ライフサイエンスコーパス: arterial

1 0-d graft loss (2% versus 5%; P = 0.66), and arterial (4% versus 12%; P = 0.19) and biliary (16% vers

2 g aptamer-based proteomics, we characterized arterial (A)-to-renal venous (V) gradients for >1,300 pr

3 To achieve that goal, we used intra-arterial administration of thrombin mixed with gadoliniu

4 COA peak velocity <2 m/s) will have a higher arterial afterload and increased left ventricular mass i

5 COA patients had higher arterial afterload compared with controls with similar S

6 e to equipment failure or abnormal pulmonary arterial anatomy.

7 Continuous arterial and discrete arterial and venous blood sampling

8 Simultaneous arterial and jugular venous bulb blood gas samples were

9 ble vasculoprotective mechanism in pulmonary arterial and lung MV (microvascular) endothelial cells i

10 tion, permits the differential assessment of arterial and venous blood flow patterns in the retina th

11 Continuous arterial and discrete arterial and venous blood sampling were performed to det

12 i) in the optic disc and in each of multiple arterial and venous segments was obtained and shown to r

13 re made by estimating, in a pair of adjacent arterial and venous segments, various temporal waveform

14 quantified the structure and composition of arterial and venous thrombi and pulmonary emboli using h

15 d organ-specific complications (for example, arterial aneurysm and dissection), integrated physical m

16 rved that while bcar1-/- zebrafish showed no arterial angiogenic or heart defects during development,

17 itulates ALI-induced proteolytic collapse of arterial architecture.

18 Afferent input from pulmonary arterial baroreceptors may contribute to sympathetic neu

19 e 1 hypertension demonstrated higher retinal arterial baseline diameter fluctuation (p = 0.0012), max

20 calcifications are a frequent finding in all arterial beds with the highest prevalence in the intracr

21 Although arterial bleeding is the main cause of postoperative hem

22 retina at PO(2)s more than ten-fold that of arterial blood (Damsgaard et al., 2019).

23 No correlation was seen between pulmonary arterial blood flow and BPD outcomes.

24 -aorta (PA/AO) diameter ratio, and pulmonary arterial blood flow were determined.

25 During multidisciplinary rounds, all arterial blood gas (ABG) results, ventilator settings an

26 Cardiorespiratory and arterial blood gases were collected throughout both exer

27 Arterial blood gases, dyspnea, and comfort were recorded

28 3 +/- 2 kg m(-2) ), FMD (Duplex ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and

29 Mechanical ventilator settings, arterial blood gases, vital signs, and use of vasopresso

30 Real arterial blood pressure (ABP) measurements from 34 traum

31 red whether the methods identify the optimal arterial blood pressure (ABPopt) and lower limit of auto

32 al mechanisms responsible for maintenance of arterial blood pressure (BP) during haemorrhage in human

33 gulation (CA) is often expressed by the mean arterial blood pressure (MAP)-cerebral blood flow (CBF)

34 Arterial blood samples were collected as a reference sta

35 Arterial blood samples were collected as the reference s

36 pted microcatheter aspiration of 3 different arterial blood samples: (1) within the core of the occlu

37 Arterial blood sampling and metabolite analysis were con

38 PET quantification of tau deposits, avoiding arterial blood sampling.

39 iably reduce CBF or CDO(2) Oxygen content in arterial blood was fully restored with acclimatisation t

40 , blood gases, and plasma-free hemoglobin in arterial blood, as well as blood entering and exiting th

41 Breast arterial calcification and calcium scores were determine

42 Generalized arterial calcification of infancy (GACI) is a rare genet

43 venous oxygen saturation, central venous-to-arterial carbon dioxide pressure difference, and oxygen

44 ane oxygenation, 4,918 of these patients had arterial carbon dioxide tension data available at 24 hou

45 Large reductions (> 20 mm Hg) in arterial carbon dioxide tension over 24 hours were assoc

46 Initial arterial carbon dioxide tension tension was independentl

47 -2.59; p = 0.04), independent of the initial arterial carbon dioxide tension.

48 ative stress, has emerged as a biomarker for arterial cardiovascular disease.

49 Arterial cardiovascular events are the leading cause of

50 icroorganisms in central venous catheter and arterial catheter-related bloodstream infections and col

51 ients were unsuitable or refractory to trans-arterial chemoembolization (TACE) and stereotactic body

52 Intra-arterial chemotherapy (IAC) has been reported to more ef

53 n her left eye, 3 years after the last intra-arterial chemotherapy (IAC) injection.

