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1 ders"); and fluid remained unchanged in 6% ("nonresponders").
2 %) occurred (i.e., changes from responder to nonresponder).
3 ients [10%] were nonevaluable and counted as nonresponders).
4 rtension (21 fluid responders and nine fluid nonresponders).
5  progression (these patients were counted as nonresponders).
6 ew York Heart Association class or worsened (nonresponders).
7 ents with BD who did not respond to lithium (nonresponders).
8 ) of pre-LTP factors associated with being a nonresponder.
9 acebo arm, all of which were observed in the nonresponders.
10 emaining regarding the optimal management of nonresponders.
11  increases postindex were more pronounced in nonresponders.
12  observed in histological responders than in nonresponders.
13  responders, and 3 patients with BD who were nonresponders.
14  16 weeks, resulting in 26 responders and 28 nonresponders.
15 oups, as well as between SSRI responders and nonresponders.
16 .7 months; HR, 0.91; 95% CI, 0.524-1.577) vs nonresponders.
17 e to recurrence of 41.2 versus 5.5 months in nonresponders.
18 rengths relative to treatment responders and nonresponders.
19 colony-stimulating factor (G-CSF) in steroid nonresponders.
20 g cells, were similar between responders and nonresponders.
21 23% +/- 9% in responders and by 8% +/- 3% in nonresponders.
22 combined response or HBsAg loss) compared to nonresponders.
23 a-glucuronidase gene abundance compared with nonresponders.
24 pressure and reliably detects responders and nonresponders.
25  was observed between treated responders and nonresponders.
26 nificantly higher expressed in the hearts of nonresponders.
27  (15%) were not assessable and assumed to be nonresponders.
28 ients missing week-13 values were considered nonresponders.
29  2.7 months; P = .01; HR, 3.1) compared with nonresponders.
30 ; P < .001) of the QLQ-C15-PAL compared with nonresponders.
31  patient gut microbiome of responders versus nonresponders.
32 e biomarkers differentiating responders from nonresponders.
33 tinguish weight and glycemic responders from nonresponders.
34 ation of Klebsiella pneumoniae compared with nonresponders.
35 rate (HR) of overall death in responders and nonresponders.
36 sor distinguished subsequent responders from nonresponders.
37 d a higher amplitude and mesor compared with nonresponders.
38  output and the proportion of responders and nonresponders.
39 duction >90%) and five partial responders or nonresponders.
40 m high-density RT-PCR between responders and nonresponders.
41 e blood of clinical responders as opposed to nonresponders.
42 36/44); 18% (8/44) were considered treatment nonresponders.
43 ers did not change in mean arterial pressure-nonresponders.
44 as moderately but significantly increased in nonresponders.
45 py showed significantly better survival than nonresponders.
46 ne was more pronounced in responders than in nonresponders.
47  condensed chromatin structure compared with nonresponders.
48 ents with persistent disease were classed as nonresponders.
49 ugh a significant number of patients will be nonresponders.
50 gnificantly different between responders and nonresponders.
51  lesion glycolysis (P = 0.04) after IC1 than nonresponders.
52 y to help predict survival of responders and nonresponders.
53 ed as responders and 15 individuals (60%) as nonresponders.
54  and 6 in the placebo group) were considered nonresponders.
55 acteristics indicated more severe disease in nonresponders.
56  score had improved (P = .025) compared with nonresponders.
57 ctive and placebo, as well as responders and nonresponders.
58 hieved SU to egg; all others were considered nonresponders.
59 ial TACE and enabled clear identification of nonresponders.
60 oosting the antitumor T cell activity of ICB nonresponders.
61 ntigen-specific TILs that was lacking in ACT nonresponders.
62 tream regulator, which was also increased in nonresponders.
63 ntravenous lidocaine treatment compared with nonresponders.
64 axin 2, differed between full responders and nonresponders.
65 n super-responders and responders but not in nonresponders.
66 of a representative subset of responders and nonresponders.
67  responders, whereas it remained elevated in nonresponders.
68                      Twenty-one percent were nonresponders.
69 mL; P = .0.042) concentrations compared with nonresponders.
