ライフサイエンスコーパス: progressor

1 ssful NGS, using samples obtained from a BE 'progressor'.

2 dividuals who did not control viremia (acute progressors).

3 ith high-grade dysplasia (HGD) or cancer (UC progressors).

4 and patients with progressive HIV infection (progressors).

5 or visual field-guided progression analysis (progressors).

6 points (p < 0.0001), but not present in non-progressors.

7 a cohort of elite controllers and in chronic progressors.

8 eated eye at 1 year were classified as being progressors.

9 s it is low to undetectable in aviremic slow progressors.

10 strointestinal tract of both controllers and progressors.

11 lymphocyte activation in controllers than in progressors.

12 fore the appearance of autoantibodies in the progressors.

13 0.007) in acute controllers but not in acute progressors.

14 apidly progressed to AIDS compared with slow progressors.

15 mia in a large cohort of HIV controllers and progressors.

16 ubgroup of 171 (59%) containing 88% of rapid progressors.

17 and 9 SIV-infected PTM, of which 3 were slow progressors.

18 responses distinguished HIV controllers from progressors.

19 A-B57-restricted response in controllers and progressors.

20 n both HIV controllers and untreated chronic progressors.

21 senescence underlies tumor progression in UC progressors.

22 rs, but less severe and transient in typical progressors.

23 nt (within 3 months) nondiabetic OGTTs in 55 progressors.

24 to approximately 50% of the sites in chronic progressors.

25 replicative capacity compared to virus from progressors.

26 es derived from chronically infected viremic progressors.

27 ver time for both progressors as well as non-progressors.

28 W9, NefMW9, and env(ARF)cRW9-in both ECs and progressors.

29 non-progressors, early progressors and late progressors.

30 ptides was commonly observed in both ECs and progressors.

31 essing macaque to the intermediate and rapid progressors.

32 inversely correlated with viral load in the progressors.

33 may focus on patients predicted to be rapid progressors.

34 ssors, who remained healthy, were matched to progressors.

35 , sustained at 48 months) compared to 58 non-progressors.

36 ea score lower than 4 compared with the slow progressors.

37 lly better helper activity than those of HIV progressors.

38 controllers but are rare or absent in HIV-1 progressors.

39 oma disease progressors and nonrapid disease progressors.

40 ssors (LTNPs), regular progressors and rapid progressors.

41 ly distinguish LTNP individuals from regular progressors.

42 that differentiated IPF progressors and non-progressors.

43 a population not commonly present in chronic progressors.

44 t is comparable to the proportion in chronic progressors.

45 by Ki-67 expression) in controllers than in progressors.

46 udy at 1 year, 22 (12.1%) were classified as progressors.

47 (+) T-cell response more frequently than PML progressors (100% versus 27.3%; P = 0.001), while only a

48 in 2 years of follow-up and were selected as progressors; 106 nonprogressors, who remained healthy, w

49 26 cognitively normal (CN), 194 MCI (39 MCI-progressors, 148 MCI-stable, 2 years after baseline), an

50 ile range: 2.1 to 7.2 years), there were 228 progressors (21%), whose annualized progression rates wi

51 elevated in fast progressors compared to non-progressors 3 months after LT.

52 The "rapid progressors" (32% of eyes) had a mean decay rate of 52.2

53 Of these progressors, 39 (53%) patients were diagnosed with ATN,

54 ate cohort of samples (median methylation in progressors 67.8% vs 96.7% in nonprogressors; P = 0.0001

55 resulting from 4.6 (3.3-5.7) months for 123 progressors, 7.3 (6.0-10.0) months in 77 with adverse ef

56 tory mutations occurred in isolates from the progressor, a superior HIV-specific CD8(+) T-cell respon

57 mory subset, whereas HIV-specific B cells in progressors accumulated in tissue-like and activated mem

58 d in antigenic-peptide-stimulated cells from progressors after blocking the PD-1/PD ligand 1 (PD-L1)

59 1 year after infection) and three were rapid progressors (AIDS within 6 months).

60 ion infectivity compared to those from acute progressors (all P<0.01).

