ライフサイエンスコーパス: small vessel

1 roke (ischemic, large artery, cardioembolic, small vessel).

2 ts, substantially affecting intermediate and small vessels.

3 rly in the endothelial cells of intratumoral small vessels.

4 through an intricate network of penetrating small vessels.

5 nvestment with mural cells of both large and small vessels.

6 y impacts the visualization of blood flow in small vessels.

7 and heterogeneity of proportion of perfused small vessels 35 [20-50]%).

8 ere markedly altered (proportion of perfused small vessels 65 [50-74]%, microvascular flow index 2.15

9 of alterations in the proportion of perfused small vessels (70% and 75% in the two upper proportion o

10 than in the earlier (proportion of perfused small vessels, 74 [57-82]% vs. 63 [48-71]%, p = 0.004) p

11 characterized by inflammatory destruction of small vessels accompanied by enhanced cleavage of membra

12 (0.68, 0.51-0.92; p=0.01), and compared with small vessel and cardioembolic subtypes, they had no exc

13 Measures of small vessel and cardiovascular disease (white matter hy

14 f socioeconomic status (SES) and measures of small vessel and cardiovascular disease on observed race

15 microinfarcts can be manifestations of both small vessel and large vessel disease, that cerebral mic

16 ds better image quality for visualization of small vessels and lung parenchyma.

17 e analysis identified proportion of perfused small vessels and sequential organ failure assessment sc

18 uring the shear stress imposed by navigating small vessels and sinusoids.

19 For discovery, 365 cases of ischemic stroke (small-vessel and large-vessel subtypes) and 809 European

20 ocated within the alveolar septa, 14% around small vessels, and 7% around the airways.

21 le-shaped erythrocytes disrupt blood flow in small vessels, and this vaso-occlusion leads to distal t

22 rent fibres located in the adventitia of the small vessels appear to respond to the level of venular

23 ECs in both large and small vessels are influenced by hyperglycemic conditions

24 provides considerable insights; although the small vessels are not easily seen themselves, the effect

25 cerebral large vessel (atherosclerosis) and small vessel (arteriolosclerosis) disease.

26 vale PVS might indicate different underlying small vessel arteriopathies according to PVS anatomical

27 reflect shared pathobiology predisposing to small vessel arteriopathy.

28 A concomitant small-vessel arteriopathy in addition to major pulmonary

29 on is to assess the presence and severity of small-vessel arteriopathy.

30 ns of large pulmonary arteries combined with small-vessel arteriopathy.

31 e-rate, which is important for contrast-free small vessel blood flow imaging.

32 We conclude that small vessel brain disease seems to affect chronic aphas

33 provides insight into the pathophysiology of small vessel brain disease, and its relationship with br

34 gnetic resonance imaging (MRI) biomarkers of small vessel brain injury, including strictly lobar cere

35 trials are probably applicable also to other small-vessel brain diseases.

36 e (CFR), an integrated measure of large- and small-vessel CAD and myocardial ischemia, identifies pat

37 Small vessel caliber, significant calcification or ather

38 of cardiovascular disease but lower odds of small-vessel cerebral vascular disease.

39 s in the retinal microvasculature may mirror small vessel cerebrovascular changes in AD.

40 aging (MRI) scans that most commonly reflect small vessel cerebrovascular disease.

41 The impact of small-vessel cerebrovascular disease, visualized as whit

42 ical mechanism of KD from the perspective of small vessels changes.

43 reperfusion, vascular density, and number of small vessels compared with nondiabetic Prkcd(+/+) mice.

44 an integrated measure of focal, diffuse, and small-vessel coronary artery disease (CAD), identifies p

45 However, perfused small-vessel density, small-vessel density, and percent perfused vessels were

46 However, perfused small-vessel density, small-vessel density, and percent

47 The most common abnormal finding was small vessel disease (20%).

48 n midlife was associated with development of small vessel disease (adjusted odds ratio [OR] = 1.47 [9

49 cognitive impairment, but also for cerebral small vessel disease (CSVD) and Abeta-positivity.

