ライフサイエンスコーパス: microvascular

1 R = 0.83 [95% CI 0.74-0.93] per 100 g/d) and microvascular (0.72 [0.61-0.87]) and macrovascular (0.87

2 or diameters (4.2 vs 5.0 cm; P = .02), fewer microvascular (17% vs 22%) and macrovascular (2% vs 9%)

3 eter [2.32 per log SD; 1.43-3.77; P = .001]; microvascular [3.07; 1.02-9.24; P = .05] and macrovascul

4 In severe NPDR, the eyes with intraretinal microvascular abnormalities (IRMA) had a significantly i

5 Patterns of microvascular ageing that develop among muscles of diver

6 These white matter microvascular alterations normalize within 1 year after

7 o evaluate the reproducibility of parafoveal microvascular anatomy of 7 different optical coherence t

8 KEY POINTS: Age-related changes in cutaneous microvascular and cardiac functions limit the extent of

9 t is unclear if these age-related changes in microvascular and cardiac functions maximally restrain t

10 strained by age-related changes in cutaneous microvascular and cardiac functions.

11 ive glycemic control to patients to minimize microvascular and cardiovascular complications in type 2

12 pective Diabetes Study Outcomes Model 2 (for microvascular and cardiovascular outcomes, C-statistics

13 , dyslipidemia and hypertension) and chronic microvascular and macrovascular complications among peop

14 n 90% of patients with diabetes and leads to microvascular and macrovascular complications that cause

15 eatment, and results in rapid progression of microvascular and macrovascular complications.

16 and hematopoietic cells in murine models of microvascular and macrovascular injury.

17 sment of disease severity, and correspond to microvascular and physiological topography.

18 Tofacitinib disrupted adventitial microvascular angiogenesis, reduced outgrowth of hyperpl

19 viability of using agonists that can improve microvascular barrier function to ameliorate trauma-indu

20 es constrict coronary capillaries and reduce microvascular blood flow after ischaemia, despite re-ope

21 modynamic quantities, which is a hallmark of microvascular blood flow, appears both in space and time

22 st circumference of <102 cm improved retinal microvascular caliber, plasma biomarkers of microvascula

23 Human dermal microvascular cells exposed to conditioned medium from m

24 d between other macrovascular parameters and microvascular changes after transfusion.

25 hyperglycemia during pregnancy, and retinal microvascular changes in pregnant women at 26-28 weeks o

26 rophil interactions play a role in mediating microvascular changes in SS and suggest that targeting M

27 g spread of melanoma cells along preexisting microvascular channels and features of both vascular co-

28 l Hey2 deletion on intestinal stem cells and microvascular compartment radiosensitivity, EndoMT and r

29 o potential new pathogenic pathways for this microvascular complication and holds translational value

30 Diabetic retinopathy (DR), a major microvascular complication of diabetes, leads to retinal

31 ormalities may lead to future development of microvascular complications among T1D pediatric patients

32 ns important for the prevention of long-term microvascular complications in adults with type 2 diabet

33 d with an increased risk of diabetes-related microvascular complications later in life, but it is unc

34 le the concept of distinct macrovascular and microvascular complications of diabetes has been useful,

35 Diabetes strongly associates with microvascular complications that ultimately promote mult

36 rther support for the importance of coronary microvascular compromise in the pathophysiology of HFpEF

37 adrenoceptor-mediated damage, epicardial and microvascular coronary vasoconstriction and/or spasm, an

38 rane anaesthesia or losartan prevented early microvascular damage and late epilepsy.

39 sets (i.e., radiomic imaging features, tumor microvascular density (MVD), and vascular endothelial gr

40 gher RPS15A expression demonstrated a higher microvascular density (MVD).

41 of distant tumor growth, proliferation, and microvascular density (P < .01).

42 tyle keeps both the vasodilator response and microvascular density high.

43 c (716/+) mice had significant reductions in microvascular density, consistent with the high expressi

44 rowth, proliferation (Ki-67 percentage), and microvascular density.

45 CBF is correlated with tumor microvascular density.

46 e to insulin, exercise and VEGF-A and reduce microvascular density.

47 ted for Ki-67 proliferative indexes and CD34 microvascular density.

