ライフサイエンスコーパス: microvascular

1 l density (VD), and presence of intraretinal microvascular abnormalities (IRMA).

2 inal vascular segments known as intraretinal microvascular abnormalities (IRMAs) are a known risk fac

3 Microaneurysms, intraretinal microvascular abnormalities (IRMAs), and neovascularizat

4 (DH), venous beading (VB), and intraretinal microvascular abnormalities (IRMAs).

5 At baseline, nePVAC is characterized by microvascular abnormalities featuring an isolated, perif

6 Nonperfusion area, SSPiM, and microvascular abnormalities in OCTA images were evaluate

7 central macular thickness and prevalence of microvascular abnormalities in the superficial and deep

8 For soft exudates, intraretinal microvascular abnormalities, and venous beading, agreeme

9 m [ma], cotton wool spot [CWS], intraretinal microvascular abnormality [IRMA]) were manually segmente

10 s on phenotypes and mechanisms that underlie microvascular aging, the greatest risk factor for cerebr

11 Our results point to the fact that microvascular alterations can be identifiable at BP valu

12 ive changes may develop independently of the microvascular alterations defining DR.

13 ch and therapeutic clinical trials targeting microvascular and endothelial alterations during septic

14 Microvascular and endothelial dysfunction in the nonculp

15 r STEMI and determine the real prevalence of microvascular and endothelial dysfunction.

16 redicting glycaemia-associated risks for the microvascular and macrovascular complications of diabete

17 s, HIFs are implicated in development of the microvascular and macrovascular complications of diabete

18 sex tended to associate with a diagnosis of microvascular angina although this was not significant (

19 Overall, 78 (52%) had isolated microvascular angina, 25 (17%) had isolated vasospastic

20 Synaptic dysfunction and microvascular angiopathy are confirmed as early progress

21 Instead, a global microvascular angiopathy was detected by immunohistochem

22 Histological analysis highlighted microvascular benefits in the training SCD patients comp

23 Decreased microvascular blood flow (MBF) increases the likelihood

24 latelet-neutrophil aggregation, and restored microvascular blood flow in lung arterioles of SCD mice

25 I/R-targeting therapeutics shown to improve microvascular blood flow in sickle transgenic mice under

26 Breathing, ECG and microvascular blood flow were simultaneously monitored f

27 Perfusion, a measure of microvascular blood flow, provides information on nutrie

28 red microvascular obstructions that impaired microvascular blood flow.

29 ces to differentiate into pericytes and form microvascular capillaries in vitro.

30 erfusion pressure that, in turn, may lead to microvascular cardiac ischemia.

31 saturation (StO(2) ) and altered patterns of microvascular cerebral blood perfusion and whether these

32 of capillaries allowing for a better view of microvascular changes and an extraction of volumetric me

33 elevant insight into the pathogenesis of the microvascular changes associated with DR.

34 to analyze relative blood flow speeds in the microvascular changes associated with DR.

35 to a diabetic milieu in mice, also mimic the microvascular changes found in patients with diabetes.

36 oninvasive measurement and quantification of microvascular changes in humans.

37 mune disease systemic sclerosis (SSc) causes microvascular changes that can be easily observed cutane

38 lopment and progression of diabetes mediated-microvascular changes, evaluation of therapeutic interve

39 lular interactions substantially compromises microvascular clotting.

40 Diabetic retinopathy (DR) is a microvascular complication of diabetes and a leading cau

41 r complications (cardiovascular disease) and microvascular complications (such as diabetic kidney dis

42 The sequelae of diabetes include microvascular complications such as diabetic kidney dise

43 Microvascular complications were present in 26% of those

44 ariate Cox analysis, early age at diagnosis, microvascular complications, high triglyceride levels, a

45 blood glucose, a primary cause of long-term microvascular complications.

46 y, characterised by increased thrombotic and microvascular complications.

47 ogy to quantify changes in muscle phenotype, microvascular composition, and oxidative capacity follow

48 Microvascular compromise was described one DM complicati

49 We discovered direct microvascular connections between PVAT and the distal mu

50 Myocardial perfusion reflects the macro- and microvascular coronary circulation.

51 tested whether this approach would decrease microvascular damage and improve allograft function.

