ライフサイエンスコーパス: hyperintense

1 had hyperintense rim; others were uniformly hyperintense.

2 hite matter on nonenhanced images and judged hyperintense.

3 erogeneous, but the lesion was predominantly hyperintense.

4 nsity that was isointense, heterogeneous, or hyperintense.

5 areas of regeneration appeared as hypo- and hyperintense.

6 8), T1-hypointense (17 of 18), and diffusion-hyperintense (15 of 15) lesions, with a sharp border tow

7 ), T2 or fluid-attenuated inversion recovery hyperintense (18 of 18), T1-hypointense (17 of 18), and

8 However, hyperintense (18)F-FDG uptake in the tumor, compared wit

9 congruent distribution of the two tracers or hyperintense activity on the leukocyte study, as compare

10 It becomes enhanced (hyperintense) after contrast administration.

11 1-weighted MR images (n = 23), 18 cysts were hyperintense and five were isointense to cerebrospinal f

12 Time to new/enlarging T2-hyperintense and gadolinium-enhancing lesions on brain m

13 was compared with the number of alternating hyperintense and hypointense lines depicted.

14 uantitative (contrast-to-noise ratio between hyperintense and hypointense liver regions, coefficient

15 close correspondence between contours of T2-hyperintense and infarcted regions, and the transmural-e

16 er, abnormal but structurally present (FLAIR-hyperintense) and rarefied or cystic (FLAIR-hypointense)

17 ense; subgrade B, inhomogeneous; subgrade C, hyperintense; and subgrade D, hyperintense with swelling

18 T2-weighted hyperintense areas and microhemorrhages did not collocat

19 a high incidence of white matter T2-weighted hyperintense areas and pituitary abnormalities, with a l

20 A pelvic MRI revealed a mass including hyperintense areas on T1-weighted images and hypointense

21 The presence of white matter T2-weighted hyperintense areas was the most common pathologic findin

22 Fluid-attenuated inversion recovery hyperintense areas were segmented and used as regions of

23 fluid-attenuated inversion recovery (FLAIR) hyperintense arteries (FLAIR-HAs) on brain MRI and progn

24 eral nodules of the posterior pole that were hyperintense at fluid-attenuated inversion-recovery imag

25 ltiple-layered appearances, with a prominent hyperintense band at the external surface of the cortex,

26 Magnetic resonance imaging studies showed hyperintense basal ganglia in 80% of patients with posts

27 Magnetic resonance imaging revealed hyperintense bilateral lesions in the dorsal brain stem

28 ator protein signal throughout the expansive hyperintense border of rim+ lesions, which co-localized

29 y neuroimaging outcome of having T2-weighted hyperintense brain lesions consistent with the 2010 McDo

30 The authors discussed a few T1-hyperintense brain lesions which did not include metasta

31 Purpose To characterize the hyperintense bronchus sign (HBS) in in vivo fetal MRI of

32 Conclusion The hyperintense bronchus sign is a frequently detectable fe

33 etween increased tau burden and white matter hyperintense burden.

34 uid-attenuated inversion recovery (FLAIR) T2-hyperintense cerebellar lesions without contrast enhance

35 -attenuated inversion recovery (or FLAIR) T2-hyperintense cerebellar lesions without contrast enhance

36 t cerebral MRI examinations with T2-weighted hyperintense cerebral (264 of 320; 82.5%), cerebellar (4

37 ere the infarcted muscles appeared diffusely hyperintense compared with adjacent muscles.

38 an diameter, 3.9 cm), including 38 benign T1 hyperintense cysts and 26 RCCs, were assessed.

39 ion with mixed-signal-intensity and multiple hyperintense droplets scattered through the cerebellar s

40 ic sources from catheter ablation can create hyperintense DWI punctate lesions in a canine model.

41 sion The amount and extension of T2-weighted hyperintense fascicular nerve lesions were greater in pa

42 Hyperintense foci on diffusion-weighted imaging (DWI) th

43 on MRI, i.e. as countless, tiny, slightly T1-hyperintense foci that did not enhance.

44 e could clearly differentiate viable glioma (hyperintense) from radiation necrosis (hypointense to is

45 Retrospective analysis of hyperintense globus pallidus lesions in 16 children and

46 Significant ADC increases were seen in hyperintense globus pallidus lesions in the NF 1 group c

47 Rate of iso- or hyperintense HCA on HPB phase gadoxetic acid-enhanced MR

48 were included to analyze the rate of iso- or hyperintense HCAs on HPB phase MR images.

