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 ients who had stable viraemia by RT-PCR (non-progressors).

7 es in 27 B(*)57(+) patients (10 LTNPs and 17 progressors).

8 apidly progressed to AIDS compared with slow progressors.

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

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

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

12 responses distinguished HIV controllers from progressors.

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

14 n both HIV controllers and untreated chronic progressors.

15 senescence underlies tumor progression in UC progressors.

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

17 oma disease progressors and nonrapid disease progressors.

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

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

20 replicative capacity compared to virus from progressors.

21 es derived from chronically infected viremic progressors.

22 lly better helper activity than those of HIV progressors.

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

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

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

26 non-progressors, early progressors and late progressors.

27 ptides was commonly observed in both ECs and progressors.

28 essing macaque to the intermediate and rapid progressors.

29 ly distinguish LTNP individuals from regular progressors.

30 inversely correlated with viral load in the progressors.

31 ed 8 long-term nonprogressors (LTNPs) and 17 progressors.

32 levels is LTNPs > HIV-uninfected subjects > progressors.

33 ation was spared by SIVmac239, even in rapid progressors.

34 a population not commonly present in chronic progressors.

35 t is comparable to the proportion in chronic progressors.

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

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

38 a cohort of elite controllers and in chronic progressors.

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

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

41 strointestinal tract of both controllers and progressors.

42 lymphocyte activation in controllers than in progressors.

43 fore the appearance of autoantibodies in the progressors.

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

45 0.007) in acute controllers but not in acute progressors.

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

47 26 cognitively normal (CN), 194 MCI (39 MCI-progressors, 148 MCI-stable, 2 years after baseline), an

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

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

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

51 PML survivors (91%) versus only 1 of 11 PML progressors (9%, P = 0.0003).

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

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

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

55 1 year after infection) and three were rapid progressors (AIDS within 6 months).

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

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

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

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

60 f interleukin 2 (IL-2), IL-4, and IL-7, both progressor and LTNP clones exhibited similar replication

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

62 46 progressors and 107 matched controls were identified in

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

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

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

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

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

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

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

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

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

72 8 months, group differences between clinical progressors and non-progressors were significant for sel

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

74 22, CTLA4, and IL2RA) did not differ between progressors and nonprogressors but were elevated in both

75 obtained over 5 years were compared between progressors and nonprogressors by Student's 2-tailed t-t

76 The mean +/- SD ages of the progressors and nonprogressors were 64.2 +/- 7.8 years a

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

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

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

80 phocyte engraftment dynamics were similar in progressors and nonprogressors.

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

82 Evolution patterns differ for progressors and nonprogressors.

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

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

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

86 te-stage R5 HIV-1 biological clones from two progressors and two long-term nonprogressors (LTNP) in f

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

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

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

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

91 tion rates compared with patients defined as progressors, and those patients in the nonprogressive jo

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

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

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

95 109P3N were recovered from a passage-3 rapid-progressor animal during chronic infection (24 weeks pos

96 In contrast, SIV-infected conventional progressor animals sustained marked but incomplete deple

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

98 ), 46 chronic progressors (CP), and 43 acute progressors (AP) were examined for their CD4, CCR5, and

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

100 tterns of progression for the early and late progressors are consistent with the hypothesis that knee

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

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

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

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

105 We found that R5 HIV-1 clones from progressors but not LTNP were cytopathic in untreated FT

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

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

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

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

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

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

112 d CIN1/CIN2 lesions that progressed to CIN3 (progressors), CIN1/CIN2 lesions that regressed spontaneo

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

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

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

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

117 he AUC/month was significantly higher in the progressors compared with the nonprogressors (12.52 +/-

118 at baseline was significantly higher in the progressors compared with the nonprogressors (14.12 +/-

119 ed with one of ten controls, while two rapid progressors controlled viremia only as long as the SIVIG

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

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

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

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

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

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

126 Progressors demonstrated higher baseline levels of gluco

127 al to or greater than the levels achieved by progressor-derived R5 HIV-1 clones in untreated FTOC.

