ライフサイエンスコーパス: responder

1 nd antiapoptosis enriched in network of poor responders).

2 ot Ultimatum Games (UG) both as proposer and responder.

3 The primary endpoint was proportion of responders.

4 icantly lower in nonresponders but higher in responders.

5 ison with EMDC-dispatched professional first responders.

6 (T2), resulting in 29 responders and 36 non-responders.

7 ith further improvements in QOL at day 42 in responders.

8 gulated tissue-residing cellular sensors and responders.

9 samples of the two responders and three non-responders.

10 ore stable EEG-vigilance regulation than non-responders.

11 group were split into Low- and High cortisol responders.

12 test to compare the proportion of treatment responders.

13 ntration increased significantly only in non-responders.

14 ic characteristics between nonresponders and responders.

15 ADC changes accurately identify noncomplete responders.

16 ns significantly reduced only in tofacitinib responders.

17 acitinib were strictly confined to treatment responders.

18 biomarker levels (76-94% elevated) than non-responders.

19 ) at 90 days, completed by patients or proxy responders.

20 expression between good responders and poor responders.

21 s as a presentation of CU and omalizumab non-responders.

22 icantly higher in IFN-responders than in non-responders.

23 significantly greater compared with those of responders.

24 health information available to humanitarian responders.

25 ng the anti-PD1 treatment were classified as responders.

26 0 at 3 wk postvaccination were designated as responders.

27 utch infants' microbiomes, assumed to be RVV responders.

28 vival after PAD by EMDC-dispatched lay first responders.

29 ing 55% (six of 11) of transplantation-naive responders.

30 revalence of EBOV infection in international responders.

31 intraventricular extension and use of proxy responders.

32 s of both copies of B2M is found only in non-responders.

33 w-derived macrophages and dendritic cells as responders.

34 t can stratify patients as responders or non-responders.

35 twork of good responders versus that of poor responders.

36 9 (19.6%) complete and 78 (80.4%) incomplete responders.

37 reefold in non-responders ( 30%) compared to responders ( 10%) and associated with poorer overall sur

38 patient fecal microbiome samples (n = 43, 30 responders, 13 nonresponders) showed significantly highe

39 Retinoic acid receptor responder 2 (RARRES2) is transcriptionally downregulated

40 ; 18 reported PAD by nondispatched lay first responders, 20 reported PAD by EMDC-dispatched professio

41 ased by a median of 4.4 g/dL in the complete responders, 3.9 g/dL in those achieving PR, and 3.7 g/dL

42 nd that B2M LOH is enriched threefold in non-responders ( 30%) compared to responders ( 10%) and asso

43 47.6%] of 273 in the naldemedine group vs 94 responders [34.6%] of 272 in the placebo group, differen

44 Seven responders (44%) proceeded to allogeneic hematopoietic s

45 demedine than with placebo in COMPOSE-1 (130 responders [47.6%] of 273 in the naldemedine group vs 94

46 hus, 12 patients were classified as complete responders (58% HCV, median age 59.7 years, 83.4% Child-

47 .0, 46.2-126.5 IU/mL, P = .008) and complete responders (73.7, 19.45-153.8 IU/mL, P = .032).

48 levels (17.9, 17.0-55.0 IU/mL) than partial responders (82.0, 46.2-126.5 IU/mL, P = .008) and comple

49 ated external defibrillators, teaching first responders about team-based CPR (eg, automated external

50 ients with the T315I mutation; 88% of CR/CRh responders achieved a complete minimal residual disease

51 In responders across 9 datasets grey matter volume (GMV) wa

52 Thirty-three patients were classified as responders after 12 weeks of antipsychotic treatment.

53 re increased in peripheral blood of clinical responders after 12 wk of treatment with KD025.

54 The responder analysis (>50% reduction from baseline HAMD on

55 mes were overall efficacy (primary outcome); responder and dropout rates; positive, negative, and dep

56 ngs in 78 Ghanaian infants, including 39 RVV responder and nonresponder pairs.

57 r time and the difference between omalizumab responder and nonresponder patients remain inconclusive.