48 This study sought to determine whether microvascular destabilization affects organ function and

49 lity of longitudinal pericyte imaging during microvascular development and aging and in models of bra

50 impair insulin sensitivity and contribute to microvascular disease in diabetes mellitus.

51 We then show that dose-dependent microvascular disease is seen in a transgenic mouse mode

52 For individuals with one, two, or three microvascular disease states versus none, the multivaria

53 Such events may arise from spasm, microvascular disease, or other pathways.

54 acute manifestations of progressive cerebral microvascular disease.

55 of macrovascular disease and 1,345 cases of microvascular disease.

56 rformed for epicardial vasospasm or coronary microvascular dysfunction (CMD) due to microvascular spa

57 Microvascular dysfunction (MVD) is considered a crucial

58 onal but viable myocardium among others (eg, microvascular dysfunction and cardiomyocyte/mitochondria

59 2016, that assessed the associations between microvascular dysfunction and depression.

60 subgroup of these patients also has coronary microvascular dysfunction and evidence of inflammation.

61 Thus, microvascular dysfunction and inadequate coronary perfus

62 at both the peripheral and cerebral forms of microvascular dysfunction are associated with higher odd

63 arasite biomass, endothelial activation, and microvascular dysfunction are associated with severe dis

64 Thus, age-related diastolic and microvascular dysfunction are reversed by late-life exer

65 lood-brain barrier suggest that white matter microvascular dysfunction contributes to the conversion

66 We investigated whether (1) microvascular dysfunction contributes to the development

67 motor function may play an important role in microvascular dysfunction in CAD or other vascular disea

68 wlesi malaria, and HRP2, angiopoietin-2, and microvascular dysfunction in falciparum malaria.

69 ntify the role of Nox1 in the development of microvascular dysfunction in metabolic disease.

70 that promotes intravascular coagulation and microvascular dysfunction in sepsis.

71 Recent evidence suggests that microvascular dysfunction is associated with depression,

72 nding may have clinical implications because microvascular dysfunction might provide a potential targ

73 The following 5 estimates of microvascular dysfunction were considered in participant

74 knowlesi malaria, IL-6, angiopoietin-2, and microvascular dysfunction were increased in severe compa

75 the associations of peripheral and cerebral microvascular dysfunction with late-life depression.

76 rs need to be considered and assessed, e.g. 'microvascular dysfunction', to calibrate individual risk

77 great promise for determination of coronary microvascular dysfunction.

78 ir application in distinct forms of coronary microvascular dysfunction.

79 nt of SIRT3 in LPS-induced pericyte loss and microvascular dysfunction.

80 training reverses age-related diastolic and microvascular dysfunction.

81 ces of coronary flow for diagnosing coronary microvascular dysfunction; in certain diseases, the degr

82 nced age, reverses age-related diastolic and microvascular dysfunction; these data suggest that late-

83 Human dermal microvascular ECs (HDMECs) treated with TLR3 [Poly(I:C)]

84 ngle guide RNA (sgRNA) in primary human lung microvascular ECs (HLMVECs) disrupted the expression of

85 Microvascular ECs instruct neighboring cells in their or

86 resistance compared with normal human dermal microvascular ECs.

87 ABSTRACT: The identity of microvascular endothelial (MVE) mechanosensors that sens

88 n Tg(fli1:EGFP) zebrafish and inhibits human microvascular endothelial cell (HMEC-1) proliferation, t

89 Microvascular endothelial cell heterogeneity and its rel

90 ABSTRACT: The human cerebral microvascular endothelial cell line hCMEC/D3 was used to

91 onolayers of the immortalized human cerebral microvascular endothelial cell line hCMEC/D3.

92 arrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC).