70 s significantly exaggerated in iPSC-ECs from nonresponders.
71 ity and a stemness program-were activated in nonresponders.
72 ld more reliably distinguish responders from nonresponders.
73 e 1, C-reactive protein, and bile acids than nonresponders.
74 t 6 months, while a decrease was observed in nonresponders (+0.2+/-0.4 L and -0.1+/-0.4 L, respective
75 esponders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010).
76 ity-time integral more in responders than in nonresponders (12% +/- 5% vs 5% +/- 2%, respectively; p
77 ers" (24-month C-peptide >/= baseline), and "nonresponders" (12-month C-peptide < baseline) were eval
78 gnificantly different between responders and nonresponders (20.3 vs. 10.6 mo, P = 0.001, for OS and 1
79 72.2 +/- 107.3 mum) was greater than that of nonresponders (209.6 +/- 85.8 mum; P = .039).
80 reatment with 5-azacytidine (40 patients; 15 nonresponders, 25 responders).
81 partial responders (17%), and 22 patients as nonresponders (31%).
82                     In contrast to prasugrel nonresponders (35 subjects), the prasugrel responders ha
83 mized crossover phase (9 responders [56%], 7 nonresponders [44%]).
84 a survival difference between responders and nonresponders (45.0 months vs 10.0 months, 84.3 months v
85 comparison, 26 patients were predicted to be nonresponders; 50.0% of these predictions were correct.
86 ders (27.2%), 55 responders (19.0%), and 156 nonresponders (53.8%) in the MitraClip arm compared with
87 response differential was observed among ECT nonresponders (59.6% compared with 34.1%).
88  P = 0.001) and better survival than the 122 nonresponders (61% vs. 39%, P = 0.001).
89 ders (10.2%), 46 responders (16.3%), and 208 nonresponders (73.5%) in the GDMT-alone arm (overall p <
90 sophageal Doppler more in responders than in nonresponders (8% +/- 2% vs 3% +/- 1%, respectively; p <
91 sophageal Doppler more in responders than in nonresponders (-8% +/- 5% vs -4% +/- 2%, respectively; p
92 provement in LVEF by >/=5 U responder versus nonresponder [95% confidence intervals] for all-cause mo
93 ntly longer OS and PFS in responders than in nonresponders according to all assessed definitions.
94 ession-free survival (PFS) in responders and nonresponders according to VTB criteria was compared by
95                                           In nonresponders across 5 datasets GMV was significantly lo
96 s was greater among responders compared with nonresponders after 2 years.
97 n 15 of 20 responders compared with 10 of 22 nonresponders after 4 cycles.
98 identified similar numbers of responders and nonresponders after ketamine or imipramine treatment.
99 rom baseline differed between responders and nonresponders after three cycles (16.6% vs 3.9%; P = .02
100                                              Nonresponders also had lower w4IgE levels and lower rati
101    TP53 gene alterations were more common in nonresponders, although this did not reach statistical s
102 D-L1 expression levels in tumor tissues from nonresponders among PD-1 mAb-treated NSCLC patients.
103 s) per additional responder patient (3-month nonresponders and 6-month responders) to aflibercept, ra
104 re contrasted between placebo responders and nonresponders and compared to healthy controls (n = 20).
105 m ADC and maximum SUV between responders and nonresponders and comparison of timing for discordant an
106  EMMA correctly classified 96% as responders/nonresponders and correctly classified 79% according to
107 omparing demographic characteristics between nonresponders and responders.
108                      Of these, 33 (25%) were nonresponders and were randomized to G-CSF or placebo (1
109 ealthy versus pathological, responder versus nonresponder) and for generation of an individual metabo
110 pertension (15 fluid responders and 15 fluid nonresponders) and 30 with intra-abdominal hypertension
111 suppression of Th17 responses by anti-TNF in nonresponders, and direct targeting of the USF2-signalin
112 cates 75% improvement in baseline PASI) from nonresponders, and gives an estimated PASI75 probability
113 aling was elevated in the CCR6(+) T cells of nonresponders, and pathogenic Th17 signature genes were
114 were categorized as anatomical responders or nonresponders, and within the responder group as rebound
115             The muscle transcriptomes of the nonresponders are further characterized by the activatio
116                         Following diagnosis, nonresponders are often passively managed, without speci
117 dian Treg cell counts 3 months post-ECP than nonresponders, as did steroid responders at 56 weeks who
118  weeks; 5 (25%) of 20 would have been deemed nonresponders at 12 weeks, the end point of the previous
119 1 second (FEV1) of omalizumab responders and nonresponders at 6 months.
