ライフサイエンスコーパス: gray

1 efrontal cortex to the dorsal periaqueductal gray, a brainstem area vital for defensive responses.

2 ks ERK MAPK activation in the periaqueductal gray and caudal brain stem.

3 estigated associations between rs9804190 and gray and white matter (GM and WM, respectively) structur

4 -induced structural brain alterations of the gray and white matter (WM).

5 terize the biophysical abnormalities in both gray and white matter regions of the brain.

6 varied positively with intracranial volume, gray and white matter volume, and cortical surface area

7 zed by grain-like tau-containing neurites in gray and white matter with heaviest burden in basal gang

8 Using surgical manipulations of the spinal gray and white matter, electrophysiological recordings,

9 d in the lesion and in adjacent perilesional gray and white matter.

10 l pontine reticular nucleus, pontine central gray, and MS, reached EC.

11 e-related findings in the brain (measured by gray- and white-matter volume, sulcal depth, and gyrific

12 eminence, infundibular stem, periaqueductal gray, area postrema, pontine raphe nucleus, gracile nucl

13 ormation on tumor infiltration into white or gray brain matter based on N-acetylaspartate (NAA) and o

14 Patients had lower gray but not white matter volumes, observed principally

15 ated gene expression, resulting in black and gray butterflies.

16 odulated in the ventrolateral periaqueductal gray by persistent inflammation differently in female an

17 ivity among avian species predicted that the gray catbird, a relevant wildlife species, is also highl

18 gmental area (VTA), habenula, periaqueductal gray, cerebellum, hypothalamus, and hippocampal CA3.

19 , with several reference regions: cerebellar gray (CG), whole cerebellum (WC), WC with brainstem (WC

20 amify extensively in two regions: the dorsal gray commissural and intermediolateral nuclei.

21 Cox proportional hazard and Fine and Gray competing risk models were used.

22 models, logistic regression models, and Fine-Gray competing risk regression for analyses.

23 , amygdala, hypothalamus, and periaqueductal gray emerge as central brain structures underlying place

24 Gray et al. observed a similar influence of the length o

25 Inspired by Gray et al.'s bottom-up approach, we conducted four larg

26 art-mind framework distinguishes itself from Gray et al.'s experience-agency framework by its clear a

27 nel Islands and is derived from the mainland gray fox (U. cinereoargenteus).

28 y weight than wild-type (wt) littermates and gray fur.

29 nd accumulating X-ray dose-levels above 2000 Gray (Gy).

30 The second was additive; in gray-headed albatrosses, not only did bycatch impact adu

31 leus of the stria terminalis, periaqueductal gray, hippocampus, and dorsal anterior cingulate cortex.

32 ated in retaliation (amygdala/periaqueductal gray) in youths with DBD and low levels of callous-unemo

33 correlation between target concentration and gray intensity were obtained to determine a limit of det

34 foliar maize diseases-southern leaf blight, gray leaf spot and northern leaf blight-has been identif

35 resistance to both southern leaf blight and gray leaf spot.

36 DG PET-derived textural feature long run low gray level emphasis, and the CT-derived textural feature

37 Short- and long-run low gray-level emphasis and surface ratio of high attenuatio

38 Skewness (asymmetry of gray-level pixel distribution), kurtosis (pointiness of

39 ity was poorest for the following high-order gray-level run-length (GLRL) gray-level zone size matrix

40 wing high-order gray-level run-length (GLRL) gray-level zone size matrix (GLZSM) and neighborhood gra

41 Set 2 comprised high-gray-level-zone emphasis and low-gray-level-zone emphasi

42 prised high-gray-level-zone emphasis and low-gray-level-zone emphasis, which were mostly sensitive to

43 quantization method, and the same number of gray levels in all quantized images, to make meaningful

44 ce of quantization method, and the number of gray levels in the quantized image.

45 ice of quantization method and the number of gray levels in the quantized images had a significant in

46 icators based on correlation and variance of gray levels were optimized and then further confirmed on

47 o September 2016); guideline registries; and gray literature (bibliographies, Google, and experts).

48 with other researchers ensured inclusion of gray literature and additional analyses as well as raw d

49 This systematic review of peer-reviewed and gray literature examines the human health impacts of exp

50 ce, ClinicalTrials.gov, reference lists, and gray literature were systematically searched.

