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

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

5 rfusion scintigraphy with (99m)Tc-MAA before lobar (90)Y radioembolization.

6 regions from ventilation in order to induce lobar absorption atelectasis.

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

8 thoracic radiologists performed independent, lobar analysis of volumetric CT images for type (centril

9 uded a case cohort of 1,681 individuals (484 lobar and 1,194 nonlobar cases) and a control cohort of

10 uded a case cohort of 1,545 individuals (664 lobar and 881 nonlobar cases) and a control cohort of 1,

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

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

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

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

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

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

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

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

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

20 2, more than 2 cm and sublobar; 3, at least lobar; and 4, hemothorax.

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

22 Lobar arteries of uni-x sheep had enhanced responsivenes

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

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

25 ollateral ventilation is present it prevents lobar atelectasis.

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

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

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

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

30 ht upper lobar bronchi 45%, left 55%; middle lobar bronchi 21%, lingula 26%; right lower lobar bronch

31 lobar bronchi 21%, lingula 26%; right lower lobar bronchi 28%, left 29%.

32 ER THAN THE TYPICAL ONES WAS IN: right upper lobar bronchi 45%, left 55%; middle lobar bronchi 21%, l

33 THE FREQUENCY OF LOBAR BRONCHI DIVISIONS OTHER THAN THE TYPICAL ONES WAS

34 Restricted lobar cerebral microbleeds (CMBs) and cortical superfici

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

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

37 ge software suites, we quantified global and lobar change in cortical thickness, outer surface area,

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

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

40 (18.4%) developed new CMBs, of whom 308 had lobar CMBs only and 178 had deep CMBs.

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

42 olysis, especially in patients with multiple lobar CMBs suggestive of cerebral amyloid angiopathy.

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

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

45 Lobar CMBs were subclassified as cortical or subcortical

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

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

48 y disease (16%) and four with frontotemporal lobar degeneration (6%).

49 been used off-label to treat frontotemporal lobar degeneration (FTD).

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

51 C9orf72 is a common cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclero

52 neity in clinical features of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclero

53 C9orf72 are a major cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclero

54 N) gene (GRN) causes familial frontotemporal lobar degeneration (FTLD) and modulates an innate immune

55 trophic lateral sclerosis and frontotemporal lobar degeneration (FTLD) characterized by TDP-43 pathol

56 been suggested that monogenic frontotemporal lobar degeneration (FTLD) due to Granulin (GRN) mutation

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

58 A significant portion of frontotemporal lobar degeneration (FTLD) is due to inherited gene mutat

59 Frontotemporal lobar degeneration (FTLD) is most commonly associated wi

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

61 ol subjects and patients with frontotemporal lobar degeneration (FTLD) to determine whether any obser

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

63 me-wide association study for frontotemporal lobar degeneration (FTLD) with TAR DNA-binding protein (

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

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

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

67 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitinated inclusions.

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

69 Frontotemporal lobar degeneration (FTLD), a neurodegenerative disease p

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

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

72 c lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD), but it is not known if they r

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

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

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

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

77 In frontotemporal lobar degeneration (FTLD)-TDP cases, CDC7 immunostaining

78 enerative disorders including frontotemporal lobar degeneration (FTLD).

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

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

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

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

83 , and patients diagnosed with frontotemporal lobar degeneration (FTLD).

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

85 ay be clinically important in frontotemporal lobar degeneration (FTLD).

86 otrophic lateral sclerosis or 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 gical overlap between ALS and frontotemporal lobar degeneration (FTLD).

90 (ALS) and several subtypes of frontotemporal lobar degeneration (FTLD).

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

92 nerative disorders, including frontotemporal lobar degeneration (FTLD-TDP) and amyotrophic lateral sc

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

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

95 ficiency are a major cause of frontotemporal lobar degeneration (FTLD-TDP).

96 rosis (ALS) and a subgroup of frontotemporal lobar degeneration (FTLD-TDP).

97 stage (N = 16 patients) from frontotemporal lobar degeneration (N = 11 patients) and normal aging (N

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

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

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

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

102 as a major cause of familial frontotemporal lobar degeneration and motor neuron disease, including c

103 er's disease diagnosis versus frontotemporal lobar degeneration and normal aging.

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

105 rms of genetically determined frontotemporal lobar degeneration ascertained at a specialist centre.

106 43 proteinopathies, including frontotemporal lobar degeneration associated with TDP-43 and amyotrophi

107 major genetic risk factor for frontotemporal lobar degeneration associated with TDP-43 deposition.

