ライフサイエンスコーパス: cerebrovascular

1 ease in 3 beds (coronary, peripheral artery, cerebrovascular).

2 he total events reduction included 177 fewer cerebrovascular, 170 fewer coronary, and 43 fewer periph

3 Cerebrovascular abnormalities have emerged as a preclini

4 is also strongly associated with subclinical cerebrovascular abnormalities, vascular cognitive impair

5 common (13% vs 8%), whereas rate of ischemic cerebrovascular accident (4% each) and venous thromboemb

6 pAF is associated with an increased risk of cerebrovascular accident (CVA) remains uncertain.

7 l infarction (HR, 6.3; 95% CI, 2.9 to 13.9), cerebrovascular accident (HR, 6.0; 95% CI, 2.6 to 14.1),

8 nt of interest was major adverse cardiac and cerebrovascular accident (MACCE) (death, myocardial infa

9 the placebo group, these adverse events were cerebrovascular accident (n=1), multiple organ dysfuncti

10 donors with treated coronary artery disease, cerebrovascular accident and nonbrain, nonskin primary m

11 patients, myocardial infarction in 9 (0.4%), cerebrovascular accident in 38 (1.5%), and acute kidney

12 gastric ulcer perforation, sudden death, and cerebrovascular accident) and the placebo group (sudden

13 cident) and the placebo group (sudden death, cerebrovascular accident, and pneumonia), with none in t

14 y mortality; nonfatal myocardial infarction, cerebrovascular accident, and stage 2 to 3 acute kidney

15 sease (a composite of myocardial infarction, cerebrovascular accident, heart failure, and peripheral

16 ine group (the most common adverse event was cerebrovascular accident, which occurred in 3 participan

17 eased after cardiac death, or deceased after cerebrovascular accident.

18 uscitated cardiac arrest; and 1 died after a cerebrovascular accident.

19 ailure (CHF), coronary artery disease (CAD), cerebrovascular accidents (CVA), chronic obstructive pul

20 Acute organ injuries such as acute cerebrovascular accidents, myocardial infarction, acute

21 rebral hemoglobin concentration, and altered cerebrovascular activity, which were reversed in part in

22 = 0.02, d = 0.50), indicating alterations in cerebrovascular activity.

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

24 Cerebrovascular alterations are a key feature of Alzheim

25 Exactly how cerebrovascular alterations contribute to Alzheimer's di

26 .p.) prevents development of parenchymal and cerebrovascular amyloid-beta (Abeta) deposits by 40-50%,

27 esolution approaching 10 microns in tortuous cerebrovascular anatomies.

28 it has been reported to increase the risk of cerebrovascular and cardiovascular problems.

29 scovery of new mechanisms and treatments for cerebrovascular and neurodegenerative diseases such as s

30 The described cerebrovascular and ocular signs are consistent with pre

31 Cerebrovascular and TDP-43 pathologies did not generally

32 in 2 beds (coronary and peripheral artery or cerebrovascular), and 149 had polyvascular disease in 3

33 ilar relative degree of benefit on coronary, cerebrovascular, and peripheral end points in patients w

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

35 the cognitive pathology under conditions of cerebrovascular beta-amyloidosis.

36 cursor protein Swedish (Tg-SwDI), a model of cerebrovascular beta-amyloidosis.

37 Existing cerebrovascular blood pressure autoregulation metrics ha

38 Stroke typically occurs on a background of cerebrovascular burden, which impacts cognition and brai

39 on and white matter integrity is mediated by cerebrovascular burden.

40 stroke patients seen in the Cleveland Clinic cerebrovascular center between September 2, 2012 and Nov

41 ed in this manuscript to detect and quantify cerebrovascular changes (i.e. blood vessel diameters and

42 on, as shown by in vivo imaging, and limited cerebrovascular changes associated with tumor growth.

43 nal microvasculature may mirror small vessel cerebrovascular changes in AD.

44 identify patients who are at higher risk for cerebrovascular complications such as aneurysm and strok

45 rtem markers of common neurodegenerative and cerebrovascular conditions.

46 CBF and cerebrovascular control were measured using middle cereb

47 o reduce these events by vascular territory (cerebrovascular, coronary, or peripheral) in SPARCL.

48 hat are considered to be most significant in cerebrovascular counter-regulation of changes in arteria

49 increases CAA and plays an important role in cerebrovascular damage in AD, we investigated the role o

50 ination and cognitive decline via CD11b link cerebrovascular damage with immune-mediated neurodegener

51 sed Alzheimer's disease risk, independent of cerebrovascular damage.