52 Here, we confirmed ACR as a marker of microvascular damage and tested whether metabolic-relate

53 accompanied by widespread macrovascular and microvascular damage.

54 ACR) is a marker of diabetic nephropathy and microvascular damage.

55 umor angiogenic heterogeneity necessitate 3D microvascular data from 'whole-tumors' as well as "ensem

56 irst choice for long-term treatment, whereas microvascular decompression is the first-line surgery in

57 nopathies are characterized by a progressive microvascular degeneration followed by a postischemic ab

58 CCA showed higher microvascular density and higher expression of nuclear f

59 urthermore, HE4 serum levels correlated with microvascular density in EOC tissue and inversely correl

60 There was a significant reduction of the microvascular density in eyes with exudative vs traction

61 erative phenotype and showed lower pulmonary microvascular density than wild-type rats.

62 Histological microvascular density was significantly correlated to UL

63 esistance is closely coupled with functional microvascular density, independent of arterial blood flo

64 ression, we analyzed the effect of prevalent microvascular disease (retinopathy, neuropathy, and neph

65 ral artery disease or microvascular disease, microvascular disease alone was associated with a 3.7-fo

66 arge cohort of veterans to determine whether microvascular disease diagnosed in any location increase

67 lar mechanisms underlying the development of microvascular disease in the memory centers of the brain

68 We investigated whether microvascular disease is associated with amputation in a

69 al to the development of diabetic macro- and microvascular disease is endothelial dysfunction, which

70 combination of peripheral artery disease and microvascular disease was associated with a 22.7-fold (9

71 art transplant patients without suspicion of microvascular disease who underwent stress cardiac MRI w

72 h those without peripheral artery disease or microvascular disease, microvascular disease alone was a

73 he retinal vasculature in the study of brain microvascular disease.

74 han patients without transplants, suggesting microvascular disease.

75 ion to the pathogenesis of macrovascular and microvascular diseases associated with old age.

76 These findings may yield insight into microvascular disorders in recipients of mechanical circ

77 Coronary microvascular dysfunction (CMD) is defined by diminished

78 Microvascular dysfunction (MVD) is a common pathophysiol

79 NAFLD independently predicted coronary microvascular dysfunction (P = .01).

80 hether there was a sex disparity in coronary microvascular dysfunction among 46 men and 27 women with

81 erlap of MS-induced myocardial ischemia with microvascular dysfunction and symptoms in the absence of

82 Endothelial activation and microvascular dysfunction are key pathogenic processes i

83 imaging could help determine the presence of microvascular dysfunction associated with increased card

84 Coronary microvascular dysfunction has been proposed as a link be

85 coronary artery disease, those with coronary microvascular dysfunction have a poor outcome.

86 he PRIMID-AS study (Prognostic Importance of Microvascular Dysfunction in Asymptomatic Patients With

87 ulticenter PROMIS-HFpEF study (Prevalence of Microvascular Dysfunction in Heart Failure With Preserve

88 ooth muscle function, directly contribute to microvascular dysfunction in MDD.

89 hese findings provide evidence that coronary microvascular dysfunction is present in HFpEF, limits O(

90 Coronary microvascular dysfunction is usually diagnosed by assess

91 Coronary microvascular dysfunction may mediate the effect of chro

92 Microvascular dysfunction plays an important role in the

93 ytokines, and chemokines), oxidative stress, microvascular dysfunction, and fibrosis in the liver.

94 Coronary microvascular dysfunction, but not eGFR, was independent

95 SVD in the heart, known as coronary microvascular dysfunction, can cause chronic or acute my

96 ons between chronic kidney disease, coronary microvascular dysfunction, cardiac dysfunction, and adve

97 the roles of inflammation, macrovascular and microvascular dysfunction, fibrosis, and tissue remodeli

98 pericyte miR-145a mediates sepsis-associated microvascular dysfunction, potentially by means of Fli-1

99 ife-threatening systemic disease with severe microvascular dysfunction.

100 dosterone in the pathophysiology of coronary microvascular dysfunction.

101 cal application, including the assessment of microvascular dysfunction.

102 yocardial ischemia in patients with coronary microvascular dysfunction.

103 gen and survival factor for bovine and human microvascular EC, with an additivity with VEGF.