120 erfusion was compared between responders and nonresponders at baseline, at week 2, after cycle 2 (12
121  coupling differences between responders and nonresponders at baseline, their correlation with sympto
122 rom nonfailing donor hearts as well as R and nonresponders at LVAD implantation (pre-LVAD) and transp
123  although the microbiota was more diverse in nonresponders at the time of vaccination.
124 ers at 1 mo had better overall survival than nonresponders, at 8.5 mo versus 4.8 mo (P = 0.018); AFP
125  care were classified into Responders versus Nonresponders based on qualitative assessment of optical
126 , and patients were defined as responders or nonresponders based on the grading scale by Salzer-Kunts
127            These baseline alterations caused nonresponder BD hippocampal neurons to drastically shift
128                       One KT recipient was a nonresponder because of nonstructural protein 5A resista
129 ertoire remodeling, which may be impaired in nonresponders because of the preexisting immune environm
130                    Limited options exist for nonresponders, because the etiology, dysregulated cell t
131 ht SFG, where GMV was significantly lower in nonresponders but higher in responders.
132 rdiography infrequently), and underestimated nonresponders by 35% compared with CCS (58% sensitivity
133 s used to classify patients as responders or nonresponders by following standard guidelines for the u
134  levels were compared between responders and nonresponders by mRECIST criteria by using unpaired Wilc
135 sion of GULP1 was observed in most cisplatin nonresponder cases.
136 FC of the RN-left MTG was also found in SSRI nonresponders compared to responders, which was a signif
137 y and profibrotic signature in the hearts of nonresponders compared with responders.
138 ion in stage 2, while sertraline and placebo nonresponders crossed over to bupropion and sertraline,
139 ignatures were not modulated by treatment in nonresponders (defined based on UAS7 longitudinal change
140 arison of overall survival of responders and nonresponders demonstrated P values of .4133, .0112, .00
141 loperidol (control group) were compared with nonresponders (dexmedetomidine group).
142                               Responders and nonresponders did not differ in the percent change of ri
143  who did not return the consent form and 163 nonresponders did not participate.
144 ammed death ligand 1 expression, whereas all nonresponders did not.
145 gnature, while the CD45(+) population in the nonresponders displayed an M2-like transcriptional signa
146 memory T cells in responding patients, while nonresponders displayed dramatic pretherapy T cell expan
147                                    Molecular nonresponders displayed limited changes in ctDNA levels
148 mL; P = .032) concentrations increased among nonresponders during therapy.
149 e VTB separated patients into responders and nonresponders, each with significantly different PFS, an
150 lity to differentiate between responders and nonresponders early in the course of treatment is essent
151  in T-cell activation between responders and nonresponders early into anti-PD-1 treatment, which may
152                              In the 15 fluid nonresponders, end-systolic pressure increased (p < 0.05
153 analyses of arterial spin-labeled (ASL) MRI, nonresponders exhibited increased cerebral blood flow (C
154                  In contrast, CD4 T cells of nonresponders exhibited increased expression of IL2 and
155 d to reveal possible responder compared with nonresponder factors.
156 008 vs 0.003) and Dutch infants and Ghanaian nonresponders (FDR, 0.002 vs 0.009).
157 ons between both Ghanaian RVV responders and nonresponders (FDR, 0.008 vs 0.003) and Dutch infants an
158 icantly different between RVV responders and nonresponders (FDR, 0.12), and Ghanaian responders were
159 mentation with A. muciniphila after FMT with nonresponder feces restored the efficacy of PD-1 blockad
160            In both volumetric responders and nonresponders, female sex remained strongly associated w
161  stem cells (iPSCs) from full responders and nonresponders, from subjects with diabetes but no DME, a
162 responders (grades I-III) and 18 patients as nonresponders (grades IV-VI).