61 and throughout the study period (P = .001); progressors also had higher IL-6 and I-FABP levels over

62 observed in HIV-1-specific CD8+ T cells from progressors, although an increase in both telomere lengt

63 evels of unmethylated INS DNA in the at-risk progressor and at-risk nonprogressor groups followed for

64 Surprisingly, we found that both progressor and regressor tumors harbored proliferating (

65 46 progressors and 107 matched controls were identified in

66 factor compared to Vif sequences from normal progressors and acutely infected individuals.

67 de were collected along the colon of nine UC progressors and analyzed for telomere length, DNA damage

68 fferences between B57-positive (B57(+)) slow progressors and B57(+) rapid progressors have largely fo

69 t cohorts of South African and Gambian adult progressors and controls.

70 egulated in HIV-specific CD8(+) T cells from progressors and correlated positively with disease progr

71 in a total of eight lesions from each of ten progressors and four nonprogressors suffering from longs

72 Here, we show that compared with HIV-1 progressors and HIV-1-negative persons, CD4+ T cells fro

73 her HOMA-IR predicted hypermetabolism in MCI-progressors and hypometabolism in AD in medial temporal

74 wo clinical datasets: non-progressors, early progressors and late progressors.

75 8 months, group differences between clinical progressors and non-progressors were significant for sel

76 proteomic signatures that differentiated IPF progressors and non-progressors.

77 d not differ significantly over time between progressors and nonprogressors (P = .60), progressors ha

78 22, CTLA4, and IL2RA) did not differ between progressors and nonprogressors but were elevated in both

79 We trained a classifier to differentiate progressors and nonprogressors on baseline cartilage tex

80 e proteins of differential abundance between progressors and nonprogressors were identified.

81 ups that were followed for 7-20 years (rapid progressors and nonprogressors), as well as a reference

82 miRs differed by more than two-fold between progressors and nonprogressors, and 12 miRs differed bet

83 levels did not differ between liver disease progressors and nonprogressors, the association of sCD14

84 phocyte engraftment dynamics were similar in progressors and nonprogressors.

85 A ploidy, and AOL most accurately identified progressors and nonprogressors.

86 s between a cohort of rapid glaucoma disease progressors and nonrapid disease progressors.

87 m long term non progressors (LTNPs), regular progressors and rapid progressors.

88 ral isolates were found in over one-third of progressors and slow progressors, but much less frequent

89 Mutations in CTNNB1 were detected in 3 of 10 progressors and VEGFA amplification in 1 of 7 responders

90 s SNP was typed in European cohorts of rapid progressors and was found to be protective for AIDS 1993

91 converted and progressed to type 1 diabetes (progressors) and those who remained autoantibody negativ

92 ly confirmed TB disease and were included as progressors, and 115 nonprogressors were included as con

93 glaucoma, can identify patients who are fast progressors, and can predict patterns of future VF loss

94 eatment, including long-term nonprogressors, progressors, and chronically infected subjects provided

95 ompared to more homogenous signatures in non-progressors, and found that non-progressors were enriche

96 ients, virologic noncontrollers, immunologic progressors, and uninfected controls (P < 0.05 for each

97 multiethnic cohort of HIV-1 controllers and progressors, and we analyzed the effects of individual a

98 f FVC over time, termed "stable low," "rapid progressor," and "slow progressor." Compared with the sl

99 Three infants were defined as "progressors," and five were defined as "slow progressors

100 109P3N were recovered from a passage-3 rapid-progressor animal during chronic infection (24 weeks pos

101 tical early weeks of acute infection only in progressor animals that did not control viral replicatio

102 ), 46 chronic progressors (CP), and 43 acute progressors (AP) were examined for their CD4, CCR5, and

103 We found that T1D progressors are characterized by a distinct cord blood l

104 fferences between Mamu-B*17-positive ECs and progressors are not readily discernible using standard a

105 s decreased significantly over time for both progressors as well as non-progressors.

106 HIV-specific CD8(+) T cell proliferation in progressors, as did silencing of necroptosis mediator RI

107 differentiated between intermediate and fast progressors at 3 months.

108 mice and humans is also evident in latent TB progressors before diagnosis, suggesting that these resp

109 r (IFNgamma) responses only in slow fibrosis progressors, both in the periphery (P = 0.003) and liver

110 remain aviremic and behave as long-term non-progressors but some progress to AIDS.

