ライフサイエンスコーパス: lobar

1 -related ICH survivors (633 nonlobar and 379 lobar).

2 , HPE is divided into alobar, semilobar, and lobar.

3 nsular, subarachnoid, subdural extension) or lobar.

4 toma location was classified as lobar or non-lobar.

5 Whole-lung and lobar (129)Xe MR imaging parameters were obtained by usi

6 centage ventilated volume and average ADC at lobar (129)Xe MR imaging showed correlation with percent

7 o higher for lobar versus non-lobar ICH (n/% lobar=20/36.4% vs 16/20.8%, p=0.047), and there was a hi

8 ere higher after lobar versus non-lobar ICH (lobar=4.0%, 2.7-7.2 vs 1.1%, 0.3-2.8; p=0.02).

9 Conclusion: Lobar ablation with (131)I is effective, especially when

10 gmentectomy involves delivering a calculated lobar activity of (90)Y microspheres selectively to trea

11 aemorrhage by location in 1813 subjects (755 lobar and 1005 non-lobar) and 1711 stroke-free control s

12 Electrographic seizures occurred in 17% of lobar and 5% of deep intraparenchymal hemorrhage (p = 0.

13 20 patients with ICH, there were 782 (55.1%) lobar and 596 (42.0%) deep haemorrhages.

14 ssed in resistance arteries, including renal lobar and arcuate arteries.

15 ic intracerebral hemorrhage and differed for lobar and deep CMBs.

16 sociated with larger ICH volume for both the lobar and deep ICH groups (odds ratios per quintile incr

17 ebral microbleeds was associated with larger lobar and deep ICHs.

18 was significantly negatively correlated with lobar and global cortical surface area and ROP was signi

19 was significantly negatively correlated with lobar and global sulcal depth in VPT infants.

20 decreased all-cause stroke incidence in both lobar and nonlobar ICH (both p < 0.01).

21 -up were associated with higher risk of both lobar and nonlobar ICH recurrence.

22 rporation of all lung segments and extensive lobar and segmental pulmonary artery reconstruction.

23 diffusivity (MD) metrics were calculated for lobar and sub-lobar regions of interest.

24 was compared between groups in whole brain, lobar and vertex-based analyses.

25 ion in 1813 subjects (755 lobar and 1005 non-lobar) and 1711 stroke-free control subjects.

26 The cohort comprised of 128 patients, 88 lobar, and 40 deep intraparenchymal hemorrhage.

27 arately for the location subcategories deep, lobar, and infratentorial (brainstem/cerebellar).

28 2, more than 2 cm and sublobar; 3, at least lobar; and 4, hemothorax.

29 structures of Arc subdomains that form a bi-lobar architecture remarkably similar to the capsid doma

30 Lobar arteries of uni-x sheep had enhanced responsivenes

31 othelium-dependent relaxation was reduced in lobar arteries of uni-x sheep, accompanied by reduced cy

32 vidence of an embolus in a main pulmonary or lobar artery or evidence of perfusion defects larger tha

33 , bronchiectasis, cicatricial emphysema, and lobar atelectasis were similar in the two patient groups

34 ollateral ventilation is present it prevents lobar atelectasis.

35 nce of bilateral pleural effusions and multi-lobar atelectasis/consolidation, which were significantl

36 d white matter lesions (WML) associated with lobar atrophy shown on magnetic resonance imaging.

37 id status in whom predominant right temporal lobar atrophy was identified based on blinded visual ass

38 tative computed tomography (CT) metrics on a lobar basis and pulmonary function test (PFT) results on

39 th quantitative CT percentage emphysema on a lobar basis and with PFT results on a whole-lung basis.