58 passed through during the interconversion of responder and nonresponder state.

59 tients, a total of 150 KD patients (126 IVIG responders and 24 IVIG nonresponders) were recruited for

60 26 (39%) of 66 haematological responders and 25 (71%) of 35 molecular responders (with

61 A RNA-sequencing in baseline samples from 25 responders and 25 non-responders to hydrochlorothiazide

62 ease was attained in 20 (80%) of 25 complete responders and 28 (57%) of 49 patients overall.

63 /- 1 days of treatment (T2), resulting in 29 responders and 36 non-responders.

64 Eight of 11 patients (72.7%) were responders and 5 were remitters after 6 months of open-l

65 eg, proapoptosis enriched in network of good responders and antiapoptosis enriched in network of poor

66 All uncrossed projecting METH responders and approximately 70% of crossed projecting M

67 ocity-time integral changed by 23% +/- 9% in responders and by 8% +/- 3% in nonresponders.

68 as a predictive diagnostic test to identify responders and guide treatment in trials of the PD-1 (pr

69 At baseline responders and non-responders differed in distribution o

70 at differed significantly (P < 0.05) between responders and non-responders including stem cell factor

71 The patients classified as responders and non-responders using QUS biomarkers demon

72 ssociated with a survival difference between responders and nonresponders (45.0 months vs 10.0 months

73 lum in comparisons between both Ghanaian RVV responders and nonresponders (FDR, 0.008 vs 0.003) and D

74 tion was significantly different between RVV responders and nonresponders (FDR, 0.12), and Ghanaian r

75 We identified similar numbers of responders and nonresponders after ketamine or imipramin

76 tory volume in 1 second (FEV1) of omalizumab responders and nonresponders at 6 months.

77 ogenesis factor levels were compared between responders and nonresponders by mRECIST criteria by usin

78 Responders and nonresponders had markedly different chan

79 g PSF and PSFEARL, we classified patients as responders and nonresponders in 60 and 40 cases versus 6

80 nts were classified using PSF and PSFEARL as responders and nonresponders in 69 and 26 cases versus 7

81 compositions between 6-week old, matched RVV responders and nonresponders in rural Ghana.

82 ion-free survival and overall survival among responders and nonresponders no matter which reconstruct

83 al studies have reported that antidepressant responders and nonresponders show different alterations

84 by levels of CRP improves differentiation of responders and nonresponders to the drug.

85 n all nonresponders; this difference between responders and nonresponders was significant (P = .001).

86 ociated circadian effects between rapid (D1) responders and nonresponders were found at baseline, D1,

87 in pretreatment sera obtained from clinical responders and nonresponders within a cohort of 82 patie

88 jor depressive disorder, both antidepressant responders and nonresponders, using the anisotropic effe

89 tures that can distinguish between treatment responders and nonresponders, we herein submit a novel a

90 nto Ab-secreting cells, were similar between responders and nonresponders.

91 djusted hazard rate (HR) of overall death in responders and nonresponders.

92 nges in cardiac output and the proportion of responders and nonresponders.

93 rved by Fluidigm high-density RT-PCR between responders and nonresponders.

94 us equilibrium pressure and reliably detects responders and nonresponders.

95 me B expression was observed between treated responders and nonresponders.

96 ed genes, which were highly expressed in non-responders and partial remission patients than in comple

97 ene regulatory networks associated with good responders and poor responders to inhaled corticosteroid

98 ferential downstream expression between good responders and poor responders.

99 ost-treatment bone marrow samples of the two responders and three non-responders.

100 registered trial units (n = 46, 1 unit had 2 responders) and a Delphi survey (n = 73 invited particip

101 Most subjects from TIV nonresponder, low responder, and high responder groups had detectable ADCC

102 e response biomarkers are needed to identify responders, and conventional imaging modalities have not

103 splenic metabolism at 3 mo were observed in responders (area under the curve > 0.85, P < 0.04).

