戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ex, age, and HLA-DR who had not progressed ("nonprogressors").
2 maining four macaques remained asymptomatic (nonprogressors).
3 and did not progress to AIDS within 9-10 yr (nonprogressors).
4  in two well-defined groups (progressors vs. nonprogressors).
5 ith chronic HIV infection, and one long-term nonprogressor.
6 se mutations was found in more than a single nonprogressor.
7 volution patterns differ for progressors and nonprogressors.
8 ise periodically in HIV-1-infected long-term nonprogressors.
9 isit were both higher in progressors than in nonprogressors.
10 unodeficiency virus (HIV)-infected long-term nonprogressors.
11 attered over the CCR5 coding sequence from 8 nonprogressors.
12 tions was silent, and each was unique to two nonprogressors.
13 ower viral load compared with CCR5 wild-type nonprogressors.
14 racterized by a larger proportion of slow or nonprogressors.
15 nodeficiency virus type 1-infected long-term nonprogressors.
16  0.83-0.88) to discriminate progressors from nonprogressors.
17 ho progressed to tuberculosis disease and 15 nonprogressors.
18 D onset and distinguish T1D progressors from nonprogressors.
19 er progressed to tuberculosis or remained as nonprogressors.
20 -independent cohort of 13 progressors and 11 nonprogressors.
21 y virus infection as well as HIV-1 long-term nonprogressors.
22  in the minority of HIV-1-infected long-term nonprogressors.
23 ent dynamics were similar in progressors and nonprogressors.
24 oviral therapy-treated patients or long term nonprogressors.
25 s of multiple phospholipids as compared with nonprogressors.
26 lated in scarring progressors relative to in nonprogressors.
27 ienced liver disease progression and 23 were nonprogressors.
28 L most accurately identified progressors and nonprogressors.
29 red with both healthy controls and long-term nonprogressors.
30 ronic HIV-1-infected patients, and long-term nonprogressors.
31 surements in discriminating progressors from nonprogressors.
32 tiating progressors from normal subjects and nonprogressors.
33 risk scores to discriminate progressors from nonprogressors.
34 acute HIV-1 infection but not from long-term nonprogressors.
35 avoided for the majority of UC patients, the nonprogressors.
36 t much less frequently in aviremic long-term nonprogressors.
37 adiographic progressors with 60 radiographic nonprogressors.
38 ronically HIV-infected individuals and elite nonprogressors.
39  than previously observed in adult long-term nonprogressors.
40 icantly higher for progressors compared with nonprogressors (-0.72 mum/y vs. 0.14 mum/y; P = 0.004),
41 ial overlap between the two groups (range of nonprogressors, 0.10-1.7%).
42  higher in the progressors compared with the nonprogressors (12.52 +/- 2.71 versus 10.82 +/- 2.71; P
43  higher in the progressors compared with the nonprogressors (14.12 +/- 3.39 units/liter versus 12.62
44  rapid progressors to AIDS (24 patients) and nonprogressors (47 controls).
45    Progressors were significantly older than nonprogressors (70.6 versus 62.5 years; P < 0.001).
46                                    Long-term nonprogressor AD-18 has been infected with human immunod
47                                              Nonprogressors also had decreased BCHE activity over tim
48                                    Many A+T+ nonprogressors also showed longitudinal cognitive declin
49             The high proportion of long-term nonprogressors among chronic lymphocytic leukemia (CLL)
50  We further compared genomic changes between nonprogressor and progressor SMM.
51 genotype was identified in 33 of 172 (19.2%) nonprogressors and 25 of 234 (10.7%) progressors from th
52               Methylation was assayed in 145 nonprogressors and 50 progressors using real-time quanti
53 progressors was readily separable from 15 UC nonprogressors and 6 normal controls.
54 ht to clarify the role of beta-chemokines in nonprogressors and AIDS patients by examination of beta-
55                             CD4+ clones from nonprogressors and CD8+ clones from AIDS patients secret
56 Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons have h
57 Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons, as we
58                                Both clinical nonprogressors and immunologically discordant progressor
59 omarkers can distinguish UC progressors from nonprogressors and improve cancer surveillance in UC.