40 nsposon-transposase complex was coupled with lobar bile duct ligation in C57BL/6 mice, followed by ad

41 tissues related with nerve, artery, and non-lobar brain, we found that experiment-wide significant (

42 Restricted lobar cerebral microbleeds (CMBs) and cortical superfici

43 topographic pattern correlated strongly with lobar cerebral microbleeds (P < 0.001, age and sex adjus

44 yperintense regions strongly correlated with lobar cerebral microbleeds suggesting that cerebral amyl

45 mall vessel brain injury, including strictly lobar cerebral microbleeds, cortical superficial sideros

46 Brain MRIs were rated for lobar cerebral microbleeds, cortical superficial sideros

47 findings suggested that restricted multiple lobar CMBs and CSS affect distinctive clinical features,

48 cantly associated with an increased risk for lobar CMBs exclusively but not for deep CMBs.

49 (18.4%) developed new CMBs, of whom 308 had lobar CMBs only and 178 had deep CMBs.

50 The relationships of restricted multiple lobar CMBs or CSS with cognitive impairment were partial

51 Presence of restricted multiple lobar CMBs was associated with impairment in all cogniti

52 In contrast, lobar CMBs were identified in 43% (21 of 49) of patients

53 Presence of restricted multiple lobar CMBs were independently associated with cortical t

54 Lobar CMBs were subclassified as cortical or subcortical

55 l infarctions, lacunar infarctions, strictly lobar CMBs, and deep/infratentorial CMBs with or without

56 and deep/infratentorial CMBs with or without lobar CMBs.

57 ion weaning and expansion recoil, Sequential Lobar Collapse, Targeted Physiotherapy, Pleural Effusion

58 0.894) and autopsy-confirmed frontotemporal lobar degeneration (area under the curve of 0.878).

59 h postmortem tau pathology in frontotemporal lobar degeneration (FTLD) and (2) tauopathy patients hav

60 rative pathologies, including frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclero

61 : haploinsufficiency leads to frontotemporal lobar degeneration (FTLD) and nullizygosity produces adu

62 CSF) has been associated with frontotemporal lobar degeneration (FTLD) in clinical series.

63 lzheimer's disease in 45% and frontotemporal lobar degeneration (FTLD) in the others, with an approxi

64 entities, including forms of frontotemporal lobar degeneration (FTLD) or Alzheimer disease (AD).

65 (n=21) and those with likely frontotemporal lobar degeneration (FTLD) pathology (n=45).

66 though sensitive detection of frontotemporal lobar degeneration (FTLD) tau inclusions has been unsucc

67 is typically associated with frontotemporal lobar degeneration (FTLD) with longTAR DNA-binding prote

68 classified pathologically as frontotemporal lobar degeneration (FTLD) with TAR DNA-binding protein o

69 ude Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD) with tau pathology (FTLD-tau),

70 is of PPA was associated with frontotemporal lobar degeneration (FTLD) with transactive response DNA-

71 ary pathological diagnosis of frontotemporal lobar degeneration (FTLD), 15 with Alzheimer's disease,

72 D), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral scler

73 he granulin (GRN) gene causes frontotemporal lobar degeneration (FTLD), and complete loss of PGRN lea

74 xpression is associated with fronto-temporal lobar degeneration (FTLD), and missense mutations in the

75 ics (disease controls (DCo)), frontotemporal lobar degeneration (FTLD), Creutzfeldt-Jakob disease (CJ

76 ALS) and approximately 50% of frontotemporal lobar degeneration (FTLD), designated as FTLD-TDP.

77 ontotemporal dementia, termed frontotemporal lobar degeneration (FTLD), is characterized by distinct

78 Unlike many other forms of frontotemporal lobar degeneration (FTLD), svPPA has a highly consistent

79 ploinsufficiency and leads to frontotemporal lobar degeneration (FTLD), the second leading cause of d

80 ical syndrome associated with frontotemporal lobar degeneration (FTLD)--and several primary psychiatr

81 DP-43 proteinopathies such as frontotemporal lobar degeneration (FTLD)-TDP are made of high-molecular

82 lateral sclerosis (ALS) and fronto-temporal lobar degeneration (FTLD).