50 lic fatty liver disease (NAFLD) and cerebral small vessel disease (CSVD) burden, especially according

51 Cerebral small vessel disease (cSVD) is a heterogeneous group of

52 pression hypothesis postulates that cerebral small vessel disease (CSVD) leads to depressive symptoms

53 In a rat model of cerebral small vessel disease (cSVD), solute transport in the per

54 us early and late manifestations of cerebral small vessel disease (eg, microbleeds and white matter h

55 tinct histopathological variants of cerebral small vessel disease (lobar for cerebral amyloid angiopa

56 Small vessel disease (mainly hypertensive arteriopathy a

57 Participants with small vessel disease (n = 118; mean age = 68.9 years; 65

58 rs than the large artery disease (p<0.0001), small vessel disease (p=0.001), and cardioembolic (p=0.0

59 Imaging markers of small vessel disease (SVD) (white matter hyperintensitie

60 Small vessel disease (SVD) and amyloid deposition may pr

61 Associations between cerebral small vessel disease (SVD) and inflammation have been la

62 led 23 patients with MS and 11 patients with small vessel disease (SVD) and performed standardized 3-

63 dy was undertaken to assess whether cerebral small vessel disease (SVD) computed tomographic (CT) bio

64 tients with late-onset AD have more comorbid small vessel disease (SVD) contributing to clinical seve

65 The term cerebral small vessel disease (SVD) describes a range of neuroima

66 Cerebral small vessel disease (SVD) is a common accompaniment of

67 Cerebral small vessel disease (SVD) is a common cause of vascular

68 Cerebral small vessel disease (SVD) is a leading cause of stroke

69 Cerebral small vessel disease (SVD) is characterised by progressi

70 Cerebral small vessel disease (SVD) is characterized by changes i

71 ular smooth muscle, is a genetic paradigm of small vessel disease (SVD) of the brain.

72 to assess whether and how single markers of small vessel disease (SVD) or a combination thereof expl

73 with loss of microvascular function, termed small vessel disease (SVD) underlying different potentia

74 arterioles (PAs), a major target of cerebral small vessel disease (SVD), and determined whether relax

75 aneous intracerebral hemorrhage (ICH) due to small vessel disease (SVD), but the association between

76 ost common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main

77 is a neurological syndrome characterized by small vessel disease (SVD), stroke, and vascular cogniti

78 association is possibly mediated by cerebral small vessel disease (SVD), which has been associated wi

79 lacunar strokes are associated with cerebral small vessel disease (SVD), which is the commonest vascu

80 he brain and may reflect underlying cerebral small vessel disease (SVD).

81 e of white matter lesion related to cerebral small vessel disease (SVD).

82 ingly recognized, particularly from cerebral small vessel disease (SVD).

83 -associated manifestations of human cerebral small vessel disease (SVD).

84 hy and magnetic resonance imaging markers of small vessel disease (white matter hyperintensities or l

85 ischaemic and haemorrhagic manifestations of small vessel disease [small vessel stroke: 11 710 cases,

86 for precisely how amyloid-beta and cerebral small vessel disease affect cognitive impairment remain

87 amyloid angiopathy is a common, well-defined small vessel disease and a largely untreatable cause of

88 we scored the severity of arteriolosclerotic small vessel disease and cerebral amyloid angiopathy, an

89 investigations into the connections between small vessel disease and delayed seizures are warranted.

90 of cognitive dysfunction in stroke, cerebral small vessel disease and dementia.

91 The resulting cerebral small vessel disease and heart failure may contribute to

92 non-demyelinating disorders such as chronic small vessel disease and other inflammatory, granulomato

93 continuum between genes underlying Mendelian small vessel disease and those contributing to the commo

94 ion, white matter microstructural changes in small vessel disease are associated with apathy but not

95 Y ON THIS ARTICLE: Amyloid-beta and cerebral small vessel disease are the two major causes of cogniti

96 pathy and depression can be distinguished in small vessel disease both in terms of their relative rel

97 ctural imaging features to gauge total brain small vessel disease burden in CAA.

98 The cerebral small vessel disease burdens were assessed with white ma

99 evelopment of vascular dementia and cerebral small vessel disease but not between atherosclerosis and

100 e considered for the prevention of ischaemic small vessel disease but the net benefit of such an appr

101 posite MRI-derived phenotype for extremes of small vessel disease can facilitate the identification o

102 CADASIL is a genetic paradigm of cerebral small vessel disease caused by NOTCH3 mutations that ste

103 nges, which may contribute to post-stroke or small vessel disease dementia.