52 f the ephrinB2-EphB4-RASA1 signaling axis in cerebrovascular development, corroborating and extending

53 Quantification of the cerebrovascular diameter and tortuosity changes may enab

54 4-1.98), and tuberculosis (1.26, 1.08-1.48); cerebrovascular disease (1.09, 1.04-1.14) and ischaemic

55 0.003); was more frequently associated with cerebrovascular disease (11.8% versus 6.0%, p = 0.006),

56 CD; e.g. prior CNS opportunistic infection), cerebrovascular disease (CVD) and HIV-associated neuroco

57 ion of apolipoprotein E (APOE) genotype with cerebrovascular disease (CVD) in a large neuropathologic

58 between various mental illnesses and cardio-cerebrovascular disease (CVD) risk, few have compared th

59 RCD; eg, prior CNS opportunistic infection), cerebrovascular disease (CVD), and HAND.

60 were acute myocardial infarction (MI), acute cerebrovascular disease (CVD), major bleeding, and all-c

61 re (HR 3.77, 95% CI: 1.79-7.95; P = 0.0005), cerebrovascular disease (HR 3.45, 95% CI: 1.72-6.92; P =

62 s not associated with an increased hazard of cerebrovascular disease (HR, 0.96; 95% CI, 0.65-1.41; P

63 t disease (HR, 1.16; 95% CI, 1.10-1.23), and cerebrovascular disease (HR, 1.15; 95% CI, 1.03-1.28).

64 D (MI, IS, PAD, and CVD death), coronary and cerebrovascular disease (MI, IS, CVD death), and individ

65 ion (P = 0.52), history of cardiovascular or cerebrovascular disease (P = 0.94) and dementia (P = 0.7

66 disease and among those without a history of cerebrovascular disease (P(interaction)=0.37).

67 opathological studies have demonstrated that cerebrovascular disease and Alzheimer disease (AD) patho

68 4 patients (5.0%) with a history of previous cerebrovascular disease and among those without a histor

69 ife remains a major concern, with death from cerebrovascular disease and cardiovascular disease accou

70 vascular aging, the greatest risk factor for cerebrovascular disease and its subsequent effects.

71 lure, earlier era of transplant, preexisting cerebrovascular disease and no previous malignancy.

72 ar disease, such as coronary artery disease, cerebrovascular disease and peripheral artery disease.

73 ]) and other atheromatous outcomes (ischemic cerebrovascular disease and peripheral vascular disease)

74 ressants (n = 420,280; 59.7% female) to have cerebrovascular disease and use anxiolytic or antipsycho

75 o a growing body of evidence that implicates cerebrovascular disease as a core feature of AD and not

76 ave higher rates of cognitive impairment and cerebrovascular disease compared with uninfected populat

77 The findings highlight the prevalence of cerebrovascular disease in adults with DS and add to a g

78 g of the epidemiology and pathophysiology of cerebrovascular disease in CKD.

79 The possible increased risk of acute cerebrovascular disease in patients with dual infection

80 ci for future functional investigations into cerebrovascular disease in sickle cell anemia.

81 ts with DS are rare, allowing examination of cerebrovascular disease in this population and insight i

82 1 and COL4A2 cause Mendelian eye, kidney and cerebrovascular disease including intracerebral haemorrh

83 The extent to which cerebrovascular disease influences the progression of AD

84 Cerebrovascular disease involves various medical disorde

85 Unexpectedly, acute cerebrovascular disease is also emerging as an important

86 Progressive cerebrovascular disease occurred in those continuing dia

87 insurance who had a history of PAD, CHD, or cerebrovascular disease on December 31, 2014.

88 ents with PAD only (33.9%) versus those with cerebrovascular disease only (43.0%) or CHD only (51.7%)

89 among patients with PAD only, CHD only, and cerebrovascular disease only was 34.7 (95% CI: 33.2 to 3

90 BMI), waist-to-hip ratio (WHR), and multiple cerebrovascular disease phenotypes.

91 y accompanied by other neuropathology, often cerebrovascular disease such as brain infarcts.

92 2, and 3 conditions including PAD, CHD, and cerebrovascular disease was 40.8 (95% confidence interva

93 Preexisting cerebrovascular disease was a potentially modifiable ris

94 rtion of the association between obesity and cerebrovascular disease was mediated by systolic blood p

95 ons, Clinical Modification billing codes for cerebrovascular disease were determined against trial-de

96 s generally characterized by the presence of cerebrovascular disease with ocular, renal, and muscular

97 rterial disease, 1.32 (95% CI 1.15-1.50) for cerebrovascular disease, and 1.93 (95% CI 1.47-2.53) for

98 lure, earlier era of transplant, preexisting cerebrovascular disease, and no previous malignancy.