54 sculature resulting from disrupted bronchial arterial circulation appears to trigger chronic lung all

55 We recently developed a bronchial-arterial-circulation-sparing (BACS) lung preservation ap

56 iving rise to HSPCs that accumulate in intra-arterial clusters (IAC) before colonizing the fetal live

57 ry pattern in response to dynamic changes in arterial CO(2) levels and, based on a learning algorithm

58 n and ventilation inhomogeneity improved but arterial CO2 increased despite unchanged respiratory rat

59 ary vascular resistance (PVR), and pulmonary arterial compliance (PAC) were measured.

60 both the usefulness and the safety of intra-arterial computed tomography angiography (IA-CTA) with u

61 The arterial connections in the Circle of Willis are a centr

62 maximum constriction (p = 0.0003) and lower arterial constriction slope (p = 0.0131).

63 PDE9a inhibition increased the ventricular-arterial coupling ratio, reflecting impaired systolic fu

64 d lusitropic reserve, as well as ventricular-arterial coupling, in the healthy heart during rest, as

65 Intra-arterial CTA with ultra-low volume of iodine contrast se

66 AVF maturation associated with preoperative arterial diameter (adjusted odds ratio [aOR], 1.50 per 1

67 AVF maturation associated with preoperative arterial diameter (aOR, 1.36 per 1-mm increase; 95% CI,

68 study evaluating the effect of preoperative arterial diameter and other hemodynamic factors on AVF m

69 Preoperative arterial diameter may be an under-recognized predictor o

70 eurons drove changes in the basal and evoked arterial diameter without corresponding changes in popul

71 orresponding increases or decreases in basal arterial diameter.

72 ed the association of early optimal brachial arterial dilatation with a successful AVF maturation and

73 ctly on smooth muscle cells (SMCs) to induce arterial dilation and increase local blood flow(1).

74 Patients with peripheral arterial disease (PAD) are at increased risk of cardiova

75 ation, cardiac revascularization, peripheral arterial disease intervention, or cardiovascular death.

76 quality of life similarly compared to other arterial disease level groups, they underwent revascular

77 -enhanced MR angiography revealed peripheral arterial disease not recognized with duplex US and was m

78 ascular risk score (Second Manifestations of Arterial Disease risk score) (RR, 1.01; 95% CI: 1.00, 1.

79 ular accident, heart failure, and peripheral arterial disease), kidney disease (a composite of ESKD o

80 tion, 1.78 (95% CI 1.53-2.07) for peripheral arterial disease, 1.32 (95% CI 1.15-1.50) for cerebrovas

81 vessels for diameter, stenosis or occlusion, arterial disease, and central stenosis.

82 ary heart disease, heart failure, peripheral arterial disease, asthma, chronic kidney disease, diabet

83 on of kidney disease, stroke, and peripheral arterial disease.

84 ith chronic coronary syndromes or peripheral arterial disease.

85 ascertainment bias, our results suggest that arterial dissection is one mechanism by which pregnancy

86 chial adipose tissue in determining brachial arterial distensibility.

87 current ischaemic event (stroke/TIA/systemic arterial embolism) and delayed symptomatic intracranial

88 initial results suggest that selective intra-arterial embolization is a safe and painless procedure t

89 ved growth factor (PDGFB) in human pulmonary arterial endothelial (HPAE) cells.

90 BATII) epithelial cells and bovine pulmonary arterial endothelial cells (BPAECs).

91 We obtain pulmonary arterial endothelial cells (PAECs) from lungs of patient

92 its oxidized phospholipid content, activates arterial endothelial cells, facilitating increased trans

93 is more effective than 600 IU/d in improving arterial endothelial function, arterial stiffness, centr

94 Arterial, endothelial, venous, angiogenic, and mural cel

95 ilia workup in patients after an unexplained arterial event.

96 S), apart from inferior OS for patients with arterial events (aHR, 1.53; 95% CI, 1.12-2.08) in Myelom

97 ), suggesting that MPN patients experiencing arterial events after MPN diagnosis deserve careful clin

98 e most significant correlate of simultaneous arterial FGF23 levels.

99 articipants, together with reference ECG and arterial finger PPG signals for validation.

