ライフサイエンスコーパス: CTE

1 CTE and AD subjects did not differ significantly at the

2 CTE and MRE are our new standard imaging modalities for

3 CTE can be caused by mutations in genes encoding EpCAM,

4 CTE can only be confidently identified at postmortem and

5 CTE images were evaluated by two radiologists.

6 CTE is characterized by intestinal epithelial cell dyspl

7 CTE is defined by an abundance of hyperphosphorylated ta

8 CTE is known to share similar neuropathological features

9 CTE may be suspected when behavior, cognition, and/or me

10 CTE pathology has been described in individuals with no

11 CTE pathology was rare in a large multicentre national d

12 CTE promotes poly(GR) stabilization, aggregation, and to

13 CTE was not associated with a different clinical present

14 CTE-associated HAI-2 mutant proteins exhibited reduced a

15 dementia pugilistica in retired boxers(1-3), CTE has since been identified in former participants of

16 bility of cooked rice incorporated with 2.5% CTE using a microwave oven.

17 A CTE severity score, maximum standardized uptake value (S

18 ons within CTE sites identified by NMR and a CTE domain swapping experiment also confirmed the functi

19 ses the levels of unspliced RNA containing a CTE and specifically promotes the association of this RN

20 me association of unspliced RNA containing a CTE.

21 ould not be viewed as a 'safer' version of a CTE.

22 ge of players under age 60 years reporting a CTE diagnosis was 2.3% versus 3.7% in participants age 6

23 n of its own intron-containing RNA through a CTE-mediated mechanism.

24 nalysis of CTE including AD and CTE with AD (CTE/AD) post-mortem human brain samples.

25 All CTE participants had co-occurring neuropathologic proces

26 on and unique transcriptome signatures among CTE, CTE/AD, and AD.

27 However, despite heightened variation among CTE neurons, CTE cases exhibited lower mean values than

28 sequencing analysis of CTE including AD and CTE with AD (CTE/AD) post-mortem human brain samples.

29 Visual interpretation of both PET/CTE and CTE images detected the presence of disease in all bowel

30 PET/CTE and CTE images were each visually assessed for Crohn disease

31 n in Alzheimer's disease, Pick's disease and CTE(17-19).

32 These localization and CTE analyses support the inference that MARCH6 and Doa10

33 ship between duration of football played and CTE risk and severity.

34 of the relationship between years played and CTE status remained consistent.

35 ciated with CTE status when years played and CTE status were both related to brain bank selection acr

36 ional/behavioural data were compared between CTE and AD subjects at the time of dementia diagnosis an

37 unprecedented negative and positive biaxial CTE (i.e., -5950 and 10 710 ppm K(-1) ), but also large

38 validated sensitive and specific biomarkers, CTE pathology might not be inexorably progressive or spe

39 um C-reactive protein (0.82, P = 0.023), but CTE score did not.

40 ntrols in brain regions that are affected by CTE and did not have elevated amyloid-beta levels.

41 lar mRNAs with retained introns use cellular CTE equivalents to overcome restrictions to their expres

42 c criteria for CTE neuropathological change (CTE-NC) were identified (athletes, n = 10; long-term sur

43 ated the ability of years played to classify CTE status using receiver operating characteristic curve

44 ly exploitable therapeutic pathway to combat CTE.

45 A conserved CTE asparagine residue is required for ubiquitylation an

46 g CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichot

47 d unique transcriptome signatures among CTE, CTE/AD, and AD.

48 agmins) were commonly down-regulated in CTE, CTE/AD, and AD.

49 be explored in former athletes demonstrating CTE-linked clinical phenotypes or symptoms as a means of

50 es as a basis for design choices for desired CTE values.

51 ers (2.8%) self-reported clinician-diagnosed CTE.

52 sented an important step for differentiating CTE from other neurodegenerative diseases.

53 in cortical layers II and III, distinguishes CTE from Alzheimer's disease and other tauopathies(10,11

54 Such selectivity suggests that the Doa10 CTE is involved in substrate discrimination and not gene

55 ividuals with neuropathologically documented CTE.