111 etion was progressive and sustained in rapid progressors, but less severe and transient in typical pr

112 nd in over one-third of progressors and slow progressors, but much less frequently in aviremic long-t

113 s of CMV-specific CD8(+) T cells in LTNP and progressors by increasing both the numbers of cells ente

114 The CFI scores between clinical progressors (CDR score, >/=0.5) and nonprogressors (CDR

115 In addition, progressor cells displayed a decreased ability to upregu

116 analysis of larger 'progressor' versus 'non-progressor' cohorts.

117 elomeres are also significantly increased in progressors (colons harbouring cancer/dysplasia and/or a

118 heterogeneous protein expression patterns in progressors compared to more homogenous signatures in no

119 RO-C3, PRO-C4, and C4M were elevated in fast progressors compared to non-progressors 3 months after L

120 decreased at study inception in 19 fibrosis progressors compared with 20 fibrosis nonprogressors (P

121 RNFL thickness were significantly higher for progressors compared with nonprogressors (-0.72 mum/y vs

122 rior to either autoantibody was lower in T1D progressors compared with nonprogressors, with simultane

123 "stable low," "rapid progressor," and "slow progressor." Compared with the slow progressors, the rap

124 mprove the function of NK cells from chronic progressors (CP) on ART.

125 s from 45 elite controllers (EC), 46 chronic progressors (CP), and 43 acute progressors (AP) were exa

126 m EC (n = 54) compared to those from chronic progressors (CP; n = 41) by constructing chimeric viruse

127 SIV-specific immune responses (conventional progressors [CP]).

128 olates from HLA-B*57 ES and HLA-B*57 chronic progressors (CPs).

129 sponse to infected CD4+ T cells than chronic progressors (CPs).

130 ells from ECs (n = 20), chronically infected progressors (CPs; n = 18), and highly active antiretrovi

131 Progressors demonstrated higher baseline levels of gluco

132 gress to disease after infection with HIV-1 (progressors) differed in their ability to inhibit viral

133 variants (R3A and R3B) isolated from a rapid progressor differentially activated pDCs to produce alph

134 f patients in the two clinical datasets: non-progressors, early progressors and late progressors.

135 Defective cytotoxicity of progressor effectors could be restored after treatment w

136 plasma viruses were similarly low in chronic progressors, elite suppressors, and HAART-treated patien

137 y HIV-1-specific CD8(+) T cells from chronic progressors even in late stages of disease, and HIV-1-sp

138 not significantly different between LTNP and progressors, even though their capacity to proliferate t

139 at antibodies from controllers and untreated progressors exhibit increased phagocytic activity, alter

140 Longitudinally, signatures of T1D progressors exhibited increasing inflammatory bias.

141 nd sustained depletion of mBAct cells, rapid progressors failed to develop SIV-specific Ab responses,

142 t that genomic biomarkers can distinguish UC progressors from nonprogressors and improve cancer surve

143 aracteristic curves (AUC) in differentiating progressors from nonprogressors and normal subjects were

144 bjects were both 0.86 and in differentiating progressors from nonprogressors were 0.68 and 0.64, resp

145 ivity and 92% specificity for distinguishing progressors from nonprogressors with optimum choice of t

146 of 0.86 (95% CI, 0.83-0.88) to discriminate progressors from nonprogressors.

147 lar thickness measurements in discriminating progressors from nonprogressors.

148 ctive ability of risk scores to discriminate progressors from nonprogressors.

149 s that precede T1D onset and distinguish T1D progressors from nonprogressors.

150 ce similar to that of TCA in differentiating progressors from normal subjects and nonprogressors.

151 TCA red pixel parameters in differentiating progressors from normal subjects were both 0.86 and in d

152 r distinguishing patients with neoplasia (UC progressors) from those without (UC nonprogressors), inc

153 The progressor group had larger baseline NV size (1834 +/- 5

154 global trend towards hypomethylation in the progressor group was observed.