104 In cultured mouse brain microvascular ECs (mBMECs), the miR-15a/16-1 cluster dir

105 ignaling and EndMT occurs in mouse pulmonary microvascular ECs in vivo under hyperglycemic conditions

106 Using lung microvascular endothelial and alveolar epithelial cells,

107 erived endothelial progenitor cells to brain microvascular endothelial cell (BMEC)-like cells with go

108 e utilised a high TEER primary porcine brain microvascular endothelial cell (PBMEC) culture to assess

109 16-1 cluster in primary mouse or human brain microvascular endothelial cell cultures enhanced in vitr

110 s of our genome-scale metabolic model of the microvascular endothelial cell function.

111 MC(TC)LUVA potentiated fetal human pulmonary microvascular endothelial cell interactions, inhibited t

112 The molecular constituents of brain microvascular endothelial cells (BMECs) and pericytes, w

113 buted to the restrictive nature of the brain microvascular endothelial cells (BMECs) that comprise th

114 egress in infected, nonpolarized human brain microvascular endothelial cells (HBMECs) and observed on

115 ivirus that persistently infects human brain microvascular endothelial cells (hBMECs), the primary ba

116 ic to neurons and persistently infects brain microvascular endothelial cells (hBMECs), which normally

117 bacteriophage (phage) K1F and human cerebral microvascular endothelial cells (hCMECs).

118 a (Caco-2) and human non-malignant intestine microvascular endothelial cells (HIMEC) was assessed.

119 cal resistance (TEER) of human or mouse lung microvascular endothelial cells (HLMVEC or MLMVEC), and

120 diated intracellular signaling of human lung microvascular endothelial cells (HLMVECs).

121 In line with these data, human microvascular endothelial cells (HMEC-1) displayed an OM

122 an macrophages, HSAEpCs, and human pulmonary microvascular endothelial cells (HPMECs) significantly a

123 We found that in human retinal microvascular endothelial cells (HRECs) vitreous activat

124 d in the vasculature, while in human retinal microvascular endothelial cells (HRMECs), TNF-alpha stim

125 Human dermal microvascular endothelial cells 1, human platelets and n

126 ic capacity of CNP was examined in pulmonary microvascular endothelial cells and aortic rings isolate

127 Silencing SIRT7 in pulmonary artery or microvascular endothelial cells attenuated LPS-induced i

128 firmed by protection of cultured human brain microvascular endothelial cells from hydrogen peroxide-i

129 Human pulmonary microvascular endothelial cells were also used to examin

130 of neurons, pericytes, astrocytes, and brain microvascular endothelial cells, in brain-like tissues a

131 , increased miR-19b expression in human lung microvascular endothelial cells, leading to a decrease i

132 ascular unit organoid containing human brain microvascular endothelial cells, pericytes, astrocytes,

133 In cultured microvascular endothelial cells, Piezo1 channel activati

134 Using monolayers of mouse primary brain microvascular endothelial cells, the permeability coeffi

135 studied using primary fetal human pulmonary microvascular endothelial cells.

136 cells to induce adhesion molecules on dermal microvascular endothelial cells.

137 lary damage was examined using primary brain microvascular endothelial cells.

138 eability in a dose-dependent manner in human microvascular endothelial cells.

139 d pluripotent stem cell (iPSC)-derived brain microvascular endothelial-like cells (iBMECs), astrocyte

140 mechanism in pulmonary arterial and lung MV (microvascular) endothelial cells in response to DNA dama

141 including macrovascular endothelium (maEC), microvascular endothelium (miECs), and a new population

142 an and mouse neutrophil adhesion patterns to microvascular endothelium were not significantly differe

143 ts, (ii) T-cell transmigration through brain microvascular endothelium, (iii) detection of T cells, B

144 by exacerbating blood-brain barrier damage, microvascular failure, brain oedema, oxidative stress, a

145 clusion plethysmography to assess peripheral microvascular filtration coefficient (measuring capillar

146 In patients with HFpEF, microvascular filtration coefficient was lower (calf: 3.

147 ogenous gas with acute mesenteric macro- and microvascular flow changes.