93 brin-Matrigel mixed gel by coculturing brain microvascular endothelial cells (BMECs) and human mesenc

94 Acute Krit1 gene inactivation in mouse brain microvascular endothelial cells (BMECs) changes expressi

95 Primary mouse brain microvascular endothelial cells (BMECs) were cultured an

96 ating leukocytes with IL-1- or TNF-activated microvascular endothelial cells (ECs) and pericytes (PCs

97 Microvascular endothelial cells (ECs) are increasingly r

98 Microvascular endothelial cells (ECs) display a high deg

99 We demonstrate that microvascular endothelial cells (ECs) from Anxa2(-/-) mi

100 Dermal microvascular endothelial cells (ECs) isolated from this

101 Human brain microvascular endothelial cells (hBMVECs) that constitut

102 ucosal biopsies and primary human intestinal microvascular endothelial cells (HIMECs) isolated from s

103 P-EA exerted antiangiogenic effects in human microvascular endothelial cells (HMVEC) and vasodilatory

104 In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increase

105 d the lipoma-preferred partner (LPP) gene in microvascular endothelial cells (MECs) and that LPP expr

106 Microvascular endothelial cells (MVEC) were developed fr

107 d functions of ICAM-1 in cerebral and dermal microvascular endothelial cells (MVECs).

108 We isolated primary renal microvascular endothelial cells (RMEC) and aortic endoth

109 all, these data show for the first time that microvascular endothelial cells in the bone marrow and s

110 We show that keratinocytes and microvascular endothelial cells show greatest NO release

111 hese exosomes alone can activate human brain microvascular endothelial cells to stimulate adhesion mo

112 of human bronchial epithelial cells and lung microvascular endothelial cells was exposed to immunosup

113 VEGF, transendothelial migration through CNS microvascular endothelial cells was regulated by VEGF.

114 transporter 1 (GLUT-1) levels in human brain microvascular endothelial cells, causing disruption of b

115 In human pulmonary microvascular endothelial cells, G was 20.4 +/- 12 Pa an

116 In human primary retinal microvascular endothelial cells, hypoxia induces the exp

117 We utilised isogenic keratinocytes, microvascular endothelial cells, melanocytes and fibrobl

118 GF, IL8, and CXCL12 leading to chemotaxis of microvascular endothelial cells, phosphorylation of VE-c

119 In retinal microvascular endothelial cells, TRPV4 channels regulate

120 esis study was evaluated in vitro with human microvascular endothelial cells-1 and in vivo with the M

121 nt, which profoundly alters the phenotype of microvascular endothelial cells.

122 erties of monocyte subsets using human brain microvascular endothelial cells.

123 and survival of BMCs or mature human cardiac microvascular endothelial cells.

124 l NanA had increased invasion of human brain microvascular endothelial cells.

125 Similar effects were observed in human brain microvascular endothelial cells.

126 microvascular caliber, plasma biomarkers of microvascular endothelial function, and the more convent

127 , cardiac radiation exposure causes coronary microvascular endothelial inflammation, a perturbation i

128 Microvascular endothelial KLF2 is significantly induced

129 The measurement of microvascular (endothelial) function is important to und

130 and hemodynamic environment of the pulmonary microvascular endothelium in vivo.

131 ne storm, oxidation, and coagulation in lung microvascular endothelium.

132 the maintenance and protection of the renal microvascular endothelium.

133 35; 2001-09) and validated the equations for microvascular events using data from the Diabetes Preven

134 ss intensive glucose control, on the risk of microvascular events.

135 To evaluate the retinal and microvascular features using OCTA in children (<18 years

136 tients, the asymptotic pressure at which the microvascular flow ceases, the reservoir pressure relate

137 and, namely cerebral blood flow increase and microvascular flow homogenization.

138 flow and permeability, ultrasound imaging of microvascular flow rate is sensitive only to changes in

139 e layer has been shown to drastically affect microvascular flow, permeability, and immune function.

140 pha, LPS, mechanical stretch/ventilation, or microvascular flow.

141 gation may have significant implications for microvascular flows and may help explain why the effects

142 Microvascular flows are often considered to be free of r

143 Increased coronary microvascular flux rate in response to chronic fetal ana

144 thened connective tissue formation, improved microvascular formation and attenuated cardiomyocyte hyp

145 odel to assess how ABCD1 alters white matter microvascular function and explores its potential as an

146 tients receiving ramipril had improvement in microvascular function as shown by a significant decreas

147 These unusual changes in microvascular function during anaemia may indicate novel

148 everal invasive modalities for interrogating microvascular function have been proposed.