99 re followed for ASCVD events comprising CHD, cerebrovascular disease, and PAD events until December 3

100 mong patients with PAD and CHD, with PAD and cerebrovascular disease, and with CHD and cerebrovascula

101 Prior cardiovascular or cerebrovascular disease, arterial hypotension at admissi

102 ate life, physical exercise, smoking, sleep, cerebrovascular disease, frailty, atrial fibrillation an

103 We identified no increased risk of cerebrovascular disease, myocardial infarction, or major

104 DS cancer, chronic renal failure, cardio and cerebrovascular disease, obesity, cachexia or hyperchole

105 r, chronic renal failure, cardiovascular and cerebrovascular disease, obesity, undernutrition, or hyp

106 diovascular disease, ischemic heart disease, cerebrovascular disease, or cardiac arrest associated wi

107 rrespective of baseline LDL-C and history of cerebrovascular disease, over a median follow-up of 2.8

108 We hypothesize that cerebrovascular disease, specifically brain large artery

109 cted patients that are at risk of developing cerebrovascular disease, such as ischemic stroke.

110 nd cerebrovascular disease, and with CHD and cerebrovascular disease, the ASCVD event rate was 72.8 (

111 s those with coronary heart disease (CHD) or cerebrovascular disease.

112 n to higher BMI did not increase the risk of cerebrovascular disease.

113 as, and cognitively unimpaired patients with cerebrovascular disease.

114 ltered also in dementias related, or not, to cerebrovascular disease.

115 be taking a statin versus those with CHD or cerebrovascular disease.

116 baseline LDL-C concentration and history of cerebrovascular disease.

117 spective of baseline LDL-C and of history of cerebrovascular disease.

118 re severe baseline upper-limb disability and cerebrovascular disease.

119 for cardiac disease, metabolic syndrome, and cerebrovascular disease.

120 ndependent from glucose levels, that lead to cerebrovascular disease.

121 e, such as headache and neuroinflammatory or cerebrovascular disease.

122 of participants with no clinical evidence of cerebrovascular disease: cognitively normal (CN) without

123 ogressive supranuclear palsy (6.4%; n = 13), cerebrovascular diseases (1%; n = 2), amyotrophic latera

124 ed more sub-phenotypes of cardiovascular and cerebrovascular diseases (e.g., angina pectoris, heart f

125 al hypertension, previous cardiovascular and cerebrovascular diseases and dementia.

126 od-brain barrier (BBB) dysfunction occurs in cerebrovascular diseases and neurodegenerative disorders

127 plications for patients with rare congenital cerebrovascular diseases and their families.

128 Cardiac and cerebrovascular diseases are currently the leading cause

129 in the research, diagnosis, and treatment of cerebrovascular diseases.

130 that migraine increases the overall risk of cerebrovascular diseases.

131 thromboembolic disease, aortic disease, and cerebrovascular diseases.

132 flammatory, neurodegenerative, traumatic and cerebrovascular diseases.

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

134 y factor for Moyamoya disease, a progressive cerebrovascular disorder that often leads to brain strok

135 obesity-induced BBB breakdown, and implicate cerebrovascular dysfunction as the mechanism for deficit

136 ts the BBB in dietary obesity, and implicate cerebrovascular dysfunction as the underlying mechanism

137 ediated astrocyte reactivity ameliorates the cerebrovascular dysfunction associated with brain metast

138 receptor in the brain helped protect against cerebrovascular dysfunction despite prolonged obesity.

139 et to pursue for prevention and treatment of cerebrovascular dysfunction in AD.

140 tially addressed the temporal progression of cerebrovascular dysfunction relative to dietary obesity

141 es to the pathogenesis of obesity-associated cerebrovascular dysfunction.

142 er several downstream pathologies, including cerebrovascular dysfunction.

143 Prolonged obesity is associated with cerebrovascular dysfunction; however, the underlying mec

144 ures did not correlate with brain hypoxia or cerebrovascular dysregulation in patients with PBC.

