ライフサイエンスコーパス: cerebrovascular

1 ischaemic heart disease 0.904, 0.882-0.927; cerebrovascular 0.942, 0.902-0.983; and respiratory 0.89

2 st the Abeta-fibrinogen interaction to treat cerebrovascular abnormalities in AD.

3 ence interval, 1.06-1.21) and a trend toward cerebrovascular accident (10-year hazard ratio, 1.08; 95

4 Cerebrovascular accident (40%) was the most prevalent ca

5 I, 3.9-6.1; OR, 2.3; 95% CI, 1.7-3.2), acute cerebrovascular accident (beta coefficient, 6.6; 95% CI,

6 rimary end point was the first occurrence of cerebrovascular accident (CVA) or death.

7 1) or having a residual deficit from a prior cerebrovascular accident (OR, 1.17; 95% CI, 1.11-1.22; P

8 ), and ischemic stroke (CV death/MI/ischemic cerebrovascular accident [iCVA]).

9 irculatory collapse, wound infection, ileus, cerebrovascular accident [possibly treatment related], a

10 ) died because of an adverse event (one [7%] cerebrovascular accident and one [7%] respiratory failur

11 l cell carcinoma in the ozanezumab group and cerebrovascular accident in the placebo group).

12 n-hospital mortality, myocardial infarction, cerebrovascular accident or transient ischemic attack, r

13 hree patients (2%) in the pravastatin group (cerebrovascular accident, arteriosclerosis coronary arte

14 ns for myocardial infarction, heart failure, cerebrovascular accident, or angina after the index angi

15 riates were defined: cardiovascular disease, cerebrovascular accident, peripheral vascular disease, d

16 ing 30-day mortality, myocardial infarction, cerebrovascular accident, rebleeding, pneumonia, or thro

17 entricular arrhythmias, current smoking, and cerebrovascular accident.

18 tcomes were death, myocardial infarction, or cerebrovascular accident.

19 mg ranibizumab yielded an increased risk for cerebrovascular accidents (OR, 2.33; 95% CI, 1.04-5.22;

20 Primary end points included cerebrovascular accidents and all-cause mortality in the

21 omposite of death, myocardial infarction, or cerebrovascular accidents, and occurrence of the key saf

22 2 years and reported the outcome measures of cerebrovascular accidents, myocardial infarctions, arter

23 increased risk for death and potentially for cerebrovascular accidents.

24 Cerebrovascular accumulation of amyloid beta-protein (Ab

25 s Dutch-E22Q and Iowa-D23N, can cause severe cerebrovascular accumulation of amyloid that serves as a

26 reactive oxygen species responsible for the cerebrovascular actions of Abeta and that CD36 and Nox2

27 Further, cerebrovascular adverse events of the anti-Abeta immunot

28 iated with an increase in cardiovascular and cerebrovascular adverse events.

29 erstanding of retinal vein occlusions and of cerebrovascular aging.

30 he cerebrovasculature, most AD patients have cerebrovascular amyloid (cerebral amyloid angiopathy (CA

31 These findings indicate that cerebrovascular amyloid can serve as an effective scaffo

32 , diabetes, smoking, heart failure, previous cerebrovascular and cardiac events, digoxin use, and tot

33 of antithrombotic treatment for known prior cerebrovascular and cardiovascular disease (0-2 points).

34 ipoprotein cholesterol (LDL-C) predicts both cerebrovascular and cardiovascular events.

35 depicting how ARBs such as losartan restore cerebrovascular and cognitive deficits in AD is unknown.

36 umerous mechanisms, serve to increase brain, cerebrovascular and cognitive reserve, thereby preservin

37 ong 9,449 deaths, we observed higher odds of cerebrovascular and respiratory mortality with greater u

38 acute ischemic syndromes (both coronary and cerebrovascular) and for the prevention of their recurre

39 demia) and diseases (ischemic heart disease, cerebrovascular, and peripheral vascular disease), muscu

40 safety end point was major adverse cardiac, cerebrovascular, and renal events at 1 month.