149 tive effect of exercise training on coronary microvascular function may result from improved endothel

150 endothelial activation (angiopoietin-2), and microvascular function, and evaluated the effects of age

151 Clinical findings, microvascular function, global hemodynamics assessed wit

152 of endothelial progenitor cells and improve microvascular function, which have been associated with

153 e-induced declines in diastolic and coronary microvascular function.

154 ecting depression, and validated measures of microvascular function.

155 sion is linked with another open question of microvascular function: how are red blood cells delivere

156 of the endothelial glycocalyx and dependent microvascular functions in vivo, and demonstrate that si

157 model as a biomimetic tool for investigating microvascular growth and function ex vivo.

158 1 deletion reduces oxidant load and restores microvascular health in db/db mice without influencing t

159 In this study, alterations in conjunctival microvascular hemodynamics were quantitatively assessed

160 sively imaged and thus enables assessment of microvascular hemodynamics.

161 d resolved cellular interactions in modeling microvascular hemodynamics.

162 ntegrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemi

163 helial KLF2 results in dysregulation of lung microvascular homeostasis and contributes to lung pathol

164 in certain diseases, the degree of coronary microvascular impairment carries important prognostic re

165 the presence of neurodegeneration and early microvascular impairment.

166 urements that increases with the presence of microvascular impairment.

167 and endothelial activation characteristic of microvascular inflammation during AMR.

168 n deposits cause endothelial dysfunction and microvascular injury and are modulated by amylin transpo

169 in elusive, studies suggest that RBC-induced microvascular injury in the distal lung plays a central

170 dies detected in the ECXM and AT1R ELISA and microvascular injury observed in antibody mediated rejec

171 let deposition, and TMA severity, as well as microvascular injury scores (glomerulitis + peritubular

172 hrombosis after carotid artery and cremaster microvascular injury without affecting parameters of hae

173 ute cor pulmonale is likely due to pulmonary microvascular injury, the mechanism of which is uncertai

174 t of hemodynamic shear stress on RBC-induced microvascular injury.

175 will improve clinical outcomes by enhancing microvascular integrity and modulating T cell tissue tro

176 conclude that ANXA2 contributes to pulmonary microvascular integrity by enabling VEC-related phosphat

177 s an important regulator of inflammation and microvascular integrity, and impaired NO bioactivity is

178 (n = 340; 283 men) had significantly higher microvascular invasion (23.8% [n = 81], P < .001), expla

179 el at the time of LT was 8.3 ng/mL; 9.4% had microvascular invasion (n = 68), and 22.1% were beyond M

180 a expression correlated with K19 expression, microvascular invasion and metastatic spread.

181 e, LRT status, serum alpha1-fetoprotein, and microvascular invasion were independent risk factors (P

182 On explantation (n = 3276), 13% had microvascular invasion, 30% had no viable tumor, and 15%

183 ndependently associated with HCC recurrence: microvascular invasion, AFP at time of LT, and the sum o

184 protein (AFP) at liver transplantation (LT), microvascular invasion, and the sum of the largest viabl

185 ribution, multiple lesions, absent necrosis, microvascular invasion, and tumors beyond the Milan crit

186 tial disease beyond MC, multinodularity, and microvascular invasion.

187 er we adjusted for potential risk factors of microvascular ischemia.

188 sine-1-phosphate (S1P), could ameliorate the microvascular leakage following alcohol intoxication plu

189 P administration ameliorated hypotension and microvascular leakage following combined alcohol intoxic

190 hemorrhagic shock and resuscitation-induced microvascular leakage using a rat model with intravital

191 ck and resuscitation-induced hypotension and microvascular leakage.

192 As, which induced the development of typical microvascular lesions in allogeneic transplants.

193 Microvascular location is likely to be biologically rele

194 320 (high Nrp-2 expression) and human dermal microvascular lymphatic endothelial cells (LECs).

195 interactions from excess collagen may affect microvascular, mechanical, and electrical function.