163 as responders (grades I-III) and 15 (41%) as nonresponders (grades IV-VI).
164 as noted, while at the 2-month follow-up the Nonresponder group had a significantly higher VEGF conce
165                              On D1, ketamine nonresponders had a lower mesor and a blunted 24-hour am
166          CCR6(+) T cells from responders and nonresponders had distinct gene expression profiles.
167                               Responders and nonresponders had markedly different changes in serum cy
168  levels after initiation of therapy, whereas nonresponders had no significant changes or an increase
169  more leukemic blasts after induction (early nonresponders) had the poorest prognosis (EFS, 22%).
170 ment had lower baseline IL-8 levels than the nonresponders (Hedge's g = -0.28; 95%CI, -0.43 to -0.13;
171  (HR = 0.59; 95% CI = 0.32-1.08) and chronic nonresponders (HR = 0.48; 95% CI = 0.23-0.99).
172 and had lower levels of peripheral IL-6 than nonresponders, implicating a role for the NF-kappaB path
173 RL, we classified patients as responders and nonresponders in 60 and 40 cases versus 63 and 37 cases,
174 fied using PSF and PSFEARL as responders and nonresponders in 69 and 26 cases versus 72 and 23 cases,
175 tween 6-week old, matched RVV responders and nonresponders in rural Ghana.
176 reater frequency in responders compared with nonresponders in the IgG(4)(+) but not the IgA(+) fracti
177             Following the blinded phase, the nonresponders in the placebo group received IVIG.
178  CI: 75%, 99%) in identifying responders and nonresponders in the treated groups compared with MR ela
179 solation of fluorescence-positive cells from nonresponders increased dynamic ranges of downstream exp
180                                              Nonresponders largely showed lesser/nonsignificant reduc
181 ferogenic TLR9 agonist, SD-101, in anti-PD-1 nonresponders led to a complete, durable rejection of es
182                       Most subjects from TIV nonresponder, low responder, and high responder groups h
183 ignificantly differed between responders and nonresponders (&lt;0.01), whereas differences in tumor size
184 ed as KIT responders (>/=25%, n = 17) or KIT nonresponders (&lt;25%, n = 11).
185 for responders than in partial responders or nonresponders (mean +/- standard deviation, 3.23 dB +/-
186 ers had higher baseline tumor perfusion than nonresponders (mean, 404 mL/100 g/min +/- 213 vs 199 mL/
187 cumulation within the tumor and converts the nonresponder mice into responders to anti-CD47 immunothe
188                       Compared with MRI-PDFF nonresponders, MRI-PDFF responders demonstrated both a s
189 ek 12 (n = 63), compared with ~30% to 65% in nonresponders (n = 12), while the residual disease genom
190 eeks of sham followed by open-label rTMS for nonresponders (n = 12).
191                         Results VTB criteria nonresponders (n = 120) according to the initial postthe
192              Results Responders (n = 31) and nonresponders (n = 19) differed (P < .05) in the percent
193 significant difference in PFS between RECIST nonresponders (n = 255) and responders (n = 20; HR = 1.5
194                        Conversely, stage III nonresponders (N = 43, 23.6%) approached stage IV outcom
195 rebleeding risk and better survival than the nonresponders (n = 72) (respective proportions: 7% vs. 3
196 ligibility criteria (responders, n = 14, and nonresponders, n = 15) and 26 healthy control subjects u
197 al and overall survival among responders and nonresponders no matter which reconstruction was used fo
198 response in all domains), 8 (15%) of 54 were nonresponders (no response in any domain), and 39 (72%)
199 ncer patients, partial responders (PR = 18), nonresponders (NR = 13), and complete responders (CR = 1
200                                              Nonresponders (NRs) were defined as having less than 15
201 achieved pCR in 35.7% compared with 19.8% in nonresponders (odds ratio, 2.2; 95% CI, 1.24 to 4.19).