83 enerative disorders including frontotemporal lobar degeneration (FTLD).

84 Mutant Tau (MAPT) can lead to frontotemporal lobar degeneration (FTLD).

85 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).

86 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).

87 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).

88 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).

89 enerative diseases, including frontotemporal lobar degeneration (FTLD).

90 tely 50% of patients dying of frontotemporal lobar degeneration (FTLD).

91 the syndromes associated with frontotemporal lobar degeneration (FTLD).

92 inicopathological spectrum of frontotemporal lobar degeneration (FTLD).

93 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).

94 ed in brains of patients with frontotemporal lobar degeneration (FTLD-tau), a disease second to Alzhe

95 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD-TDP) are two neurodegenerative

96 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD-TDP).

97 for a cohort of patients with frontotemporal lobar degeneration (n = 58, 25 female, aged 52-84 years,

98 l proportion of patients with frontotemporal lobar degeneration (~45%) exhibit TDP-43 positive neuron

99 ascular brain injury = 1, and frontotemporal lobar degeneration = 2).

100 tions in the PGRN gene causes frontotemporal lobar degeneration accompanied by TDP-43 accumulation, a

101 Alzheimer's disease, 19 with frontotemporal lobar degeneration and 54 healthy individuals (HIs).

102 ogenetic mechanisms with both frontotemporal lobar degeneration and Alzheimer's disease, but also sug

103 nificant risk factor for both frontotemporal lobar degeneration and Alzheimer's disease.

104 EV-DEMALS (Predict to Prevent Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis) st

105 nerative diseases, especially frontotemporal lobar degeneration and amyotrophic lateral sclerosis.

106 gates in distinct subtypes of frontotemporal lobar degeneration and amyotrophic lateral sclerosis.

107 odegenerative diseases beyond frontotemporal lobar degeneration are enriched in CTCF-binding sites fo

108 trophic lateral sclerosis and frontotemporal lobar degeneration are incurable motor neuron diseases a

109 osis and approximately 60% of frontotemporal lobar degeneration cases.

110 3 in neurons is a hallmark of frontotemporal lobar degeneration caused by haploinsufficiency in the g

111 on analyses with the modified frontotemporal lobar degeneration clinical dementia rating score and CS

112 The modified frontotemporal lobar degeneration clinical dementia rating was obtained

113 correlated with the modified frontotemporal lobar degeneration clinical dementia rating.

114 d morphometry analysis of the frontotemporal lobar degeneration cohort, pain and temperature symptoms

115 Frontotemporal lobar degeneration comprises a group of disorders charac

116 hat syndromes associated with frontotemporal lobar degeneration do not form discrete mutually exclusi

117 The syndromes caused by frontotemporal lobar degeneration have highly heterogeneous and overlap

118 Frontotemporal lobar degeneration is a neurodegenerative disease charac

119 stic; 20 non-amnestic) and 64 frontotemporal lobar degeneration patients (five amnestic; 59 non-amnes

120 avioural changes arising from frontotemporal lobar degeneration provides new insights into apathy and

121 eimer tauopathies and non-tau frontotemporal lobar degeneration showed a range of tracer retention th

122 enotypes, particularly in the frontotemporal lobar degeneration spectrum, but the basis for these sym

123 c approach to the spectrum of frontotemporal lobar degeneration syndromes provides a useful framework

124 of apathy and impulsivity in frontotemporal lobar degeneration syndromes.

125 AV-1451, which is elevated in frontotemporal lobar degeneration tauopathies.

126 generative disorder, known as frontotemporal lobar degeneration tauopathy (FTLD-Tau), which presents

127 gyrophilic grain disease, and frontotemporal lobar degeneration with MAPT mutations), and three had n

128 athy and multiple subtypes of frontotemporal lobar degeneration with tau inclusions.

129 sues among LATE-NC, ADNC, and frontotemporal lobar degeneration with TDP-43 (FTLD-TDP).