41 procedural or 1-month major adverse cardiac, cerebrovascular, and renal events in the IASD group and

42 dentified all nonaccidental, cardiovascular, cerebrovascular, and respiratory deaths (2009-2013) with

43 seases that primarily involves the renal and cerebrovascular arteries.

44 an detect the effects of stimuli employed in cerebrovascular autoregulation (CVA) tests on the brain,

45 ytes couples neuronal activity to changes in cerebrovascular blood flow.

46 inversely with measures of glycemic control, cerebrovascular burden and depression scores.

47 oke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt-beta-catenin signaling.

48 n between omalizumab and cardiovascular (CV)/cerebrovascular (CBV) events in EXCELS.

49 Cerebrovascular changes occur in Alzheimer's disease (AD

50 e high pulsatility could represent prodromal cerebrovascular changes that damage the brain over time,

51 ral blood flow and probably underlie several cerebrovascular clinical conditions in the SCI populatio

52 prostaglandin E2 (PgE2) plays a key role for cerebrovascular CO2 reactivity, and that preserved synth

53 xtent of early signs of metabolic and cardio-cerebrovascular complications affecting multiple organs

54 velop a wide range of pathologies, including cerebrovascular complications and stroke.

55 The risk of cerebrovascular complications is less well understood.

56 eters are associated with cardiovascular and cerebrovascular conditions.

57 Additionally, cerebrovascular contributions to dementia are increasing

58 ropathy, and nephropathy) and macrovascular (cerebrovascular, coronary artery, and peripheral arteria

59 n the maintenance of BBB integrity following cerebrovascular damage.

60 adgra2 mutants and exhibit highly penetrant cerebrovascular defects.

61 at could restore Abeta-related cognitive and cerebrovascular deficits in AD.SIGNIFICANCE STATEMENT An

62 epigenetic variations, white matter disease, cerebrovascular deregulation, altered neuroplasticity, a

63 te that Rdh10 mutants have severe defects in cerebrovascular development and that this phenotype corr

64 235.7 deaths per 100000 persons) and 1.7 for cerebrovascular disease (40.3 vs 68.1 deaths per 100000

65 S caused the most deaths (29.1%) followed by cerebrovascular disease (7.5%) and lower respiratory inf

66 0.72; 95% CI: 0.55 to 0.94; p = 0.02), acute cerebrovascular disease (adjusted OR: 0.36; 95% CI: 0.31

67 re significantly higher for 18 patients with cerebrovascular disease (CeVD) than for 18 age- and gend

68 Cerebrovascular disease (CVD) is consistently associated

69 95% confidence interval [CI]: 1.45 to 1.54), cerebrovascular disease (HR: 1.07; 95% CI: 1.04 to 1.11)

70 (odds ratio [OR], 0.31; 95% CI, 0.12-0.80), cerebrovascular disease (OR, 0.10; 95% CI, 0.01-0.78), c

71 a (NHL) (RR = 2.69; 95% CI: 1.33, 5.45), and cerebrovascular disease (RR = 1.49; 95% CI: 1.11, 2.01).

72 Ischemic heart disease and cerebrovascular disease age-standardized death rates (as

73 irment in LLD seems to be related to greater cerebrovascular disease along with abnormalities in immu

74 of the association between these lesions and cerebrovascular disease and dementia.

75 novel approaches to slow the progression of cerebrovascular disease and lessen both the frequency an

76 heart failure, or combination of preexisting cerebrovascular disease and mild cognitive impairment in

77 function among individuals with established cerebrovascular disease and preserved estimated glomerul

78 d provide insight into inflammation-mediated cerebrovascular disease and stroke.

79 15 provinces had cerebrovascular disease and two (Hong Kong and Macao) ha

80 The consequences of cerebrovascular disease are among the leading health iss

81 INTRODUCTION: Patients with cerebrovascular disease are at increased risk for cognit

82 By 2013, 27 provinces had cerebrovascular disease as the leading cause, five had i

83 a low, intermediate or high likelihood that cerebrovascular disease contributed to cognitive impairm

84 whereas Mexicans experienced higher rates of cerebrovascular disease deaths.

