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1  likely to be lacunar if the index event was lacunar.
2 I (tumor-like) - 2, II (honeycomb) - 5, III (lacunar) - 23, IV (cystic-like) - 34.
3 odosome belt that forms a gasket to restrict lacunar acid leakage, and (iii) basolateral chloride upt
4                              We recruited 51 lacunar and 46 cortical stroke patients.
5   We compared the enhancement (leak) between lacunar and cortical patients, and associations with key
6        Beneath, the epithem is composed of a lacunar and highly vascularized parenchyma offering a di
7 ircle of Willis was strongly associated with lacunar and large brain infarcts.
8                                  At autopsy, lacunar and larger brain infarcts were identified, and s
9 glial signalling in white matter adjacent to lacunar and microinfarcts.
10 hite matter ischaemic lesions in the form of lacunar and microinfarcts.
11                   We recruited patients with lacunar and mild cortical stroke.
12                  Differences in prognosis of lacunar and non-lacunar infarction patients might suppor
13 e pattern of recurrent stroke subtypes after lacunar and non-lacunar infarction.
14 t AF) were used to compare the prevalence of lacunar and non-lacunar infarcts, periventricular and de
15 tiple stroke subtypes (e.g. atherosclerotic, lacunar and non-lacunar of undetermined etiology).
16         Similar proportions of patients with lacunar and non-lacunar stroke (16 studies, n=6478) had
17 sents differences in immune response between lacunar and nonlacunar stroke.
18 Is of unclear cause, 15 were predicted to be lacunar, and 17 were predicted to be nonlacunar.
19 king this domain glial processes forming the lacunar area appear to collapse and closely apposed stac
20 teocytes prevented the increase in osteocyte lacunar area seen during lactation, as well as the effec
21 ning which small deep infarcts (SDIs) are of lacunar, arterial, or cardioembolic etiology is challeng
22  relevant entity, which are defined as a non-lacunar brain infarct without proximal arterial stenosis
23 into their lumina and are penetrated by thin lacunar branches and by side lines of the venous lumen.
24               Interstitial fluid flow in the lacunar canalicular system produces focal strains at loc
25  flow through the pericellular matrix in the lacunar-canalicular porosity due to mechanical loading c
26            Solute transport through the bone lacunar-canalicular system is believed to be essential f
27                            Osteocytes in the lacunar-canalicular system of the bone are thought to be
28 he characteristic anatomical features of the lacunar-canalicular system.
29 ement has been measured directly in the bone lacunar-canalicular system.
30 that osteocytes respond to fluid flow in the lacunar-canalicular system.
31 ructure, including the sizes of vascular and lacunar (cellular) spaces, provide useful indicators of
32 life span, as well as collapse of nephrocyte lacunar channels and effacement of nephrocyte slit diaph
33 scular spaces, but these did not explain the lacunar-cortical difference.
34 clastic resorption 2- to 3-fold in assays of lacunar dentine resorption, without affecting osteoclast
35                The factor most predictive of lacunar development was age less than 5 years at the tim
36 d with lacunes and the factors predictive of lacunar development.
37                    A significant increase in lacunar dimensions was observed when 1% w/v sodium laury
38 ed hypomineralization occurs 14 um away from lacunar edges, past a hypermineralized barrier.
39                     We sought to distinguish lacunar from nonlacunar causes of SDIs using a gene expr
40              A 41-gene profile discriminated lacunar from nonlacunar stroke with >90% sensitivity and
41 fferentially expressed genes can distinguish lacunar from nonlacunar stroke.
42     Recurrent strokes were more likely to be lacunar if the index event was lacunar.
43       Periodontitis has been associated with lacunar infarct (LI), a type of cerebral small vessel di
44 planted with human hNT neurons adjacent to a lacunar infarct 27 months after surgery.
45 ependent predictors of processing speed were lacunar infarct count and brain atrophy.
46 predictors of executive function in SVD were lacunar infarct count and diffusivity of normal appearin
47 ence risks are higher among non-lacunar than lacunar infarct patients, the risks appear not to differ
48 creening and randomisation, had brainstem or lacunar infarct, a substantial comorbid disease, an inab
49 forating artery associated with the relevant lacunar infarct.
50 nts showed evidence of no infarct; seven, of lacunar infarct; and 24, of acute cortical infarct.