104 AFP responders at 1 mo had better overall survival than nonr

105 tatus and 69.7% (85 of 122) deemed treatment responders at 1 year based on Insomnia Severity Index da

106 The proportion defined as responders at 24 h (primary study endpoint) was 16% for

107 semide regimen did not improve the number of responders at 24 h, despite greater weight loss and flui

108 nt was the proportion of patients considered responders at 24 h.

109 Skin and global organ responders at 28 weeks had higher median Treg cell count

110 (18)F-FDG PET/CT detected all responders at 3 mo and reclassified best overall respons

111 rs, at 8.5 mo versus 4.8 mo (P = 0.018); AFP responders at 3 mo had overall survival of 13.3 mo, vers

112 Among suboptimal (<5-letter) responders at 3 months, 6.7% showed >/=10-letter gains a

113 post-ECP than nonresponders, as did steroid responders at 56 weeks who were 12 months post-ECP.

114 prebronchodilator FEV1 showed improvement in responders at 6 months, while a decrease was observed in

115 ter deglucuronidation capabilities in strong responders, based on differential gut microbial composit

116 that BAT is negative or the patient has non-responder basophils, OFC may still be indicated.

117 Selectively bred high-responder (bHR) and low-responder (bLR) male rats are kn

118 While loss to follow-up was low, there was responder bias with patients injured in intentional even

119 tion factors (TFs) function as genomic first responders, binding to inaccessible regions of chromatin

120 electively bred high-responder (bHR) and low-responder (bLR) male rats are known to differ in their e

121 In responders, both drugs reversed susceptibility-associate

122 sting our model performed well at predicting responders, but not non-responders (i.e. many non-respon

123 Secondary end points included percentage of responders by age strata and treatment-emergent adverse

124 studied, 20 had been classified as complete responders by the centers, but eight of these patients w

125 (+) T cells inhibited IFNgamma production by responder CD8(+) T cells.

126 13 responders ceased all therapy; among these all 11 minima

127 GPCRs that are only expressed in the PGE2-G responder cell lines.

128 irus (VZV) ex vivo restimulation measured by responder cell-frequency and flow cytometry, but the res

129 The Wnt responder cells showed increased tumour propagation abil

130 of miR-301a-3p and miR-145-5p were higher in responders (combined response or HBsAg loss) compared to

131 After restaging, complete responders continued with four courses of rituximab cons

132 PAD by EMDC-dispatched lay first responders could be a promising strategy, but evidence i

133 = 18), nonresponders (NR = 13), and complete responders (CR = 14) to CRT, as defined by a tumor regre

134 eriod, subjects meeting stabilization/stable-responder criteria were randomized to asenapine or place

135 Median corticosteroid dose in responders decreased from 0.29 mg/kg per day at baseline

136 y received bystander-initiated CPR and first-responder defibrillation (odds ratio, 1.55; 95% CI, 1.01

137 re patients received bystander CPR and first-responder defibrillation at home and in public, which wa

138 ardiopulmonary resuscitation (CPR) and first-responder defibrillation for OHCAs stratified by home vs

139 to 70.5% [424 of 601], P = .01), while first-responder defibrillation increased at home (from 42.2% [

140 ek 24 among the intent-to-treat sample, with responders defined as having a 25% or greater improvemen

141 The proportion of responders (defined as having a reduction >/=50% in SSI

142 At baseline responders and non-responders differed in distribution of overall EEG-vigil

143 baseline to 0.12 mg/kg per day at week 49; 5 responders discontinued corticosteroids.

144 Medical Dispatch Center (EMDC), or lay first responders dispatched by the EMDC.

145 eive a platelet donation from a high- or low-responder donor when both were available, or when only 1

146 from low-responder donors, and 49 from high-responder donors (47 of which were randomized and 53 non

147 ts in vitro assessed by flow cytometry (high-responder donors) are cleared more quickly from the circ

148 were assigned to receive platelets from low-responder donors, and 49 from high-responder donors (47

149 kly from the circulation than those from low-responder donors, resulting in lower platelet count incr

150 The causes of this non-responder effect are not well understood due to the cost

151 ured by fMRI as a potential cause of the non-responder effect.