85 This results in an increased burden of cerebrovascular disease in CKD patients, who consistentl

86 Given the role of cerebrovascular disease in dementia risk, geographic pat

87 to the post-mortem assessment and scoring of cerebrovascular disease in relation to vascular cognitiv

88 Comorbidity of AD/SDAT and various types of cerebrovascular disease is a major theme in dementia res

89 [CI, 0.68 to 0.90]; P for trend < 0.001) and cerebrovascular disease mortality (HR, 0.70 [CI, 0.55 to

90 France has the lowest present-day cerebrovascular disease mortality for both males and fem

91 Analysis of cerebrovascular disease mortality revealed that Austria

92 The melanoma, NHL, and cerebrovascular disease mortality risks are possibly due

93 c retinopathy OR macular edema AND stroke OR cerebrovascular disease OR coronary artery disease OR he

94 rt disease, venous thromboembolic event, and cerebrovascular disease than inactivity.

95 ential role of choline in cardiovascular and cerebrovascular disease through its involvement in lipid

96 tribution of cardiovascular disease (CV) and cerebrovascular disease to the risk for late-onset Alzhe

97 Cerebrovascular disease typically manifests with stroke,

98 p), the HRs of death from cardiovascular and cerebrovascular disease were 1.5 (95% CI, 1.4 to 1.7) an

99 Patients with ischemic cerebrovascular disease were enrolled into our study.

100 ith moyamoya vasculopathy or atherosclerotic cerebrovascular disease who had undergone (15)O-water PE

101 6 x (renal insufficiency) + 0.46 x (previous cerebrovascular disease) + 0.352 x (prior tobacco use) +

102 id congestive heart failure, cardiomyopathy, cerebrovascular disease, and chronic lung disease.

103 Risk of CHD, cerebrovascular disease, and heart failure in normal wei

104 had a higher risk of coronary heart disease, cerebrovascular disease, and heart failure than normal w

105 e immune signalling in the pathogenesis of a cerebrovascular disease, as well as strategies for its t

106 blood pressure, blood urea nitrogen, sodium, cerebrovascular disease, chronic obstructive pulmonary d

107 The prevalence of diabetes, hypertension, cerebrovascular disease, chronic obstructive pulmonary d

108 k of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary d

109 disease, heart failure, cardiac arrhythmia, cerebrovascular disease, congenital heart disease, or ad

110 and the new occurrence of cardiovascular and cerebrovascular disease, especially the brain infarction

111 presentations (coronary heart disease [CHD], cerebrovascular disease, heart failure, and peripheral v

112 hite matter hyperintensities, a biomarker of cerebrovascular disease, in several brain areas.

113 associations between neuroimaging markers of cerebrovascular disease, including lesion topography and

114 diseases, including ischemic heart disease, cerebrovascular disease, ischemic stroke, hemorrhagic st

115 from a distant embolism rather than in situ cerebrovascular disease, leading to the recent formulati

116 cerebral alpha-synuclein scores, presence of cerebrovascular disease, MAPT haplotype, and APOE genoty

117 harmful) to the risk for cardiovascular and cerebrovascular disease, mortality, or all-cause mortali

118 forms of cognitive disorder associated with cerebrovascular disease, regardless of the specific mech

119 ic resonance imaging (MRI) manifestations of cerebrovascular disease, such as lacunes and white matte

120 who had a primary or secondary diagnosis of cerebrovascular disease, who underwent magnetic resonanc

121 ld be useful for treatment and prevention of cerebrovascular disease.

122 ly onset of TAAD and occlusive moyamoya-like cerebrovascular disease.

123 lin sensitivity, might benefit patients with cerebrovascular disease.

124 cribed for patients with coronary artery and cerebrovascular disease.

125 may offer a potential therapeutic target in cerebrovascular disease.