108 rs, including the majority of frontotemporal lobar degeneration cases (FTLD-TDP), motor neuron diseas

109 entified, representing 35% of frontotemporal lobar degeneration cases with identified mutations, 36%

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

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

112 Frontotemporal lobar degeneration comprises a group of disorders charac

113 that alpha-synucleinopathies, frontotemporal lobar degeneration due to tau and TAR DNA-binding protei

114 agnosis (Alzheimer's disease, frontotemporal lobar degeneration due to tau, and TAR DNA-binding prote

115 pathological changes found in frontotemporal lobar degeneration involving the microtubule-associated

116 Frontotemporal lobar degeneration is a neurodegenerative disease charac

117 Frontotemporal lobar degeneration is associated with cytoplasmic or nuc

118 asis for neuroinflammation in frontotemporal lobar degeneration pathogenesis.

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

120 that the recently identified frontotemporal lobar degeneration risk factor TMEM106B undergoes regula

121 ight on the regulation of the frontotemporal lobar degeneration risk factor TMEM106B.

122 ith C9ORF72 mutation from the frontotemporal lobar degeneration series identified histomorphological

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

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 s might instead be related to frontotemporal lobar degeneration with abnormal TARDBP.

128 icient, is linked to cases of frontotemporal lobar degeneration with TAR DNA-binding protein-43 (TDP-

129 Alzheimer's disease (AD) and frontotemporal lobar degeneration with tau pathologies, are neurodegene

130 Four subtypes of frontotemporal lobar degeneration with TDP-43 immunoreactive inclusions

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

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

133 and, at autopsy, showed both frontotemporal lobar degeneration with TDP-43 inclusions and AD.

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

135 trophic lateral sclerosis and frontotemporal lobar degeneration with TDP-43 inclusions.

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

137 c lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP-43(+) inclusions (FTLD-TDP).

138 ) and frontotemporal dementia-frontotemporal lobar degeneration with TDP-43-positive inclusions (FTLD

139 pe of frontotemporal dementia-frontotemporal lobar degeneration with TDP-43-positive inclusions (FTLD

140 GRN mutations cause frontotemporal lobar degeneration with TDP-43-positive inclusions.

141 a unique association between frontotemporal lobar degeneration with type C pathology and corticospin

142 oprotein, is a major cause of frontotemporal lobar degeneration with ubiquitin (FTLD-U) positive incl

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

144 phic lateral sclerosis (ALS), frontotemporal lobar degeneration with ubiquitin-positive inclusions (F

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

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

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

148 ncluding Alzheimer's disease, frontotemporal lobar degeneration, and Parkinson's disease, with risk f

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

150 lymorphism is associated with frontotemporal lobar degeneration, but little is known about how it aff

151 ce of the C9ORF72 mutation in frontotemporal lobar degeneration, delineate phenotypic and neuropathol

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

153 myotrophic lateral sclerosis, frontotemporal lobar degeneration, inclusion body myopathy, and multisy

154 c lateral sclerosis (ALS) and frontotemporal lobar degeneration, is important for the DNA damage resp

155 ddition to autosomal-dominant frontotemporal lobar degeneration, mutations in the progranulin gene ma

156 7p21 locus linked by GWASs to frontotemporal lobar degeneration, nominating a causal variant and caus

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

158 trophic lateral sclerosis and frontotemporal lobar degeneration, suggesting that either loss or gain

159 tion in 53 control cases with frontotemporal lobar degeneration-TAR DNA-binding protein.

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

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

162 trophic lateral sclerosis and frontotemporal lobar degeneration.

163 in addition to ALS, including frontotemporal lobar degeneration.

164 trophic lateral sclerosis and frontotemporal lobar degeneration.

165 ich TMEM106B confers risk for frontotemporal lobar degeneration.

166 trophic lateral sclerosis and frontotemporal lobar degeneration.

167 the neurodegenerative disease frontotemporal lobar degeneration.

168 l sclerosis and some types of frontotemporal lobar degeneration.

169 syndromes, all attributed to frontotemporal lobar degeneration.

170 cluding Parkinson disease and frontotemporal lobar degeneration.

171 trophic lateral sclerosis and frontotemporal lobar degeneration.

172 rotein 2B (CHMP2B) gene cause frontotemporal lobar degeneration.

173 s and other clinical forms of frontotemporal lobar degeneration.

174 erosis and ubiquitin-positive frontotemporal lobar degeneration.

175 tation, which causes familial frontotemporal lobar degeneration.

176 trophic lateral sclerosis and frontotemporal lobar degeneration.

177 and track different types of frontotemporal lobar degeneration.

178 and disabling consequences of frontotemporal lobar degeneration.

179 ied in patients with familial Frontotemporal Lobar Degeneration.