152 ficacy end point was percentage of treatment responders (eliciting dose: >/=10-times increase and/or

153 In responders eliminated food groups were reintroduced indi

154 patients clinically classified as a complete responder eventually recur and succumb to the disease.

155 igilance levels from baseline to T1 than non-responders (F2,130 = 4.978, p = 0.005).

156 the large-scale deployment of international responders, few cases of Ebola virus disease have been d

157 approximately 70% of crossed projecting METH responders fired with the concurrent ipsilateral motor o

158 hed lay first responders, professional first responders (firefighters/police) dispatched by the Emerg

159 lation by EMDC-dispatched professional first responders (firefighters/police) was associated with a m

160 ed PAD by EMDC-dispatched professional first responders (firefighters/police), and 3 reported both.

161 ase), followed by monotherapy maintenance in responders for a 2-year period.

162 te response and another 5 (36%) were partial responders for an overall response rate of 72% (10 of 14

163 cision medicine approach for differentiating responders from non-responders to BCL-2/MCL-1 targeted t

164 Imaging distinguished treated responders from nonresponders with excellent predictive

165 nabled us to distinguish weight and glycemic responders from nonresponders.

166 ern and lower mesor distinguished subsequent responders from nonresponders.

167 hanges in ctDNA content during therapy and a responder given a checkpoint inhibitor-based regimen bec

168 om TIV nonresponder, low responder, and high responder groups had detectable ADCC antibodies prevacci

169 Sensitive responders >/=65 and <65 and highly sensitive responders

170 esponders >/=65 and <65 and highly sensitive responders >/=65 years old required pharmacogenomic-guid

171 provided well-controlled INR only in normal responders >/=65, whereas for normal responders <65 year

172 at month 6, patients were classified as KIT responders (>/=25%, n = 17) or KIT nonresponders (<25%,

173 In responders, H1N1 stimulation at T0 also resulted in CXCR

174 A responder had at least three spontaneous bowel movements

175 Overall, 55 (91.6%) of 60 of the TFGED/FFGED responders had 1 or 2 food triggers.

176 Responders had higher biomarker levels (76-94% elevated)

177 ring changes in QOL from baseline to day 42, responders had significantly greater improvements in the

178 ed with poor responders, the network of good responders has differential connectivity and distinct on

179 genetic marks, and pathways activated in non-responders have been identified for therapeutic developm

180 d well at predicting responders, but not non-responders (i.e. many non-responders were predicted to r

181 sis by modified intention to treat, with non-responder imputation.

182 The proportion of responders in both trials was significantly higher with

183 an fluid challenge modify the proportions of responders in postoperative patients.

184 erval [CI], 43%-71%) using RECIST 1.1 (17/34 responders in the (18)F-FMISO-positive group).

185 As the primary immune responders in the brain, glial cells are implicated as k

186 health effects amongst marine life and spill responders in the northern Gulf of Mexico.

187 baseline of 3 or greater at 24 weeks (termed responders), in patients with a baseline ACT score less

188 cantly (P < 0.05) between responders and non-responders including stem cell factor, platelet-derived

189 ed functional differences in gut bacteria in responders, including enrichment of anabolic pathways.

190 nd a fluid bolus was given to identify fluid responders (increase in cardiac index > 15%).

191 The proportion of responders increased from 20% in the group of 1 mL/kg to

192 h initiatives to improve bystander and first-responder interventions included training members of the

193 ting multiple factors downstream of the core responder kinase ATM/ATR.

194 th after the intervention, the percentage of responders (LBP intensity <40) was higher in the GC IDI

195 However, highly sensitive responders <65 years old did not achieve well-controlled

196 normal responders >/=65, whereas for normal responders <65 years old, a clinically guided protocol w

197 dose maintenance, 8 weeks), lisdexamfetamine responders (</=1 binge eating day per week for 4 consecu

198 gative at a threshold of 10(-5) Among the 62 responders, median duration of response was not estimabl

199 For partial metabolic responders (n = 19), the median OS was 22.8 mo.

200 Nonmetabolic responders (n = 6) (stable metabolic disease or progress

201 levels did not differ significantly between responders, nonresponders, or controls.