126 cans that most commonly reflect small vessel cerebrovascular disease.

127 le for myeloperoxidase in the progression of cerebrovascular disease.

128 ment of pregnancy, and strategies to prevent cerebrovascular disease.

129 ial cell-derived exosomes in atherosclerotic cerebrovascular disease.

130 ve had previous revascularization or carotid/cerebrovascular disease; and were more likely to have th

131 VD deaths), hypertensive diseases (27%), and cerebrovascular diseases (10%).

132 eaths, with ischemic heart disease (31%) and cerebrovascular diseases (30%) being the leading CVD cau

133 dependent risk factor for cardiovascular and cerebrovascular diseases (adjusted HR, 2.27 [95% CI, .97

134 Cardiovascular and cerebrovascular diseases (CVDs) related to overwork are

135 ffects, their mechanisms and implications in cerebrovascular diseases are not known.

136 ons found in inflammatory cardiovascular and cerebrovascular diseases associated with an elevated blo

137 and the new occurrence of cardiovascular and cerebrovascular diseases in the study.

138 e same role in predicting cardiovascular and cerebrovascular diseases, especially in China.

139 s to neuronal injury during stroke and other cerebrovascular diseases.

140 parameter for treatment decisions in chronic cerebrovascular diseases.

141 n clinical application on cardiovascular and cerebrovascular diseases.

142 nt of therapeutics for neuroinflammatory and cerebrovascular diseases.

143 s the reactive oxygen species production and cerebrovascular dysfunction induced by Abeta applied dir

144 complications are associated in part with a cerebrovascular dysfunction.

145 ar matrix in CADASIL is a key contributor to cerebrovascular dysfunction.

146 leads to cerebral cavernous malformation, a cerebrovascular dysplasia occurring in up to 0.5% of the

147 duces these peripheral risk factors, but its cerebrovascular effect is less documented, especially by

148 sion of adhesion molecules in primary murine cerebrovascular endothelial cells and, in a wound-healin

149 or the first time, the regulation of MCT1 in cerebrovascular endothelial cells by the multifunctional

150 domized patients, 1270 patients (5.1%) had a cerebrovascular event >1 year old, including 650 assigne

151 vestigate the risks of hospitalization for a cerebrovascular event among 5-year survivors of cancer d

152 evaluate the risks of hospitalization for a cerebrovascular event among long-term survivors of teena

153 patients in the CHAMPION trials with a prior cerebrovascular event at least 1 year before the percuta

154 mptomatic, 41 urgent, and 24 patients with a cerebrovascular event between 5 and 180 days of the caro

155 peri-procedural or major adverse cardiac or cerebrovascular event or need for cardiac surgical inter

156 tely symptomatic patients ([urgent] ischemic cerebrovascular event within the previous 5 days) underg

157 event (a composite of any coronary event, a cerebrovascular event, peripheral vascular disease, or h

158 782 cancer survivors were hospitalized for a cerebrovascular event-40% higher than expected (SHR=1.4,

159 s, respectively, had been hospitalized for a cerebrovascular event.

160 for acute coronary syndromes after a recent cerebrovascular event.

161 articularly at risk of hospitalization for a cerebrovascular event.

162 r risk for an acute major adverse cardiac or cerebrovascular event.

163 cardial infarction [major adverse cardiac or cerebrovascular event] by day 30 plus ipsilateral stroke

164 al, 1.32-1.90) and major adverse cardiac and cerebrovascular events (2.62; 2.28-3.01; all P<0.001).

165 , P=0.003), major adverse cardiovascular and cerebrovascular events (4.6% versus 5.7%, P=0.007), and

166 0.034), and major adverse cardiovascular or cerebrovascular events (40.2% vs. 47.9%, respectively; p

167 Those with CM-associated cerebrovascular events (8%) may benefit from short-term

168 y; p < 0.001), and major adverse cardiac and cerebrovascular events (8.7% vs. 23.9%, respectively; p

169 replacement (TAVR) patients at high risk for cerebrovascular events (CVE) is of major clinical releva

170 hard, patient-centered outcomes of death and cerebrovascular events (CVEs) after heart rhythm disorde

171 nd points included major adverse cardiac and cerebrovascular events (ie, death from any cause, stroke

172 rimary outcome was major adverse cardiac and cerebrovascular events (MACCE) (i.e., death, stroke, myo

173 the risk of major adverse cardiovascular and cerebrovascular events (MACCE) among those with AF.