148 We focus primarily on studies of microvascular flow, mural cell control of vessel diamete

149 The association between ACR and microvascular function (responses to acetylcholine [ACH]

150 c hypotension and impaired macrovascular and microvascular function accompanied by both systolic and

151 ACR was robustly associated with microvascular function measures in SUMMIT.

152 On longer-term follow-up, impaired microvascular function predicts adverse cardiovascular o

153 Retinal microvascular function was assessed in 201 participants

154 Microvascular function was assessed using peripheral art

155 in skin microvessels, resulting in improved microvascular function, as assessed by laser Doppler ima

156 icrocirculation in both organs, with loss of microvascular function, termed small vessel disease (SVD

157 ded changes in the endothelial glycocalyx or microvascular function.

158 ave developed to detect impairments in brain microvascular function.

159 ues of investigation, including the study of microvascular function.

160 with hyperglycemia and impairment of retinal microvascular function.

161 ges in measures of endothelial glycocalyx or microvascular function.

162 testing, echocardiography, and assessment of microvascular function.

163 of adiposity-related traits in causing lower microvascular function.

164 ACR is a valid marker for microvascular function.

165 Abnormal retinal microvascular geometry has been associated with cardiac

166 orer cardiac function and suboptimal retinal microvascular geometry, among Chinese without CVD.

167 against constitutively expressed antigens of microvascular glomerular cells in patients with AMVR.

168 VE-cad-p120 binding, reduced VE-cad levels, microvascular hemorrhaging, and decreased survival.

169 y endothelial damage, SAR247799 improved the microvascular hyperemic response without reducing lympho

170 permits the reconstruction of super-resolved microvascular images at clinically relevant penetration

171 Non-invasive, contrast-free microvascular imaging of human thyroids can be potential

172 ual microbubbles (MBs), offers unprecedented microvascular imaging resolution at clinically relevant

173 .032) and a higher extent (g>=1 + ptc>=1) of microvascular inflammation (67% vs 9%, P = 0.02).

174 ncreased graft survival after accounting for microvascular inflammation (adjusted hazard ratio =0.967

175 omerular area was associated with indices of microvascular inflammation (glomerulitis, peritubular ca

176 onor-specific antibody (DSA) negative (DSA-) microvascular inflammation (MVI).

177 These data support comorbidity-driven microvascular inflammation as a pathophysiologic mechani

178 cells can also trigger antibody-independent microvascular inflammation by sensing the absence of sel

179 Sessions on ABMR focused on biopsies showing microvascular inflammation in the absence of C4d stainin

180 Comorbidity-driven microvascular inflammation is posited as a unifying path

181 Activated NK cells contribute to microvascular inflammation leading to chronic antibody-m

182 y, splenic, and bone marrow involvement, and microvascular injury and thrombosis were also detected.

183 a-FcRn mAb prevented fibrin deposition after microvascular injury in a murine model of HIT in which h

184 superior to prasugrel in preventing coronary microvascular injury in the infarct-related territory as

185 hology studies suggest a pathogenic role for microvascular injury, specifically blood-brain barrier d

186 t is suspected to be related to myocarditis, microvascular injury, systemic cytokine-mediated injury,

187 e and race-matched controls, suggesting that microvascular insult may precede structural thinning.

188 -2alpha in transplant donors promoted airway microvascular integrity and diminished alloimmune inflam

189 has a functionally relevant influence on the microvascular integrity of orthotopic tracheal allograft

190 and it is followed by the rapid recovery of microvascular integrity.

191 Corresponding microvascular invasion rates were 37.2% and 50.0%, compa

192 ly, we provide a brief perspective on future microvascular investigations within the framework of the

193 We further show that pathologic microvascular leakage in CD31-deficient mice can be corr

194 Collectively, we demonstrate that increased microvascular leakage reverses the localization of direc

195 nteen weeks post infection revealed coronary microvascular leakage, fibrosis and immune cell infiltra

196 Although neutrophils can promote microvascular leakage, the impact of vascular permeabili

197 ducing endothelial contraction and transient microvascular leakage.

198 icantly improved tissue oxygenation, limited microvascular leakiness, and prevented airway ischemia.

199 (AMI), reperfusion injury is associated with microvascular lesions and myocardial edema.