202 h response to CRT (25% of responders, 47% of nonresponders; odds ratio 0.3 [0.12-0.76]; P=0.01).
203 d patients were categorized as responders or nonresponders on the basis of the 6-stage regression sca
204  2006, local radiotherapy was introduced for nonresponders or patients with classic medulloblastoma (
205  x 10 min remote ischemic preconditioning in nonresponders) or sham-remote ischemic preconditioning (
206 lonoscopy and invitation for FIT for initial nonresponders); or choice (invitation offering a choice
207  predict the outcome at 52 weeks: responder, nonresponder, or indeterminate.
208 not differ significantly between responders, nonresponders, or controls.
209 s was more significant in responders than in nonresponders (P < .001).
210 VGPR/CR, 64 months for PR, and 28 months for nonresponders (P < .001).
211 re significantly lower in responders than in nonresponders (P < .001): clinical response, 156 vs 725
212 rum levels were higher in responders than in nonresponders (P < 0.001).
213  in responders' cells compared with those of nonresponders (P = .0011).
214 ders were more similar to Dutch infants than nonresponders (P = .002).
215 on of donor material than fecal samples from nonresponders (P = .04) and distinct baseline compositio
216 S >/= 18.8 degrees as opposed to only 16% of nonresponders (P = 0.001).
217 erall survival of 13.3 mo, versus 6.9 mo for nonresponders (P = 0.021).
218 ore decreased TNF-alpha levels compared with nonresponders (P = 0.046).
219 responders vs mean decrease of 2.2 points in nonresponders, P = .04).
220 y outcome vs an increase of 0.10 +/- 0.98 in nonresponders; P < .001).
221 aian infants, including 39 RVV responder and nonresponder pairs.
222 esponse index to differentiate responder and nonresponder patients and had substantial agreement with
223  difference between omalizumab responder and nonresponder patients remain inconclusive.
224 o hippocampal neurons that were derived from nonresponder patients that we also observed when re-exam
225 ndex for the discrimination of responder and nonresponder patients was evaluated by receiver operatin
226                Extending the loading dose in nonresponder patients would cost euro 214,862.57, euro 2
227 46 and 18 clinically diagnosed responder and nonresponder patients, the quantitative response index a
228 mite AIT were compared between responder and nonresponder patients.
229 old correctly identified 42 responder and 17 nonresponder patients.
230 tions; these dynamic patterns were absent in nonresponder patients.
231                     At day 10, compared with nonresponders, patients with a pain response had a great
232                      A high incidence of CRT nonresponders persists despite good patient selection an
233 t-LVAD R (post-R) as compared with post-LVAD nonresponders (post-NR).
234             Nine patients were classified as nonresponders (PSA decline <50%), and 25 patients were c
235                                      Chronic nonresponders received nadolol+prazosin and had a third
236              Remarkably, 44% of site-defined nonresponders received no additional treatment.
237 rouracil/vincristine/doxorubicin (C5VD), and nonresponders received six cycles of C5VD alone.
238                   Overall, more site-defined nonresponders received treatment (55.9% vs. 38.3% of res
239 were classified as responders (score 0-2) or nonresponders (score 3).
240  reported that antidepressant responders and nonresponders show different alterations in brain grey m
241 icrobiome samples (n = 43, 30 responders, 13 nonresponders) showed significantly higher alpha diversi
242 artial response, n = 5) and 11 patients were nonresponders (stable disease, n = 9; progressive diseas
243 esponders (complete or partial response) and nonresponders (stable or progressive disease) according
244  during the interconversion of responder and nonresponder state.
245  of 10(-3) or greater before allo-HSCT (late nonresponders) still had an EFS of 50% and OS of 63%, wh
246 howed greater deviation from baseline in ICS nonresponders than in ICS responders.
247                   Results: In responders and nonresponders, the 2-y OS was 66% versus 29% for imPERCI
248                                           In nonresponders, the percent change in IL-6 on the day aft
249                            In responders and nonresponders, the respective progression-free survival
250 n tDV, while no decrease was observed in all nonresponders; this difference between responders and no
251 edictable differences between samples (e.g., nonresponder to treatment).