100 HGPS-iPSC SMCs cultured under arterial flow conditions detach from the chip after a fe

101 sponses, as well as thrombus formation under arterial flow conditions on collagen and atherosclerotic

102 n significantly decreased perfusion (DCE MRI arterial flow, P = .002; IVIM pseudodiffusion coefficien

103 l conduit that returns filtered interstitial arterial fluid and tissue metabolites to the blood circu

104 Standard deviation of DCE MRI parameter arterial fraction was selected as the optimal predictor

105 crophages thereby maintaining a strengthened arterial framework refractory to AAA.

106 ssfully demonstrated the putative human para-arterial glymphatic transports and meningeal lymphatics

107 d-term patency rates between vein grafts and arterial grafts when veins are used as a composite graft

108 enable improved mechanistic understanding of arterial growth and remodeling in health and disease, an

109 , that can achieve instant and durable intra-arterial hemostasis regardless of coagulopathy, is devel

110 nary arteries (PAAF) of idiopathic pulmonary arterial hypertension (IPAH) patients and healthy donors

111 PAE cells isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those

112 existing coronary artery disease (n=31), 33% arterial hypertension (n=75), and 12% diabetes mellitus

113 prevalence of diabetes mellitus (P = 0.16), arterial hypertension (P = 0.45), chronic obstructive pu

114 Pulmonary arterial hypertension (PAH) is a disease characterized b

115 Pulmonary arterial hypertension (PAH) is a fatal disease character

116 Pulmonary arterial hypertension (PAH) is a lethal vasculopathy.

117 Rationale: Pulmonary arterial hypertension (PAH) is a life-shortening conditi

118 Pulmonary arterial hypertension (PAH) is a rare, fatal, and incura

119 Pulmonary Arterial Hypertension (PAH) is overrepresented in People

120 In pulmonary arterial hypertension (PAH), endothelial dysfunction and

121 Another is pulmonary arterial hypertension (PAH), where gravitational gradien

122 namic characteristics, response to pulmonary arterial hypertension (PAH)-approved drugs, and transpla

123 le on racial/ethnic differences in pulmonary arterial hypertension (PAH).Objectives: Determine effect

124 dysfunction is a characteristic of systemic arterial hypertension (SAH) and an early marker of ather

125 a rare, inherited disorder characterized by arterial hypertension and hyperkalemia with metabolic ac

126 and/or genetic conditions (such as systemic arterial hypertension and phaeochromocytoma), which vari

127 Arterial hypertension is the most prevalent modifiable r

128 15 patients per center; three centers) with arterial hypertension underwent standardized 3-T baselin

129 A clinical history of arterial hypertension was present in 10 857 (78%) partic

130 tion, iSM-Gprc5b-KO mice were protected from arterial hypertension, and this protective effect was ab

131 previously genetically linked with pulmonary arterial hypertension, as a major component of the mamma

132 f any systemic parameter including diabetes, arterial hypertension, previous cardiovascular and cereb

133 mutations have been implicated in pulmonary arterial hypertension, whereas the role of TGFbeta in th

134 fibrosis in human and experimental pulmonary arterial hypertension.

135 Because arterial hypotension is frequently a trigger for adminis

136 Intra-arterial (IA) infusion of mannitol induces osmotic blood

137 Valvulo-arterial impedance (Z(va)), which reflects total left ve

138 eta [95% CI]: 0.192 [0.030-0.353], P=0.020), arterial inflammation (0.203 [0.055-0.351], P=0.007), an

139 tomography; AmygA, bone marrow activity, and arterial inflammation were quantified.

140 o through decreased bone marrow activity and arterial inflammation.

141 uction in MACE risk, potentially via reduced arterial inflammation.

142 on studies before and after acute intrarenal arterial infusion of candesartan (4.2 mug kg(-1) ) or in

143 Additionally, we demonstrate that intra-arterial infusion of capsaicin results in a dose-related

144 in vascular conductance (FVC) to local intra-arterial infusion of phenylephrine (PE; alpha(1) -agonis

145 od reconstructs 3D neointima formation after arterial injury and allows for volumetric analysis of re

146 od, isolated platelets, and animal models of arterial injury.

147 ted as a reference standard representing the arterial input function (AIF).

148 es were collected as the reference standard (arterial input function [AIF]).

149 mouse brain without the need to consider an arterial input function and may find potential applicati

150 concentration (BP(P)) were derived using an arterial input function-based kinetic analysis.