200 the highest average relative risks comprised microvascular, macrovascular, and miscellaneous complica

201 ilarly do not fit neatly into the historical microvascular/macrovascular paradigm.

202 ating lymphocytes, tissue-based hypoxia, and microvascular markers were analyzed and correlated with

203 this paper, we describe the protocols of the microvascular measurements applied in the Maastricht Stu

204 summarize our main findings involving these microvascular measurements through the end of 2018.

205 Using human skin as a microvascular model, we hypothesized that cutaneous vaso

206 cused on developing treatments to halt renal microvascular (MV) rarefaction in RVD, a major feature o

207 dentifying signalling components that impact microvascular network morphology as well as endothelial

208 usly to cellular elements in the neighboring microvascular network through gap junctions, where it re

209 gnals within the highly interconnected brain microvascular network to increase local CBF.

210 propagate over significant distances in the microvascular network, thus dramatically increasing the

211 s shown potential to noninvasively visualize microvascular networks in vivo.

212 formation and controlled 3D organization of microvascular networks.

213 nesis in response to injury and regulate the microvascular niche as well as subsequent distal lung ti

214 ons are presumably mediated by the increased microvascular O(2) availability.

215 ositive effects on muscle contraction force, microvascular O(2) delivery and skeletal muscle oxidativ

216 and redistribute muscle QO2 and thus defend microvascular O(2) partial pressures and capillary blood

217 The primary outcome was the amount of microvascular obstruction (MVO) (percentage of left vent

218 he relationship among smoking, infarct size, microvascular obstruction (MVO), and adverse outcomes af

219 d coronary flow reserve (CFR) for predicting microvascular obstruction (MVO), myocardial hemorrhage,

220 eperfusion due to the occurrence of coronary microvascular obstruction (MVO).

221 Microvascular obstruction affects one-half of patients w

222 Sonothrombolysis reduces microvascular obstruction and improves myocardial dynami

223 In the primary analysis, the mean microvascular obstruction did not differ between the 20-

224 The occurrence of microvascular obstruction was not different in patients

225 ection fraction, global longitudinal strain, microvascular obstruction, and infarct size (AUC compari

226 e reduction but also attenuation of coronary microvascular obstruction, as well as longer-term target

227 with hypokinetic myocardial wall motion and microvascular obstruction, demonstrating potential for c

228 r pump strains; and infarct size, edema, and microvascular obstruction.

229 declined human kidneys on NMP, we discovered microvascular obstructions that impaired microvascular b

230 reduced intravascular thrombin activity and microvascular occlusion as compared with untreated S aur

231 ore, the relationships between metabolic and microvascular oscillators were examined during phenyleph

232 o in CARMELINA (The Cardiovascular and Renal Microvascular Outcome Study With Linagliptin), a cardiov

233 stigate the renal component of the composite microvascular outcome, defined as the first occurrence o

234 nnels support skeletal muscle blood flow and microvascular oxygen delivery-to-utilization matching du

235 The macular microvascular parameters on OCTA may serve as biomarkers

236 rdised retinal photographs to assess retinal microvascular parameters.

237 the endothelium in maintaining perfusion and microvascular patency in the ischemic penumbra that is c

238 1P(1) supports blood-brain barrier function, microvascular patency, and the rerouting of blood to hyp

239 sensitivity, and color perception before any microvascular pathologies on the fundus become detectabl

240 nhanced-MRI can be used to diagnose specific microvascular pathology after traumatic brain injury and

241 Microvascular pathology and ischemic lesions contribute

242 MRI, often with an ovoid shape suggestive of microvascular pathology and with a predilection for the

243 ADMA treatment also exacerbated brain microvascular pathology in Tg-SwDI mice as observed by i

244 ce of the vasculature and are key players in microvascular pathology.

245 its precursor, arginine, contributes to the microvascular pathophysiology of severe falciparum malar

246 d normal vascular permeability but displayed microvascular patterning defects.