145 ion of cerebral blood vessels, but how these cerebrovascular effects lead to cognitive impairment and

146 It is unclear, however, whether the cerebrovascular effects of APOE4 contribute to cognitive

147 er to determine whether Ang-(1-7) has direct cerebrovascular effects, laser speckle contrast imaging

148 of miR-34a in a stroke, we purified primary cerebrovascular endothelial cells (pCECs) from mouse bra

149 ied RGD ligands in platelet adherence to the cerebrovascular endothelium and highlight the ability of

150 Inhibition of miR-15a/16-1 function in cerebrovascular endothelium may be a legitimate therapeu

151 in the studied cohort, CM is associated with cerebrovascular engagement of CD3+CD8+ T cells, which is

152 oth Alzheimer's disease-related dementia and cerebrovascular etiologies.

153 e and the primary (major adverse cardiac and cerebrovascular event [MACCE] or all-cause mortality) an

154 Major adverse cardiovascular and cerebrovascular event rates were not statistically diffe

155 782 cancer survivors were hospitalized for a cerebrovascular event-40% higher than expected (SHR=1.4,

156 rimary endpoint was major adverse cardiac or cerebrovascular events ([MACCE] the composite of all-cau

157 Cerebrovascular events (CVEs) are devastating complicati

158 P=0.036) and major adverse cardiovascular or cerebrovascular events (hazard ratio, 1.97 [95% CI, 1.08

159 composite of major adverse cardiovascular or cerebrovascular events (MACCE) including all-cause death

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

161 including any CVD, major adverse cardiac and cerebrovascular events (MACCE), myocardial infarction (M

162 posite end point of major adverse cardiac or cerebrovascular events (major adverse cardiac event or i

163 ctors of stroke at 30 days were a history of cerebrovascular events (odds ratio, 2.2; 95% CI, 1.4-3.6

164 e, or death (termed major cardiovascular and cerebrovascular events [MACCEs]) were compared between t

165 the rate of major adverse cardiovascular and cerebrovascular events after a median follow-up of 3.8 y

166 Prior cerebrovascular events and a low glomerular filtration r

167 Fatal cerebrovascular events are often caused by rupture of at

168 increased risk of major adverse cardiac and cerebrovascular events as compared with SAVR (42.5% vers

169 omposite of major adverse cardiovascular and cerebrovascular events at 30 days.

170 from any cause and major adverse cardiac and cerebrovascular events at 5 years.

171 wer rate of major adverse cardiovascular and cerebrovascular events compared with FFR-guided PCI, dri

172 occurrence and/or outcomes of patients with cerebrovascular events in association with their SARS-Co

173 The CENTER (Cerebrovascular EveNts in patients undergoing Transcathe

174 symptomatic OSA to reduce cardiovascular and cerebrovascular events is not currently supported by hig

175 ne cells in plaques that are associated with cerebrovascular events may enable the design of more pre

176 ower mortality and major adverse cardiac and cerebrovascular events rates than transfemoral TAVR perf

177 HIV-associated cerebrovascular events remain highly prevalent even in t

178 ) and have found a stronger association with cerebrovascular events than global stiffness measures.

179 ncidence of major adverse cardiovascular and cerebrovascular events was higher in the FFR-guided PCI

180 arction, and major adverse cardiovascular or cerebrovascular events were 43.0%, 4.1%, 15.2%, and 52.6

181 All cerebrovascular events were less frequent after PCI than

182 and overall major adverse cardiovascular or cerebrovascular events were recorded.

183 d go on to develop major adverse cardiac and cerebrovascular events with an area under the curve of 0

184 absolute hazard of major adverse cardiac or cerebrovascular events with PCI compared with CABG rose

185 Emerging data indicate an increased risk of cerebrovascular events with severe acute respiratory syn

186 rel in High-Risk Patients With Non-disabling Cerebrovascular Events), a similar trial treating with c

187 0.9-1.6%, I(2) = 87%) were hospitalized for cerebrovascular events, 1.1% (95% CI = 0.8-1.3%, I(2) =

188 ower rates of new-onset atrial fibrillation, cerebrovascular events, and readmissions.

189 d point was major adverse cardiovascular and cerebrovascular events, defined as all-cause death, myoc

190 all-cause mortality, coronary artery events, cerebrovascular events, heart failure, nephropathy, and

191 all-cause mortality, coronary artery events, cerebrovascular events, heart failure, nephropathy, and

192 at risk of future major adverse cardiac and cerebrovascular events, highlighting the great potential

193 We recorded cardiac and cerebrovascular events, mortality, and clinical progress

194 The cumulative incidence of cerebrovascular events, myocardial infarction, and coron

195 cular disease and ensuing cardiovascular and cerebrovascular events, the leading causes of death worl

196 ficant benefit on rates of cardiovascular or cerebrovascular events.