130 Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) is

131 tein haploinsufficiency cause frontotemporal lobar degeneration with TDP-43 inclusions.

132 e genetically associated with frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP), and

133 LATE is distinguished from frontotemporal lobar degeneration with TDP-43 pathology based on its ep

134 c lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin positive inclusions (F

135 c lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin-positive inclusions (F

136 Lewy bodies, 55 patients with frontotemporal lobar degeneration), and scans from 73 healthy controls.

137 nerative disorders, including frontotemporal lobar degeneration, amyotrophic lateral sclerosis and Al

138 myotrophic lateral sclerosis, frontotemporal lobar degeneration, and Alzheimer's disease, were found

139 from pathologically confirmed frontotemporal lobar degeneration, and in silico techniques to identify

140 myotrophic lateral sclerosis, frontotemporal lobar degeneration, and sporadic inclusion body myositis

141 was relatively insensitive to frontotemporal lobar degeneration, and these patients were likely to be

142 stic Alzheimer's disease from frontotemporal lobar degeneration, compared to discrimination of amnest

143 ndrome likely to be caused by frontotemporal lobar degeneration, including behavioural variant fronto

144 human Alzheimer's disease and frontotemporal lobar degeneration, including beta-amyloid senile plaque

145 7p21 locus linked by GWASs to frontotemporal lobar degeneration, nominating a causal variant and caus

146 include Alzheimer's disease, frontotemporal lobar degeneration, Pick's disease, progressive supranuc

147 the neurodegenerative disease frontotemporal lobar degeneration, while homozygous loss-of-function of

148 tal State Examination (MMSE), Frontotemporal Lobar Degeneration-Clinical Dementia Rating scale and MR

149 gions, but not with change in Frontotemporal Lobar Degeneration-Clinical Dementia Rating scale score

150 agnosis of Alzheimer disease, frontotemporal lobar degeneration-tau, frontotemporal lobar degeneratio

151 poral lobar degeneration-tau, frontotemporal lobar degeneration-transactive response DNA binding prot

152 scriminating both groups from frontotemporal lobar degeneration.

153 d or autopsy-confirmed AD and frontotemporal lobar degeneration.

154 the neurodegenerative disease frontotemporal lobar degeneration.

155 erosis and ubiquitin-positive frontotemporal lobar degeneration.

156 and track different types of frontotemporal lobar degeneration.

157 and disabling consequences of frontotemporal lobar degeneration.

158 ied in patients with familial Frontotemporal Lobar Degeneration.

159 trophic lateral sclerosis and frontotemporal lobar degeneration.

160 in addition to ALS, including frontotemporal lobar degeneration.

161 trophic lateral sclerosis and frontotemporal lobar degeneration.

162 stic Alzheimer's disease from frontotemporal lobar degeneration.

163 rms of non-amyloid-associated frontotemporal lobar degeneration.

164 entified as a risk factor for frontotemporal lobar degeneration.

165 tions), and three had non-tau frontotemporal lobar degeneration.

166 vestigations of patients with frontotemporal lobar degenerations who show unusual white matter hyperi

167 conditions distinct from the frontotemporal lobar degenerations, TDP-43 appears to progress in a ste

168 many patients suffering from frontotemporal lobar dementia (FTLD) with ubiquitinated inclusion bodie

169 c Lateral Sclerosis (ALS) and Frontotemporal Lobar Dementia (FTLD).

170 c lateral sclerosis (ALS) and frontotemporal lobar dementia (FTLD).

171 rf72 gene were found in major frontotemporal lobar dementia and amyotrophic lateral sclerosis patient

172 rophic lateral sclerosis, and frontotemporal lobar dementia are among the most pressing problems of d

173 myotrophic lateral sclerosis, frontotemporal lobar dementia, and Alzheimer's disease.

174 trophic lateral sclerosis and frontotemporal lobar dementia.