196 nnel occlusion risk and an "endothelialized" microvascular model that measures alterations in sRBC/en

197 works provide insights into peripheral nerve microvascular morphogenesis, restrictive barrier formati

198 ntrol in children with T1D can cause evident microvascular morphological changes long before any path

199 Our findings showed that abnormal retinal microvascular morphology was evident in pediatric patien

200 Transmural inflammation induces microvascular neoangiogenesis and results in lumen-occlu

201 trated by PD-1(+) effector T cells developed microvascular neoangiogenesis as well as hyperplasia of

202 athological analysis revealed high levels of microvascular nestin immunoreactivity in the same region

203 ), the 3D construct containing the lymphatic microvascular network can be analyzed by microscopy (sta

204 reporter protein expression across a dynamic microvascular network in an adult mammal.

205 showed the absence of a radial peripapillary microvascular network in these 12 eyes.

206 lular organisation, extracellular matrix and microvascular network mimic human heart tissue.

207 liomas are indistinguishable on imaging, the microvascular network of pilomyxoid astrocytoma, a subty

208 ns confirmed the presence of a peripapillary microvascular network only in MGS cases supports the hyp

209 cs involved in angiogenesis within an intact microvascular network using time-lapse imaging.

210 of transport costs may be prioritized by the microvascular network.

211 of the peripapillary retina revealed a dense microvascular network.

212 We study occlusive dynamics within a model microvascular network: the embryonic zebrafish trunk.

213 he microdevice features self-organized human microvascular networks formed over 4-5 d, after which th

214 ells (RBCs) are performed in three realistic microvascular networks from the mouse cerebral cortex.

215 flow and pressure distribution in realistic microvascular networks is needed for improving our under

216 her vascular smooth muscle cells in cultured microvascular networks maintain the ability to constrict

217 On Day 0 and Day 3 live microvascular networks were visualized with FITC conjuga

218 cale blood flow in physiologically realistic microvascular networks.

219 fraction </=47%, infarct size >/=19%LV, and microvascular obstruction >/=1.4%LV were identified as t

220 for infarct size >/=19%LV, and 2 points for microvascular obstruction >/=1.4%LV.

221 Myocardial salvage index and microvascular obstruction (MVO) are markers for reperfus

222 incidence of angiographic no reflow (NR) and microvascular obstruction (MVO) at cardiac magnetic reso

223 ion on infarct size, myocardial salvage, and microvascular obstruction (MVO) in patients with STEMI.

224 re, being able to predict the development of microvascular obstruction at the time of PPCI may identi

225 Although microvascular obstruction can be detected by cardiac ima

226 Microvascular obstruction during a VOC leads to impaired

227 Myocardial hemorrhage and microvascular obstruction follow distinct time courses p

228 The association between neutrophil count and microvascular obstruction is abolished in metoprolol-tre

229 Eighteen of 28 (64%) patients had microvascular obstruction on the acute scan, of whom 15/

230 measures out to 2 years and the influence of microvascular obstruction present at baseline on these l

231 Microvascular obstruction region on acute late gadoliniu

232 mediately after contrast administration, the microvascular obstruction region was 3.2+/-1.1 times lar

233 ze, salvage, intramyocardial hemorrhage, and microvascular obstruction should be standardized accordi

234 the extent of intramyocardial hemorrhage and microvascular obstruction varied dramatically according

235 Exponential fit to the microvascular obstruction volume was found to be the bes

236 Microvascular obstruction was associated with reduced re

237 Microvascular obstruction was present in 48 patients at

238 acute scan, of whom 15/18 (83%) patients had microvascular obstruction with IMH.

239 ze, salvage, intramyocardial hemorrhage, and microvascular obstruction) is not well understood.

240 Edema, microvascular obstruction, and enhanced volumes were ide

241 Acute myocardial infarct size, extent of microvascular obstruction, and IMH correlated with the c

242 tribution, infarct size, myocardium at risk, microvascular obstruction, and intramyocardial hemorrhag

243 s is partly attributed to the development of microvascular obstruction, which occurs in around 50% of

244 ar (LV) ejection fraction, infarct size, and microvascular obstruction.

245 and anti-inflammatory agents that may reduce microvascular obstruction.

246 segments with intramyocardial hemorrhage or microvascular obstruction.

247 ce imaging results and their modification by microvascular obstruction.

248 the degree of intramyocardial hemorrhage or microvascular obstruction.