174 e of perioperative major adverse cardiac and cerebrovascular events (MACCE) and bleeding and its rela

175 Major adverse cardiovascular and cerebrovascular events (MACCE) are a significant source

176 point consisted of major adverse cardiac and cerebrovascular events (MACCE) at 30 days, and the prima

177 rimary endpoint was major adverse cardiac or cerebrovascular events (MACCE), a composite of all-cause

178 ombosis and major adverse cardiovascular and cerebrovascular events (MACCE).

179 status, or major adverse cardiovascular and cerebrovascular events (MACCEs) in older adults undergoi

180 .84-1.29; P=0.73), major adverse cardiac and cerebrovascular events (OR, 1.05; 95% CI, 0.80-1.38; P=0

181 ids had a significant reduction in secondary cerebrovascular events (P = .0049).

182 e primary endpoint (major adverse cardiac or cerebrovascular events [MACCE]) was a composite of all-c

183 cardiac endpoint (major adverse cardiac and cerebrovascular events [MACCE]), and quality of life (QO

184 eduction in major adverse cardiovascular and cerebrovascular events and increased bleeding.

185 yocardial infarction, revascularization, and cerebrovascular events at 12 months.

186 e early events and major adverse cardiac and cerebrovascular events at 3 years.

187 er rates of major adverse cardiovascular and cerebrovascular events at 7 years.

188 n the subgroup of patients with a history of cerebrovascular events at least 1 year prior to randomiz

189 nt mortality and nonfatal cardiovascular and cerebrovascular events for those with ST-segment-elevati

190 zard ratio, 0.32; 95% CI, 0.20 to 0.54), and cerebrovascular events in 0 and 4 patients (0 vs. 0.7%).

191 Major adverse cardiovascular and cerebrovascular events occurred most frequently in patie

192 in terms of major adverse cardiovascular and cerebrovascular events of 2 different complete coronary

193 ereas freedom from major adverse cardiac and cerebrovascular events was 80.9% after SAVR and 67.3% af

194 o, rates of major adverse cardiovascular and cerebrovascular events were 4.2% versus 5.0% among patie

195 served numbers of first hospitalizations for cerebrovascular events were compared with that expected

196 l and freedom from major adverse cardiac and cerebrovascular events were observed after SAVR compared

197 l infarction, coronary revascularization, or cerebrovascular events) independently of each other, wit

198 infarction, major adverse cardiovascular and cerebrovascular events, and Global Utilization of Strept

199 eenage and young adult cancer are at risk of cerebrovascular events, but the magnitude of and extent

200 -cause mortality, cardiovascular disease and cerebrovascular events, diabetes, cognitive impairment,

201 identify all women aged 12 to 55 years with cerebrovascular events, including transient ischemic att

202 y safety end point was a composite of death, cerebrovascular events, or serious treatment-related adv

203 As endothelial activation is a hallmark of cerebrovascular events, we postulated that this may also

204 ncidence of major adverse cardiovascular and cerebrovascular events, which were defined as cardiac de

205 in terms of major adverse cardiovascular and cerebrovascular events.

206 be a marker of increased risk for recurrent cerebrovascular events.

207 es based on specific diagnostic data, demand cerebrovascular expertise on big data approaches to clin

208 Previous work suggests that impairments of cerebrovascular flow or reactivity might be early marker

209 as well as how they act in concert to modify cerebrovascular function and permeability in health and

210 cular unit (NVU), and their consequences for cerebrovascular function, are implicated as driving cogn

211 cyte mobility, which is vital in maintaining cerebrovascular function.

