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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
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
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
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
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
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
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
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
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
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
129 ertoire remodeling, which may be impaired in nonresponders because of the preexisting immune environm
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
136 FC of the RN-left MTG was also found in SSRI nonresponders compared to responders, which was a signif
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
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
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
153 analyses of arterial spin-labeled (ASL) MRI, nonresponders exhibited increased cerebral blood flow (C
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
161 stem cells (iPSCs) from full responders and nonresponders, from subjects with diabetes but no DME, a
164 as noted, while at the 2-month follow-up the Nonresponder group had a significantly higher VEGF conce
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;
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,
176 reater frequency in responders compared with nonresponders in the IgG(4)(+) but not the IgA(+) fracti
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
181 ferogenic TLR9 agonist, SD-101, in anti-PD-1 nonresponders led to a complete, durable rejection of es
183 ignificantly differed between responders and nonresponders (<0.01), whereas differences in tumor size
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
189 ek 12 (n = 63), compared with ~30% to 65% in nonresponders (n = 12), while the residual disease genom
193 significant difference in PFS between RECIST nonresponders (n = 255) and responders (n = 20; HR = 1.5
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
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
211 re significantly lower in responders than in nonresponders (P < .001): clinical response, 156 vs 725
215 on of donor material than fecal samples from nonresponders (P = .04) and distinct baseline compositio
222 esponse index to differentiate responder and nonresponder patients and had substantial agreement with
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
227 46 and 18 clinically diagnosed responder and nonresponder patients, the quantitative response index a
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
245 of 10(-3) or greater before allo-HSCT (late nonresponders) still had an EFS of 50% and OS of 63%, wh
250 n tDV, while no decrease was observed in all nonresponders; this difference between responders and no
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
257 her PRM(-) and a lack of change in PRM(+) in nonresponders to bevacizumab therapy implies that tumors
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
264 or 3 HCV, those with cirrhosis, and/or prior nonresponders to pegylated interferon-based regimens.
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
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
280 vity index score compared with baseline) and nonresponders were compared with Mann-Whitney test.
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
300 t sera obtained from clinical responders and nonresponders within a cohort of 82 patients with grass