151 aphical analysis with a metabolite-corrected arterial input function.

152 Metabolite-corrected arterial input functions were measured.

153 In comparison to SBP, Doppler-derived arterial load indices correlate more strongly with LV hy

154 ared with controls, and that Doppler-derived arterial load indices would be a better predictor of LVM

155 sponders after fluid bolus were similar, the arterial load parameters did not change in mean arterial

156 c filling pressure-central venous pressure), arterial load properties (systemic vascular resistance i

157 ment led to the deposition of NETs along the arterial lumen, and inhibition of NET release annulled l

158 cluding Bowman's capsule, tubules, arteries, arterial lumina, and veins.

159 ALI-induced HMGB1 leaks and is captured by arterial macrophages thereby altering their mitochondria

160 tablish an inter-organ circuitry that alerts arterial macrophages to regulate vascular remodeling.

161 its application to mouse-specific models of arterial mechanics using an experimentally informed four

162 ar smooth muscle cells (VSMCs) in the normal arterial media continually express contractile phenotypi

163 LP expression (mineralization marker) in the arterial media.

164 he lineage relationships between epicardium, arterial mesothelial cells (AMCs), and the coronary vasc

165 Arterial %MT and %IT of nonobstructed lung territories a

166 e-activation in pericytes, without affecting arterial mural cells.

167 Arterial myeloid cell adhesion was quantified by intravi

168 itability, [Ca(2+)](i), and myogenic tone in arterial myocytes.

169 receptors to induce Ca(2+) sparks in native arterial myocytes.

170 at it is based exclusively on data from male arterial myocytes.

171 nase anchoring protein 5 (AKAP5) function in arterial myocytes.

172 es at the plasma membrane of human and mouse arterial myocytes.

173 eased blood flow are prevented in AKAP5 null arterial myocytes/arteries.

174 Peripheral arterial narrowing is associated with increasing nonperf

175 g create an O(2) delivery (i.e. blood flow x arterial [O(2) ], QO2 ) dependency that slows VO2 kineti

176 ertension (CTEPH) is the result of pulmonary arterial obstruction by organized thrombotic material st

177 ammation (IOI), endophthalmitis, and retinal arterial occlusion in the phase 3 HAWK and HARRIER trial

178 Major arterial or venous thromboembolism, major adverse cardio

179 acent arterioles than venules, supporting an arterial origin for DH.

180 nstrated slower flow speeds, whereas that of arterial origin showed relatively high flow speeds.

181 erformance in acute hypoxia through a higher arterial oxygen content and an unchanged pulmonary gas e

182 During maximal KE, both convective arterial oxygen delivery to the skeletal muscle microvas

183 ne, in patients with COPD who have nocturnal arterial oxygen desaturation without qualifying for long

184 Despite no difference in end-exercise arterial oxygen tension in hypoxia (59 +/- 6 vs. 59 +/-

185 radiological and partial pressure of oxygen, arterial (Pao2)/fraction of inspired oxygen (Fio2) crite

186 ingeal lymphatics by clear depiction of para-arterial, parasinus, and paravenous meningeal contrast e

187 as those with a lowest achievable first-day arterial partial pressure of CO2 of >=60 mm Hg.

188 utrophil-derived microvesicles may influence arterial pathophysiology.

189 TN selectively controls lung ventilation and arterial Pco(2) stability.

190 F; +10-20%) mediated via small elevations in arterial PCO2 and metabolism.

191 arkedly increasing CMRO(2) , irrespective of arterial pH.

192 ination, including pre-contrast phase (PCP), arterial phase (AP), and portal venous phase (PVP) scans

193 responders were defined as CI >=10% and mean arterial pressure >=10%, respectively.

194 usion or intervention, hypotension (systolic arterial pressure <=90 mm Hg), and pneumonia.

195 ation, terlipressin decreased mean pulmonary arterial pressure (-6.5 +/- 1.8 mm Hg; p = 0.005) and te

196 Hypotension was defined as a mean arterial pressure (MAP) below 65 mm Hg for at least 1 mi

197 The measured mean arterial pressure (MAP) exhibited measurable deviation f

198 BP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) were significantly (P < 0.05) re

199 class (WHO FC); and change in mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance

200 1) and a two-fold increase in mean pulmonary arterial pressure (p < 0.0001) compared with baseline.