51 Surveys, meeting abstracts, "gray" literature, studies not available in English, and

52 ere referenced to a subsection of cerebellar gray matter (cere-crus) as well as a parametrically deri

53 hin the external capsule and the surrounding gray matter (claustrum and amygdala).

54 the median signal intensity in basal ganglia gray matter (DGErho = 4.59%) was significantly increased

55 arily due to a global difference in cortical gray matter (F1,70 = 9.10, p = .004).

56 Patterns of gray matter (GM) and white matter (WM) atrophy at presen

57 lied voxel-based morphometry methods to test gray matter (GM) and white matter (WM) volume difference

58 Gray matter (GM) anomalies may represent a critical path

59 lerosis (MS) is characterized by progressive gray matter (GM) atrophy that strongly correlates with c

60 we compared the results with MRI measures of gray matter (GM) atrophy.

61 of sensitivity to both white matter (WM) and gray matter (GM) demyelination.

62 ntia (bvFTD) in individual patients by using gray matter (GM) density maps computed from standard T1-

63 g changes and remission status using pre-ECT gray matter (GM) in 38 MDD patients and validate in two

64 Modeling gray matter (GM) microstructural properties is now possi

65 otal, 71 cerebral areas were mapped onto the gray matter (GM) of an averaged T1-weighted structural M

66 By contrast, regional gray matter (GM) thickness and volume are not found to m

67 ata for estimating total brain volume (TBV), gray matter (GM) volume (GMV), and white matter (WM) vol

68 Gray matter (GM) volume of distribution (VT) derived fro

69 cross-sectional association of rs162008 with gray matter (GM) volume variation in cortices, including

70 maps (nlTPMs) of cerebrospinal fluid (CSF), gray matter (GM), and white matter (WM) tissues; 3) deli

71 of normal-appearing white matter (NAWM) and gray matter (GM).

72 d with that in control subjects in the total gray matter (P < .05) and cortex (P = .03).

73 ylaspartate to creatinine levels in parietal gray matter (r = -0.352 and P < .001 at baseline and r =

74 min after injection, using either cerebellar gray matter (SUVRCB) or whole subcortical white matter (

75 Patients showed a global downregulation of gray matter [(11) C]PBR28 binding of 26 +/- 26% (mean +/

76 Four RRs (cerebellar gray matter [CGM], whole cerebellum [WCER], pons, and su

77 ed to investigate the histological origin of gray matter alterations for every distinct clinical enti

78 SIGNIFICANCE STATEMENT: Regional gray matter alterations in chronic pain, as detected wit

79 tion on the histological origins of cerebral gray matter alterations in fibromyalgia, this study adva

80 Chronic pain patients present with cortical gray matter alterations, observed with anatomical magnet

81 healthy individuals (11 women), whether the gray matter anatomy and volume of the hippocampus were r

82 D-only showed volumetric reductions in total gray matter and (mainly) frontal brain areas.

83 numerous complex abnormalities of white and gray matter and a high incidence of long-term neurocogni

84 rolled studies have found regionally greater gray matter and persistence of structural alterations fo

85 The relation between regional gray matter and T1 relaxation times suggests decreased t

86 found with advancing age, the trajectory of gray matter and white matter changes during the disease

87 compounds, Cr, and mI concentrations in the gray matter and white matter of the four cerebral lobes

88 PFC and NAA concentrations in multiple lobar gray matter and white matter regions and subcortical nuc

89 p = .001) even after controlling for global gray matter and white matter volume.

90 ion model that used volumetric predictors of gray matter and white matter was 94.3% accurate.

91 hip did not hold; thus, baseline measures of gray matter and white matter were not significantly rela

92 te (Pi) varied in opposite directions across gray matter and white matter when MDD subjects were comp

93 as well as measuring the differences between gray matter and white matter.

94 pical of the nfvPPA-PSP group, while greater gray matter atrophy and a trend toward greater sentence

95 substrate involving cortical demyelination, gray matter atrophy, and meningeal inflammation.

96 but rather formed 1 week later at the white-gray matter border, preferentially including the ventral

97 e brain was segmented according to white and gray matter by using a dual-clustering algorithm.

