increased LacZ staining in multiple vascular beds.

29 markable target tissue tropisms for selected vascular beds.

30 into new clinical treatments across multiple vascular beds.

31 cted to compare risk factor relations across vascular beds.

32 gulates vascular tone in multiple peripheral vascular beds.

33 elated to the presence of aneurysms in other vascular beds.

34 nnuli is related to atherosclerosis in other vascular beds.

35 marked differences in lectin binding between vascular beds.

36 ly extends vessel length in these developing vascular beds.

37 es, but differences are evident in different vascular beds.

38 gnaling in the development of organ-specific vascular beds.

39 c acid (20-HETE) in blood vessels of several vascular beds.

40 or actions in fetal essential and peripheral vascular beds.

41 ctural and functional abnormalities of other vascular beds.

42 primary human EC from different tissues and vascular beds.

43 tensively and colonized the appropriate host vascular beds.

44 le of proteins in several well-characterized vascular beds.

45 dhesion molecules expressed within different vascular beds.

46 ntial recruitment of leukocytes at different vascular beds.

47 planes in arteries explanted from different vascular beds.

48 an arteries and veins of different sizes and vascular beds.

49 constricts with hypoxia in contrast to other vascular beds.

50 hemostatic regulatory pathways in individual vascular beds.

51 what leads to fibrin formation in different vascular beds.

52 tablishment of late-forming, tissue-specific vascular beds.

53 for developing distinct arterial and venous vascular beds.

54 inking on active vasodilatation in these two vascular beds.

55 GE2 regulates regional blood flow in various vascular beds.

56 in the degradation of bradykinin in several vascular beds.

57 , expression of vWF varies between different vascular beds.

58 s, including coronary, mesenteric, and renal vascular beds.

59 rences in response to these hormones between vascular beds.

60 othelial channels in the endothelia of these vascular beds.

61 EPCR expression varies dramatically among vascular beds.

62 involved in estrogen responsiveness in other vascular beds.

63 er inflammatory cells or stimuli or to other vascular beds.

64 adhesion molecules (ECAMs) within different vascular beds.

65 thromboembolic occlusions affecting diverse vascular beds.

66 wn maturation factors act universally in all vascular beds.

67 and neovascularization but spared quiescent vascular beds.

68 ctors in splanchnic, hepatic, and collateral vascular beds.

69 l-ankle PWV), and mixed (brachial-ankle PWV) vascular beds.

70 heterogeneity of F8 expression in different vascular beds.

71 p of angiogenic sprouts in several mammalian vascular beds.

72 relative values of resistances in different vascular beds.

73 fied in the extracted lipid portion from all vascular beds.

74 and reduced deposition in deep postcapillary vascular beds.

75 ry, cerebral, splanchnic and skeletal muscle vascular beds.

76 VSMC in a spatiotemporal fashion across all vascular beds.

77 small resistance arteries in the splanchnic vascular beds.

78 and vascular endothelial function in several vascular beds.

79 gand-receptors common or specific to certain vascular beds.

80 as drastically different effects on distinct vascular beds.

81 involvement of cephalocervical and/or renal vascular beds (32% in males versus 80% in females).

82 culature of adjacent, nonischemic mesenteric vascular beds, a phenomenon well established in other or

83 In many vascular beds, adhesive interactions between leukocytes

84 otch1DeltaEC/Notch4(-/-)) had defects in all vascular beds affected in Adam10DeltaEC mice.

85 ve as an important mechanism that protects a vascular bed against the damaging effects of nitrogen mo

86 were correlated with quantity of CAP in all vascular beds (all p<0.05); no differences in the streng

87 on varies depending upon the anatomical site/vascular bed analyzed.

88 ccording to the anatomical sites and diverse vascular beds analyzed.

89 rteries extending the depth of the placental vascular bed and accelerating vessel remodeling.

90 at statins have benefits beyond the coronary vascular bed and are capable of reducing ischemic stroke

91 mp2 gene in odontoblasts on formation of the vascular bed and associated pericytes in the pulp.

92 f the native portal inflow despite a reduced vascular bed and dramatically elevated blood flow may re

93 Blood flow was homogeneous through the vascular bed and replicated native flow patterns.

94 onsiderable thickening of both the choroidal vascular bed and scleral coat, which provide nutritive a

95 CTGF is expressed in vascular beds and acts on multiple cell types.

96 calcium due to atherosclerosis in 5 distinct vascular beds and calcium in the aortic and mitral annul

97 a mosaic pattern in the capillaries of many vascular beds and in the aorta.