201 as low recruiters experienced lower systolic arterial pressure (P = 0.008).Conclusions: A single-brea

202 sin II caused a significant increase in mean arterial pressure and a rapid reduction in catecholamine

203 assessed for each time-weighted-average-mean arterial pressure and cumulative-time-below mean arteria

204 timate Pglom in patients from combined renal arterial pressure and flow measurements.

205 and the hypoxia-induced CR (O(2) -CR), mean arterial pressure and heart rate were significantly grea

206 ru), a setting that increases both pulmonary arterial pressure and sympathetic outflow.

207 l mice, Pkd1 knockout mice exhibited reduced arterial pressure during high salt intake; this associat

208 s the need for vasopressors to maintain mean arterial pressure greater than or equal to 65 mm Hg and

209 ained by transcranial Doppler sonography and arterial pressure in the radial artery was obtained by t

210 Mean arterial pressure is critically important in patients wi

211 In humans, pulmonary arterial pressure is positively related to basal muscle

212 nificant associations only remained for mean arterial pressure less than 65 mm Hg (odds ratio, 1.07;

213 oach, we demonstrate that reducing pulmonary arterial pressure lowers basal MSNA in healthy humans.

214 These data suggest that maintaining a mean arterial pressure of greater than 65 mm Hg may be a reas

215 The mean arterial pressure response to fluid bolus in cardiac ICU

216 eat fluid bolus based solely on lack of mean arterial pressure response to the initial fluid, since t

217 rial pressure and cumulative-time-below mean arterial pressure threshold (55, 60, 65, 70, and 75 mm H

218 ters, grafting RN-NSCs restored resting mean arterial pressure to normal levels and remarkably allevi

219 Mean arterial pressure was slightly higher in SHR but within

220 pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen satura

221 s to describe changes in cardiac index, mean arterial pressure, and their relationship to other indic

222 tcomes included 24-hour survival rates, mean arterial pressure, lactate, hemoglobin, and estimated in

223 erial load parameters did not change in mean arterial pressure-nonresponders.

224 Cardiac index responders and mean arterial pressure-responders were defined as CI >=10% an

225 Cardiac index-responsiveness and mean arterial pressure-responsiveness rates were 33% and 56%,

226 etween cardiac index-responsiveness and mean arterial pressure-responsiveness.

227 Neither candesartan nor CAP affected arterial pressure.

228 strongly correlated with pulse and systolic arterial pressures and with total arterial stiffness, re

229 reduction of right ventricular and pulmonary arterial pressures, toward normal levels of right-side p

230 match the experimental results and show that arterial pulsations only drive oscillatory motion of CSF

231 The arterial pulse recording morphology was compared against

232 paB occurred within 30 min after exposure to arterial rates of shear stress.

233 ultaneous venous resections, and 101 (85.5%) arterial reconstructions.

234 of the largest cohort of pancreatectomy with arterial resection (P-AR).

235 r, there remains unmet therapeutic needs for arterial revascularization and ischemic tissue repair.

236 For example, some hotspots were on arterial roads with an upstream signalized intersection

237 Arterial sampling was used to measure plasma input funct

238 n characterization of 88 of 236 (37%) of the arterial sections examined as unsuitable for AVF creatio

239 Resected arterial segments included the coeliac trunk (50), hepat

240 racterization of such complex, heterogeneous arterial segments.

241 In cultured coronary arterial smooth muscle cells (CASMCs) from Asah1(fl/fl)/

242 tion, as well as the expression of CD47 from arterial smooth muscle cells in mice.

243 The accepted role of the protein Kv2.1 in arterial smooth muscle cells is to form K(+) channels in

244 s) and raised intracellular Ca(2+) levels in arterial smooth muscle cells, constricted arterioles ex

245 he expression of CD47 and other oncogenes in arterial smooth muscle cells.