60 patients but have been reported in long-term nonprogressors and in patients treated with highly activ
61 r results show that cocaine-using, long-term nonprogressors and normal progressors of HIV infection m
62 IGN compared with cocaine-nonusing long-term nonprogressors and normal progressors, respectively.
63 es (AUC) in differentiating progressors from nonprogressors and normal subjects were compared to the
64 ts showed no evidence of differences between nonprogressors and progressors (mean, -5.5 g/L +/- 9.5 v
65 of HIV-specific CD8+ T cells were present in nonprogressors and progressors, only those of nonprogres
66 ogous isolate than were sera from short-term nonprogressors and progressors.
67 d in human TB progressors when compared with nonprogressors and rapidly decreased S100A8/A9 protein l
68 gressive HIV disease compared with long-term nonprogressors and responders.
69                             Lymphocytes from nonprogressors and seronegative controls also showed neg
70                 Twenty biopsies from four UC nonprogressors and twenty-one biopsies from control indi
71     It distinguished between progressors and nonprogressors and was associated with a greater decline
72 sequence (CCR5-Delta32) was found in 4 of 13 nonprogressors, and 12 different point mutations were fo
73 y more than two-fold between progressors and nonprogressors, and 12 miRs differed between late presen
74 nfection (clinical progressors), 10 clinical nonprogressors, and 3 immunologically discordant progres
75                     HIV-1-infected long-term nonprogressors are a heterogeneous group of individuals
76 re their third birthday (>89%) and long-term nonprogressors are rare.
77 ed that these patients, as well as long-term nonprogressors, are infected with defective HIV-1 varian
78 llowed for 7-20 years (rapid progressors and nonprogressors), as well as a reference panel of normoal
79 gressors at corresponding visits or those of nonprogressors at any visit.
80     We further show that in a rare long-term nonprogressor, both an HIV-1-specific CD4(+)-T-cell clon
81 L2RA) did not differ between progressors and nonprogressors but were elevated in both groups relative
82  who had CD4 cell counts similar to those of nonprogressors but with a high likelihood of disease pro
83 d 20 QuantiFERON-positive progressors and 40 nonprogressors by sex, age, and exposure duration.
84  years were compared between progressors and nonprogressors by Student's 2-tailed t-test.
85 ), while 265 children remained disease free (nonprogressors) by December 2011.
86 tion of both progressor (BALB) and long term nonprogressor (C57BL) mouse strains is characterized by
87 4 down-modulation, and a subset of long-term nonprogressors carry viruses defective in this function.
88 clinical progressors (CDR score, >/=0.5) and nonprogressors (CDR score, 0) and between APOE epsilon4
89              In comparison with HIV-positive nonprogressor chimpanzees, progressors have higher plasm
90 ific proliferative responses in the clinical nonprogressor cohort that correlated with significant nu
91 is increased among HIV-1- infected long-term nonprogressors compared with progressors; however, the h
92 eristics were not different in this group of nonprogressors compared with those with low AIRg who did
93 worsened Sepsis 3 category compared with 141 nonprogressor controls.
94 istance to ADA infection in CD4+ clones from nonprogressors could be partially reversed by treatment
95          Differences between progressors and nonprogressors diminished with worsening disease severit
96 differed significantly in progressors versus nonprogressors (DQB*0302, 42.6 vs. 34.7%, P = 0.0047; DQ
97 activity was observed in sera from long-term nonprogressors (elite controllers).
98 in CD4(+) T cells from HIV-1 elite long-term nonprogressors (eLTNPs), naive patients, and multiply ex
99 atients and discusses them in the context of nonprogressors enrolled in other cohorts.
