ライフサイエンスコーパス: small vessel

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

2 nts (PES) for the reduction of restenosis in small vessels.

3 f large vessels and decreasing the number of small vessels.

4 g neutrophils adhere to and thereby obstruct small vessels.

5 ked decrease in vasculature, particularly in small vessels.

6 of cancer cell migration and deformation in small vessels.

7 ts, substantially affecting intermediate and small vessels.

8 rly in the endothelial cells of intratumoral small vessels.

9 7.7% versus 37.7%, P=0.01) and in those with small vessels (23.6% versus 35.2%, P=0.02), long lesions

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

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

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

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

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

15 (0.68, 0.51-0.92; p=0.01), and compared with small vessel and cardioembolic subtypes, they had no exc

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

17 rly period of sepsis, proportion of perfused small vessels and lactate were independent predictors of

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

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

20 Ang-2 was strongly expressed in small vessels and spindle tumor cells in KS tumors.

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

22 fail to remodel into a network of large and small vessels, and embryonic vessels show defective angi

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

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

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

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

27 We aimed to investigate whether these small vessels are specialized in terms of structure and

28 ted ischemic hearts had more capillaries and small vessels around the injection site, smaller infarct

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

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

31 nfarcts and leukoencephalopathy), a cerebral small-vessel arteriopathy, which thus complicates the ge

32 uggesting that they result from an occlusive small-vessel arteriopathy.

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

34 ction in endothelial cells of both large and small vessels, as well as in the myocardium.

35 TA selectively inhibited the growth of new, small vessels because L(v) decreased from 13.14 +/- 0.61

36 Synthetic vascular grafts cannot be used in small vessels because of graft failure caused by thrombo

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

38 lesions as markers for, and contributors to, small-vessel brain disease.

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

40 bbles normally pass freely through large and small vessels but are retained in regions with ED.

41 Plaque remodeling is overestimated in small vessels by 12-detector row MDCTA, whereas 16- and

42 and tissue damage due to the obstruction of small vessels by sickled cells.

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

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

45 europsychological impairment associated with small vessel cerebrovascular disease and Alzheimer's dis

46 s indicate that the cognitive effects of the small vessel cerebrovascular disease are variable and no

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

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

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

50 (NO) and is postulated as a primary cause of small vessel complications as a result of poor glycemic

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

52 gate marker of ongoing ischaemic injury from small-vessel damage.

53 by multiple arterial thromboses in large and small vessels despite maximal anticoagulation, immunosup

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

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

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

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

58 Small vessel disease (mainly hypertensive arteriopathy a

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

60 types cardioembolism (OR: 1.03; p = 0.69) or small vessel disease (OR: 1.06; p = 0.52).

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

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

63 Patients with cerebral small vessel disease (SVD) can present as isolated lacun

64 Cerebral small vessel disease (SVD) causes focal lacunar infarcti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 sms remain unclear, but may include cerebral small vessel disease caused by COPD.

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

97 patients, 33% of stroke was due to cerebral small vessel disease compared with 14% in the white stro

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

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

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

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

102 Evidence of small vessel disease in the retina increases the likelih

103 Cerebral small vessel disease is a common condition associated wi

104 Small vessel disease is a stroke subtype characterized b

105 Small vessel disease is associated with high rates of ap

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

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

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

109 =3 sulci; disseminated, >/=4 sulci), and key small vessel disease markers.

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

111 Although severe small vessel disease or cerebral amyloid angiopathy may

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

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

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

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

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

117 e gave a higher estimate of the frequency of small vessel disease stroke, particularly in white patie

118 A relative excess of small vessel disease was observed in black patients with

119 , hypertension, lacunar stroke and ischaemic small vessel disease, and have generated interest as a m

120 validated mutations that cause porencephaly, small vessel disease, and hereditary angiopathy, nephrop

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

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

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

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

125 pathy (CAA) is a common age related cerebral small vessel disease, characterised by progressive depos

126 nt membrane and COL4A1 mutations cause adult small vessel disease, familial porencephaly and heredita

127 cts of cerebrovascular disease, particularly small vessel disease, from those of Alzheimer's disease

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

129 nce of magnetic resonance imaging markers of small vessel disease, including cerebral microbleeds and

130 Cerebral small vessel disease, including microvascular lesions, i

131 ere protein mutations (ie, myocyte disarray, small vessel disease, myocardial scarring).

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

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

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

135 ld identify a homogeneous subpopulation with small vessel disease.

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

137 ebrovascular diseases secondary to large and small vessel disease.

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

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

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

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

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

143 rns of brain injury supported both large and small vessel disease.

144 ascular risk factors known to cause sporadic small vessel disease.

145 neuroimaging and genetic markers of cerebral small vessel disease.

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

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

148 whole brain atrophy in symptomatic cerebral small vessel disease.

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

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

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

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

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

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

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

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

157 imaging markers of the severity and type of small-vessel disease (hypertensive arteriopathy or cereb

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

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

160 CADASIL and their mechanistic connection to small-vessel disease and GOM accumulation remain enigmat

161 an age at which white matter findings due to small-vessel disease are common.

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

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

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

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

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

167 The most common monogenic cause of small-vessel disease leading to ischemic stroke and vasc

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

169 Treatment of small-vessel disease with a paclitaxel DEB was associate

170 ss of Notch signaling with ischemic cerebral small-vessel disease, a prevalent human condition.

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

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

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

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

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

176 thrombotic material or coexistent intrinsic small-vessel disease, remains a major determinant of poo

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

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

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

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

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

182 ent type of stroke caused mainly by cerebral small-vessel disease.