197 AD) are at risk of major adverse cardiac and cerebrovascular events.

198 es that were likely to affect NfL, including cerebrovascular events.

199 likely to develop major adverse cardiac and cerebrovascular events.

200 ters can generate the largest changes in the cerebrovascular flow resistance of all brain vessel segm

201 However, it remains unclear whether cerebrovascular function (measured via grey-matter cereb

202 the association between genetic variants and cerebrovascular function after injury.

203 with CMS (CMS+) is associated with impaired cerebrovascular function and adverse neurological outcom

204 as the potential to significantly compromise cerebrovascular function and contribute to the neurologi

205 CD36 deficiency is associated with restored cerebrovascular function in an Alzheimer's disease (AD)

206 but also prevents age-associated decline of cerebrovascular function in mice.

207 Cerebrovascular function is critical for brain health, a

208 These results suggest that acute post-TBI cerebrovascular function is worse in males, and that thi

209 bioavailability, is associated with impaired cerebrovascular function, accelerated cognitive decline

210 ivity in rats with brain metastases restored cerebrovascular function, as shown by in vivo imaging, a

211 c risk alleles is associated with attenuated cerebrovascular function, during young adulthood.

212 grity and plasticity, glucose metabolism and cerebrovascular function.

213 mproved musculoskeletal, cardiopulmonary and cerebrovascular function.

214 ession of apoE4 in mice impairs behavior and cerebrovascular function.

215 disease (HR: 0.56; 95% CI: 0.35 to 0.87) and cerebrovascular (HR: 0.39; 95% CI: 0.20 to 0.75) death r

216 n vivo models, the feasibility of HF-OCT for cerebrovascular imaging was demonstrated.

217 iplex immunohistochemistry, we characterized cerebrovascular immune cells in brain sections from 34 c

218 eads to hematopoietic, gastrointestinal, and cerebrovascular injuries.

219 Background Blunt cerebrovascular injury (BCVI) is associated with increas

220 ats subjected to recurrent seizures or focal cerebrovascular injury suggest that increased cellular t

221 Conclusion Most blunt cerebrovascular injury-related changes occurred within 3

222 enzyme of amyloidogenesis, is upregulated by cerebrovascular insult; moreover, its activity is increa

223 and cerebral blood flow responses, improved cerebrovascular integrity, and diminished neuroinflammat

224 LNM) has been applied to true lesions (e.g., cerebrovascular lesions in stroke) to identify functiona

225 Magnetic resonance angiogram demonstrated cerebrovascular lesions resembling but distinct from Moy

226 Conclusion In addition to cerebrovascular lesions, perfusion abnormalities, cytoto

227 -specific deletion of Cdc42 elicits CCM-like cerebrovascular malformations and that CDC42 is engaged

228 dothelial-specific deletion of Cdc42 elicits cerebrovascular malformations reminiscent of cerebral ca

229 s relative importance for the development of cerebrovascular malformations.

230 ptom burden and increased cardiovascular and cerebrovascular mortality.

231 its pial collateral arteriogenesis following cerebrovascular occlusion.

232 with sickle cell anemia and known pediatric cerebrovascular outcomes.

233 rinogen and Abeta, which might be central to cerebrovascular pathologies observed in HCAA.

234 resonance imaging (MRI)-based biomarkers of cerebrovascular pathology in adults with DS, and determi

235 s disease, there is increasing evidence that cerebrovascular pathology is also abundant in Alzheimer'

236 ism underlying CAA formation and CAA-induced cerebrovascular pathology is unclear.

237 We derived MRI-based biomarkers of cerebrovascular pathology, including white matter hyperi

238 uropathology, usually Alzheimer disease with cerebrovascular pathology.

239 rd scores were associated with Lewy body and cerebrovascular pathology.

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

241 Cognitive function depends on adequate cerebrovascular perfusion and control.

242 Here, we aim to review the human cerebrovascular phenotypes associated with ephrinB2-EphB

243 e of crosstalk between neurodegenerative and cerebrovascular processes.

244 ion or diabetes dampen this response, making cerebrovascular reactivity a useful diagnostic marker fo

245 Hence, an impaired cerebrovascular reactivity amplifies the CO(2) effect on

246 4 mmHg), we investigated arterialized PCO2 , cerebrovascular reactivity and the hypercapnic ventilato

247 t atmospheric CO(2) concentrations, impaired cerebrovascular reactivity caused longer apneic episodes

248 Compared to pre-HDTBR, cerebrovascular reactivity during and after HDTBR did no

249 1) proteins mediate the CO(2)/H(+) effect on cerebrovascular reactivity in mice.