246 Delta-like ligand 4 (Dll4), the arterial-specific Notch ligand, is expressed by second h

247 Purpose To determine if arterial spin labeled (ASL) MRI perfusion changes are as

248 Arterial spin labeling (ASL) is a neuroimaging technique

249 MR angiography, carotid plaque imaging, and arterial spin labeling (ASL) to identify imaging paramet

250 Arterial spin labeling (ASL), as a non-invasive and non-

251 Magnetic resonance imaging with pulsed arterial spin labelling provided serial measurements of

252 In a subset of 112 participants who received arterial spin labelling scans, faster aortic stiffening

253 In analyses of arterial spin-labeled (ASL) MRI, nonresponders exhibited

254 R 1.42, 95% CI 0.96 to 2.10) and ipsilateral arterial stenosis with 50%-99% narrowing (HR 1.54, 95% C

255 Strategies to prevent arterial stiffening prior to this point may be required

256 femoral pulse-wave velocity (cfPWV) measured arterial stiffness 2, 12, 24, and 42 weeks post-ART init

257 There are sex differences in arterial stiffness and neural control of blood pressure

258 induce an amelioration in vascular function, arterial stiffness and vascular remodelling by improving

259 Vascular function, arterial stiffness and vascular remodelling were evaluat

260 e if vitamin K supplementation might improve arterial stiffness in patients in CKD, we conducted a pa

261 Vascular function improved and arterial stiffness reduced in the arteries involved and

262 Arterial stiffness was assessed in two medical examinati

263 pheral (carotid-radial artery PWV, PWV(CR) ) arterial stiffness was measured by pulse-wave velocity (

264 ng heart contractility, myocyte hypertrophy, arterial stiffness, and systemic resistance.

265 in improving arterial endothelial function, arterial stiffness, central and systemic blood pressure

266 d systolic arterial pressures and with total arterial stiffness, regardless of the preload dependence

267 anges at 3 and 6 mo in endothelial function, arterial stiffness, systemic-systolic BP, lipids, and in

268 aser Doppler imaging with iontophoresis, and arterial stiffness, using pulse wave analysis.

269 tween residential surrounding greenspace and arterial stiffness.

270 12 suppression in ALI-inflicted mice repress arterial stress and brake MMP12 release by transmural ma

271 Our data demonstrate that an arterial surgical approach is effective in LAPC with pro

272 th factor (VEGF) could be implanted into the arterial system of a pre-clinical ovine animal model, wh

273 ti-Platelet Trialists' Collaboration-defined arterial thromboembolic events was 1.9%, 0.9%, 1.1%, 2.1

274 of the role of hypercoagulable disorders in arterial thrombosis and discuss our approach to thrombop

275 incidence of and risk factors for venous and arterial thrombosis in patients hospitalized with COVID-

276 nticoagulant therapy for suspected pulmonary arterial thrombosis or thromboembolism.

277 djustment for confounders, the occurrence of arterial thrombosis remained independently associated wi

278 erial thrombus stability in a mouse model of arterial thrombosis using intravital microscopy.

279 botic or pro-inflammatory conditions such as arterial thrombosis.

280 platelet aggregates is a critical process in arterial thrombosis.

281 fect that impacts on platelet reactivity and arterial thrombosis.

282 We found that rivaroxaban reduced arterial thrombus stability in a mouse model of arterial

283 ding microstructural insight into changes in arterial tissue by exploring how cell, collagen and elas

284 hanges in the microstructural composition of arterial tissue, specifically pointing to cell, not coll

285 blood flow is altered systemically, from the arterial to the venous circulation.

286 id, since the implications include decreased arterial tone even if the cardiac index increases.

287 tial effect of arrhythmias on the peripheral arterial tonometry (PAT) amplitude and pulse rate change

288 est attention but, over the past decade, the arterial toxic effects, which can present as acute vasos

289 t diffusion coefficient (ADC) parameters and arterial tumor enhancement were tested for ability to ch

290 ns and other mammals identified differential arterial-venous proteoglycan dynamics as a determinant o

291 d Western blot confirmed PTH1R expression in arterial VSM that was reduced by Cre-mediated knockout.

292 n and the atherogenic gene expression in the arterial wall and aortic sinus induced by severe periodo

293 minent autofluorescent particles in the pial arterial wall and in neocortical parenchyma of young, dr

294 he presence of CD8+CD161+ lymphocytes in the arterial wall of two unruptured intracranial aneurysms.

295 eir peaceful integration within the coronary arterial wall.

296 elimination of solutes from the brain along arterial walls is driven by low-frequency arteriolar osc

297 ection and pathologic invasion of venous and arterial walls were 52.4%, 74.2%, and 58%, respectively.

298 with this, ex vivo exposure of LSVs to acute arterial WSS promoted monocyte interactions with the ves

299 ion of the NF-kappaB pathway prevented acute arterial WSS-induced CCL2 production and reduced monocyt

300 is necessary for the induction of the acute arterial WSS-induced pro-inflammatory response.