51 d on brain imaging into two groups: isolated lacunar infarction (n = 47) and ischaemic leukoaraiosis,
52 on (P < 0.0005)] in comparison with isolated lacunar infarction [4.22 (95% CI 1.29-13.73), P = 0.02]
53 and for two different SVD subtypes: isolated lacunar infarction and ischaemic leukoaraiosis.
54 bral small vessel disease (SVD) causes focal lacunar infarction and more diffuse ischaemia, referred
55  ratio (P = 0.01) compared with the isolated lacunar infarction group.
56                                              Lacunar infarction is associated with distinct clinical
57 vessel disease (SVD) can present as isolated lacunar infarction or with diffuse white matter changes,
58  Differences in prognosis of lacunar and non-lacunar infarction patients might support distinct arter
59 ificantly greater following non-lacunar than lacunar infarction, but the difference decreased thereaf
60 ), cerebral ischaemia, neuroinflammation and lacunar infarction, further worsening neurological dysfu
61                 We compared non-lacunar with lacunar infarction, using study-specific and summary odd
62 urrent stroke subtypes after lacunar and non-lacunar infarction.
63 for a distinct arterial pathology underlying lacunar infarction.
64  risk of cardiac death in non-lacunar versus lacunar infarction.
65 tions for gaining insights into the cause of lacunar infarction.
66  vessel disease determined by WMHV and acute lacunar infarction.
67 ntensities, dilated perivascular spaces, and lacunar infarction.
68 0 large-artery occlusive infarctions and 142 lacunar infarctions were identified.
69 racterized by white matter hyperintensities, lacunar infarctions, and microhemorrhages), APOE4 genoty
70 correlate with global cognitive performance (lacunar infarctions, P = .060; acute lesions, P = .088;
71 reviewed all scans for cortical infarctions, lacunar infarctions, strictly lobar CMBs, and deep/infra
72 olved after treatment, but seven resulted in lacunar infarctions.
73 ion: 2 patients presented with small-vessel (lacunar) infarctions, whereas 1 patient presented with a
74 osclerosis patients were more likely to have lacunar infarcts (21% vs 26%; P = .001).
75     AF patients were more likely to have non-lacunar infarcts (22% vs 10%; P < .001), and atheroscler
76 val [CI] 1.86-2.81; P < .001), lower odds of lacunar infarcts (OR 0.66, 95% CI 0.56-0.79; P < .001),
77 patients had a higher odds ratio (OR) of non-lacunar infarcts (OR 2.28, 95% confidence interval [CI]
78 s (OR = 1.4, 95% CI = 1.1-1.9), multiple old lacunar infarcts (OR = 1.9, 95% CI = 1.5-2.5), and moder
79 rsenic]; and between cadmium and presence of lacunar infarcts [relative risk (RR) = 1.024 (95% CI: 1.
80  organization of axons in tissue adjacent to lacunar infarcts and in the regions surrounding microinf
81 sease include white matter hyperintensities, lacunar infarcts and microhaemorrhages, all of which are
82 t-mortem brain tissue from six patients with lacunar infarcts and tissue from two patients with autos
83                 We examined the influence of lacunar infarcts and white matter lesions (WML) on sever
84                                              Lacunar infarcts are a frequent type of stroke caused ma
85 s), enlarged perivascular spaces (PVSs), and lacunar infarcts are common findings in the elderly popu
86                                              Lacunar infarcts are commonly found in the basal ganglia
87 ts with recent (within 6 months) symptomatic lacunar infarcts from 81 centres in North America, Latin
88 olving 3020 patients with recent symptomatic lacunar infarcts identified by magnetic resonance imagin
89 timating equation models, a relation between lacunar infarcts in deep white matter and an increased s
90 er during 3 years follow-up in patients with lacunar infarcts in deep white matter and that symptom s
91 appeared to result in dementia in those with lacunar infarcts in the basal ganglia, thalamus, or deep
92                            Participants with lacunar infarcts in the basal ganglia, thalamus, or deep
93                         A high percentage of lacunar infarcts occur in the BG, yet the relationship b
94 sulting in ischaemic damage that ranges from lacunar infarcts to white matter hyperintensities seen o
95                                              Lacunar infarcts were not associated with severity or co
96  magnetic resonance imaging (MRI)-documented lacunar infarcts were randomly assigned in a factorial d
97                         In axons adjacent to lacunar infarcts yet extending up to 150% of the infarct
98 37 patients had had previous small-vessel or lacunar infarcts, 576 had had cryptogenic infarcts, and
99 SF), and white matter hyperintensity volume, lacunar infarcts, and cerebral microbleeds were estimate
100  White matter hyperintensities (WMH) volume, lacunar infarcts, and gray matter atrophy were quantifie
101 's disease pathology or larger infarcts (ie, lacunar infarcts, and large cortical and non-lacunar sub
102 ter hyperintensity (T(2)-weighted scans) and lacunar infarcts, but no intracerebral haemorrhage.