49 , low-grade destruction of vertebral bodies, hyperintense/homogeneous signal from the vertebral bodie

50 (n = 7); hypointense, hyperintense (n = 2); hyperintense, hyperintense (n = 1).

51 ely: HCC, hyperintense, hypointense (n = 3); hyperintense, hyperintense (n = 1); hypointense, isointe

52 - and T2-weighted images, respectively: HCC, hyperintense, hypointense (n = 3); hyperintense, hyperin

53 Small HCC, hyperintense, hypointense (n = 7); hypointense, hyperint

54 Both dysplastic nodules with subfoci of HCC, hyperintense, hypointense.

55 All three high-grade dysplastic nodules, hyperintense, hypointense.

56 n nonsiderotic low-grade dysplastic nodules, hyperintense, hypointense.

57 tially progressive T1-shortened/enhancing T2-hyperintense-immature components.

58 cular pressure (IOP) elevation, CSS appeared hyperintense in both freshly prepared ovine eyes and liv

59 nly used biphasic contrasts agents behave as hyperintense in T2 and hypointense in T1.

60 found to be hypointense in T1 sequences and hyperintense in T2 sequences, mimicking the findings of

61 (particle-induced synovitis), lamellated and hyperintense (infection), and a homogeneous effusion wit

62 The hyperintense layer 1 closest to the vitreous likely cons

63 er and the inner and outer segments; and the hyperintense layer 3, the choroid.

64 magnetic resonance imaging detected a single hyperintense lesion in the left temporal lobe.

65 data do, however, give clear clues that the hyperintense lesion is likely to be inflammatory.

66 s or less from symptom onset, spinal cord T2-hyperintense lesion less than 3 vertebral segments, AQP4

67 ortion to the total cerebral T2-weighted MRI hyperintense lesion load.

68 trophy, disability, and advancing disease; a hyperintense lesion may be a clinically relevant biomark

69 group with extreme new or newly enlarging T2 hyperintense lesion numbers (>=25) contributed most of t

70 -executive/attention had higher mean (SE) T2-hyperintense lesion volume (51.33 [31.15] mL vs 99.69 [3

71 ociation between miRNA and brain lesions (T2 hyperintense lesion volume [T2LV]), the ratio of T1 hypo

72 at baseline was correlated with enlarging T2-hyperintense lesion volumes over the subsequent year (rh

73 At least one T1 hyperintense lesion was found in 113 patients (total, 34

74 he numbers of new or enlarging T(2)-weighted hyperintense lesions (all P<0.001) and new T(1)-weighted

75 daily BG-12), new or enlarging T(2)-weighted hyperintense lesions (both BG-12 doses), and new T(1)-we

76 n for treating acute ICH, might increase DWI hyperintense lesions (DWIHLs).

77 =0.008, respectively) or new or enlarging T2 hyperintense lesions (each p<0.0001).

78 esions and of new or enlarging T(2)-weighted hyperintense lesions (P<0.001 for the comparison of each

79 In addition to gliomas and other tumors, T2 hyperintense lesions (unidentified bright objects or UBO

80 he proportion of patients with no N or NE T2 hyperintense lesions among 103 trial completers was 16.1

81 ed with MS, including perivenous T2-weighted hyperintense lesions and focal leptomeningeal enhancemen

82 cant ADC increases were measured both in the hyperintense lesions and in the normal-appearing areas o

83 n immunosuppressed patients, especially when hyperintense lesions are seen in the insular region and

84 the mean number of new or newly enlarging T2 hyperintense lesions at week 72 between the once every 6

85 a, mean numbers of new or newly enlarging T2 hyperintense lesions at week 72 were 0.20 (95% CI 0.07-0

86 was the number of new or newly enlarging T2 hyperintense lesions at week 72, assessed in all partici

87 free of new or newly enlarging (N or NE) T2 hyperintense lesions at week 96 among trial completers.

88 T1 hyperintense lesions had lower ADCs compared with their

89 ity signal in globi pallidi in all patients; hyperintense lesions in midbrain were observed in three

90 onia with dysphagia, choreoathetosis, and T2-hyperintense lesions in striatum.

91 ocations were performed, with and without T2-hyperintense lesions included.