100 y, B27- and B57-restricted CD8+ T cells from nonprogressors exhibited greater expansion than those re
101 se parameters from the progressors, the four nonprogressors exhibited more individual variability wit
102 utant identified in HIV-1-infected long-term nonprogressors failed to promote TERT destabilization.
103 in 8 QuantiFERON-positive progressors and 12 nonprogressors from India.
104 sed genes was identified that distinguished "nonprogressors" from "progressors" with an estimated 100
105                                              Nonprogressors generally had high titers of ADCC Abs at
106 d programmed death ligand -1 compared to the nonprogressor group at baseline, months 4 and 12.
107 plantation biopsies were classified as IF/TA nonprogressors (group 1) or progressors (group 2) using
108 NS DNA in the at-risk progressor and at-risk nonprogressor groups followed for 4 years.
109 , progressors had a higher risk category and nonprogressors had a lower risk category when genetic fa
110                  Although long-term survivor nonprogressors had a significantly higher percentage of
111 lin G (IgG) from rapid progressors, IgG from nonprogressors had no suppressive effects on glycoprotei
112                          Patients defined as nonprogressors had significantly lower baseline levels o
113 d because genetic studies of long-term HIV-1 nonprogressors have associated specific HLA-B alleles wi
114                                    Long-term nonprogressors have high titer antibody responses to HIV
115                                Compared with nonprogressors, hazard ratios for mortality were 1.42 (9
116 ) T cells in coinfected HLA-DR7(+) long-term nonprogressor HIV subjects with undetectable HCMV plasma
117 ) of 73% for distinguishing progressors from nonprogressors in a cohort of 596 individuals with knee
118 ells are elevated in blood of HIV+ long-term nonprogressors in comparison to HIV- donors.
119  a community-based cohort of HIV-2 long-term nonprogressors in rural Guinea-Bissau, we performed what
120 ressed, no difference was seen compared with nonprogressors in spine BMD, but hip BMD was modestly re
121 asia (UC progressors) from those without (UC nonprogressors), including assays of telomere length, an
122 r (P) and C57BL/10-H-2(k) (B10.BR) long-term nonprogressor (LTNP) mice.
123  in intestinal mucosal biopsies of long-term nonprogressor (LTNP) patients as compared to chronically
124 ation in elite controller (EC) and long-term nonprogressor (LTNP) patients has been associated with e
125                                    Long-term nonprogressors (LTNP) and seronegative controls had leve
126                Undiluted sera from long-term nonprogressors (LTNP) had broad neutralizing antibodies
127 lones from two progressors and two long-term nonprogressors (LTNP) in fetal thymic organ culture (FTO
128 -mediated control over HIV, termed long-term nonprogressors (LTNP) or elite controllers, and patients
129  A unique cohort of HIV-1-infected long term nonprogressors (LTNP) with normal CD4(+) T cell counts a
130 tetanus toxoid in normal controls, long-term nonprogressors (LTNP), and HIV-infected patients with pr
131 ed Rx <50) and untreated patients (long-term nonprogressors [LTNP]) matched for very low HIV RNA leve
132 jects; the latter group included 8 long-term nonprogressors (LTNPs) and 17 progressors.
133 ture by autologous CD8+ T cells in long-term nonprogressors (LTNPs) and in patients whose viremia was
134                              Seven long-term nonprogressors (LTNPs) have been identified in a cohort
135                                    Long-term nonprogressors (LTNPs) of human immunodeficiency virus t
136 cation in rare individuals, termed long-term nonprogressors (LTNPs) or elite controllers.
137 V type 1-infected, untreated white long-term nonprogressors (LTNPs) with a cohort of 605 HIV-1-infect
138 an immunodeficiency virus (HIV) in long-term nonprogressors (LTNPs) with protective human leukocyte a
139 11 healthy donors, 360 +/- 69 in 3 long-term nonprogressors (LTNPs), 186 +/- 52 in 9 newly diagnosed
140 nts including typical progressors, long-term nonprogressors (LTNPs), and vertically HIV-infected subj
141 unodeficiency virus (HIV)-infected long-term nonprogressors (LTNPs), it is also present at the expect
142 t been evaluated in HIV-1-infected long-term nonprogressors (LTNPs), who maintain high CD4(+) T cell
143 (Abs) from a panel of HIV-infected long-term nonprogressors (LTNPs).