252 al were also apparent between responders and nonresponders to anti-PD-1 therapy.
253 P values < .001), and 15% were identified as Nonresponders to anti-VEGF therapy over 51.4 +/- 18.7 mo
254  protein levels were significantly higher in nonresponders to antihistamines as compared to responder
255            Here we identified early and late nonresponders to be considered as events in future trial
256 stratification of tumors into responders and nonresponders to BETi are lacking.
257 her PRM(-) and a lack of change in PRM(+) in nonresponders to bevacizumab therapy implies that tumors
258 sis, and may prioritise future therapies for nonresponders to current approaches.
259 s, which could be exploited for treatment of nonresponders to current immunotherapies.
260 x, and applied separately for responders and nonresponders to ECT.
261 ity-time integral more in responders than in nonresponders to fluid administration (11% +/- 5% vs 3%
262 es in pain phenotypes between responders and nonresponders to intravenous lidocaine treatment using q
263                                              Nonresponders to omalizumab had significantly lower bIgE
264 or 3 HCV, those with cirrhosis, and/or prior nonresponders to pegylated interferon-based regimens.
265 isional surgery for OAG or OHT; and no known nonresponders to prostaglandins.
266 of hematologic response is vital to shifting nonresponders to rescue treatments.
267 P improves differentiation of responders and nonresponders to the drug.
268                                              Nonresponders to the n-3 FA supplementation had a higher
269 ated RA patients classified as responders or nonresponders to therapy.
270 nses demonstrated prolonged OS compared with nonresponders.TRIAL REGISTRATIONClinicalTrials.gov NCT02
271 al (OS) were compared between responders and nonresponders using Kaplan-Meier and log-rank analyses.
272 disorder, both antidepressant responders and nonresponders, using the anisotropic effect size version
273 ation as a vaccine responder (VR) or vaccine nonresponder (VNR).
274 ve of central venous pressure was smaller in nonresponders was 0.12.
275 ders; this difference between responders and nonresponders was significant (P = .001).
276 pitalizations, and death, among site-defined nonresponders was significantly higher than responders.
277 distinguish between treatment responders and nonresponders, we herein submit a novel animal experimen
278                    The percentage changes in nonresponders were -6.2% in tumor size, -17.3% in SUV(pe
279                ADC changes in responders and nonresponders were compared (Wilcoxon rank sum tests).
280 vity index score compared with baseline) and nonresponders were compared with Mann-Whitney test.
281 an effects between rapid (D1) responders and nonresponders were found at baseline, D1, and D3.
282                                              Nonresponders were gradually offered a 4-food-group elim
283 showed that CD11b(+) cells in responders and nonresponders were markedly different.
284                                    Confirmed nonresponders were randomly assigned to treatment with e
285                                              Nonresponders were those who either died, were hospitali
286                                       If all nonresponders were without complaints, the prevalence wo
287                              Following LTP, "nonresponders" were those with <20% IOP reduction after
288 KD patients (126 IVIG responders and 24 IVIG nonresponders) were recruited for this study.
289 ectivity between these regions compared with nonresponders, whereas venlafaxine responders had lower
290 ifference in survival between responders and nonresponders, whereas vRECIST (hazard ratio, 0.6; 95% C
291 d increased mitochondrial mass compared with nonresponders, which positively correlated with the expa
292 ateral hippocampus and surrounding tissue in nonresponders, while responders showed increased GMV in
293 inuation (arm A) and proportion of nivolumab nonresponders who converted to PR/CR after ipilimumab (a
294                                              Nonresponders who received placebo on day 1 were randoml
295                                           In nonresponders with at least 1 medication at baseline, 76
296 maging distinguished treated responders from nonresponders with excellent predictive ability.
297           We previously reported 3 anti-IL-6 nonresponders with increased mTOR activation who respond
298 sponders were treated with nadolol and acute nonresponders with nadolol+nitrates.
299 ter IC1 were compared between responders and nonresponders with the Mann-Whitney U test.
300 t sera obtained from clinical responders and nonresponders within a cohort of 82 patients with grass

 
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