92 Magnetic resonance imaging indicated T2-hyperintense lesions of her splenium.

93 ymphoma in the peripheral retina (n = 2) and hyperintense lesions on brain magnetic resonance imaging

94 To retrospectively document hyperintense lesions on nonenhanced T1-weighted magnetic

95 The number of new or newly enlarged hyperintense lesions on T2-weighted magnetic resonance i

96 After adjustment for disease course, T1 hyperintense lesions remained associated with brain atro

97 , 59%), nonconfluent multifocal white matter hyperintense lesions seen with fluid-attenuated inversio

98 Hyperintense lesions were observed on DWI (median maximu

99 hancing (Gd+) lesions or new or enlarging T2 hyperintense lesions) over 2 years in these trials.

100 ifocal, punctate diffusion restricting or T2 hyperintense lesions) was seen on MRI in all children, b

101 ifocal, punctate diffusion restricting or T2 hyperintense lesions) was seen on MRI in all children, b

102 allosum normal appearing white matter and T2-hyperintense lesions, a significant difference was found

103 = 0.002) and number (p = 0.017) of T2-FLAIR hyperintense lesions, and altered integrity of normal-ap

104 from the NAWM to the perilesional areas, T2 hyperintense lesions, and T1 hypointense lesions (38.1%

105 owed characteristic bilateral symmetrical T2 hyperintense lesions, histologically representing enceph

106 With exclusion of hyperintense lesions, significant ADC increases were mea

107 We found that hyperintense (light) areas in MTC images were coextensiv

108 d computer simulations demonstrated that the hyperintense magnetic signal correlates with Abeta(1-42)

109 lso associated with increasing numbers of T2 hyperintense MRI lesions (OR = 2.36; 95% CI 1.21 to 4.59

110 Hyperintense MS plaques on T1-weighted MR images are com

111 To test whether the hyperintense myocardium would exhibit partial functional

112 observed 2 days later, that the T2-weighted hyperintense myocardium would show partial functional re

113 intense, hyperintense (n = 2); hyperintense, hyperintense (n = 1).

114 rintense, hypointense (n = 3); hyperintense, hyperintense (n = 1); hypointense, isointense (n = 1).

115 erintense, hypointense (n = 7); hypointense, hyperintense (n = 2); hyperintense, hyperintense (n = 1)

116 ing: all lesions were hypointense on T2- and hyperintense (n=12) and isointense (n=6) on T1-weighted

117 The amount and extension of T2-weighted hyperintense nerve lesions correlated positively with th

118 T2w hyperintense nerve lesions were detectable in all MS pat

119 Inner retinal cell swelling was hyperintense on diffusion-weighted images at 3 hours and

120 1H images (tumors) or regions that were only hyperintense on fluid-attenuated inversion recovery (FLA

121 Cast appeared hyperintense on nonenhanced T1-weighted images.

122 Gadolinium enhancement in lesions that are hyperintense on precontrast FLAIR images, such as intrap

123 e on T1-weighted images and iso- to slightly hyperintense on proton-density- and T2-weighted images.

124 showed exaggerated OC responses which became hyperintense on T(2)-weighted MRI at 24h.

125 Melanotic melanomas are hyperintense on T1-weighted images because of paramagnet

126 on T2-weighted images and were predominantly hyperintense on T1-weighted images.

127 Normal myocardium appeared hyperintense on T1-weighted inversion-recovery SE MR ima

128 es (from -4.87 +/- 6.1 to -1.79 +/- 5.7) and hyperintense on T2-weighted images (from 10.12 +/- 7.9 t

129 ges (from -5.77 +/- 5.9 to -7.8 +/- 6.8) and hyperintense on T2-weighted images (from 8.73 +/- 5.4 to

130 led multiple, disseminated lesions that were hyperintense on T2-weighted images and did not enhance a

131 mainly hypointense on T1-weighted images and hyperintense on T2-weighted images and significant restr

132 ghted images in all six patients and iso- to hyperintense on T2-weighted images in five patients.

133 atter immediately adjacent to the enhancing (hyperintense on T2-weighted images, but not enhancing on

134 t were hypointense on T1-weighted images and hyperintense on T2-weighted images.

135 ith the liver on T1-weighted images and were hyperintense on T2-weighted images.

136 the liver on T1-weighted images and slightly hyperintense on T2-weighted images.

137 he deep supratentorial white matter that are hyperintense on T2-weighted/FLAIR sequences.

138 rticularly in the setting of masses that are hyperintense on unenhanced MR images.