103 hese regions to both large lesions and small lacunar infarcts, creating specific symptoms based on st
104 llary tangles (NFTs), hippocampal sclerosis, lacunar infarcts, hyaline atherosclerosis, siderocalcino
105 ippocampal sclerosis of ageing pathology and lacunar infarcts, large infarcts, Circle of Willis ather
106 perintensities, dilated perivascular spaces, lacunar infarcts, microbleeds, and spontaneous intracere
107 cerebral amyloid angiopathy, large infarcts, lacunar infarcts, microhaemorrhage, larger haemorrhage,
108 cerebral amyloid angiopathy, large infarcts, lacunar infarcts, microinfarcts, arteriolosclerosis, per
109    Patients with AF had a higher rate of non-lacunar infarcts, multi-infarct patterns and more severe
110                    As in regions adjacent to lacunar infarcts, nodal and paranodal length in white ma
111 to compare the prevalence of lacunar and non-lacunar infarcts, periventricular and deep white matter
112 se features can be assessed on MRI including lacunar infarcts, T2 lesion volume, brain atrophy, and c
113  differences by Hp were noted for atrophy or lacunar infarcts.
114 ascular beds could account structurally for "lacunar" infarcts.
115       DESIGN, SETTING, AND PARTICIPANTS: The Lacunar Intervention Trial-2 (LACI-2) was an investigato
116        Primary intracerebral haemorrhage and lacunar ischaemic stroke are acute manifestations of pro
117 SUS) is used to describe patients with a non-lacunar ischaemic stroke without any identified embolic
118           Included participants had clinical lacunar ischemic stroke, were independent, were aged old
119 s, livedo reticularis, polyarteritis nodosa, lacunar ischemic strokes, and intracranial hemorrhages),
120 bnormalities (white matter hyperintensities, lacunar lesions suggestive of ischemic infarcts, and atr
121 re pigment mottling in 27 patients (63%) and lacunar maculopathy in 3 (6.9%).
122 ast acid secretion across the ruffled border lacunar membrane, the result of mutations in the vH(+)-A
123       Genes differentially expressed between lacunar (n = 30) and nonlacunar strokes (n = 86) were id
124  participants, respectively, as follows: for lacunar, n = 23 and n = 43 (adjusted RR, 0.53; 95% CI, 0
125 types (e.g. atherosclerotic, lacunar and non-lacunar of undetermined etiology).
126 cognitive impairment (MCI) or dementia after lacunar or cortical ischaemic stroke.
127 rom inpatient and outpatient services with a lacunar or minor cortical ischaemic stroke (National Ins
128 on of tissue strains to specific chondrocyte lacunar organizations within intact loaded joints and to
129 ution X-ray nanoCT studies revealed signs of lacunar osteolysis, including increases in cross-section
130                                              Lacunar resorption and filamentous actin ring formation
131 oncentrations that are sufficient to inhibit lacunar resorption.
132 ssion of TSG-6 correlated with inhibition of lacunar resorption; this effect was ameliorated by an an
133 es and sodium lauryl sulfate showed that the lacunar spaces expanded significantly more and the secre
134 nce of the otherwise scattered and separated lacunar spaces in the SC.
135 mechanical waves induce the expansion of the lacunar spaces within the stratum corneum leading to the
136 ectron microscopy showed an expansion of the lacunar spaces within the stratum corneum lipid bilayers
137                Here we show that a series of lacunar spinel compounds, GaM4X8 (M=Nb, Mo, Ta and W and
138                                          The lacunar spinel GaTa4Se8 was theoretically predicted to f
139 proportions of patients with lacunar and non-lacunar stroke (16 studies, n=6478) had MCI or dementia
140  (HR, 1.49; 95% CI: 1.07-2.07) as opposed to lacunar stroke (HR, 0.89; 95% CI: 0.57-1.40).