104 ee of apathy and depression found within the small vessel disease group.

105 ut suggest that an excess burden of cerebral small vessel disease in multiple sclerosis may explain t

106 kely harbor a more advanced form of cerebral small vessel disease in need of efficacious therapeutic

107 ease; 2) that imaging biomarkers of cerebral small vessel disease in POAG and NTG will show different

108 ns in older adults with and without cerebral small vessel disease in vivo.

109 Cerebral small vessel disease is a common condition associated wi

110 Small vessel disease is a disorder of cerebral microvess

111 Cerebral small vessel disease is a major cause of stroke and deme

112 Small vessel disease is a stroke subtype characterized b

113 Small vessel disease is associated with high rates of ap

114 cally atherosclerosis, is lower and cerebral small vessel disease is higher in multiple sclerosis cas

115 fected by pathological changes when cerebral small vessel disease is present.

116 suggest that apathy, but not depression, in small vessel disease is related to damage to cortical-su

117 tween systemic vascular disease and cerebral small vessel disease is stronger in patients with multip

118 MR evidence of cerebral small vessel disease is strongly associated with a diagn

119 thy (CARASIL), an inherited form of cerebral small vessel disease leading to early-onset stroke and p

120 =3 sulci; disseminated, >/=4 sulci), and key small vessel disease markers.

121 we hypothesized that CSF markers related to small vessel disease may also be applicable as biomarker

122 on testing for acquired causes, on excluding small vessel disease mimics, and detailed advice on meta

123 Moreover, small vessel disease of the brain has been estimated to

124 integrity; and (iii) the effect of cerebral small vessel disease on cognition.

125 predict concurrent beta-amyloid deposition, small vessel disease or Alzheimer's disease-pattern neur

126 Although severe small vessel disease or cerebral amyloid angiopathy may

127 e lowest in cortex from patients with severe small vessel disease or cerebral amyloid angiopathy, nei

128 se (i.e. atherosclerosis) and/or of cerebral small vessel disease or worse multiple sclerosis patholo

129 with SVS, we assessed its influence on other small vessel disease phenotypes, as well as on messenger

130 , and targets for lipid-modifying drugs with small vessel disease phenotypes.

131 atherosclerosis, but their role in cerebral small vessel disease remains largely elusive.

132 evidence of concept validity of a total MRI small vessel disease score in CAA.

133 nd pons was used to obtain a global cerebral small vessel disease score that captured the presence an

134 corporated into a prespecified ordinal total small vessel disease score, ranging from 0 to 6 points.

135 independently associated with the total MRI small vessel disease score.

136 us on systemic vascular disease and cerebral small vessel disease scores and, in the multiple scleros

137 mes throughout 5 years between patients with small vessel disease treated with ultrathin-strut BP-SES

138 es at known pathogenic variants for familial small vessel disease within NOTCH3 and HTRA1.

139 with progression of WMH burden (a marker of small vessel disease).

140 rly during sleep, and in the pathogenesis of small vessel disease, Alzheimer disease and other neurod

141 artery atherosclerosis, cardioembolism, and small vessel disease, and defined shared genetic influen

142 sights into the longitudinal pathogenesis of small vessel disease, and imply that therapies aimed at

143 dentification of genetic variants underlying small vessel disease, both common variants and those wit

144 uent measurements of MRI markers of cerebral small vessel disease, brain tissue volumes, and white ma

145 e potential neuroimaging markers of cerebral small vessel disease, but their functional significance

146 e severity of structural vascular pathology (small vessel disease, cerebral amyloid angiopathy or VWF

147 In small vessel disease, cerebrospinal fluid (CSF) markers

148 to detect novel genetic factors for cerebral small vessel disease, elucidating underlying disease mec

149 gnitive impairment, and other MRI markers of small vessel disease, in a patient cohort of ischaemic s

150 Cerebral small vessel disease, including microvascular lesions, i

151 l changes, including MRI markers of cerebral small vessel disease, smaller brain tissue volumes, and