144                               True long-term nonprogressors (LTNPs)/elite controllers (ECs) maintain
145 a lack of disease progression (ie, long-term nonprogressors [LTNPs]) through 7 years of follow-up (LT
146                     Here we tested long-term nonprogressors' (LTNPs') susceptibility to superinfectio
147 unodeficiency virus (SIV)-infected long-term-nonprogressor macaque.
148                            Compared with the nonprogressor macaques, the two progressor macaques exhi
149 onprogressors and progressors, only those of nonprogressors maintained a high proliferative capacity.
150 ns with progressive disease, suggesting that nonprogressors may not target unique epitopes.
151 mean age, 72 years +/- 7; five women) and 13 nonprogressors (mean age, 70 years +/- 10; 11 men).
152 ral therapy (n = 21), HIV-infected long-term nonprogressors (n = 10), and HIV-seronegative volunteers
153  decline > 5 ml/min/1.73 m2/year, n = 23) or nonprogressors (n = 23)-and 23 healthy controls (HC) wer
154 gressors had lower baseline FPIR values than nonprogressors (n = 270), with adjustments made for age
155 ); and tuberculosis progressors (n = 22) and nonprogressors (n = 34; 0.75; 0.63-0.87).
156 = 63), elite controllers (n = 19), long-term nonprogressors (n = 7), and HIV-infected patients affect
157 were stratified as progressors (n = 200) and nonprogressors (n = 751) and compared.
158  "Progressors" (N = 41) did not differ from "nonprogressors" (N = 156) in terms of hours per day spen
159  diagnosis with BE were matched to controls (nonprogressors, n = 291), for age, sex, and year of BE d
160   All others were considered nonprogressing (nonprogressors; n = 210 eyes).
161                Thus, in contrast to clinical nonprogressors, neither progressors nor immunologically
162 ere classified as progressors (P = F0/F1) or nonprogressors (NP = F3/F4) according to the severity of
163  were compared: eight progressors (P) and 45 nonprogressors (NP), using Cox proportional hazards mode
164  classifier to differentiate progressors and nonprogressors on baseline cartilage texture maps, which
165  seen in HIV-1-infected cohorts of long-term nonprogressors or patients with AIDS.
166                                    Long-term nonprogressors or slow progressors may remain asymptomat
167 tuberculosis infection who remained healthy (nonprogressors) or who progressed to microbiologically c
168 s/y in progressors versus -8,808 cells/y for nonprogressors (P < 0.001).
169 in progressors versus an increase of 0.6% in nonprogressors (P < 0.05).
170 brosis progressors compared with 20 fibrosis nonprogressors (P < 0.05).
171 nificantly over time between progressors and nonprogressors (P = .60), progressors had significantly
172 methylation in progressors 67.8% vs 96.7% in nonprogressors; P = 0.0001, z = 3.85, Wilcoxon rank-sum
173 cells from PBMCs from HIV-positive long-term nonprogressors; partial blocking of infection with chemo
174 endent manner, with discordant and long-term nonprogressor patients showing elevated SLAMF7 levels, a
175  PWH with CD4 count >200 cells/uL, long-term nonprogressors, people with idiopathic CD4 lymphopenia,
176                      In studies of long-term nonprogressors - persons who have stable CD4+ T-cell cou
177  downregulation; how this contributes to the nonprogressor phenotype of these infected individuals re
178                                              Nonprogressor plasma cells showed significantly lower mu
179 progression in SMM and those with a low-risk nonprogressor precursor condition.