247 Deletion of mPges-1 impairs cardiac microvascular perfusion and increases inflammatory cell

248 Impaired microvascular perfusion is central to the development of

249 An increased and more effective microvascular perfusion is postulated to play a key role

250 f injury biomarker NGAL (P = .012), improved microvascular perfusion on contrast-enhanced ultrasound

251 adjusts endothelium-mediated vasorelaxation, microvascular perfusion, and blood pressure during acid-

252 insulin signalling, and associated enhanced microvascular perfusion, contributes to glycaemic contro

253 l standards for best practices when studying microvascular perfusion, partly motivated by recent cont

254 Furthermore, mice with a selective defect in microvascular permeability enhancement (VEC-Y685F-ki) sh

255 Increased microvascular permeability to plasma proteins and neutro

256 T2-weighted magnetic resonance imaging, and microvascular permeability was estimated by strain gauge

257 rough microbubble potentiated enhancement of microvascular permeability.

258 e introduced to recapitulate tissue-specific microvascular physiology.

259 relating with red blood cell aggregation and microvascular plugging.

260 on data localized DCN expression to areas of microvascular proliferation and immunohistochemical stud

261 To what extent microvascular rarefaction contributes to impaired skelet

262 ates that angiogenic treatments to alleviate microvascular rarefaction may be key to restoring exerci

263 e were to: (1) quantify the effect of random microvascular rarefaction on limb perfusion and muscle p

264 r endothelial function as it participates in microvascular reactivity, endothelium interaction with b

265 ion biomarkers were measured, in addition to microvascular reactivity, using laser Doppler imaging wi

266 Insulin-mediated microvascular recruitment (IMVR) regulates delivery of i

267 nd incredibly robust local electro-metabolic microvascular regulation of blood flow in heart.

268 n, provides a quantitative metric of macular microvascular remodeling with a strong physiological und

269 infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus lim

270 Microvascular reserve over the wave-free period of diast

271 if conducted vasodilation, which coordinates microvascular resistance longitudinally to match tissue

272 ate the recovery of blood flow regulation in microvascular resistance networks.

273 The change in microvascular resistance post-TAVI was equivalent to tha

274 endotypes were distinguished by a hyperemic microvascular resistance threshold of 2.5 mm Hg/cm/s.

275 described, with normal and elevated minimal microvascular resistance, respectively.

276 resses the ratio between basal and hyperemic microvascular resistance.

277 hms targeting HbA(1c) from 6.5% to 8%, lower microvascular risk, or higher HbA(1c) for those aged 75

278 terns and degrees of flow changes in various microvascular settings, such as middle cerebral artery o

279 Physiological integrity of microvascular smooth muscle and endothelium recovers in

280 to the endosteal surface and adjacent to the microvascular space the marrow adipocyte can store or pr

281 rombin significantly attenuates heme-induced microvascular stasis in mouse models of VOC.

282 ther coagulation directly contributes to the microvascular stasis that causes VOC.

283 expression, which has been shown to mediate microvascular stasis.

284 ULM, by providing non-invasive in vivo microvascular structural information, has the potential

285 This technique was applied to evaluate the microvascular structure, vascular perfusion, and hypoxia

286 sualization and quantification of lymph node microvascular structures and blood flow dynamics with re

287 culation and suggest that restoring impaired microvascular supply, regardless of disease co-morbiditi

288 e possibilities of fabricating sophisticated microvascular systems by enabling precise spatiotemporal

289 We show that, in COVID-19, inflammatory microvascular thrombi are present in the lung, kidney, a

290 rumental for the prevention and treatment of microvascular thromboembolic pathologies, which are inac

291 r these rheological effects are relevant for microvascular thrombogenesis remains elusive.

292 om inflammation, endothelial activation, and microvascular thrombosis occur in the context of coronav

293 isk of thrombotic complications ranging from microvascular thrombosis, venous thromboembolic disease,

294 heterogeneous angiogenic landscape from the microvascular to tumor ensemble scale in terms of vascul

295 ersies about the precise location within the microvascular tree where neurovascular coupling is initi

296 The response to endothelium-dependent microvascular vasodilation was greater after the apples

297 th capillary rarefaction and impaired muscle microvascular vasoreactivity, due to reduced nitric oxid

298 Spinal loading elevated a microvascular volume as well as VEGF expression.

299 bly, knee loading significantly improved the microvascular volume, type H vessel formation, and bone

300 of tumor and blood flow mapping of the tumor microvascular with improved sensitivity up to 11.09 dB f