152 Background Lesions of cerebral small vessel disease, such as white matter hyperintensit

153 WMHs) are a common manifestation of cerebral small vessel disease, that is increasingly studied with

154 have an impact in diseases such as cerebral small vessel disease, the leading cause of vascular deme

155 oke and is a major manifestation of cerebral small vessel disease, the primary cause of vascular cogn

156 dinal cohort of 99 subjects with symptomatic small vessel disease, who were followed-up for >/=1 year

157 re the most acute manifestations of cerebral small vessel disease, with no established preventive app

158 atter lesions (WMLs)-an imaging surrogate of small vessel disease-are associated with a higher rate o

159 n candidate gene studies with other cerebral small vessel disease-related traits strengthens the cred

160 ith lacunar infarct (LI), a type of cerebral small vessel disease.

161 (MRI) are a neuroimaging marker of cerebral small vessel disease.

162 r spaces may reflect the underlying cerebral small vessel disease.

163 d venular diameter, and markers for cerebral small vessel disease.

164 dase pathway in the pathogenesis of cerebral small vessel disease.

165 neuroimaging and genetic markers of cerebral small vessel disease.

166 Disease-type disease rather than to cerebral small vessel disease.

167 , which belongs to the continuum of cerebral small vessel disease.

168 whole brain atrophy in symptomatic cerebral small vessel disease.

169 finding appears to be related to underlying small vessel disease.

170 ibutions to quality of life in patients with small vessel disease.

171 ld identify a homogeneous subpopulation with small vessel disease.

172 ebrovascular diseases secondary to large and small vessel disease.

173 bnormalities, resemble symptoms and signs of small vessel disease.

174 function over time in patients with cerebral small vessel disease.

175 EPVS) are a promising neuroimaging marker of small vessel disease.

176 ding of the biological mechanisms underlying small vessel disease.

177 ge for verbal memory performance in cerebral small vessel disease.

178 g 2109 patients, 1234 (59%) were treated for small vessel disease.

179 f older persons for gene-mapping of cerebral small vessel disease.

180 percutaneous coronary revascularization for small vessel disease.

181 improve risk prediction for individuals with small vessel disease.

182 neuroimaging and genetic markers of cerebral small vessel disease: APOE variants epsilon2/epsilon4, c

183 nes known to harbour mutations for Mendelian small vessel disease: NOTCH3, HTRA1, COL4A1, COL4A2 and

184 coma is associated with evidence of cerebral small vessel disease; 2) that imaging biomarkers of cere

185 ith the hypothesis that PVS reflect cerebral small vessel disease; the different associations for bas

186 This radiological detection of small vessels disease is important because there are no

187 because of chronic joint pain or evidence of small-vessel disease (0.7%).

188 Patients with cerebral small-vessel disease (CSVD) exhibit perturbed end-artery

189 ear if and how associations between cerebral small-vessel disease and Alzheimer disease (AD) patholog

190 ebral amyloid angiopathy is a common form of small-vessel disease and an important risk factor for co

191 luable technique for assessing the degree of small-vessel disease and postoperative outcome after PEA

192 bidities, cognition, hippocampal volume, and small-vessel disease but not on gait speed (0.85 vs 0.92

193 sought to assess the presence and degree of small-vessel disease in patients with chronic thromboemb

194 adjuvant therapies and subclinical cerebral small-vessel disease in survivors of breast cancer.

195 and to magnetic resonance imaging markers of small-vessel disease including increased white matter hy

196 Although cerebral small-vessel disease is an important cause of cognitive

197 of frontal-subcortical circuits by cerebral small-vessel disease is thought to predispose to depress

198 The mechanisms linking small-vessel disease to cognitive impairment are not wel

199 abetes, dyslipidemia, smoking, infarcts from small-vessel disease, and "other definite" causes and wo

200 appears aggravated in patients with cerebral small-vessel disease, especially in apolipoprotein E eps

201 alent CMBs, and markers of cerebral ischemic small-vessel disease, heavy alcohol consumption (vs ligh

202 lopathy (CADASIL), the most common inherited small-vessel disease, is associated with vascular aggreg

203 bnormal vascular development, which triggers small-vessel disease, recurrent hemorrhagic strokes, and

204 l large-vessel disease compared with that of small-vessel disease.