250 c episodes and more anxiety, indicating that cerebrovascular reactivity is essential for normal brain

251 The consequential washout of CO(2), if cerebrovascular reactivity is impaired, reduces respirat

252 r cognitive performance and CBF, but similar cerebrovascular reactivity to CO(2) and dynamic cerebral

253 demonstrate no change in arterialized PCO2 , cerebrovascular reactivity to CO(2) or the hypercapnic v

254 Cerebrovascular reactivity was assessed in the superior

255 bral vasculature to increase its blood flow (cerebrovascular reactivity) are relatively new areas of

256 nd cortical spreading depression might drive cerebrovascular reactivity.

257 trates and their potential role in mediating cerebrovascular reactivity.

258 erebral blood vessels, a phenomenon known as cerebrovascular reactivity.

259 Neurovascular coupling, cerebrovascular remodeling and hemodynamic changes are c

260 ter of intra-cerebral vessels, which control cerebrovascular resistance (CVR).

261 to the dynamic relationship between MAP and cerebrovascular resistance (CVR).

262 An estimated cerebrovascular resistance index was then calculated as

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

264 the potential to influence a given patient's cerebrovascular response to an injury.

265 tween reactive astrocytes and changes in the cerebrovascular response to electrical and physiological

266 ty associated with brain metastases impaired cerebrovascular responses to stimuli at both the cellula

267 matter integrity, stroke characteristics and cerebrovascular risk (root mean square error of approxim

268 hed statements addressing cardiovascular and cerebrovascular risk and disparities among racial and et

269 but attenuated, to the associations between cerebrovascular risk factors and Alzheimer disease.

270 We also evaluated the association between cerebrovascular risk factors and subsequent renal colic

271 Cerebrovascular risk factors are associated with Parkins

272 ctional anisotropy and mean diffusivity) and cerebrovascular risk factors better explain executive dy

273 These findings suggest cerebrovascular risk factors impact on brain structure a

274 Cerebrovascular risk factors increase the likelihood of

275 g the validity of our analytical model, most cerebrovascular risk factors were not associated with th

276 We analyzed demographics, cerebrovascular risk factors, clinical findings, and pro

277 Most evaluated cerebrovascular risk factors, including prior stroke (ha

278 in this sample are detrimentally affected by cerebrovascular risk factors.

279 oke can be both considered manifestations of cerebrovascular risk factors.

280 Structural equation modelling revealed that cerebrovascular risk is associated with reduced cerebral

281 The cerebrovascular safety of these agents must therefore be

282 ome marker CD81-normalized EDE levels of the cerebrovascular-selective biomarkers large neutral amino

283 ortant role in alpha-SMA function within the cerebrovascular smooth muscle cell.

284 auses of death included head trauma (39.4%), cerebrovascular/stroke (25.8%), and anoxia (31.8%).

285 Cerebrovascular structural changes that occur as a resul

286 cocorticoid receptors, neuroimmune outcomes, cerebrovascular structure, and cognition/behavior.

287 Cerebrovascular surgery can benefit from an intraoperati

288 eceiving EVT for acute posterior circulation cerebrovascular syndromes.

289 model, to investigate whether changes in the cerebrovascular system in the PFC contribute to cocaine

290 how coupling of pre-existing neurons to the cerebrovascular system regulates hippocampal neurogenesi

291 unction (CDF) of the 3-D distance map of the cerebrovascular system to quantify alterations in cerebr

292 l information and appearance features of the cerebrovascular system; 2) Estimating the cumulative dis

293 directed nanocarriers provide a platform for cerebrovascular targeting to inflamed brain, with the go

294 resolution atlas, showing the supratentorial cerebrovascular territories and the inter-territorial bo

295 from the cerebral cortex and tau pathology, cerebrovascular territories, plasma anti-AN1792 antibody

296 075 improves microvascular circulation after cerebrovascular thrombosis.

297 of mean and Gaussian curvatures to quantify cerebrovascular tortuosity; and 4) Statistical and corre

298 ion between intracranial aneurysms and other cerebrovascular traits.

299 Other pathologies (cerebrovascular, transactive response DNA-binding protei

300 Therefore, we hypothesize that cerebrovascular TRPC3 channels may contribute to seizure