212 detect brain pulsatility changes related to cerebrovascular functioning, and TPI identified an incre

213 We show that RA is permissive for cerebrovascular growth via suppression of WNT inhibitor

214 ical clinical conditions related to impaired cerebrovascular health, including: 300-400% increased ri

215 l to generate a precise approach to optimise cerebrovascular health.

216 lication of precision medicine to stroke and cerebrovascular health.

217 ta increased neuroinflammation and disrupted cerebrovascular homeostasis.

218 cerebral blood flow, and clinical markers of cerebrovascular impairment in adults with sickle cell an

219 2 in myeloid cells (Tgfbr2(Myeko)) developed cerebrovascular inflammation in the absence of significa

220 Cerebrovascular injury from a variety of causes, rather

221 One thousand one hundred forty-six blunt cerebrovascular injury patients over 10 years.

222 We identified 1,146 blunt cerebrovascular injury patients; 54 (4.7%) experienced s

223 r hospital arrival among patients with blunt cerebrovascular injury.

224 on arising from neurodegenerative disease or cerebrovascular insufficiency.

225 ontinuous letrozole group) had grade 3-5 CNS cerebrovascular ischaemia, 16 (nine [<1%] vs seven [<1%]

226 Fabry disease leads to renal, cardiac, and cerebrovascular manifestations.

227 ate; all-cause mortality; cardiovascular and cerebrovascular morbidity and mortality; retinopathy, ne

228 : 0.88, 1.33); within 151-300 m, the odds of cerebrovascular mortality were 1.05 (95% CI: 0.98, 1.12)

229 upwind congestion within 150 m, the odds of cerebrovascular mortality were 1.08 (95% confidence inte

230 The role of the cerebrovascular network and its acute response to TBI is

231 hways and effector systems across the entire cerebrovascular network in a highly orchestrated manner.

232 death because of coronary heart disease and cerebrovascular or other atherosclerotic diseases.

233 ng-term risks of ischemic cardiovascular and cerebrovascular outcomes by MI classification among olde

234 es, further exploration of potential adverse cerebrovascular outcomes may be warranted.

235 e mortality and composite cardiovascular and cerebrovascular outcomes through 2 years after hospital

236 a Nox2-containing NADPH oxidase, leading to cerebrovascular oxidative stress.

237 rapeutic target for diseases associated with cerebrovascular oxidative stress.

238 ic marker for non-small cell lung cancer, in cerebrovascular pathogenesis of ischemic stroke.

239 iopathy' now encompasses not only a specific cerebrovascular pathological finding, but also different

240 osis pathologies; this group was enriched in cerebrovascular pathologies.

241 ic analysis of MRI was used to determine the cerebrovascular pathology (white-matter hyperintensities

242 neurodegenerative pathologies tended to have cerebrovascular pathology and carry the MCI diagnosis fo

243 ustrating mechanisms associated with amyloid cerebrovascular pathology and neurological dysfunction.

244 vel and highly useful technique for studying cerebrovascular pathology following experimental SAH.

245 selected ARVd can exacerbate HIV-associated cerebrovascular pathology.

246 jor gaps in the extent of sex differences in cerebrovascular pathology.

247 tors, history of cardiovascular disease, and cerebrovascular pathology.A cross-sectional subset of th

248 vascular disease, and radiologic evidence of cerebrovascular pathology.Higher concentrations of plasm

249 anisms of other classes of noncoding RNAs in cerebrovascular pathophysiology after stroke are less st

250 nique for assessing cerebral vasospasm using cerebrovascular perfusion with ROX, SE (5-Carboxy-X-Rhod

251 These data indicate that a subset of cerebrovascular pericytes derive from mature macrophages

252 Here, we show a new source of cerebrovascular pericytes during neurogenesis.

253 ntiated into NG2/PDGFRbeta/desmin-expressing cerebrovascular pericytes, enwrapping and associating wi

254 he present study was to define mechanisms of cerebrovascular permeability and associated reduction in

255 have a prevailing role in overall increased cerebrovascular permeability in HFg mice.