183 ied a COL4A1 mutation in a human family with small-vessel disease.

184 tify CTEPH patients with significant distal, small-vessel disease.

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

186 Several hereditary small vessel diseases (SVDs) of the brain have been repo

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

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

189 Small-vessel diseases of the brain underlie 20 to 30 per

190 ts for rational therapies for this enigmatic small vessel disorder is provided.

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

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

193 glycemic index (high-GI) diets could lead to small vessel dysfunction.

194 developing large vessel atherothrombosis and small vessel dysfunction.

195 Small-vessel dysfunction may be an important consequence

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

197 l differentiation, contributing to large and small vessel formation.

198 temporal (<200 ms per frame) resolution for small-vessel imaging are achieved at 1-3 mm deep in the

199 yeloid cells colocalized with Thy-1(+) EC of small vessels in microabscesses, suggesting an interacti

200 of large blood vessels and cells surrounding small vessels in the CNS also strongly expressed EGFP, a

201 also stained for E-selectin in RPE cells and small vessels in the periphery.

202 ound predominantly on RPE cells, but also on small vessels in the periphery.

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

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

205 o evaluate complement in the pathogenesis of small vessel injury in children receiving HSCT.

206 recipients with kidney disease secondary to small vessel injury.

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

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

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

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

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

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

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

214 his effect is driven by improved outcomes in small vessels, long coronary stenoses, and possibly saph

215 at risk for restenosis, including those with small vessels, long lesions, and diabetes mellitus.

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

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

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

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

220 pretation, and patients with emboli in these small vessels may have deep vein thrombosis or recurrent

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

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

223 Vascular contraction was measured using small vessel myography.

224 Using small-vessel myography, aorta from these mice exhibited

225 lasmic antibody-associated (ANCA-associated) small vessel necrotizing vasculitis is caused by immune-

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

227 n-1 (an antiangiogenic agent) production and small vessel occlusion in untreated juvenile dermatomyos

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

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

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

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

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

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

234 ng a striking anemia, especially apparent in small vessels of the yolk sac.

235 3 to 15 mum in diameter that could represent small vessels or scleral fibroblasts.

236 l PAD (LV-PAD) progression might differ from small-vessel PAD (SV-PAD).

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

238 ed twofold in ANIT-fed rats, suggesting that small vessels preferentially undergo proliferation.

239 tly attenuated the deterioration in perfused small vessel proportion and density, microvascular flow

240 75% in the two upper proportion of perfused small vessel quartiles compared with 3% and 44% in the t

241 Small vessel reactivity was assessed by measuring the ab

242 domized 182 patients with lesions located in small vessels (reference diameter <2.8 mm) to treatment

243 In the subgroup of small vessels (reference diameter <3 mm) OCT showed a si

244 vessel (atherosclerosis, cardiomyopathy) and small vessel (retinopathy, nephropathy and neuropathy) c

245 helial cell (PAEC) apoptosis and the loss of small vessels seen in idiopathic pulmonary arterial hype

246 gistration (16%), motion artifacts (30%), or small vessel size (54%).

247 The clinical significance of small-vessel stenoses is therefore questionable.

248 pes of stents (bare-metal, drug-eluting, and small-vessel stents).

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

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

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

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

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

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

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

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

257 tes are recruited into the tissues mainly in small vessels such as capillaries and venules.

258 /MRA) findings into large-vessel (LV) versus small-vessel (SV) disease stroke subgroups.

259 In de novo lesions (small vessels), the TLR rate was low and did not differ

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

261 characterized by histopathologic evidence of small vessel thrombosis, dysfunction of multiple organs

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

263 Skin biopsies revealed a predominantly small-vessel thrombotic vasculopathy with varying degree

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

265 l-established risk factor for both large and small vessel vascular changes, and conversely other vasc

266 ulin resistance and predicts both large- and small-vessel vascular complications, independent of a pa

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

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

269 nase 3 are detected in sera of patients with small vessel vasculitis and participate in the pathogene

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

271 neutrophil cytoplasm autoantibody-associated small vessel vasculitis based on antineutrophil cytoplas

272 entic glomerulonephritis (NCGN) and systemic small vessel vasculitis in humans.

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

274 ischemic infarctions, presumed secondary to small vessel vasculitis.

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

276 ic antibodies (ANCAs) can result in systemic small vessel vasculitis.

277 ophil cytoplasmic antibody (ANCA)-associated small-vessel vasculitis (ANCA-SVV) and to gather evidenc

278 NOTCH activation did not occur in small-vessel vasculitis affecting branches of the vasa v

279 angiitis (Churg-Strauss, EGPA) is a systemic small-vessel vasculitis associated with asthma and eosin

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

281 Microscopic polyangiitis is an autoimmune small-vessel vasculitis that often manifests as focal an

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

283 een consistently detected in ANCA-associated small-vessel vasculitis, and this association prompted u

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

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

286 (ANCA) causes vascular injury that leads to small-vessel vasculitis.

287 A large number of entities can mimic small-vessel vasculitis.

288 ophil cytoplasmic antibody (ANCA)-associated small-vessel vasculitis.

289 ten than other patients with ANCA-associated small-vessel vasculitis.

290 autoimmunity; an obliterative, proliferative small vessel vasculopathy; and fibrosis.

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

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

293 irculatory variables, proportion of perfused small vessels was the strongest predictor of outcome (re

294 articulate character of blood, especially in small vessels where the red blood cells must substantial

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

296 Small vessel wire myography was used to measure isometri

297 te high-spatial-resolution MR angiography of small vessels with low blood flow and thus has potential

298 ause adherence of leukocytes to the walls of small vessels with subsequent injury.

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.