155 ssified as IF/TA nonprogressors (group 1) or progressors (group 2) using graft function and histology

156 Rapid progressors had a faster component rate of >25%/year.

157 Generally, progressors had a higher risk category and nonprogressor

158 those who were designated to be slow disease progressors had an increased proportion of autoreactive,

159 Progressors had faster chamber remodeling, functional cl

160 mal immune activation; high viral load HIV-2 progressors had high values, similar to or exceeding tho

161 decreased corneal nerve fiber density, rapid progressors had increased levels of SIV RNA and CD68-pos

162 By contrast, rapid disease progressors had increased numbers of islet-specific CD8(

163 This small subset of slow progressors had limited innate immune activation in muco

164 The 74 progressors had lower baseline FPIR values than nonprogr

165 ompared with the slow progressors, the rapid progressors had shorter diagnosis delay, more bulbar-ons

166 en progressors and nonprogressors (P = .60), progressors had significantly higher plasma levels of sC

167 on the early CTL responses of eventual slow progressors have been available.

168 e (B57(+)) slow progressors and B57(+) rapid progressors have largely focused on cytotoxic T lymphocy

169 HIV-2 non-progressors have low rates of T-cell turnover (both CD4(

170 For MCI-progressors, higher HOMA-IR predicted higher FDG in the

171 ms and HLA-B haplotypes within Long Term Non-Progressor HIV-1-controllers ((LTNP-C), defined by maint

172 ms and HLA-B haplotypes within Long Term Non-Progressor HIV-1-controllers ((LTNP-C), defined by maint

173 and T cells only slightly differ among HIV-1 progressors, HIV-1 elite controllers, and HIV-1-negative

174 In contrast to those in progressors, HIV-specific CD4(+) T-cell responses in the

175 d may assist in the identification of "rapid progressors." However, the absence of CC-16 does not app

176 longitudinal viral sequences from high-risk progressors (HRPs) and low-risk progressors (LRPs).

177 ence the emergence of mutations in high-risk progressors (HRPs) versus low-risk progressors (LRPs).

178 The identification of "rapid progressors" identifies high-risk patients for appropria

179 globulin class switching than cells from HIV progressors.IMPORTANCE Dissecting the factors that are i

180 still has a relevant role in detecting fast progressors in advanced disease.

181 nt differences were detected between ECs and progressors in any measured parameter.

182 these LTA were as pathogenic as viruses from progressors in organ culture.

183 drop in alpha-diversity was observed in T1D progressors in the time window between seroconversion an

184 riants were primarily found in slow/standard progressors in the URF group, whereas they predominated

185 in a regression analysis of the 48 remaining progressors in whom the rate of decline became more mark

186 the integration profile of HIV-1 in viremic progressors, individuals receiving antiretroviral therap

187 as "slow progressors." We observed that slow-progressor infants carry HIV isolates with significantly

188 al profile of HIV-specific CD8(+) T cells in progressors is limited compared to that of nonprogressor

189 lack of diagnostic specificity for MCI 'non-progressors' is a weakness inherent in framing MCI prima

190 aseline OAI visits in 58 future radiographic progressors (joint space narrowing at 24 months, sustain

191 liferating and activated T cells compared to progressors, like other LTA.

192 dred seventy-four patients including typical progressors, long-term nonprogressors (LTNPs), and verti

193 high-risk progressors (HRPs) versus low-risk progressors (LRPs).

194 om high-risk progressors (HRPs) and low-risk progressors (LRPs).

195 ART-naive seroconverters, and long-term non-progressors (LTNPs) who have spontaneous virological con

196 HIV miRNAs in human PBMCs from long term non progressors (LTNPs), regular progressors and rapid progr

197 C109P4 was recovered from a passage-4 normal-progressor macaque at 22 wpi and is a tier 2 virus, more

198 Early identification of "rapid progressors" may enable targeted intervention to preserv

199 Relative risk (RR) of being a "rapid progressor" (mean deviation [MD] loss >=1.5 dB/year) was

200 -1-infected African American controllers and progressors (n = 1107), and tested them for association

201 r cells from HIV elite controllers (n = 10), progressors (n = 12), and antiretroviral-treated individ

202 of <or=70 mg/dl (n = 951) were stratified as progressors (n = 200) and nonprogressors (n = 751) and c

203 ts with levels of >10,000 copies/mL (chronic progressors, n = 30).