202 a patients, EMMA correctly classified 96% as responders/nonresponders and correctly classified 79% ac

203 but IL-17A was significantly reduced only in responders of either treatment.

204 hoid cells (ILCs) are tissue-resident "first responders" of the immune system that function to protec

205 cal signatures that can stratify patients as responders or non-responders.

206 rounding area for responders than in partial responders or nonresponders (mean +/- standard deviation

207 umor volume reduction >90%) and five partial responders or nonresponders.

208 feration and effector cytokine production by responders or through conversion of Tregs into T helper

209 w4IgE/bIgE levels than partial and complete responders (P < .001).

210 nresponders to antihistamines as compared to responders (P < .001).

211 to hydrochlorothiazide compared with 25 poor responders (P=0.01).

212 mab initiation, FEV1 improved at 6 months in responder patients and then remained stable for 2 years.

213 In the omalizumab responder patients, lung function parameters were also o

214 Here we examined the non-responder phenomenon in an aggressive MCF10-CA1a breast

215 Of 275 randomized lisdexamfetamine responders (placebo, n = 138; lisdexamfetamine, n = 137)

216 hese patients, classified as prednisone poor responders (PPR), have poorer outcome than do the other

217 Forty-five rectal cancer patients, partial responders (PR = 18), nonresponders (NR = 13), and compl

218 d the defibrillator: nondispatched lay first responders, professional first responders (firefighters/

219 Primary endpoints were responder rate defined as 50% reduction in migraine atta

220 ot meet the primary endpoint of reduction in responder rate in patients with frequent migraine.

221 There was no difference in responder rate in the PFO closure (45 of 117) versus con

222 dine treatment led to a significantly higher responder rate than did placebo and was generally well t

223 Responder rates for each active treatment were not signi

224 cally significant, as shown by the following responder rates: joint treatment group, 47.2%; single ac

225 6-8 weeks after R-CHOP, responders received two doses of 15 mCi/m(2) (555 MBq/m(

226 Conclusion For IC responders, reduced-dose IMRT with concurrent cetuximab

227 ese all 11 minimal residual disease-negative responders remain progression-free off therapy.

228 r, with a particular focus on the 260-bp and Responder satellites.

229 Poor responders should be identified and offered a detailed e

230 Exploratory analyses revealed that responders showed a stronger decline in EEG-vigilance le

231 onths, best overall response was 67%; 71% of responders showed a sustained response for >/=20 weeks.

232 group (including both Low and High cortisol responders) showed reduced P300 amplitude to target onse

233 nce stages (F2,133 = 4.780, p = 0.009), with responders showing significantly more high vigilance sta

234 Among the responders, six patients achieved a partial response, tw

235 ects of MSC-Exo on immune cell migration and responder T cell proliferation were examined by chemotac

236 A expression was significantly higher in IFN-responders than in non-responders.

237 ion decreased velocity-time integral more in responders than in nonresponders (12% +/- 5% vs 5% +/- 2

238 ion increased velocity-time integral more in responders than in nonresponders to fluid administration

239 n the tumor than in the surrounding area for responders than in partial responders or nonresponders (

240 igher systemic exposure to tacrine in strong responders that experienced transaminitis, revealing enh

241 improvement seemed restricted to a group of responders that included 40% of the cohort.

242 When compared with poor responders, the network of good responders has different

243 cordance (5.0%) occurred (i.e., changes from responder to nonresponder).

244 lts in early identification of a majority of responders to an empiric diet with few food triggers, av

245 Therefore, it was hypothesized that responders to antidepressants show a) a high level of EE

246 Higher brain arousal level in responders to antidepressants supports the concept that

247 oach for differentiating responders from non-responders to BCL-2/MCL-1 targeted therapy.