175 trophic lateral sclerosis and frontotemporal lobar dementia.

176 The lobar distribution of hepatic metastases from colorectal

177 location of colorectal adenocarcinoma on the lobar distribution of its hepatic metastases based on th

178 obar for cerebral amyloid angiopathy and non-lobar for arteriolosclerosis), we performed GWAS of intr

179 l variants of cerebral small vessel disease (lobar for cerebral amyloid angiopathy and non-lobar for

180 the DLPFC and NAA concentrations in multiple lobar gray matter and white matter regions and subcortic

181 excitable patterns were more frequent in the lobar group (44.3% vs 17.5%; p = 0.005).

182 In multivariable analyses in the lobar group, lateralized rhythmic delta activity predict

183 ty (AD) for these 151 individual regions and lobar groups were calculated and averaged across partici

184 1.36, P = 0.044), history of multiple prior lobar haemorrhages (hazard ratio 2.50, P = 0.038), exclu

185 bral hemorrhage (ICH) care, particularly for lobar hemorrhages related to amyloid angiopathy.

186 portal vein revascularization who underwent lobar hepatectomy, median OS was not reached yet exceede

187 of the visual apparatus and basal forebrain, lobar holoprosencephaly, and CP.

188 in and a likely mechanism for the underlying lobar holoprosencephaly.

189 Areas of cortical lobar hypo (hyper)-metabolism in the cerebrum that were

190 inding on brain (18)F-FDG PET/CT imaging was lobar hypometabolism, being observed in 21 of 23 (91.3%)

191 ALYs) were also lower after lobar versus non-lobar ICH (2.9 vs 3.8 for non-lobar, p=0.04).

192 patient-years); and 39 in patients with non-lobar ICH (AER 2.97 per 100 patient-years).

193 tient-years); 29 in patients presenting with lobar ICH (AER 3.12 per 100 patient-years); and 39 in pa

194 ssociated with admission haematoma volume in lobar ICH (beta, 0.25; SE, 0.12; p=0.03), but there was

195 iated with higher risk of recurrence of both lobar ICH (hazard ratio [HR], 3.53 [95% CI, 1.65-7.54])

196 rrent ICH were higher after lobar versus non-lobar ICH (lobar=4.0%, 2.7-7.2 vs 1.1%, 0.3-2.8; p=0.02)

197 sults: This study analyzed 254 patients with lobar ICH (mean [SD] age, 75 [11] years and 140 [55.1%]

198 ementia was also higher for lobar versus non-lobar ICH (n/% lobar=20/36.4% vs 16/20.8%, p=0.047), and

199 tient-years); 35 in patients presenting with lobar ICH (n=447, AER 3.77 per 100 patient-years); and 9

200 ears); and 9 in patients presenting with non-lobar ICH (n=580, AER 0.69 per 100 patient-years).

201 , 109 (42.7%) had lobar ICH, 144 (56.5%) non-lobar ICH and 2 (0.8%) had uncertain location.

202 recurrent ICH events among 505 survivors of lobar ICH and 44 recurrent ICH events among 640 survivor

203 We separately analyzed nonlobar and lobar ICH cases using propensity score matching and Cox

204 ble associated with larger ICH volume in the lobar ICH group (odds ratio per quintile increase in fin

205 ectively) and with hematoma expansion in the lobar ICH group (odds ratio, 1.70; 95% CI, 1.07-2.92; P

206 rrent stroke, dementia and lower QALYs after lobar ICH highlight the need for more effective preventi

207 In ICH survivors, lobar ICH location was associated with a higher risk of

208 p was associated with increased risk of both lobar ICH recurrence (HR, 1.33 per 10-mm Hg increase [95

209 g increase [95% CI, 1.01-1.47]) but not with lobar ICH recurrence (HR, 1.36 [95% CI, 0.90-2.10]).

210 /633 (28%) resumed OAT, whereas 86/379 (23%) lobar ICH survivors did.