139 ed as benign at quantitative assessment were hyperintense on unenhanced MR images; all were diagnosed

140 Fibroids were classified as hyperintense or hypointense relative to skeletal muscle

141 ncing fibroids selected for treatment had no hyperintense or hypointense signal intensity changes on

142 ly than have traditional measures such as T2 hyperintense or T1 hypointense lesion volumes.

143 rized with DW imaging than lesions that were hyperintense or well defined.

144 ism was denoted by the presence of multiple, hyperintense pleural spots on high-b-value DW images.

145 Based on the classical findings of hyperintense pulmonary cystic lesion with T2-weighted hy

146 er was visually scored as percentage normal, hyperintense, rarefied, or cystic on fluid-attenuated in

147 uences need to be included to determine if a hyperintense region is an extrascleral invasion.

148 cclusion would be similar to the T2-weighted hyperintense region observed 2 days later, that the T2-w

149 Infarctlike lesion was defined as a nonmass, hyperintense region on spin-density- and T2-weighted ima

150 s consistent with meningioma and an adjacent hyperintense region on T2-weighted MR images were examin

151 LV) ischemic myocardium at risk (T2-weighted hyperintense region) early after myocardial infarction,

152 from isotropic DW images of enhancing tumor, hyperintense regions adjacent to enhancing tumor, normal

153 tionship between the transmural-extent of T2-hyperintense regions and that of the AAR (bright-blood-T

154 e-regression analyses to detect white matter hyperintense regions associated with Alzheimer's biomark

155 ultiregional (contrast-enhancing regions and hyperintense regions at nonenhanced fluid-attenuated inv

156 he difference in FA decreases in peritumoral hyperintense regions between these tumors approached but

157 Ablated areas of myocardium appeared as hyperintense regions directly adjacent to the catheter t

158 d the finding that the lateral borders of T2 hyperintense regions frequently extend far beyond that o

159 thology images were well correlated with the hyperintense regions measured on T1-weighted GRE images

160 s were also well correlated with the smaller hyperintense regions measured on those IR images with in

161 ADC maps, and (iii) visual determination of hyperintense regions on DWI.

162 Infarcts appeared as hyperintense regions on T2-weighted, fluid-attenuated in

163 In contrast, there were no white matter hyperintense regions significantly associated with incre

164 urther, the amyloid-associated, white matter hyperintense regions strongly correlated with lobar cere

165 ontralateral tissue, and 98 +/- 12 for FLAIR hyperintense regions surrounding tumors.

166 Mean FA values in peritumoral hyperintense regions were 0.178 (43% of normal WM value)

167 Mean ADCs in peritumoral hyperintense regions were 1.309 x 10(-3) mm2/sec (mean p

168 lysis demonstrated a fingerprint match of T2-hyperintense regions with the intricate contour of infar

169 ncing tumor, normal-appearing WM adjacent to hyperintense regions, and analogous locations in the con

170 ancement ratio in the characterization of T1 hyperintense renal lesions, with both methods having low

171 ed in 41 patients with non-fat-containing T1 hyperintense renal lesions.

172 Results DWI revealed a hyperintense rim at the margin of the ablation zone.

173 ltiple sclerosis lesions, characterized by a hyperintense rim of iron-enriched, activated microglia a

174 active rim+ lesions, identified as having a hyperintense rim on QSM, and both clinical disability an

175 study aimed to validate that lesions with a hyperintense rim on quantitative susceptibility mapping

176 were detected, and 43 chronic lesions with a hyperintense rim on quantitative susceptibility mapping

177 study provides evidence that suggests that a hyperintense rim on quantitative susceptibility measure

178 "Penumbra sign" (hyperintense rim on T1W images), diffusion restriction,

179 A hyperintense rim surrounding lesions on R2* maps was onl

180 : a central lesion with hypointense core and hyperintense rim with or without contrast enhancement; a

181 Two-thirds of lesions had hyperintense rim; others were uniformly hyperintense.

182 All tumours showed T2 hyperintense signal and presented with marked contrast e

183 ween the rostro-caudal location of the FLAIR hyperintense signal and seizure severity, based on the C

184 On MRI there was mass showing both T1 and T2 hyperintense signal area suggestive of fat component.

185 plasty demonstrated an acellular zone with a hyperintense signal consistent with a mild interface opa

186 l CA3 [F(1,34) = 16.87, P < 0.0001], despite hyperintense signal evident in 5 of 18 patients on prese

187 Diffusion restriction (hyperintense signal in DWI) was shown in the cortex of t

188 within the modular brain neuropil, revealing hyperintense signal in synapse-rich microdomains.