56 truncated EAAT2 and COOH terminus of EAAT2 (CTE).

57 lic cells to demonstrate ultra-low effective CTE with a wide temperature range.

58 ted but highly conserved C-terminal element (CTE) in Doa10; this cytosolically disposed 16-residue mo

59 at contain a constitutive transport element (CTE), a cis-acting 2-fold symmetric RNA stem-loop motif.

60 monkey virus constitutive transport element (CTE), an element that enables export of unspliced, intro

61 virus (MPMV) constitutive transport element (CTE).

62 known as the constitutive transport element (CTE).

63 lar or viral constitutive transport element (CTE).

64 ies are needed to determine whether elevated CTE-associated tau can be detected in individual persons

65 isease and chronic traumatic encephalopathy (CTE) (in which both 3R and 4R isoforms are found in the

66 lopment of chronic traumatic encephalopathy (CTE) and Alzheimer's disease.

67 The term chronic traumatic encephalopathy (CTE) has recently entered public consciousness via media

68 stent with chronic traumatic encephalopathy (CTE) have been reported in ASF players, there are curren

69 Chronic traumatic encephalopathy (CTE) in particular is associated with repetitive mild TB

70 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with expo

71 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that has been associ

72 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is associated w

73 Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder that is associated

74 Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy that is associated

75 Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of

76 Chronic traumatic encephalopathy (CTE) is associated with repeated traumatic brain injurie

77 Chronic traumatic encephalopathy (CTE) refers to pathologic changes that have been found i

78 h century, chronic traumatic encephalopathy (CTE) was conceptualized as a neurological disorder affec

79 lopment of chronic traumatic encephalopathy (CTE), a neurodegenerative disorder histopathologically c

80 rticularly chronic traumatic encephalopathy (CTE).

81 described chronic traumatic encephalopathy (CTE).

82 ficits, or chronic traumatic encephalopathy (CTE).

83 iteria for chronic traumatic encephalopathy (CTE).

84 including chronic traumatic encephalopathy (CTE).

85 ocusing on chronic traumatic encephalopathy (CTE).

86 hy (PET/CTE), compared with CT enterography (CTE) alone, in the assessment of patients with Crohn dis

87 based imaging, specifically CT enterography (CTE) and magnetic resonance enterography (MRE), transcut

88 Computed tomography enterography (CTE) images in a three-year period were included randoml

89 parable to computed tomography enterography (CTE).

90 Syndromic congenital tufting enteropathy (CTE) is a life-threatening recessive human genetic disor

91 Congenital tufting enteropathy (CTE) is a rare autosomal recessive diarrheal disorder pr

92 Congenital tufting enteropathy (CTE) is a severe autosomal recessive human diarrheal dis

93 ations (FE) and charge-transfer excitations (CTE) coupled nonadiabatically to local intramolecular vi

94 Exogenous CTE peptide increased PR-binding affinity for PRE as did

95 The coefficient of thermal expansion (CTE) is a physical quantity that indicates the thermal e

96 Ultra-low coefficient of thermal expansion (CTE) is an elusive property, and narrow temperature rang

97 tween the coefficients of thermal expansion (CTE) of the consecutive device layers of field-effect tr

98 ating, its coefficient of thermal expansion (CTE) smoothly increases, leading to a room temperature C

99 r ultralow coefficient of thermal expansion (CTE), achieving a broad range of CTE values with access

100 The redox regulated C-terminal extension (CTE) and the associated alternate splicing mechanism, wh

101 and the impact of the C-terminal extension (CTE) by contrasting HP1a to its paralogue, HP1b.

102 VirD2 proteins and the C-terminal extension (CTE) domain of Arabidopsis thaliana telomerase reverse t

103 -box proteins, while a C-terminal extension (CTE) induces a second bend, resulting in RNA crimping.