211 independent variable associated with larger lobar ICH volume, and the absence of cerebral microbleed

212 The event rate for lobar ICH was 84 per 1000 person-years among patients wi

213 OAT resumption after lobar ICH was also associated with decreased mortality (

214 Multivariable Cox regression found that lobar ICH was associated with ICH recurrence (HR 8.96, 9

215 ontrol group having noninflammatory CAA with lobar ICH, 1 of 21 (5%) met the criteria for possible CA

216 ICH (mean/SD age 75.5/13.1), 109 (42.7%) had lobar ICH, 144 (56.5%) non-lobar ICH and 2 (0.8%) had un

217 Compared with non-lobar ICH, the substantially higher 10-year risks of rec

218 frequent hematoma expansion in patients with lobar ICH.

219 sociated with admission haematoma volumes in lobar ICH.

220 higher risk of recurrent ICH events than non-lobar ICH; ICH location did not influence risk of subseq

221 tion was complicated by pulmonary emboli and lobar infarction, all contributing to rapid deterioratio

222 amyloid angiopathy (CAA) is associated with lobar intracerebral haemorrhage (ICH).

223 more than two times higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23.

224 23.4%, 14.6-33.3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2

225 While the association between CAA and lobar intracerebral haemorrhage (with its high recurrenc

226 rates novel genome-wide associations for non-lobar intracerebral haemorrhage at 2q33 and 13q34.

227 gnificant associations were observed for non-lobar intracerebral haemorrhage enhanced by SVS with rs2

228 mptoms in patients with probable CAA without lobar intracerebral haemorrhage.

229 a strong independent risk factor for future lobar intracerebral haemorrhage.

230 oup was further divided into those with past lobar intracerebral hemorrhage (ICH) (n = 21) and those

231 13 without neurologic symptoms, 6 with prior lobar intracerebral hemorrhage) and 17 mutation noncarri

232 Patients with lobar intraparenchymal hemorrhage and lateralized rhythm

233 Electrographic seizures are frequent in lobar intraparenchymal hemorrhage, occurring in one in s

234 rographic seizures predicted poor outcome in lobar intraparenchymal hemorrhage.

235 s (score of 1-2 on Glasgow Outcome Scale) in lobar intraparenchymal hemorrhage.

236 tissue complication probability (NTCP) after lobar irradiation of the liver results in highly variabl

237 At the lobar level, inter- and intrareader reproducibility were

238 , 1.09-1.97; P < .001 for heterogeneity) and lobar location of ICH (HR, 2.04; 95% CI, 1.06-3.91; P =

239 hese regions were grouped according to their lobar location within the brain (frontal, occipital, tem

240 factors for developing CMBs, especially in a lobar location, in the general population of older peopl

241 nset CMBs, particularly those occurring in a lobar location.

242 d with having no microbleeds, microbleeds in lobar locations were associated with an increased risk f

243 Performing lobar lung transplantation (LLT) can circumvent issues w

244 Lobar lung transplantation recipients were older (54 +/-

245 rved no functional communication between the lobar lymphatics.

246 (hazard ratio 2.50, P = 0.038), exclusively lobar microbleeds (hazard ratio 2.22, P = 0.008) and pre

247 atients with an intracerebral hemorrhage had lobar microbleeds at baseline; 4 of them used antithromb

248 Patients with lobar microbleeds had an increased risk for stroke and s

249 In addition, lobar microbleeds were associated with an increased risk

250 ctionated whole-liver (n = 1), or sequential lobar (n = 16) RE.

251 en) underwent unilobar (n = 5) or sequential lobar (n = 19) RE.

252 otein in the biliary epithelium coupled with lobar obstruction and IL-33 administration results in th

253 e either valves placed to achieve unilateral lobar occlusion (bronchoscopic lung volume reduction) or

254 Unilateral lobar occlusion with endobronchial valves in patients wi

255 hich were further categorized as exclusively lobar or as deep.