205 resting-state CBF is a marker of CMB-related small-vessel disease.

206 other magnetic resonance imaging markers of small-vessel disease.

207 bal brain atrophy and an increased burden of small-vessel disease.

208 arge-vessel and cardioembolic stroke but not small-vessel disease.

209 the brain are important markers of aging and small-vessel disease.

210 shown mixed results, with a major benefit in small-vessel disease.

211 es of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are

212 Our results also support the view that small vessel diseases such as CAA can cause cortical atr

213 wever, deep ICHs are rare in some aggressive small vessel diseases that are characterized by signific

214 inding and may be a useful endophenotype for small vessel diseases.

215 a common and important age-related cerebral small vessel disorder leading to intracerebral haemorrha

216 The small-vessel disorder cerebral autosomal dominant arteri

217 trends seen in the original images, whereas small vessels displayed different trends, with length an

218 Small-vessel dysfunction may be an important consequence

219 ent hyperglycemia during pregnancy may cause small-vessel dysfunction.

220 Microcirculatory blood flow in small vessels increased (2.8 [2.6; 3.0] vs 3.0 [3.0; 3.0

221 s a systemic autoimmune disease resulting in small-vessel inflammation caused by pathogenic autoantib

222 recipients with kidney disease secondary to small vessel injury.

223 c changes (i.e. morphological changes to the small vessels) instead of frank haemorrhages on histolog

224 RF/MRTF activity for maintenance of cerebral small vessel integrity.

225 kedly increased capacity to remodel existing small vessels into larger conduits.

226 Intracerebral haemorrhage and small vessel ischaemic stroke (SVS) are the most acute m

227 ed significant association of rs2293871 with small vessel ischaemic stroke, and two blood expression

228 ring the follow-up, or further adjusting for small-vessel ischaemic disease volumes.

229 association of diabetes characteristics with small vessel ischemic disease in the brain.

230 a 57% (95% CI = 29-91%) increase in risk for small vessel ischemic stroke, a 197% increase (95% CI =

231 s of presentation: 2 patients presented with small-vessel (lacunar) infarctions, whereas 1 patient pr

232 d IS, and the three subtypes (cardioembolic, small vessel, large vessel), using genome-wide SNP data.

233 R, sO2, cerebral BF and cerebral MRO2 at the small vessel level in a rodent model.

234 se deficiency may increase susceptibility to small vessel loss in IPAH.

235 ndothelial-pericyte interactions and prevent small vessel loss in PAH.

236 icyte interactions are linked to progressive small vessel loss in pulmonary arterial hypertension (PA

237 othelial-pericyte interaction contributes to small vessel loss in pulmonary arterial hypertension (PA

238 versible encephalopathy syndrome (PRES) is a small vessel microangiopathy of the cerebral vasculature

239 e absence of pretone by using a conventional small vessel myograph.

240 For small vessel occlusion (17.8%), outcomes tended to vary

241 classified as large artery atherosclerosis, small vessel occlusion, or cardioembolism.

242 atherosclerosis (LAA), cardio-embolism (CE), small-vessel occlusion (SVO), other determined aetiologi

243 performed GWAS for a major subtype of stroke-small-vessel occlusion (SVO)-to identify potential genet

244 thromboembolism rather than in situ cerebral small-vessel occlusion.

245 Conversely, small vessel occlusions (SVOs) had low levels of all imp

246 tes regulate VSMCs and vascular integrity in small vessels of deep brain regions.

247 shock patients improves density and flow in small vessels of sublingual microcirculation.

248 rt that >30% of the endothelial cells in the small vessels of the bone marrow and spleen of patients

249 ere are no technical possibilities to assess small vessels of the brain using computed tomography (CT

250 In small vessels of the retina, brain, and skeletal muscle,

251 d allows the majority of cells to escape the small vessels of the tissues before fibers form.