189 gra and globus pallidus, with a 'halo' of T1 hyperintense signal in the substantia nigra.

190 There was a significant association of hyperintense signal of solid components on T2W and DWI w

191 The T2 relaxometry demonstrated no hyperintense signal of the amygdala in any patient with

192 An artificially hyperintense signal on FLAIR images can result from magn

193 , 74 cystic hemorrhagic adnexal lesions with hyperintense signal on T1-weighted images were identifie

194 Hyperintense signal on T1W MRI and comparison of axial T

195 ypointense signal on T1-weighted imaging and hyperintense signal on T2- and proton-density weighted i

196 Acute axonal nerve lesions cause a hyperintense signal on T2-weighted images at and distal

197 e to slow flow, thrombosis or occlusion, and hyperintense signal within the vessel wall due to intram

198 This was consistent with the lack of hyperintense signals in the anterior temporal pole and e

199 Most commonly, PRES presents with hyperintense signals on T2 and FLAIR sequences.

200 reviewed for the HBS, a tubular or branching hyperintense structure within a lung lesion on T2-weight

201 t (necrotic core, enhancing tumor, and FLAIR-hyperintense subcompartments), 1008 radiomic descriptors

202 ansfer-prepared T1-weighted MRI can depict a hyperintense subregion of the substantia nigra involved

203 Volumetric measurement of hyperintense substantia nigra from magnetization transfe

204 ensity as an internal reference was used for hyperintense substantia nigra volumetry normalized to in

205 Thermal lesions appeared hypointense with hyperintense surrounding rims with all sequences in both

206 ries of patients, the presence of lamellated hyperintense synovitis at MR imaging of knee arthroplast

207 The sensitivity of lamellated hyperintense synovitis for infection was 0.86-0.92 (95%

208 radiologists for the presence of lamellated hyperintense synovitis.

209 FCI scans below 0.2 T exhibited hyperintense T1 regions corresponding to the infarct reg

210 /fluid-attenuated inversion recovery (FLAIR) hyperintense, T1-hypointense, and appeared as perivascul

211 mated the percentage of tumor volume showing hyperintense T2 signal at baseline.

212 The percentage of baseline tumor volume with hyperintense T2 signal defined by a validation radiologi

213 ite, or age, it was strongly associated with hyperintense T2 signal in >=90% versus <90% of baseline

214 The percent tumor volume characterized by hyperintense T2 signal is associated with desmoid progre

215 resonance imaging of the brain demonstrated hyperintense T2-weighted signal in the dorsomedial aspec

216 hypointense band deeper in the cortex, and a hyperintense third band.

217 t test for both tumors and surrounding FLAIR hyperintense tissues versus GM, WM, CSF, and contralater

218 All local recurrences were hyperintense to adjacent pelvic muscles on T2-weighted M

219 yma, 1 = isointense to brain parenchyma, 2 = hyperintense to brain parenchyma) by a pediatric neurora

220 images (n = 18), 17 cysts were isointense or hyperintense to cerebrospinal fluid.

221 to liver on T1-weighted images (n = 11) and hyperintense to liver on T2-weighted images (n = 10).

222 mages, the lesion was isointense or slightly hyperintense to muscle.

223 On T1-weighted images, hyperintense tubal fluid was significantly correlated wi

224 T1-weighted images showed hyperintense vagus medullar striae, coursing towards the

225 White matter hyperintense volumes in the detected topographic pattern

226 Neuroimaging showed hyperintense white matter abnormalities on T2 and fluid

227 Hyperintense white matter foci were seen on MR images in

228 assification into normal white matter and T2-hyperintense white matter hyperintensity volume was perf

229 d volumetric correlates, as well as T2-FLAIR hyperintense white matter lesion burden and microstructu

230 le for CL and CVS assessment; presence of T2-hyperintense white matter lesions (WMLs).

231 nuated inversion recovery magnetic resonance hyperintense white matter voxels was performed using cer

232 s; subgrade C, hyperintense; and subgrade D, hyperintense with swelling.

233 bnormality (Modic changes), posterior anular hyperintense zone (HIZ), and facet arthropathy.

234 animals), was comparable to the size of the hyperintense zone on T2-weighted images 2 days later (43

235 Edema, as detected by a hyperintense zone on T2-weighted images, resolved, and r