204 urthermore, we assessed the impact of EC and progressor Nef on the ADCC susceptibility of HIV-1-infec

205 y enhance such effector functions in chronic progressor NK cells without inhibiting their general CD8

206 Ten of these infected monkeys became normal progressors (NPs) and had gradual losses of both memory

207 iously classified patients as rapid and slow progressors on the basis of clinical features and expres

208 activity in HIV-1-specific CD8+ T cells from progressors or controllers to determine underlying molec

209 rapy compared with their levels in untreated progressors or controllers.

210 rs were Mamu-B*08 positive compared to 3% of progressors (P = 0.00001).

211 itive CD4(+) T cells in HIV controllers than progressors (P = 0.0001), and these expanded Gag-specifi

212 ed progressors (P = 0.01) as well as treated progressors (P = 0.0003).

213 sly undetectable (new) responses compared to progressors (P = 0.0008).

214 breadth of Gag responses than did untreated progressors (P = 0.01) as well as treated progressors (P

215 rogressors versus 31.5% of moderate and fast progressors (P = 0.04).

216 Patients were classified as progressors (P = F0/F1) or nonprogressors (NP = F3/F4) a

217 and frequently is superior to that of HIV-1 progressors, partially due to the HLA class I alleles B*

218 similar viral isolates obtained from a rapid progressor patient with significantly different pathogen

219 Notably, in antiretroviral-treated aviremic progressor patients (TAPPs), no induction of NKp46 or NK

220 er progression and antiretroviral treatment (progressor patients [PP]).

221 Among progressor patients, 20% of sera neutralized more than 7

222 Three macaques exhibiting a rapid progressor phenotype experienced rapid and irreversible

223 D8-depleted animals, three were conventional progressors (progressing to AIDS >1 year after infection

224 .37 D vs -0.73 +/- 0.48 D; P < .001), but in progressors, progression was more similar between eyes (

225 rnover would be critical determinants of non-progressor/progressor status.

226 th plasma collected at necropsy from a rapid-progressor PTM was consistently highly pathogenic, with

227 Furthermore, rapid disease progressors (RDPs) had earlier and more robust cytokine

228 F were significantly upregulated in scarring progressors relative to in nonprogressors.

229 ecificity in normals, and specificity in non-progressors, respectively, were POD-Bonferroni = 100%, 0

230 of envelope sequences from the conventional progressors revealed compartmentalization of viral popul

231 postdepletion in both CD4(+) TCM and TEM in progressor RMs but decrease in the CD4(+) TCM of control

232 D4(+) effector memory T lymphocytes (TEM) in progressor RMs but decreased in the CD4(+) TCM of 4 out

233 ns of CD8(+) T lymphocytes in controller and progressor RMs.

234 s of env in three SIVsmE543-3-infected rapid-progressor (RP) macaques suggest the evolution of a comm

235 nvergent Env mutations evolve in these rapid progressor (RP) macaques.

236 ently described a coreceptor switch in rapid progressor (RP) R5 simian-human immunodeficiency virus S

237 esponses and progress rapidly to AIDS (rapid progressors [RP]).

238 cytokine storms, compared with slow disease progressors (SDPs) (49.6 days vs. 74.9 days, respectivel

239 lymphocyte depletion between controller and progressor SIV-infected RMs, emphasizing the complexity

240 For detecting fast progressors (slope faster than 2 mum/year), the ROC curv

241 isual field progression was identified using Progressor software version 3.7 (Medisoft, Leeds, United

242 Visual field progression was assessed by PROGRESSOR software version 3.7 (Medisoft, Leeds, United

243 supernatants from HCV-stimulated IHL of slow progressors specifically increased fibrolytic gene expre

244 Sensitivity in progressors, specificity in normals, and specificity in

245 T-cell turnover, immune activation, and progressor status were closely associated.

246 cells from elite controllers than from HIV-1 progressors supports the crucial role of effective HIV-s

247 , whereas they predominated in long-term non-progressors/survivors in the remaining cohort (p = 0.037

248 AD8)-inoculated macaques experienced a rapid-progressor syndrome characterized by sustained plasma vi

249 n progressive multifocal leukoencephalopathy progressors than in survivors (12.8% versus 3.4% P = 0.0

250 ural defect in HIV-1-specific CD8 T cells in progressors that cannot be overcome by manipulation of i

251 a property of HIV-specific CD8(+) T cells of progressors that is not shared with responses to other v

252 ent elevations in plasma sphingolipids in AS progressors that, together with plasma Cav-1, yield a pr

253 nd "slow progressor." Compared with the slow progressors, the rapid progressors had shorter diagnosis

254 In the longitudinal analysis of the 26 progressors, there was a greater decline in the FPIR fro

255 as significantly different at early and late progressor time points (p < 0.0001), but not present in

256 ed the relative abilities of Nef from EC and progressors to downmodulate NKG2D ligands.