98 ive sleep apnea severity are associated with gray matter changes among middle-aged and older individu

99 studies investigating the cellular origin of gray matter changes are lacking.

100 Regression analyses were performed between gray matter characteristics and markers of obstructive s

101 Regional gray matter decreases were largely explained by T1 relax

102 sed tissue water content underlying regional gray matter decreases.

103 Unraveling gray matter degeneration is critical for developing trea

104 A growing body of evidence suggests that gray matter demyelination, cortical atrophy, and leptome

105 alongside conventional diagnoses, examining gray matter density (GMD) as an independent validator fo

106 Gray matter density (GMD), a measure often assumed to be

107 matter integrity (diffusion tensor imaging); gray matter density (voxel-based morphometry); and hippo

108 resonance imaging was used to determine the gray matter density changes across groups and their rela

109 Muller-Lyer illusions, correlated with local gray matter density in the parahippocampal cortex, but n

110 Instead, reduction of gray matter density in ventrolateral prefrontal cortex c

111 hometry analysis, we found that reduction of gray matter density in ventrolateral prefrontal cortex c

112 It is shown for the first time that gray matter density increases from childhood to young ad

113 demonstrated structural similarities to the gray matter distribution on conventional T1-weighted (1)

114 age at onset and the atrophy of subcortical gray matter fraction in women with relapsing-onset MS (s

115 Gray matter hypertrophy and thickening were associated w

116 st atlas applied to the spatially normalized gray matter image obtained from segmentation of the base

117 velopmental abnormalities, including reduced gray matter in both human patients and rodent models and

118 We found decreased gray matter in fibromyalgia to be associated with T1 rel

119 We previously reported that gray matter increases in these regions were associated w

120 In contrast, regional gray matter increases were explained by GABAA receptor c

121 In contrast, regional gray matter increases were partly explained by GABAA rec

122 ng the first 6 months, the growth pattern of gray matter is anisotropic and spatially inhomogeneous w

123 n summary, we found specific visual cortical gray matter loss in Retinitis Pigmentosa patients associ

124 The spatial pattern of gray matter loss is consistent with disuse-driven neuron

125 and likely cognition and that periadolescent gray matter loss may be less pronounced than previously

126 s characterized by an initial, rapid rate of gray matter loss that slows in middle life, followed by

127 parcellation were used to extract GMD, GMV, gray matter mass (GMM; defined as GMD x GMV), and CT fro

128 effects and sex differences in four regional gray matter measures in 1189 youths ranging in age from

129 tudy demonstrates that different MRI-derived gray matter measures show distinct age and sex effects a

130 roitinase injections into the contralesional gray matter of the cervical spinal cord administered 28

131 T1 of the gray matter of the whole brain (P < .001), globus pallid

132 ring the motor neurons, identified as mature gray matter oligodendrocytes.

133 In contrast, no abnormalities of cortical gray matter or white matter were found.

134 T1 segmentation and a novel high-resolution gray matter parcellation were used to extract GMD, GMV,

135 However, little is known about their role in gray matter pathology.

136 (18)F-T807 in gray matter peaked quickly (SUV > 2 at approximately 5 m

137 In addition, within the MDD group, gray matter Pi, a regulator of oxidative phosphorylation

138 psychosis showed a steeper rate of cortical gray matter reduction compared with non-converters and h

139 ated to be transdiagnostically vulnerable to gray matter reduction.

140 e calculated (t = 80-100 minutes, cerebellum gray matter reference).

141 n sides) connections between all 77 cortical gray matter regions in each hemisphere of the rat brain.

142 d by a network of axonal connections between gray matter regions within and between right and left ce

143 high ( approximately 25-55 mL/cm(3)) in all gray matter regions, consistent with the ubiquitous expr

144 levels of analysis: macroconnections between gray matter regions, mesoconnections between neuron type

145 s in TSPO VT (22%-29%) were present in other gray matter regions.

146 The claustrum is a telencephalic gray matter structure with various proposed functions, i

147 ing hand muscles and extensively sprout into gray matter structures after SCI; therefore, it has been

148 ion with prior GBCA exposure, especially for gray matter structures.