104 We show here that this C-terminal extension (CTE) mediates in vivo localization of the protein to the

105 ction is mediated by a C-terminal extension (CTE) of the DNA binding domain and is unique to the estr

106 ally disordered carboxyl-terminal extension (CTE) of the DNA binding domain.

107 short flexible carboxyl terminal extension (CTE) that interacts with the minor groove flanking the P

108 C and CAT-tailing-like C-terminal extension (CTE).

109 terminus, known as the C-terminal extension (CTE).

110 tes are located in the C-terminal extremity (CTE) of the receptor following its palmitoylation site.

111 Signatures of FE/CTE mixing and the extent of electron/hole separation ar

112 rs a repressive conformation of the flexible CTE enabling it to bind to preferred sequences flanking

113 The effect of Clitoria ternatea flower (CTE) incorporated into cooked rice using domestic cookin

114 een implicated as a potential antecedent for CTE amongst Iraq and Afghanistan Warfighters.

115 Among 339 subjects assessed for CTE in the National Alzheimer's Coordinating Center data

116 reliminary consensus diagnostic criteria for CTE neuropathological change (CTE-NC) were identified (a

117 ment of pathological diagnostic criteria for CTE represented an important step for differentiating CT

118 stablished premortem diagnostic criteria for CTE.

119 et neuropathological diagnostic criteria for CTE.

120 e a unifying neuropathological criterion for CTE, and support the hypothesis that the formation and p

121 f the new mixture were good or excellent for CTE.

122 RBT represents the greatest risk factor for CTE pathological features, although clinicopathological

123 udy was to identify the gene responsible for CTE.

124 ns in the gene for EpCAM are responsible for CTE.

125 in the brains of living persons at risk for CTE has not been well studied.

126 a prospective study of a cohort at risk for CTE.

127 The sumoylated CTE fragment (CTE-SUMO-1) accumulates in the spinal cord of these mice

128 show that the Tap gene contains a functional CTE in its alternatively spliced intron 10.

129 ntaining RNA through the use of a functional CTE within intron 10.

130 Furthermore, CTE is widely considered to be a consequence of exposure

131 ed by heterologous RNA export elements, e.g. CTE of simian type D retroviruses.

132 polyamides in both the upstream minor groove CTE site and the minor groove of the ERE half-site.

133 football played were associated with having CTE (odds ratio [OR] = 1.30 per year played, 95% confide

134 ing to the CTE, indicating that DNA and HMGB-CTE interactions are mutually exclusive.

135 We conclude that a transient HMGB-CTE interaction alters a repressive conformation of the

136 actors may have a role in tau aggregation in CTE.

137 totagmin 1 (SYT1) were markedly decreased in CTE and AD compared to normal.

138 owever, the morphologies of tau filaments in CTE and the mechanisms by which brain trauma can lead to

139 Moreover, filaments in CTE have distinct protofilament interfaces to those of A

140 rain tau isoforms assemble into filaments in CTE, and residues K274-R379 of three-repeat tau and S305

141 es (CAMs) associated genes was only found in CTE.

142 tion and post-translational modifications in CTE remain largely unexplored.

143 that the early pathological loci of NFTs in CTE brains are regions of high deformation during injury

144 demonstrate that astroglial tau pathology in CTE is composed of 4R-immunoreactive thorn-shaped astroc

145 e is known about the molecular properties in CTE.

146 ion, radiological confidence, and quality in CTE evaluations.

147 aptotagmins) were commonly down-regulated in CTE, CTE/AD, and AD.

148 ses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropath

149 on during acute and chronic phases including CTE-like pathology and dysfunction after repetitive TBI.

150 Accordingly, the measured instantaneous CTE of polystyrene resin varied from 5.86 x 10(-5) degre

151 ved and recorded to derive the instantaneous CTE of the packaged LED under different injected current

152 t the use of conventional materials with low CTE.

153 bout the neuropathological aspects that make CTE unique.