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

181 Y90RE treatments aimed at a lobar delivery of 120 Gy.

182 enerative diseases, including frontotemporal lobar dementia (FTLD) and amyotrophic lateral sclerosis

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

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

185 s (UBIs) in diseased cells of frontotemporal lobar dementia (FTLD-U) and amyotrophic lateral sclerosi

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

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

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

189 arious dementias-most notably frontotemporal lobar dementia, stroke, Parkinson's disease, autism and

190 trophic lateral sclerosis and frontotemporal lobar dementia.

191 c lateral sclerosis (ALS) and frontotemporal lobar dementia.

192 c lateral sclerosis (ALS) and frontotemporal lobar dementia.

193 trophic lateral sclerosis and frontotemporal lobar dementia.

194 trophic lateral sclerosis and frontotemporal lobar dementia.

195 rosphere liver radioembolizations delivering lobar doses of 70 and 120 Gy, respectively, display hepa

196 le session (n = 8 patients), in a sequential lobar fashion (n = 10 patients), or to only 1 liver lobe

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

198 non-invasively localize seizure onset at sub-lobar/gyral level when ictal scalp-electroencephalograph

199 1.36, P = 0.044), history of multiple prior lobar haemorrhages (hazard ratio 2.50, P = 0.038), exclu

200 Median ICH volume was larger in lobar hemorrhages (39 mL; interquartile range, 16-75 mL)

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

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

203 located to 4 groups: 1.Sham; 2.IR: 40 min of lobar hepatic ischemia and 2 hr reperfusion; 3.RIPC+IR:

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

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

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

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

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

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

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

211 re centrum semiovale EPVS are more common in lobar ICH attributed to CAA than other ICH.

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

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

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

215 his risk was higher after lobar ICH than non-lobar ICH in two of three hospital-based studies.

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

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

218 /633 (28%) resumed OAT, whereas 86/379 (23%) lobar ICH survivors did.

219 nine studies and this risk was higher after lobar ICH than non-lobar ICH in two of three hospital-ba

220 Independent predictors of lobar ICH volume were intensity of anticoagulation (beta

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

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

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

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

225 CAA was significantly associated with lobar ICH, both overall (OR 2.21, 95% CI 1.09 to 4.45; s

226 and identified two susceptibility loci: for lobar ICH, chromosomal region 12q21.1 (rs11179580, odds

227 OE-epsilon4 and epsilon2 are associated with lobar ICH.

228 frequent hematoma expansion in patients with lobar ICH.

229 s in the underlying biology between deep and lobar ICHs, limited data are available on location speci

230 e the extent of bleeding differ for deep and lobar ICHs.

231 lume only partially overlap between deep and lobar ICHs.

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

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

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

235 23.4%, 14.6-33.3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2

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

237 tion for conscious patients with superficial lobar intracerebral haemorrhage of 10-100 mL and no intr

238 ng brain and is associated with dementia and lobar intracerebral haemorrhage.

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

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

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

242 ing, and luminal area were quantified at the lobar level by using commercial software.

243 haemodynamic cluster was localizable at sub-lobar level within the presumed seizure onset zone in si

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

245 With a partial lobar liver warm ischemia (90 minutes) model, ASC-defici

246 , 1.09-1.97; P < .001 for heterogeneity) and lobar location of ICH (HR, 2.04; 95% CI, 1.06-3.91; P =

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

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

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

250 le LTX (n=7), size-reduced double LTX (n=8), lobar LTX (n=16), split LTX (n=2), and lobar LTX after e

251 n=8), lobar LTX (n=16), split LTX (n=2), and lobar LTX after ex vivo lung perfusion (n=1).

252 described, but pregnancy after living donor lobar lung transplantation (LDLT) has not been reported.

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

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

255 Recipients of multivisceral, redo, and lobar lung transplants and those who underwent pretransp

256 Lobar microbleed count, another marker of CAA severity,

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

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

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

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

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

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

263 Unilateral lobar occlusion with endobronchial valves in patients wi

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

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

266 8 consecutive patients admitted with primary lobar or deep ICH to a single tertiary care medical cent

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

268 s blinded to genotype data and classified as lobar or nonlobar based on brain computed tomography.

269 ICH is classified as lobar or nonlobar based on the location of ruptured bloo

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

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

272 l pneumonia and non-invasive pneumococcal or lobar pneumonia in children and adults, indicating herd

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

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

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

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

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

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

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

280 s of previously described, genetically based lobar regionalization patterns.

281 y of cortical regions, most commonly midline lobar regions in the default mode network, cerebellum, i

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

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

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

285 Lobar segmentations delineated by major fissures on both

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

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

288 Lobar transplantation and ex-vivo lung perfusion techniq

289 Sequential lobar treatment and absence of prior angiosuppressive th

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

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

292 Conclusion Lobar ventilation and ADC values obtained from hyperpola

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

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

295 rom the change in inspiratory and expiratory lobar volumes.

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

297 rm outcome, accounting for ICH location (ie, 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