149 Adults with MDD had thinner cortical gray matter than controls in the orbitofrontal cortex (O

150 entation, all of which could damage cerebral gray matter that can be indirectly assessed by neuroimag

151 formed the largest study to date of cortical gray matter thickness and surface area measures from bra

152 al gray matter were investigated by means of gray matter VBM.

153 o), was quantitatively investigated in brain gray matter versus white matter of healthy volunteers an

154 s in humans have long described decreases in gray matter volume (GMV) and cortical thickness (CT) dur

155 used magnetic resonance imaging to quantify gray matter volume (GMV) and the N-acetylaspartate and N

156 effects of rs1137070 and heroin addiction on gray matter volume (GMV) based on 78 heroin abusers and

157 7; P = .003) and was predominantly driven by gray matter volume (mean difference in z score per stand

158 f inhibitory control was conducted comparing gray matter volume and activation abnormalities between

159 (1) voxel-based morphometry, which measures gray matter volume and concentration; and (2) FreeSurfer

160 ildhood to young adulthood, in contrast with gray matter volume and cortical thickness, and that fema

161 resonance imaging studies have found reduced gray matter volume and cortical thinning in acutely unde

162 pters with bipolar disorder demonstrate less gray matter volume and decreased structural and function

163 on was used to model the influence of age on gray matter volume and fractional anisotropy at a whole-

164 METHOD: Gray matter volume and fractional anisotropy were mapped

165 Between-group differences in gray matter volume and fractional anisotropy were region

166 The rates of reduction of gray matter volume and fractional anisotropy were signif

167 dicted smaller increases in both subcortical gray matter volume and global fractional anisotropy over

168 matter integrity of the pons and cerebellar gray matter volume associated with higher 'p factor' sco

169 morphometry was applied to study whole brain gray matter volume changes in 27 Retinitis Pigmentosa pa

170 elease were associated with less hippocampal gray matter volume compared with moderate cortisol relea

171 range: 50-75 years) to test whether regional gray matter volume decreases in chronic pain are associa

172 The impact of this retinal loss in cortical gray matter volume has not been addressed before in Reti

173 ability were each negatively associated with gray matter volume in an overlapping region of the ventr

174 try analysis to determine where reduction of gray matter volume in healthy female and male adults ove

175 es of individual human subjects, we assessed gray matter volume in the frontal polar area, a region t

176 elwise analyses revealed significantly lower gray matter volume in the medial temporal lobe (maximum

177 p factor' scores are associated with reduced gray matter volume in the occipital lobe and left cerebe

178 mpter group showed significant reductions in gray matter volume in the orbitofrontal cortex, hippocam

179 relates with economic irrationality: reduced gray matter volume in this area correlates with the freq

180 The anteromedial pattern of reduced gray matter volume in visual primary and association cor

181 The inferred rate of gray matter volume loss was significantly accelerated in

182 s that cortical thickness of PFC regions and gray matter volume of the hippocampus and amygdala diffe

183 anticipatory strategies correlated with the gray matter volume of the hippocampus.

184 nd that females, who are known to have lower gray matter volume than males, have higher density throu

185 We found significant reductions in gray matter volume that were restricted to the occipital

186 Significant loss of gray matter volume was evident in schizophrenia, progres

187 with SNAP, sustained glucose metabolism and gray matter volume were associated with disproportionate

188 sure, whole-brain voxelwise regressions with gray matter volume were calculated.

189 ality, an older age, lower gait speed, lower gray matter volume, and greater global mean diffusivity

190 Cognitive impairment, lower gray matter volume, and white matter microstructural abn

191 -related variation in global measurements of gray matter volume, thickness, and surface area.

192 Regional gray matter volume, white matter integrity, and function

193 release correlated with reduced hippocampal gray matter volume.

194 eripheral visual loss can lead to changes in gray matter volume.

195 ported in a transdiagnostic meta-analysis of gray matter volume.

196 Compared with controls, PLWH had lower gray matter volumes (-13.7 mL; 95% confidence interval,

197 The presence of lower gray matter volumes and more white matter microstructura

198 These findings suggest that decreased gray matter volumes are not explained by compromised neu

199 Reduced regional gray matter volumes are often interpreted to reflect neu

200 rtical thickness measurement and subcortical gray matter volumetry could provide an early and accurat

201 puted on the whole cortical ribbon, and deep gray matter volumetry was performed after automatic segm

202 of correlations of each voxel with all other gray matter voxels in the brain.