154 conserved Asn residue (N890A) in the MARCH6 CTE stabilized the normally short lived enzyme to the sa

155 Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms

156 Moreover, CTE significantly reduced the level of rapidly digestibl

157 on from a pNL4-3 provirus that used the MPMV CTE for RNA export.

158 o the Tap/Nxf1 pathway, utilized by the MPMV CTE, through the expression of a RevM10-Tap fusion prote

159 pite heightened variation among CTE neurons, CTE cases exhibited lower mean values than Control cases

160 s, and low testosterone when compared to non-CTE respondents.

161 The presence and accumulation of CTE-SUMO-1 is specific to ALS mice, since it does not oc

162 nducted transcriptome sequencing analysis of CTE including AD and CTE with AD (CTE/AD) post-mortem hu

163 These unresolved aspects of CTE underlie disparate claims about its clinical and pat

164 ia are developed, the clinical assessment of CTE should be informed by modern research that is of rel

165 ical findings described as characteristic of CTE, in studies published before 2016, were not included

166 n toto, as the pathology 'characteristic' of CTE.

167 iomarkers of pathological characteristics of CTE and longitudinal tracking with neuropsychological ev

168 urrent neuropathological characterization of CTE is acknowledged as preliminary.

169 hological and assumed clinical correlates of CTE have been well characterized, its effects on cortica

170 anism, and clinicopathological correlates of CTE reflect the current reliance on postmortem case seri

171 rkers in diagnosis, and existing criteria of CTE are reviewed.

172 e as a causative agent in the development of CTE and may provide a new target for the treatment of CT

173 mild TBI and autopsy-confirmed diagnosis of CTE.

174 such, the immunohistochemical distinction of CTE neuropathology from other mixed 3R/4R tauopathies of

175 proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior partici

176 an replace Nxt1 to enhance the expression of CTE-containing mRNA and promote its association with pol

177 ast to general impressions, the incidence of CTE is unknown, the clinical diagnostic criteria have no

178 criteria define the pathognomonic lesion of CTE as patchy tau pathology within neurons and astrocyte

179 ral brain regions, a typical localization of CTE tauopathy.

180 vidence about the clinical manifestations of CTE has been accumulating via post-mortem medical record

181 ique information about the manifestations of CTE, including clinical and preclinical stages.

182 s may represent a new pathological marker of CTE, and further examination of dendritic changes could

183 eration of a Spint2-deficient mouse model of CTE.

184 criteria for defining the neuropathology of CTE were forged in 2015 and published in 2016.

185 The odds of CTE double every 2.6 years of football played.

186 glial and neurofibrillary tau pathologies of CTE are phenotypically distinct from each other and reca

187 few studies have compared the pathologies of CTE with those of other neurodegenerative disorders or o

188 tochemistry, we performed tau phenotyping of CTE neuropathologies and compared this to a range of tau

189 tion, characterization, and/or prediction of CTE.

190 expansion (CTE), achieving a broad range of CTE values with access to large thermally induced dimens

191 stantially enlarging the accessible range of CTE.

192 of NXF1:NXT1 facilitates the recognition of CTE-RNA and promotes its nuclear export.

193 review discusses the state of the science of CTE and raises considerations for researching and interp

194 Neuropathological severity of CTE was distributed across the highest level of play, wi

195 In contrast, neurofibrillary tangles of CTE contain both 3R and 4R tau, with post-translational

196 mote polysome association and translation of CTE-RNA, we investigated the effect of 9G8 on cytoplasmi

197 ay provide a new target for the treatment of CTE in individuals carrying SPINT2 mutations.This articl

198 Research on CTE would benefit greatly from incorporating principles

199 s of consciousness (LOC) was reported in one CTE and one AD subject; information about injuries witho

200 s enterocolic fistula, not evident on PET or CTE alone.

201 PET/CTE also may reveal clinically significant findings, suc

202 PET/CTE and CTE images were each visually assessed for Crohn

203 Visual interpretation of both PET/CTE and CTE images detected the presence of disease in a

204 combined (18)F-FDG PET/CT enterography (PET/CTE), compared with CT enterography (CTE) alone, in the

205 and underwent abdominal-pelvic (18)F-FDG PET/CTE using neutral oral and intravenous contrast medium.