98 tial response of endothelial cells in distal vascular beds and large central blood vessels is establi

99 imary endothelial cells derived from various vascular beds and mouse retinal explants.

100 the maintenance of distinct arterial-venous vascular beds and that attenuation of the Alk1 signaling

101 d by endothelial cell activation in multiple vascular beds and the appearance of activated immune cel

102 to apoptosis and subsequent growth at target vascular beds and tissues in distant organs.

103 bute the cardiac output away from peripheral vascular beds and towards essential circulations, such a

104 n alpha(1)AR subtype expression differs with vascular bed, and (2) age influences human vascular alph

105 s have a significant impact on the heart and vascular bed, and descriptions of echocardiographic find

106 lial cell expression of CAMs in a particular vascular bed, and other factors must influence their lev

107 lve a direct peptide effect on the choroidal vascular bed, and the AII-mediated potentiation of sympa

108 transduce signaling events, in particular in vascular beds, and how endothelial cell integrins can be

109 de maintains differentiated smooth muscle in vascular beds, and its synthetic enzyme cystathionine-ga

110 Formation and remodeling of vascular beds are complex processes orchestrated by mult

111 ery of oxygen and nutrients, but independent vascular beds are highly specialized to meet the individ

112 thod in which peptides that home to specific vascular beds are identified after administration of a p

113 vasodilatation of the uterine and placental vascular beds are important at all stages of pregnancy,

114 Vascular beds are known to differ in structure and metab

115 ditional high-resolution studies in multiple vascular beds are required to address the therapeutic po

116 Endothelial cells of two vascular beds are specified, but the aortae are distende

117 ss we develop new hypotheses about why these vascular beds are susceptible to sequestration of parasi

118 nesis by using the readily visualized ocular vascular bed as a surrogate to test pro- and antiangioge

119 of adherent leukocytes in the rat mesenteric vascular bed, as assessed by video microscopy.

120 parenchyma of the brain, leptomeninges, and vascular beds, as well as through secretion of biologica

121 an extravasation pathway for lymphocytes in vascular beds at sites of inflammation.

122 ed in the sublingual, intestinal, and muscle vascular beds at the different time points and included

123 Adjustment for calcification in other vascular beds attenuated this association (HR: 1.40 [95%

124 tients are unable to vasoconstrict locomotor vascular beds beyond NB when presented with a respirator

125 for VEGF not only in the formation of ocular vascular beds but also in the differentiation of the len

126 We observed an association in the carotid vascular beds but not the coronary, abdominal, or periph

127 Tbdn-1 is not detected in most adult vascular beds but persists at high levels in the adult o

128 sities in gastrointestinal, uterine and skin vascular beds, but had mild effects in the brain.

129 differentially expressed in tissue-specific vascular beds, but its expression is induced in hematopo

130 se (SK) pathway is an important regulator of vascular beds, but its role in the survival and function

131 ration of infected erythrocytes (IE) in deep vascular beds, but the endothelial receptors involved in

132 ced vessel diameter and normalization of the vascular bed by coverage of mature pericytes and immunor

133 Impaired blood flow in the tumor vascular bed caused by structurally and functionally abn

134 rdigitated with quail vascular cells in most vascular beds colonized by graft cells.

135 er vessels leading to circumscribed terminal vascular beds could account structurally for "lacunar" i

136 Event rates including all vascular beds declined from 0.61 to 0.16 (P<0.0001).

137 that CGRP-stimulated vasodilation in several vascular beds depends, at least in part, on nitric oxide

138 ation of perivascular cells selectively in a vascular bed destined to regress.

139 atherosclerotic stimuli might contribute to vascular bed differences in susceptibility to atheroscle

140 adenosine affects both systemic and coronary vascular beds differentially.

141 al determinant of vasorelaxation in numerous vascular beds, drugs influencing H(2)S biosynthesis offe

142 osis serves to open capillary lumens in this vascular bed during glomerular development.

143 a selective permeability barrier in certain vascular beds (e.g., brain), as well as in the preservat

144 monoclonal antibody technique) in different vascular beds (eg, lung, small intestine, and spleen) we

145 l cell networks into patterns reminiscent of vascular beds, even on plastic and glass.