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

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

130 Here, we show that progressors displayed a gain of 3q whereas none of the r

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

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

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

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

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

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

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

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

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

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

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

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

143 lar thickness measurements in discriminating progressors from nonprogressors.

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

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

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

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

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

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

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

151 At the time of their death, two SIV rapid progressors had experienced a nearly complete loss of th

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

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

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

155 The 74 progressors had lower baseline FPIR values than nonprogr

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

157 Non-progressors had small numbers of persistently active nod

158 These long-term survivors or long-term non-progressors have an immune system that can control HIV i

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

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

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

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

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

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

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

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

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

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

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

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

171 Unlike immunoglobulin G (IgG) from rapid progressors, IgG from nonprogressors had no suppressive

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

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

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

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

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

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

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

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

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

181 Whether B57(+) progressors lack restriction of viral replication becaus

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

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

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

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

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

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

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

189 ese studies show that the SIV-infected rapid progressor macaques initially mounted an appropriate but

190 ay 2 and at the end of cycle 1 compared with progressors (mean difference in % of baseline Ki, 47%, P

191 -1-infected African American controllers and progressors (n = 1107), and tested them for association

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

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

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

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

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

197 e-using, long-term nonprogressors and normal progressors of HIV infection manifest significantly high

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

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

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

201 serum samples could be correctly assigned as progressors or nonprogressors using random sample cross-

202 In all rapid progressors (P <0.0001), production of these cells initi

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

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

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

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

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

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

209 nt at 5 years postinfection, excluding rapid progressors (P = 0.05).

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

211 Two patient groups were compared: eight progressors (P) and 45 nonprogressors (NP), using Cox pr

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

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

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

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

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

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

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

219 .37 D vs -0.73 +/- 0.48 D; P < .001), but in progressors, progression was more similar between eyes (

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

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

222 genic mechanisms of an envelope from a rapid progressor (R3A Env) in the NL4-3 backbone (NL4-R3A) whi

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

224 Moreover, R5 HIV-1 clones from progressors replicated to higher levels than LTNP-derive

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

226 nonusing long-term nonprogressors and normal progressors, respectively.

227 Immunologically discordant progressors responded strongly to clade B Gag p24 with a

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

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

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

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

232 from sequential plasma samples of one rapid progressor (RP) macaque.

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

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

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

236 17 animals (88.2%), including 12 of 12 rapid progressors (RP) and 3 of 5 slow progressors (SP).

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

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

242 of 12 rapid progressors (RP) and 3 of 5 slow progressors (SP).

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 memory T cells that best distinguished rapid progressors, suggesting that mechanisms of the CD4+ memo

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

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

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

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

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

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

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

254 lution in three SIVsmE543-3-inoculated rapid progressors to determine the contribution of viral evolu

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

256 ntial abilities of HLA B(*)5701(+) LTNPs and progressors to restrict virus replication.

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

260 However, progressor tumors contained a higher percentage of Tregs

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 gh Tregs are activated in both regressor and progressor tumors, the ratio of regulatory to effector T

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

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

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

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

269 0302 and DQB1*0301 differed significantly in progressors versus nonprogressors (DQB*0302, 42.6 vs. 34

270 Progressors versus nonprogressors were compared using th

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

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

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

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

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

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 Twenty-three (82%) of 28 stage III progressors were correctly identified by MALDI-ToF combi

281 Progressors were more likely to have worked as machinist

282 Rapid progressors were older, had significantly lower CCT and

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

284 Progressors were significantly older than nonprogressors

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

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

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

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

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

290 Among 98 progressors whose DYSOGTTs and NLOGTTs were synchronized

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

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

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

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

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

296 ed that distinguished "nonprogressors" from "progressors" with an estimated 100% accuracy.

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)