252 ocation may relate to the type of underlying small vessel pathology: those in the white matter centru

253 75% in the two upper proportion of perfused small vessel quartiles compared with 3% and 44% in the t

254 success in the biofabrication of large- and small-vessel replacements, functional microvasculature h

255 compared with patients with cardioembolic or small vessel stroke (CES/SVS) as a combined reference gr

256 nhibitors were associated with lower risk of small vessel stroke (OR: 0.82, 95% CI = 0.75-0.89) and l

257 a shared genetic contribution between AD and small vessel stroke (rG(SE)=0.37(0.17); p=0.011).

258 yet identified any associations solely with small vessel stroke (SVS).

259 cardioembolic (CES), large artery (LAS), and small vessel stroke (SVS).

260 y levels may be particularly associated with small vessel stroke (SVS).

261 L-C levels was associated with lower risk of small vessel stroke [odds ratio (OR) per standard deviat

262 cate shared genetic susceptibility to AD and small vessel stroke and highlight potential causal pathw

263 sification of stroke, 4 loci influenced both small vessel stroke and intracerebral hemorrhage.

264 les, is associated with both a lower risk of small vessel stroke and lower WMH volume.

265 ge were negatively correlated with those for small vessel stroke and WMH volume across all lipid trai

266 ny ischemic stroke, large artery stroke, and small vessel stroke but not cardioembolic stroke or intr

267 and pathway analysis in the combined AD and small vessel stroke datasets to identify the SNPs and mo

268 A meta-analysis of AD IGAP and METASTROKE+ small vessel stroke GWAS data highlighted a region (ATP5

269 ny ischemic stroke, large artery stroke, and small vessel stroke in all univariable MR analyses, but

270 ny ischemic stroke, large artery stroke, and small vessel stroke in the main and sensitivity univaria

271 chemic stroke, particularly large artery and small vessel stroke.

272 hemic stroke, in particular large artery and small vessel stroke.

273 agic manifestations of small vessel disease [small vessel stroke: 11 710 cases, 287 067 controls; whi

274 p = < 0.001, respectively) but not seen with small-vessel stroke (p = 0.811).

275 Compared with large artery and small vessel subtypes combined, patients with cryptogeni

276 olic stroke (23% vs 27% for large artery and small vessel subtypes combined; p=0.26) as was the 10-ye

277 In BVS-assigned patients, treatment of very small vessels (those with quantitatively determined refe

278 c-uremic syndrome (HUS) features episodes of small-vessel thrombosis resulting in microangiopathic he

279 parotomy often had ischemia, possibly due to small-vessel thrombosis.

280 est: a stream of the liquor is poured into a small vessel to induce surface bubbles.

281 In particular, small vessels treated with smaller stents were associate

282 icular are associated with distinct forms of small vessel vasculitides.

283 we discuss the differences between these two small-vessel vasculitides, focusing especially on possib

284 microdissected glomeruli from patients with small vessel vasculitis (SVV) had markedly higher levels

285 ic or soft plaques of the coronary arteries, small vessel vasculitis and small aneurysm.

286 omerular lesions with crescents, mimicking a small vessel vasculitis such as ANCA-associated GN, are

287 ischemic infarctions, presumed secondary to small vessel vasculitis.

288 arthritis, systemic lupus erythematosus, and small vessel vasculitis.

289 oup of disorders involving severe, systemic, small-vessel vasculitis and are characterized by the dev

290 strointestinal disease, febrile attacks, and small-vessel vasculitis characteristic of Behcet disease

291 three patients with polyarteritis nodosa or small-vessel vasculitis were homozygous for the p.Gly47A

292 granulomatosis with polyangiitis (eGPA) is a small-vessel vasculitis where 40% of patients present wi

293 th polyarteritis nodosa and one patient with small-vessel vasculitis.

294 patients with clinical manifestations due to small-vessel vasculitis.

295 nce in the sarcoma model, a higher amount of small vessels was detected in the tumor regions with hig

296 Blood velocity in the small vessels was estimated by tracking microbubbles, de

297 The proportions of perfused small vessels were (mean +/- scanning electron microscop

298 partmentalization of embolisms that occur in small vessels, while promoting high hydraulic conductivi

299 Histological features included lobules of small vessels within the dermis, resembling a tufted ang

300 ement of alveolar septa, distal airways, and small vessels within the secondary lobules of the lung.