257 Seventy-four oral insulin trial progressors to T1D from the Diabetes Prevention Trial-Ty

258 d fluctuations between states of glycemia in progressors to type 1 diabetes and studied whether those

259 ded into groups of fast, intermediate or non-progressors towards RC (<1 year, 3-5 years or no advance

260 lite controllers (ECs) compared with typical progressors (TPs), but sufficient viral replication pers

261 were actively proliferating, suggesting that progressor tumors recruited and/or activated endogenous

262 The Tregs in progressor tumors were derived from peripheral CD25+ nat

263 ced tumors, which either grow progressively (progressor tumors) or are rejected by the immune system

264 buted to the progressive growth phenotype of progressor tumors, we monitored tumor outgrowth in naive

265 ion was assayed in 145 nonprogressors and 50 progressors using real-time quantitative methylation-spe

266 estimated RGC counts was -18,987 cells/y in progressors versus -8,808 cells/y for nonprogressors (P

267 vessel shift was present in 12.1% of minimal progressors versus 31.5% of moderate and fast progressor

268 0302 and DQB1*0301 differed significantly in progressors versus nonprogressors (DQB*0302, 42.6 vs. 34

269 Progressors versus nonprogressors were compared using th

270 d enable the comparative analysis of larger 'progressor' versus 'non-progressor' cohorts.

271 eparated samples in two well-defined groups (progressors vs. nonprogressors).

272 ion analysis showed that the risk of being a progressor was 40% lower with each year of increased age

273 oring pairs analysis, classification of such progressors was observed with a high success rate.

274 A total of 14 UC progressors was readily separable from 15 UC nonprogress

275 gression to >=moderate-severe AR (stage C/D; progressors) was 12%, 30%, and 53%, respectively.

276 T cells were significantly diminished in HIV progressors, we found that a small subset of gp120-speci

277 In viremic controllers and progressors, we found variant recognition to be associat

278 progressors," and five were defined as "slow progressors." We observed that slow-progressor infants c

279 the chemokines CXCL9 and CXCL10 in the slow progressor were elevated at each of the three oral mucos

280 tures in non-progressors, and found that non-progressors were enriched for proteomic processes involv

281 Rapid progressors were older, had significantly lower CCT and

282 erences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P<

283 Progressors were significantly older than nonprogressors

284 lengths of HIV-1-specific CD8+ T cells from progressors were significantly shorter compared with aut

285 ponders and 10 patients who did not respond (progressors) were analyzed by next-generation sequencing

286 8 and S100A9 mRNA in whole blood in human TB progressors when compared with nonprogressors and rapidl

287 blood mDCs of HIV-infected rapid and classic progressors, whereas it is low to undetectable in avirem

288 cation, more prominently in controllers than progressors, which correlated inversely with predepletio

289 was diagnosed in 201 of these children (43%, progressors), while 265 children remained disease free (

290 The FPIR was examined longitudinally in 26 progressors who had FPIR measurements during each of the

291 Among 98 progressors whose DYSOGTTs and NLOGTTs were synchronized

292 iori to permit comparison of 60 radiographic progressors with 60 radiographic nonprogressors.

293 n this report, an analysis of 2 conventional progressors with encephalitis is described.

294 at higher frequencies than those of treated progressors with equally low amounts of HIV.

295 Of 135 progressors with four or more OGTTs, 30 (22%) went from

296 At day 70 postinfection, the animals (10 progressors with high viremia and 5 controllers with low

297 s who developed active tuberculosis disease (progressors) with those who remained healthy (matched co

298 ntolerant without viral hepatitis, sorafenib progressor without viral hepatitis, HCV infected, and HB

299 In contrast, on average, slow progressors would lose 0.8, 2.1, and 4.1 dB MD under the

300 Our models predicted that, on average, fast progressors would lose 2.1, 6.7, and 11.2 decibels (dB)