206 Low-dose (18)F-FDG PET/CTE, compared with CTE, may improve the detection and gr

207 The effective dose from PET/CTE was 17.7 mSv for the first 4 patients and 8.31 mSv f

208 ith biopsies within 27 d (mean, 12 d) of PET/CTE.

209 ) of 13 patients, (18)F-FDG uptake using PET/CTE revealed active inflammation in a bowel segment not

210 parate risk scores were developed to predict CTE (defined as the composite of stent thrombosis or myo

211 rate similar clinical phenotypes to putative CTE.

212 At the present time, evidence regarding CTE has not been confirmed in a prospective study of a c

213 Comorbidities in participants self-reporting CTE were significantly more common, including sleep apne

214 cantly higher in participants self-reporting CTE.

215 structively determine the spatially resolved CTE of the packaged LED device, which offers significant

216 prepared from mutant G93A-SOD1 mice reveals CTE to be of a higher molecular weight than expected bec

217 Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms

218 nding surface of the HP1a CSD plus its short CTE provide the needed discrimination among HP1a's partn

219 ng former players may be inclined to suggest CTE without a thorough exploration of comorbid factors t

220 The sumoylated CTE fragment (CTE-SUMO-1) accumulates in the spinal cord

221 NP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distributi

222 nal American football players with suspected CTE (n = 14) and compared results with those of cognitiv

223 key virus-CTE or the recently discovered Tap-CTE.

224 hly increases, leading to a room temperature CTE that is similar to that of ZrW(2)O(8) and positive t

225 ed the field have asserted definitively that CTE is a delayed-onset and progressive neurodegenerative

226 progressive, and there is now evidence that CTE neuropathology might not be progressive in some indi

227 Overall, the results show that CTE is a useful ingredient to incorporate with cooked ri

228 ue samples from G93A-SOD1 mice, we show that CTE-SUMO-1 is targeted to promyelocytic leukemia nuclear

229 These findings suggest that CTE may not have a distinct clinical profile when other

230 athological evidence of CTE, suggesting that CTE may be related to prior participation in football.

231 This evidence suggests that CTE is manifested clinically by changes in cognition (es

232 One key finding was that CTE neurons exhibited increased variability and distribu

233 The CTE interacts directly with the Tap protein (also known

234 The CTE-associated loss of the cell junctional proteins EpCA

235 tween active site residues of Rv0805 and the CTE that determine its association with the cell wall.

236 of minor groove DNA contacts mediated by the CTE and by changing the helical geometry of DNA such tha

237 y of the Rca complex can be modulated by the CTE of the alpha isoform, particularly in relation to a

238 s; and indicate that the bend induced by the CTE results primarily from a steric block.

239 may be specific pathological markers for the CTE pathology.

240 mmation per bowel segment was higher for the CTE score (0.79, P < 0.0001) than the SUVmax ratio (0.62

241 However, the CTE (only 4 residues in HP1a as compared with 87 residue

242 tal deletion of phosphoacceptor sites in the CTE affected proper receptor regulation.

243 ced single point mutations of Lys-428 in the CTE of Rca-alpha from wheat (Triticum aestivum) (TaRca2-

244 osphorylation of Ser and Thr residues in the CTE of the receptor in a redundant fashion, able to inco

245 on in the helicase core and the other in the CTE-that may help displace or sequester the opposite RNA

246 al coherence tomography (OCT) to measure the CTE of an InGaN-based (lambda = 450 nm) high-power LED e

247 from naturally intronless genes, but not the CTE or RRE from intron-containing genes, significantly e

248 The importance of the CTE for binding JDP2 was confirmed by peptide competitio

249 to the role and functional importance of the CTE for co-activator interactions.