141  Cerebral small vessel disease (cSVD) causes lacunar stroke (LS) and intracerebral haemorrhage and is
142             The prevalence of dementia after lacunar stroke (six studies, n=1421) was 20% (95% CI 9 t
143 d ten white Caucasian patients with previous lacunar stroke and 50 community control subjects were st
144                INTERPRETATION: Patients with lacunar stroke and CMBs likely harbor a more advanced fo
145                    Consecutive patients with lacunar stroke and confluent leukoaraiosis were recruite
146     In a longitudinal study of patients with lacunar stroke and confluent white matter hyperintensiti
147 e generalized BBB leakiness in patients with lacunar stroke and control patients with cortical ischem
148  patients with an MRI-confirmed diagnosis of lacunar stroke and existing genome-wide association stud
149 been observed at postmortem in patients with lacunar stroke and have not been noted previously on ima
150 ith intracerebral haemorrhage, hypertension, lacunar stroke and ischaemic small vessel disease, and h
151 chaemic leukoaraiosis, defined as a clinical lacunar stroke and leukoaraiosis on brain imaging (n = 6
152              We identified participants with lacunar stroke and MRI-confirmed RSSI from 3 prospective
153                       In patients with prior lacunar stroke and relatively preserved kidney function,
154 troke, and their incidence and prevalence in lacunar stroke as a pooled proportion.
155                     TMAO was associated with lacunar stroke but not other ischemic stroke subtypes in
156                                              Lacunar stroke has a substantial heritable component, wi
157                                Patients with lacunar stroke have subtle, diffuse BBB dysfunction in w
158               We observed nine patients with lacunar stroke imaged with computed tomography and magne
159 = 0.49); and for other nonlacunar stroke and lacunar stroke in CKB, the ORs were 0.89 (0.80, 1.00; p
160 14-EPB41L3) were found to be associated with lacunar stroke in the European or transethnic meta-analy
161                   These studies suggest that lacunar stroke is a heterogeneous disease with various m
162                                              Lacunar stroke is a marker of cerebral small vessel dise
163                                              Lacunar stroke is common (25% of ischemic strokes) and m
164                         The genetic basis of lacunar stroke is poorly understood, with a single locus
165  review, we provide an overview of potential lacunar stroke mechanisms and discuss therapeutic implic
166  can cause an acute stroke syndrome known as lacunar stroke or more subtle pathological alterations o
167             These loci provide insights into lacunar stroke pathogenesis, highlighting disruption of
168  characterize cerebral microbleeds (CMBs) in lacunar stroke patients in the Secondary Prevention of S
169                     Cognitive dysfunction in lacunar stroke patients may commonly be overlooked in cl
170 tory comparative studies and case series) on lacunar stroke patients with a focus on more recent stud
171  In this large, well-characterized cohort of lacunar stroke patients, MCI was present in nearly half,
172 cterize the neuropsychological impairment in lacunar stroke patients.
173 reased primary intracerebral haemorrhage and lacunar stroke risk.
174 om hospitals in the UK as part of the UK DNA Lacunar Stroke studies 1 and 2 and from collaborators wi
175 ity in the basal ganglia was associated with lacunar stroke subtype (p<0.0001).
176         Age and hypertension (but not WMH or lacunar stroke subtype) were independently associated wi
177                                              Lacunar stroke was defined as a lacunar syndrome with in
178 thrombotic stroke, cardioembolic stroke, and lacunar stroke were associated with recurrent stroke (ha
179 ng to stroke subtype; gains in patients with lacunar stroke were best predicted by a measure of intra
180                Ten patients with symptomatic lacunar stroke were recruited (mean age, SD, 64 +/- 9.9
181 cal and magnetic resonance imaging confirmed lacunar stroke with radiological leukoaraiosis were recr
182  disease (cSVD) is a common cause of stroke (lacunar stroke), is the most common cause of vascular co
183 ts with different stroke subtypes (including lacunar stroke).
184 lerotic stroke, 1.71 (95% CI, 0.80 to 3.63); lacunar stroke, 2.32 (95% CI, 1.48 to 3.63); and cardioe
185 lerotic stroke, 3.18 (95% CI, 1.42 to 7.13); lacunar stroke, 3.09 (95% CI, 1.86 to 5.11); and cardioe
186  of patients with acute left hemisphere, non-lacunar stroke, 40 with and 40 without insular damage; (
187 ve impairment/dementia in lacunar versus non-lacunar stroke, and their incidence and prevalence in la
188 , dependence, and cognitive impairment after lacunar stroke, and they could prevent other adverse out
189 isease is a common condition associated with lacunar stroke, cognitive impairment and significant fun
190 isk of primary intracerebral haemorrhage and lacunar stroke, directly implicate the myeloperoxidase p
191  sequencing and available data pertaining to lacunar stroke-related diseases, namely stroke, dementia
192 the microvascular and brain abnormalities in lacunar stroke.