180 rts of HIV-1-infected individuals: long-term nonprogressors, progressors to disease, acute seroconver
181 ogression and treatment, including long-term nonprogressors, progressors, and chronically infected su
182 apid progressors and nonrapid progressors or nonprogressors remained when longitudinal changes within
183 biopsy samples from long-term HIV-1-infected nonprogressors showed maintenance of normal CD4(+) T-cel
184 progressor phenotype are akin to MM, whereas nonprogressor SMM has monoclonal gammopathy of undetermi
185 tion in Vif contributes significantly to the nonprogressor status of this mother and child.
186 decrease virus burden, whereas the long term nonprogressor strains do not.
187 esions from each of ten progressors and four nonprogressors suffering from longstanding UC.
188 mechanisms by which long-term HIV-1-infected nonprogressors suppress HIV-1 infection and maintain imm
189                                Among sibling nonprogressors, temporal decreases were measured in the
190  seen in HIV elite controllers and long-term nonprogressors that does not require combined antiretrov
191 differ between liver disease progressors and nonprogressors, the association of sCD14, I-FABP, and IL
192                                           In nonprogressors, the myopia progression at 1 year was les
193 , in a cohort of 33 HIV-1-infected long-term nonprogressors, those who were heterozygous for the muta
194 aseline NAS between fibrosis progressors and nonprogressors, though NAS rose over time in the progres
195 ed in unrelated cohorts (including long-term nonprogressors), thus confirming their independence from
196 ort Study, enriched with rapid and long-term nonprogressors to increase statistical power.
197 assified as glaucoma progressors or glaucoma nonprogressors using event-based analysis.
198 ty risk was compared between progressors and nonprogressors using four definitions.
199 ould be correctly assigned as progressors or nonprogressors using random sample cross-validation stat
200              However, IL-4 production in the nonprogressors was restricted to a limited number of p24
201 ost striking attribute of long-term survivor nonprogressors was the detection of HIV-1-specific CD4(+
202 dly, biologic clones from an adult long-term nonprogressor were noncytopathic in spite of similar lev
203 0.86 and in differentiating progressors from nonprogressors were 0.68 and 0.64, respectively; the AUC
204  The mean +/- SD ages of the progressors and nonprogressors were 64.2 +/- 7.8 years and 63.3 +/- 10.6
205                           Progressors versus nonprogressors were compared using the two-sample t-test
206                 These results indicated that nonprogressors were differentiated by increased prolifer
207                                     Clinical nonprogressors were found to respond to a wide range of
208 fferential abundance between progressors and nonprogressors were identified.
209 se and were included as progressors, and 115 nonprogressors were included as controls.
210 on to beta-chemokine production; clones from nonprogressors were poorly susceptible to ADA replicatio
211       The recent discovery of long term AIDS nonprogressors who harbor nef-attenuated HIV suggests th
212                         We hypothesized that nonprogressors who were heterozygous for the mutant CCR5
213             An estimated 25-30% of long-term nonprogressors (who avoid clinical AIDS for 10 or more y
214 n progressors is limited compared to that of nonprogressors, who consistently maintain highly functio
215 low-up and were selected as progressors; 106 nonprogressors, who remained healthy, were matched to pr
216  mutant CCR5 gene might define a subgroup of nonprogressors with higher CD4+ T cell counts and lower
217 ere secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated.
218 udied including a unique cohort of long-term nonprogressors with low levels of plasma viral RNA and s
219 tion favoring nonsynonymous mutations, while nonprogressors with low viral loads selected against the
220 cificity for distinguishing progressors from nonprogressors with optimum choice of threshold.
221 e were indistinguishable from CCR5 wild-type nonprogressors with regard to all measured immunologic a
222 c CD8+ T cells were not limited to long-term nonprogressors with restriction of plasma virus.
223                       Furthermore, long-term nonprogressors with the wild-type CCR5 genotype are indi
224 y was lower in T1D progressors compared with nonprogressors, with simultaneous lower diglycerides, ly
225 cer/dysplasia and/or aneuploidy) compared to nonprogressors (without cancer/dysplasia/aneuploidy), wh

 
Page Top