146 venous circulation of an arterially occluded vascular bed evokes sympathetic activation in healthy in

147 Of the five vascular beds examined, atherosclerosis was present in o

148 ock does not impair blood flow to any of the vascular beds examined.

149 ursor that gives rise to VSMC in vivo in all vascular beds examined.

150 the Flt-1 promoter directs expression in all vascular beds except for the liver.

151 Limb vascular beds exhibit a graded dilatation in response to

152 r coagulopathy, endothelial dysfunction, and vascular bed failure.

153 elivery, and suggest that one can create new vascular beds for a variety of applications with this ma

154 ng-(1-7) was measured in perfused mesenteric vascular beds from rats after bile-duct ligation.

155 ion of vascular endothelial growth factor to vascular beds generated immediate and robust vascular tr

156 n the absence of a preexisting or developing vascular bed, i.e., in the absence of angiogenesis, in t

157 lation in patients with a reactive pulmonary vascular bed in a selective, safe and expeditious fashio

158 tical component in the reorganization of the vascular bed in response to angiogenic stimuli.

159 ombosis or pregnancy loss), depending on the vascular bed in which this interaction occurs.

160 The model should deal with vascular beds in all tissues, and the computational infr

161 expression triggers the formation of ectopic vascular beds in embryos.

162 n to be a major component of EDHF in several vascular beds in multiple species, including in humans.

163 , irregular plaques should occur in multiple vascular beds in some individuals more frequently than w

164 ns had exited the blood stream and docked at vascular beds in the brain, the application of an extern

165 odilator actions in essential and peripheral vascular beds in the fetus in late gestation.

166 OX-1 pathway in the pulmonary and peripheral vascular beds in the rat and that TXA2 is a major prosta

167 to a provisional matrix during formation of vascular beds in tumors expressing TSP1.

168 ree to four beds in 11 (8%), and in all five vascular beds in two (1%).

169 f this hemostatic factor in ECs in different vascular beds in vivo.

170 ory enzyme in hemostasis and is generated in vascular beds in which inflammatory responses are ongoin

171 on factor in cells removed from a functional vascular bed; in this regard there is evidence indicatin

172 organ-specific phenotypes in representative vascular beds including arteries and veins, heart, lung,

173 brain; similar processes can occur in other vascular beds, including the lung.

174 hat regardless of developmental stage of the vascular bed, increased expression of VEGF in the retina

175 venous circulation of an arterially occluded vascular bed induces sympathetic activation and an incre

176 observation suggests that, if an appropriate vascular bed is available, a tumor can exploit it and gr

177 ce (CVC) during whole-body heat stress, this vascular bed is important in the regulation of blood pre

178 ll arterioles and the functional size of the vascular bed is increased.

179 tivity also influences the patterning of the vascular bed is not known.

180 reserve blood flow capacity of the coronary vascular bed is preserved.

181 wever, thrombotic occlusion of the placental vascular bed is rarely observed and the mechanistic rele

182 ternal and fetal systems, development of its vascular beds is essential to normal placental function,

183 Although analysis of changes in vascular beds is helpful for developing strategies for c

184 esenteric arteries, but involvement in other vascular beds is unclear.

185 rterial administration of EGCG to mesenteric vascular beds isolated ex vivo from WKY rats caused dose

186 Because 15-HETE is a constrictor in this vascular bed, it may play an important role in hypoxia-i

187 rin-B2 expression patterns vary in different vascular beds, it can extend into capillaries about midw

188 pinephrine induces vasoconstriction in other vascular beds, it may decrease visceral blood flow, impa

189 ing on the particular inflammatory stimulus, vascular bed, leukocyte subset, and species; most data s

190 The hepatic sinusoid is a unique vascular bed lined by hepatic sinusoidal endothelial cel

191 M-1, E-selectin, and P-selectin in different vascular beds (lung, heart, stomach, mesentery, small in

192 Upon encountering the relevant vascular bed, lymphocytes attach to endothelial adhesion

193 hesis that full recruitment of the pulmonary vascular bed may decrease evidence of lung injury by rec

194 nduced NO-dependent effects in the umbilical vascular bed may provide an important mechanism in the c

195 ., local cytokine production within inflamed vascular beds may enhance surface hyaluronan expression

196 ascribed to its ability to sequester in deep vascular beds, mediated by the variant surface antigen f

197 ries in skeletal muscle, and is unlike other vascular beds (mesentery).