249 gly, the levels of LEP secretion predict the microvascular outcome of APCs transplantation in a mouse

250 Microvascular outcomes were nephropathy, retinopathy, an

251 ast sensitivity, and color perception before microvascular pathologies become apparent.

252 Microvascular pathology and related blood-brain barrier

253 r single-legged exercise in humans increased microvascular perfusion (determined by contrast-enhanced

254 The change in microvascular perfusion after transfusion correlated neg

255 steric CD11b/CD18 inhibitor mAb107, improves microvascular perfusion and histopathology, reduces intr

256 a coordinated increase in insulin-stimulated microvascular perfusion and molecular signaling at the l

257 after establishment of AKI rapidly restores microvascular perfusion and small molecule accessibility

258 adhesion may prevent the impairment of renal microvascular perfusion and the heightened inflammatory

259 on perfusion is critical for optimization of microvascular perfusion and to define which patients can

260 The effects of RBC transfusion on microvascular perfusion are not well documented.

261 oids have an immediate and massive effect on microvascular perfusion because of formation of RBC aggr

262 reversed the insulin-stimulated increase in microvascular perfusion in both legs and abrogated the g

263 perfusion imaging revealed markedly improved microvascular perfusion in response to the blockade of N

264 ischaemia, a prolonged decrease of coronary microvascular perfusion often occurs even after flow is

265 metabolic syndrome, issues such as aggregate microvascular perfusion resistance, mass transport and e

266 Microvascular perfusion was evaluated by low-power contr

267 o effects of several particulate steroids on microvascular perfusion were assessed.

268 , reduced platelet aggregation, and improved microvascular perfusion.

269 nsfusion correlated negatively with baseline microvascular perfusion.

270 ormed immediately after HIFD showed improved microvascular perfusion.

271 However, the origin of CNS microvascular pericytes and the mechanism of their recru

272 helial glycocalyx are critical regulators of microvascular permeability to both water and albumin.

273 /0 (but not 45/10), there was an increase in microvascular permeability, cyclical abolition of preloa

274 lycocalyx to one critical vascular function, microvascular permeability, remains unclear.

275 endothelial cell proliferation and increased microvascular permeability.

276 , showing the impact of CXCR7 on stabilizing microvascular permeability.

277 will describe basic concepts of coronary and microvascular physiology, review available modalities fo

278 a, and organ ischemia linked to disseminated microvascular platelet rich-thrombi.

279 d by significant intratumoral heterogeneity, microvascular proliferation, immune system suppression,

280 uptake to be highest in the area with marked microvascular proliferation.

281 -VEGF drugs collapsed MV to form glomeruloid microvascular proliferations (GMP), accompanied by only

282 /clonogenic epithelial cell loss mediated by microvascular protection.

283 tion, neutrophil infiltration, fibrosis, and microvascular pruning.

284 l changes in white matter integrity or brain microvascular pulsatility.

285 y induced by levodopa within areas of active microvascular remodeling, and that such changes correlat

286 -17A, pathologic neutrophil recruitment, and microvascular remodeling.

287 by carotid artery cannulation and increased microvascular resistance measured using a tail-cuff.

288 on-derived measure of the minimum achievable microvascular resistance-is relatively easy to measure,

289 We investigated regional cerebral microvascular responses to acute (2 h) and prolonged (10

290 onary microvascular dysfunction (CMD) due to microvascular spasm.

291 s, GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-spe

292 ogenic and slight angiogenic activities in a microvascular sprouting assay using choroid explants.

293 ate how this system can be used to phenotype microvascular structures in gliomas to predict survival,

294 duction, replenishing ADAMTS13, and blocking microvascular thrombosis despite persistent ADAMTS13 def

295 lial antithrombogenic properties and induces microvascular thrombosis in a perfusion system.

296 cellular histones, with widespread pulmonary microvascular thrombosis.

297 agulants directly within grafts and decrease microvascular thrombotic sequelae, while avoiding system

298 c cells (DCs) are highly mobile, going along microvascular tracks, while static macrophages (MF) form

299 lecular regulators that drive organ-specific microvascular transcriptional programs and thereby regul

300 Diabetes mellitus destabilized microvascular vessels of the heart, affecting the amplit