203 In BD, cortical gray matter was thinner in frontal, temporal and parieta

204 In all analyses, cerebellar gray matter was used as the reference region.

205 Alterations in occipital gray matter were investigated by means of gray matter VB

206 Results T1 values of gray matter were significantly shorter for patients with

207 d morphometry, FreeSurfer revealed increased gray matter with obstructive sleep apnea.

208 uage-processing network is cortically (i.e., gray matter) well defined.

209 2LV [T1:T2]), brain atrophy (whole brain and gray matter), and cervical spinal cord lesions (T2LV) an

210 n a given region relative to the whole-brain gray matter, a pseudotemporal accumulation rate for each

211 largely explained by T1 relaxation times in gray matter, a surrogate measure of water content, and n

212 is found in neurons, astrocytes, and glia in gray matter, and antisense QAGR proteins accumulate with

213 also evaluated: whole cerebellum, cerebellar gray matter, atlas-based white matter, and subject-speci

214 iated with structural abnormalities in total gray matter, basal ganglia, and cerebellum.

215 ler neuroanatomical volumes, including total gray matter, cerebral cortex, and putamen.

216 are associated with neuron death and loss of gray matter, especially in the frontal cortex and hippoc

217 ly expressed within the anterior horn of the gray matter, in both cervical and lumbar sections.

218 ury at their synaptic connections within the gray matter, independent of the white matter pathology,

219 In contrast to the gray matter, these diffusion abnormalities correlated wi

220 cal MRI optimized for myelin contrast within gray matter, we also observe a stripe pattern.

221 Volumetric segmentation of global gray matter, white matter, ventricles, and hippocampi wa

222 perficial brain white matter and neighboring gray matter.

223 y projections to the midbrain periaqueductal gray matter.

224 anged, in parvalbumin interneurons and DLPFC gray matter.

225 tem plasticity have primarily focused on the gray matter.

226 parvalbumin interneurons, and in total DLPFC gray matter.

227 connectivity patterns within the spinal cord gray matter.

228 lues in white matter and 1.5 times higher in gray matter.

229 iated with changes in cerebral perfusion and gray matter.

230 showing lesions predominantly restricted to gray matter.

231 works are highly correlated to resting-state gray-matter networks, highlighting their functional role

232 orks correlated with signals from functional gray-matter networks, providing missing knowledge on how

233 The claustrum is a gray-matter structure that underlies neocortex and recip

234 group, but no association was found between gray-matter thickness and BPnd for either dopamine recep

235 atively associated with global mean cortical gray-matter thickness in the methamphetamine group, but

236 In the methamphetamine group, mean cortical gray-matter thickness was negatively associated with cum

237 d D2-type receptor availability and cortical gray-matter thickness, respectively.

238 1, smoking relapse was associated with less gray-matter volume (F1,74 = 28.32; familywise error P th

239 iations between corticothalamic-mediated IC, gray-matter volume, and smoking lapse/relapse.

240 rks of interacting functional modules in the gray-matter, limited research was directed to the functi

241 signal fluctuations similar to those of the gray-matter.

242 le to vCu-Au as validated by both the Harvey-Gray method of crystallographic-distance-to-force-consta

243 The Fine and Gray method was used to estimate the incidence of SCD ac

244 In a multivariate Fine and Gray model based on the external cohort, the presence of

245 e patterns generated on an identical uniform gray model in direct versus diffuse illumination.

246 In the Fine-Gray model, all 3 risk factors were independently associ

247 ed significantly increased resistance toward gray mold (Botrytis cinerea), a pathogen responsible for

248 The midline central gray of the pons and nucleus incertus receive input from

249 The lateral central gray of the pons receives bilateral input from the later

250 Finally, occipital white (OWM) and gray (OGM) human brain matter were quantified in vivo us

251 ury, neuroinflammation, or cell death in the gray or white matter.

252 xpectancy have identified the periaqueductal gray (PAG) as a key brainstem structure implicated in en

253 ated neuroinflammation in the periaqueductal gray (PAG) drives tolerance.