256 Relevance: In patients admitted with primary lobar or deep ICH to a single tertiary care medical cent

257 8 consecutive patients admitted with primary lobar or deep ICH to a single tertiary care medical cent

258 matoma volume and expansion in patients with lobar or deep ICH.

259 Haematoma location was classified as lobar or non-lobar.

260 talizations coded as pneumonia (pneumococcal/lobar, other specified, unspecified, and all-cause) usin

261 bar versus non-lobar ICH (2.9 vs 3.8 for non-lobar, p=0.04).

262 For multiple fronto-temporal lobar pathologies and tauopathies, e2 was not significan

263 on the comparison between gravitational and lobar perfusion data, perfusion was not redistributed to

264 es in a mouse model of Klebsiella pneumoniae lobar pneumonia.

265 ich appeared ischemic with a flattened right lobar portal vein and vena cava without any visible acti

266 tumor involvement who were treated by right-lobar PVE (n = 141) or RE (n = 35) at two centers were m

267 mo (12-28.7 mo) for those with segmental or lobar PVT (not statistically significant).

268 Conclusion: Although lobar quantification parameters differed significantly b

269 Conclusion: Although lobar quantification parameters differed significantly b

270 wed correlation with percentage emphysema at lobar quantitative CT (r = -0.32, P < .001 and r = 0.75,

271 Whole-lung and lobar quantitative CT-derived metrics for emphysema and

272 However, there was no significant lobar redistribution (P < 0.89).

273 D) metrics were calculated for lobar and sub-lobar regions of interest.

274 e frontal and temporal lobes and several sub-lobar regions previously associated with ASD pathology.

275 rPHs were mostly (74%) located in lobar regions.

276 n of contralateral hypertrophy to facilitate lobar resection.

277 This study revealed the advantages of lobar-segmental analysis in structure-function correlati

278 ocellular carcinoma PVT patients (main = 12; lobar/segmental = 29).

279 Lobar segmentations delineated by major fissures on both

280 lateral ventilation (13 patients) or because lobar segments were inaccessible to the endobronchial va

281 bnormalities of cerebral amyloid angiopathy (lobar structures) and hypertensive vasculopathy (deep br

282 Lobar transplantation and ex-vivo lung perfusion techniq

283 Sequential lobar treatment and absence of prior angiosuppressive th

284 especially in those patients with sequential lobar treatment or without prior angiosuppressive therap

285 estimates of thickness and surface area and lobar values were compared, focusing on overall differen

286 Conclusion Lobar ventilation and ADC values obtained from hyperpola

287 Purpose To compare lobar ventilation and apparent diffusion coefficient (AD

288 Percentage lobar ventilation estimated by the FAN model was compare

289 The ratios of lobar ventilations in the models were linearly correlate

290 ted life years (QALYs) were also lower after lobar versus non-lobar ICH (2.9 vs 3.8 for non-lobar, p=

291 ual rates of recurrent ICH were higher after lobar versus non-lobar ICH (lobar=4.0%, 2.7-7.2 vs 1.1%,

292 ulative rate of dementia was also higher for lobar versus non-lobar ICH (n/% lobar=20/36.4% vs 16/20.

293 tion)=0.75), or cerebral microbleed strictly lobar versus other location (HR 0.52 [0.004-6.79] vs 0.3

294 A lobar volume reduction greater than 350 ml at 3 months w

295 rom the change in inspiratory and expiratory lobar volumes.

296 rm outcome, accounting for ICH location (ie, lobar vs nonlobar).

297 rrent ICH and its location within the brain (lobar vs nonlobar).

298 eductions in pneumonia coded as pneumococcal/lobar were statistically significant in all age groups a

299 s suggestive of cerebral amyloid angiopathy (lobar with or without cerebellar microbleeds) were at in

300 Lobar (with or without cerebellar) microbleeds were asso