250 accurate and immediate determination of the CTE of packaging materials is gaining importance because

251 Rv0805 and a truncated mutant devoid of the CTE produce different phenotypic effects when expressed

252 An Ashby plot of the CTE versus density serves as a quantitative comparison o

253 Functional conservation of the CTE was investigated in the human ortholog of Doa10, MAR

254 ding affinity for PRE as did deletion of the CTE.

255 mination among HP1a's partners, and that the CTE is important for differentiating the interactions of

256 sults with the yeast enzyme suggest that the CTE is involved in the recognition and/or ubiquitylation

257 Here we show that the CTE of PR contains a specific binding site for HMGB that

258 Here, we show that the CTE-associated early-onset intestinal failure and lethal

259 ecific PRE DNA inhibited HMGB binding to the CTE, indicating that DNA and HMGB-CTE interactions are m

260 While the CTE and RRE primarily enhance nucleocytoplasmic export,

261 onal importance of JDP2 interaction with the CTE for enhancement of PR transcriptional activity.

262 Vmax (0.67, P = 0.013), as compared with the CTE score (0.62, P = 0.024).

263 nvolved in binding of JDP2 reside within the CTE.

264 of candidate symptoms in retired athletes to CTE is complicated by the presence of multiple premorbid

265 ayers described neuropathology attributed to CTE that was broad and diverse.

266 all diagnostic yield of MRE is comparable to CTE.

267 Compared to CTE the image quality is not quite as good, and there is

268 at the neuropathology described as unique to CTE may not be unique.

269 fers significant advantages over traditional CTE measurement techniques.

270 These engineered tunable CTE thin film can be applied to minimize thermal fatigue

271 go on to show that insertion of an ultrathin CTE buffer layer mitigates this problem and can help ach

272 mmation in a bowel segment not evident using CTE (n = 2) or revealed an enterocolic fistula missed wi

273 The incorporation of 1.25% and 2.5% (w/v) CTE caused a reduction in the starch digestibility of co

274 id indicator of neuropathologically verified CTE.

275 taining either the Mason-Pfizer monkey virus-CTE or the recently discovered Tap-CTE.

276 euroimaging or laboratory evaluations, while CTE currently only can be definitively diagnosed postmor

277 A family with 2 children affected with CTE was identified.

278 CI] = 1.19-1.41; p = 3.8 x 10(-9) ) and with CTE severity (severe vs mild; OR = 1.14 per year played,

279 erpreting cognitive outcomes associated with CTE and for developing preventive treatment programs.

280 ing the clinical syndrome(s) associated with CTE and the necessary and sufficient symptoms needed for

281 at can affect cognition were associated with CTE diagnoses in both older and younger players.

282 rs played remained adversely associated with CTE status when years played and CTE status were both re

283 se that has been cognitively associated with CTE.

284 europathologic processes are coexistent with CTE pathology.

285 Low-dose (18)F-FDG PET/CTE, compared with CTE, may improve the detection and grading of active inf

286 players have been clinically diagnosed with CTE, a postmortem condition.

287 ts from the brains of three individuals with CTE at resolutions down to 2.3 angstrom, using cryo-elec

288 revealed an enterocolic fistula missed with CTE (n = 1).

289 of the Agrobacterium bait proteins, or with CTE.

290 Participants with CTE were 1/10th as likely to have played <4.5 years (neg

291 association of years of football played with CTE pathological status and severity.

292 l features of deceased football players with CTE.

293 The sensory evaluation of cooked rice with CTE given by panelists demonstrated a good overall accep

294 cteristics, the hardness of cooked rice with CTE remained unchanged, whereas a reduction in stickines

295 reduction in stickiness of cooked rice with CTE was observed.

296 Coordinating Center dataset, 6 subjects with CTE and 25 subjects with AD neuropathologic change match

297 Point mutations within CTE sites identified by NMR and a CTE domain swapping ex

298 9.8-10.7) compared with participants without CTE.

299 d 5 cases without (M(age) = 76 +/- 11 years) CTE.

300 6 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87