198 ed apoptosis of endothelial cells within the vascular bed of a tumor, we show that a chemotherapeutic

199 We analyzed MAIT cells resident in the vascular bed of livers and showed that they represented

200 improved endothelial function in the forearm vascular bed of patients with type 1 diabetes and smoker

201 potent vasopressor activity in the pulmonary vascular bed of the cat and that this response may be me

202 e conditions in the isolated left lower lobe vascular bed of the cat, N omega-I-nitro-L-arginine meth

203 nephrine and other agonists in the pulmonary vascular bed of the cat.

204 ficant vasodilator activity in the pulmonary vascular bed of the cat.

205 blocker, were investigated in the pulmonary vascular bed of the cat.

206 AngII were investigated in the hindquarters vascular bed of the cat.

207 re "spare" AT1 receptors in the hindquarters vascular bed of the cat.

208 to have remarkable effects on the primitive vascular bed of the chick chorioallantoic membrane, whic

209 ion is proximal and distal within the muscle vascular bed of the human thigh.

210 pressing cells docked exclusively within the vascular bed of the ipsilateral carotid artery and that

211 In the feline pulmonary vascular bed of the isolated left lower lobe, norepineph

212 ve apoptosis of endothelial cells within the vascular bed of tumors.

213 llel mechanisms regulate angiogenesis in the vascular beds of both the heart and bone marrow.

214 ith impaired functional sympatholysis in the vascular beds of contracting forearm muscle in healthy m

215 mpathetic vasoconstriction is blunted in the vascular beds of contracting skeletal muscles.

216 e endothelial and smooth muscle cells in the vascular beds of skeletal muscle.

217 dase activity was consistently absent in the vascular beds of the liver, kidney, and spleen.

218 Accurate mapping of the vascular beds of the septal perforators was successfully

219 s, allowing parasites to sequester into deep vascular beds of various organs.

220 In the vascular beds of vertebrate animals blood flow is regula

221 of the environmental influence of different vascular beds on the in vivo endothelial responses to an

222 rct volumes, in the distribution of affected vascular beds or in the clinical severity of strokes.

223 g the value of radiologic screening of other vascular beds, particularly in asymptomatic males, in pa

224 nimal models and in human disease in various vascular beds, particularly the carotid arteries, is pre

225 rectly quantify atherosclerosis in different vascular beds performed in a single cohort.

226 Blood flow to vascular beds perfused by this artery does not seem to b

227 cal mechanisms controlling blood flow in the vascular beds perfused by this artery.

228 echanism of vascular repair may differ among vascular beds, pointing to the importance of coronary ar

229 t the loss of O2 from the arterioles in this vascular bed primarily is caused by O2 consumption in th

230 , GPR124 overexpression throughout all adult vascular beds produced CNS-specific hyperproliferative v

231 Arsenic exposure affects multiple vascular beds, promoting liver sinusoidal capillarizatio

232 The correlation in CAP scores across vascular beds ranged from 0.59 to 0.72.

233 ovessels of different types and in different vascular beds regulate the passage of small and large mo

234 g1 acts to maintain the endothelium in other vascular beds, regulating some actions of VEGF, these ob

235 signaling as a pathway controlling choroidal vascular bed relaxation and provide a pathogenic link wi

236 ee the reproducible anatomy of stereotypical vascular beds remains unclear.

237 to pump blood to the pulmonary and systemic vascular beds, respectively.

238 ses of haemodynamic changes in the umbilical vascular bed reveal an initial decrease in umbilical vas

239 cific T-cell interactions in the cremasteric vascular bed revealed that cognate recognition of the en

240 indicate that vasodilatation occurs in other vascular bed(s) to account for the lack of increase in a

241 ul model system, because it contains several vascular beds sandwiched between avascular tissue.

242 llution with markers of atherosclerosis in 4 vascular beds simultaneously in an all-African-American

243 tion of the skin or lung, thereby uncovering vascular bed-specific differences in the prevention of i

244 information for environmentally responsive, vascular bed-specific expression in the heart, skeletal

245 indicate that distinct DNA modules regulate vascular bed-specific expression of VWF.

246 us targeting is a valuable tool for studying vascular bed-specific gene regulation, (2) the VWF and F

247 he local endothelial components that dictate vascular bed-specific hemostatic regulation.

248 AT1R-Abs acted in a vascular bed-specific manner and caused small contractio

249 to the liver and other organs is directed by vascular bed-specific mechanisms, including blood flow-r

250 use and human vWF promoters are regulated by vascular bed-specific mechanisms.