256 hat at an elevated blood level, Fg increases cerebrovascular permeability via mainly caveolar protein

257 upper" cerebral perfusion pressure limits of cerebrovascular pressure autoregulation (assessed with p

258 ebral perfusion pressure management based on cerebrovascular pressure reactivity index has the potent

259 Both intracranial pressure (ICP) and the cerebrovascular pressure reactivity represent the dysreg

260 We observed that regions of reduced cerebrovascular reactivity (CVR) in the white matter of

261 Cerebrovascular reactivity and whisker-evoked neurovascu

262 Cerebrovascular reactivity can provide a continuously up

263 Cerebrovascular reactivity effects were also measured wi

264 defined and emerging evidence suggests that cerebrovascular reactivity is altered.

265 Amelioration of cerebrovascular reactivity or white matter lesions in th

266 s, dependent on glutathione, are involved in cerebrovascular reactivity to CO2 Reductions in glutathi

267 ad no effect on resting cerebral blood flow, cerebrovascular reactivity, and neuronal responses to se

268 important for (1) the basic understanding of cerebrovascular regulation and (2) interpretation of fun

269 the most profound effects as it may lead to cerebrovascular remodelling and result in memory reducti

270 as identified as mediating the cognitive and cerebrovascular rescue of losartan, a commonly prescribe

271 Cerebrovascular reserve capacity (CVRC) is an important

272 ation of cerebral blood flow, and to measure cerebrovascular reserve, will be reviewed.

273 ope (CA slope) between percentage changes in cerebrovascular resistance (CVR = MAP/CBF) and MAP relat

274 ession slope of proportionate (%) changes in cerebrovascular resistance (CVR) in response to proporti

275 Further, we predicted that increased cerebrovascular resistance and amyloid retention would s

276 theses, we investigated associations between cerebrovascular resistance and amyloid retention, cognit

277 Lastly, we anticipated associations between cerebrovascular resistance and later brain atrophy, prio

278 Increased baseline cerebrovascular resistance index also predicted greater

279 Furthermore, cerebrovascular resistance index group differences were

280 Finally, increased cerebrovascular resistance index predicted greater regio

281 In contrast, the cerebrovascular resistance index was significantly eleva

282 An estimated cerebrovascular resistance index was then calculated as

283 llow-up was accelerated by elevated baseline cerebrovascular resistance index, particularly for amylo

284 Findings suggest that increased cerebrovascular resistance may represent a previously un

285 essure to cerebral blood flow, indicative of cerebrovascular resistance, would exhibit earlier and mo

286 a unique insight into the nuanced localized cerebrovascular response to hypoxia that is not attainab

287 es, should be considered for surveillance of cerebrovascular risk factors and potential pharmacologic

288 sisted when further adjusted for genetic and cerebrovascular risk factors.

289 ns included 1 for all key cardiovascular and cerebrovascular safety end points.

290 To evaluate the cardiovascular and cerebrovascular safety of ranibizumab, 0.5 mg and 0.3 mg

291 angiopoietin-1, and lysyl oxidase-2 and the cerebrovascular-selective proteins glucose transporter 1

292 of high-thoracic (T3 spinal segment) SCI on cerebrovascular structure and function, as well as molec

293 nd evidence for both flow diversion and open cerebrovascular surgery for complex aneurysms that may n

294 For these cases, open cerebrovascular surgery remains important.

295 es cerebrovasodilation through the trigemino-cerebrovascular system and trigemino-parasympathetic ref

296 diabetes leads to maladaptive changes in the cerebrovascular system that ultimately limit neuronal re

297 intaining blood pressure-dependent change in cerebrovascular tone, and perhaps also in blood vessel-t

298 erfibrinogenic (HFg) mice were used to study cerebrovascular transcellular and paracellular permeabil

299 Our data indicate that congenital cerebrovascular variants in the posterior circulation an

300 we report a higher prevalence of congenital cerebrovascular variants; vertebral artery hypoplasia, a