193 ers in a prospective series of patients with lacunar stroke.
194 revent long-term disability in patients with lacunar stroke.
195  due to PAMM followed a few weeks later by a lacunar stroke.
196 troke prevention strategies in patients with lacunar stroke.
197 non-lobar intracerebral hemorrhage (ICH) and lacunar stroke.
198 history of smoking, and type 2 diabetes with lacunar stroke.
199 rs in trials aiming to improve outcome after lacunar stroke.
200 A44, ULK4, CARF, FAM117B, ICA1L, NBEAL1) and lacunar stroke.
201 A2 and HTRA1) that are involved in monogenic lacunar stroke.
202 ncluding cardioembolic) ischemic stroke, and lacunar stroke.
203 duction in fairly young patients with recent lacunar stroke.
204 tudies of 7575 patients, including 2860 with lacunar stroke; 24% had MCI or dementia post stroke.
205 enes for which expression is associated with lacunar stroke; identified significantly enriched pathwa
206 hypertension and diabetes became stronger in lacunar strokes after adjusting for confounders, but not
207 syndrome of intermittent fevers, early-onset lacunar strokes and other neurovascular manifestations,
208                                              Lacunar strokes are a leading cause of cognitive impairm
209 severe, larger cortical strokes, except that lacunar strokes are associated with cerebral small vesse
210 nitive impairment appears to be common after lacunar strokes despite their small size, suggesting tha
211                                              Lacunar strokes might be less likely to affect cognition
212                        The average number of lacunar strokes per person was 0.9 in the AS group and 0
213 c subtypes, large artery atherosclerotic and lacunar strokes were associated with hypertension, diabe
214                                              Lacunar strokes were found in 35% of AS patients and 16%
215  (DWM), enlarged perivascular spaces (ePVS), lacunar strokes, and cerebral microbleeds (CMBs).
216                   Among patients with recent lacunar strokes, the addition of clopidogrel to aspirin
217             Among ischaemic stroke subtypes, lacunar strokes, which were once the commonest variety,
218 ents with ischaemic stroke, more commonly in lacunar strokes.
219 rent ischemic strokes, 71% (133 of 187) were lacunar strokes.
220  of both hemorrhagic and ischemic (including lacunar) strokes.
221 vered by a mesh of glial processes forming a lacunar structure that possibly serves as an ion reservo
222 he formation of the nephrocyte diaphragm and lacunar structure, which is essential for protein uptake
223 lacunar infarcts, and large cortical and non-lacunar subcortical infarcts).
224 etic risk score was strongly associated with lacunar subtype only (odds ratio, 1.05, P = 0.0012).
225 ents with a right pure motor or sensorimotor lacunar syndrome after a subcortical stroke and eight ag
226              Lacunar stroke was defined as a lacunar syndrome with infarction <15mm in a region suppl
227 he basilar pons to determine whether pontine lacunar syndromes conform to discrete clinical entities,
228 of action of peptide modulators, including a lacunar system and multiple types of intercellular junct
229 l enhancement after gadolinium was higher in lacunar than cortical stroke patients in white matter (p
230 stroke recurrence risks are higher among non-lacunar than lacunar infarct patients, the risks appear
231 oke were significantly greater following non-lacunar than lacunar infarction, but the difference decr
232 isability and stroke subtype (lacunar vs non-lacunar) to examine the association of late improvement
233 rebral blood flow, and a higher incidence of lacunar type infarcts.
234 t difference in risk of cardiac death in non-lacunar versus lacunar infarction.
235  the OR for cognitive impairment/dementia in lacunar versus non-lacunar stroke, and their incidence a
236  number and length as well as an increase in lacunar volume and area in AIS.
237 the metabolic demand, resulting in increased lacunar volume, quantifiable with synchrotron X-ray radi
238  sex, 3-month disability and stroke subtype (lacunar vs non-lacunar) to examine the association of la
239 one and cementum is abnormal, with irregular lacunar walls and fewer canaliculi.
240                              We compared non-lacunar with lacunar infarction, using study-specific an

 
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