254 STATEMENT We demonstrate that periaqueductal gray (PAG) microglia contribute to the sexually dimorphi

255 d microglia activation in the periaqueductal gray (PAG), a central locus mediating the antinociceptiv

256 eurons (LepRb neurons) in the periaqueductal gray (PAG), the largest population of LepRb neurons in t

257 forebrain structures plus the periaqueductal gray (PAG).

258 Mutations in the human NBEAL2 gene cause gray platelet syndrome (GPS), a bleeding diathesis chara

259 he scaffolding protein Nbeal2, are causal of gray platelet syndrome (GPS), a rare recessive bleeding

260 EAL2 gene or Nbeal2 deficiency in mice cause gray platelet syndrome, a bleeding disorder characterize

261 ity that therapeutic interventions targeting gray rami might be useful in some chronic inflammatory p

262 ity that therapeutic interventions targeting gray rami might be useful in some inflammatory condition

263 crosympathectomy" by cutting the ipsilateral gray rami where they entered the spinal nerves near the

264 Using cerebellar gray reference, 18F-T807 data were expressed as standard

265 Fine and Gray regression analysis was conducted to determine the

266 return to work were assessed using Fine and Gray regression analysis.

267 ival was evaluated with a multivariable Fine-Gray regression model.

268 e and fatal CHD events using Cox regression, Gray's model, and competing risks analysis, adjusting fo

269 Using Gray's model, negative fluid balance, compared with even

270 Two approaches were used: gray scale level (GSL), measured from the ultrasound ima

271 smartphone camera and analyzed with a simple gray scale quantification procedure.

272 However, gray scale ultrasound and color Doppler measurements rev

273 The aim of this study was to describe the gray-scale and color Doppler ultrasonography (US) and ma

274 enital adrenal hyperplasia were evaluated by gray-scale and color Doppler ultrasonography.

275 Gray-scale and color Doppler US and MR findings of the p

276 ed to a complete ophthalmologic examination, gray-scale and Doppler ultrasonography, and nuclear magn

277 with varying levels of experience evaluated gray-scale CT scans for the presence of fractures and th

278 Using gray-scale images as the reference, multivariate analyse

279 Because of that, gray-scale thyroid ultrasonography and a fine-needle asp

280 t 4 cm proximal to the medial malleolus with gray-scale ultrasonography and SWE.

281 esticular lesions that were indeterminate on gray-scale US scans were further characterized with colo

282 arametric ultrasonography (US) consisting of gray-scale US, color Doppler US, strain elastography, an

283 On the basis of these results, a gray-scale-correction procedure was developed to achieve

284 tient CT scan again after application of the gray-scale-correction procedure.

285 on of a correction procedure to the template gray scales allowed for a linear correlation (r = 0.9946

286 an exponential correlation between template gray scales and printer deposition.

287 stigated by printing geometric phantoms with gray scales ranging from 0% (white) to 100% (black).

288 In a second step, gray scales, iodine deposition, and Hounsfield units wer

289 implantation in eutherian mammals using the gray short-tailed opossum (Monodelphis domestica) as a m

290 We reanalyze data for Gray Squirrels (Sciurus carolinensis), native to North A

291 el zone size matrix (GLZSM) and neighborhood gray-tone difference matrix (NGTDM) parameters: GLRL int

292 In this study of Cope's gray treefrog (Hyla chrysoscelis; Hylidae), we investiga

293 t consisting of four larval amphibian hosts [gray treefrogs, American toads (Anaxyrus americanus), le

294 dditionally, survival rates of hosts (larval gray treefrogs; Hyla versicolor) infected with Echinopar

295 a linear relationship between the ECL image gray value and the logarithmic concentration of the AFM1

296 ial GABAergic neurons in the pontine central gray; ventromedial, small GABAergic neurons that express

297 , including the ventrolateral periaqueductal gray (vlPAG) and locus ceruleus (LC).

298 ses in insular cortex and the periaqueductal gray, were noted.

299 ly 40 years later and across territory where gray wolves have been historically absent and remnant re

300 r hypertrophic substrates, especially in the gray zone of mild hypertrophy (maximum wall thickness </