248 R at baseline showed a trend to being better responders to capsaicin treatment compared with patients

249 markers for the prediction and monitoring of responders to clinical checkpoint blockade has been the

250 to subpopulations of good and poor treatment responders to delineate response-associated signature tr

251 ased English General Practice Patient Survey responders to explore the prevalence of self-reported di

252 nd that hepatocytes themselves were the main responders to hepatocyte death, increasing transcription

253 seline samples from 25 responders and 25 non-responders to hydrochlorothiazide (HCTZ) or chlorthalido

254 ASP mRNA was significantly higher in 25 good responders to hydrochlorothiazide compared with 25 poor

255 Complete or partial responders to induction chemotherapy received 54 Gy in 2

256 for the key role of neutrophils as the first responders to inflammatory stimuli.

257 rks associated with good responders and poor responders to inhaled corticosteroids based on a subset

258 Responders to ketamine showed increased GBCr in the late

259 To identify patients among exceptional responders to NCT with a low risk for axillary metastase

260 Pteropods are among the first responders to ocean acidification and warming, but have

261 All six responders to olaparib showed a decrease in tDV, while n

262 A retrospective analysis of responders to subcallosal cingulate deep brain stimulati

263 tion, and of exposure events, among returned responders to the West African Ebola epidemic 2014-2016.

264 ease assay to Nexvax2 peptides was negative (responders to treatment) in two (22%) of nine placebo-tr

265 rivative that is especially effective in non-responders to triptan derivatives.

266 Responders to VI received two additional cycles of VI in

267 r data identify cerebellar astrocytes as key responders to viral infection and highlight the existenc

268 n of rhotekin 2 (RTKN2), an oxysterol stress responder, to optimize cell survival.

269 Patients' imaging outcomes consisted of six responders (tumor volume reduction >90%) and five partia

270 phage library screening in mice bearing non-responder tumors showed that compared to untreated and t

271 he patients classified as responders and non-responders using QUS biomarkers demonstrated significant

272 composition of the patient gut microbiome of responders versus nonresponders.

273 between the gene regulatory network of good responders versus that of poor responders.

274 social aspects (mean increase, 1.2 points in responders vs mean decrease of 2.2 points in nonresponde

275 Defibrillation by nondispatched lay first responders was associated with the highest survival with

276 Defibrillation by nondispatched lay first responders was found to correlate with the highest impac

277 At week 24, the odds of being a responder were higher for patients who initiated treatme

278 uration of response was not yet reached; all responders were alive, and eight had responses lasting 1

279 gh (>/=14) NIHSS score, larger ICH and proxy responders were associated with low scores in all five d

280 criptome profiles of good and poor treatment responders were compared in the murine model.

281 Spatial clusters of high-IgG responders were identified across space and time within

282 Food triggers in TFGED responders were milk (52%), gluten-containing grains (16

283 and nonresponders (FDR, 0.12), and Ghanaian responders were more similar to Dutch infants than nonre

284 Transcriptional profiles in treatment responders were most similar in the PFC.

285 nders, but not non-responders (i.e. many non-responders were predicted to respond).

286 Three of the responders were refractory to previous immune checkpoint

287 ot reached for treated patients overall; all responders were still alive at data cutoff.

288 In the HVPG-guided group, acute responders were treated with nadolol and acute nonrespon

289 on in approximately 30% of the patients, and responders were typically coadministered additional anti

290 Responders were withdrawn from treatment (for up to 36 w

291 ce to first-line drugs relative to treatment responders when both groups are matched for symptom seve

292 rted by male General Practice Patient Survey responders who endorsed gay or bisexual orientation comp

293 DS AND We used snowball sampling to identify responders who had returned to the UK or Ireland, and us

294 mean value 42.25 mug/mL) compared to delayed responders with lower sIgG titers (mean value 14.79 mug/

295 response; there were eight confirmed partial responders with MET-driven disease (18%), but none with

296 sed English Cancer Patient Experience Survey responders with sexual orientation as a binary outcome,

297 lly increased were correctly predicted to be responders with SHAPE and subharmonic imaging after comp

298 ved with nivolumab; 10 (37%) of 27 confirmed responders with squamous NSCLC and 19 (34%) of 56 with n

299 ical responders and 25 (71%) of 35 molecular responders (with the JAK2 Val617Phe mutation) have maint

300 At one year, 9 of 11 patients (81.8%) were responders, with 6 of them in remission.