251 cal and systemic elements that contribute to vascular bed-specific prothrombotic potential.

252 neity and to use this information to develop vascular bed-specific therapies.

253 Vascular bed-specific TLR fingerprints were functionally

254 The architecture of an organ's vascular bed subserves its physiological function and me

255 BACKGROUND-Peripheral cutaneous vascular beds, such as the fingertips, contain a high co

256 om peripheral circulations towards essential vascular beds, such as the umbilical, cerebral, myocardi

257 justment for vascular calcification in other vascular beds, suggesting partial confounding by systemi

258 that resembled wild-type and colonized host vascular beds, suggesting that host-derived signals can

259 The vascular beds supplying the retina may sustain injury as

260 factors have a greater impact on CAP in one vascular bed than another.

261 te to pathologic alterations in nonplacental vascular beds that are associated with fibrinolysis.

262 a the HIF transcription factors in one large vascular bed, that underlying the skin, influences cardi

263 In contrast to any other vascular bed, the coronary circulation receives its perf

264 In contrast, in the umbilical vascular bed, the dilator response was not only prevente

265 ffuseness of TV involvement in the allograft vascular bed, the only currently definitive therapy requ

266 In marked contrast to other essential vascular beds, the mechanisms mediating maintained perfu

267 erosclerotic lesion size was quantified in 2 vascular beds: the ascending aorta and the aortic arch.

268 sodilates and O2 vasoconstricts the cerebral vascular bed; the opposite is true in the lungs.

269 that as the extent of CAA progressed in this vascular bed, there was increased prevalence of propagat

270 n hemostasis may be associated with distinct vascular beds, thus implying that the relative combined

271 episodes of ischemia with reperfusion in one vascular bed, tissue, or organ confer a global protectiv

272 The nature of this imbalance varies from one vascular bed to the next according to the local set poin

273 loss of an angiogenesis inhibitor, can prime vascular beds to be more responsive to an angiogenic sti

274 or determining the heterogeneous response of vascular beds to NO and NO-based vasodilators, thereby p

275 s of organization extending over scales from vascular beds to single cells, subcellular structures, a

276 arameter circulatory model with two parallel vascular beds; two distinct control mechanisms for both

277 ply to the caudal ventral artery of the same vascular bed under comparable conditions.

278 ring transitional circulation, the pulmonary vascular bed undergoes a rapid and profound reduction in

279 circulating leukocytes in the rat peritoneal vascular bed using intravital microscopy.

280 y, acetylcholine, a powerful dilator of most vascular beds, virtually lost the ability to dilate cere

281 pressure-flow relationship in the pulmonary vascular bed was shifted to the right in animals transfe

282 ake of leptin by the splanchnic or pulmonary vascular beds was detected; leg tissue was a net leptin

283 Subsequent angiographic imaging of other vascular beds was negative.

284 e of changes over time between the different vascular beds was similar in both models, but the endoto

285 l infarction of the left anterior descending vascular bed were excluded from the study.

286 vessels distal to the coarctation, yet both vascular beds were exposed to the same circulating facto

287 Vascular beds were imaged selectively based on clinical

288 Endothelial cells cultured from several vascular beds were superfused with normoxic (equilibrate

289 In vitro-perfused SMA vascular beds were tested for the cumulative dose-respon

290 found to be expressed in VSMCs from several vascular beds where they contribute to the regulation of

291 lates basal blood flow in the human coronary vascular bed, whereas substance P-stimulated vasodilatat

292 tment for the extent of calcium in the other vascular beds, whereas the thoracic aorta was significan

293 posing effects on the pulmonary and cerebral vascular beds, which are connected after BSCC.

294 or vasculature, Ang-2 destabilizes the tumor vascular bed while improving perfusion in surviving tumo

295 ed pattern of arterial branching in multiple vascular beds while the venous system remained normal.

296 er birth, and to remodel the fetal pulmonary vascular bed whose outlet is obstructed.

297 s that long-term PGI2 remodels the pulmonary vascular bed with subsequent decreases in endothelial ce

298 veness to vasoconstrictors in the splanchnic vascular bed, with several vasoactive molecules, control

299 venular distension and to recruitment of the vascular bed within the skeletal muscles.

300 x data, measured across the human splanchnic vascular bed, within a genome-scale model of human metab