ライフサイエンスコーパス: posttreatment

1 during the training sessions and at pre- and posttreatment.

2 4, 48, and 72 hours and 5, 7, 9, and 14 days posttreatment.

3 tionnaires before, during, and up to 2 years posttreatment.

4 recorded at baseline, 3 hours, and 24 hours posttreatment.

5 mine and underwent repeated rs-fcMRI at 24 h posttreatment.

6 the same amount of initial DNA damage by 3 h posttreatment.

7 erienced vision loss; however, most improved posttreatment.

8 h a sustained virologic response at 12 weeks posttreatment.

9 er treatment, and this remained elevated 3 h posttreatment.

10 ; 12 (31%) reported residual visual symptoms posttreatment.

11 not predictive of clinical failure assessed posttreatment.

12 t randomization, biweekly, midtreatment, and posttreatment.

13 n the CD group during anticipatory phases at posttreatment.

14 4 and follow-up visits occurred for 9 months posttreatment.

15 incentive delay task (MIDT) pretreatment and posttreatment.

16 ore treatment and at 2 d and 1, 4, and 16 wk posttreatment.

17 Patients were followed until 1 year posttreatment.

18 g administration (baseline), 2 h, and 7 days posttreatment.

19 ially those experiencing persistent symptoms posttreatment.

20 ups with no significant differences pre- and posttreatment.

21 h a model Ag and monitoring immune responses posttreatment.

22 eek 4, end of treatment, and 6 and 12 months posttreatment.

23 nd levels contracted toward baseline by 4 wk posttreatment.

24 centrations of CO applied as pretreatment or posttreatment.

25 xiety symptoms were assessed at baseline and posttreatment.

26 and adverse events monitored 3 and 24 hours posttreatment.

27 went an (18)F-FDG PET/CT scan at baseline, a posttreatment (166)Ho SPECT/CT scan, and another (18)F-F

28 estimated using the activity distribution on posttreatment (166)Ho SPECT/CT.

29 The posttreatment (166)Ho-microsphere activity distributions

30 All patients underwent systematic posttreatment (18)F-FDG PET/CT and were followed with at

31 oradiation for NSCLC, involving baseline and posttreatment (18)F-FDG PET/CT imaging, were conducted b

32 For this, the performance of posttreatment (18)F-FDG PET/CT, the impact on patient ca

33 urine at diagnosis who became sIFE-negative posttreatment, 3 (1.8%) were uIFE positive.

34 volume increased (pretreatment, 412.7 cm(3); posttreatment, 577.6 cm(3); P = 0.005).

35 WAZ score were examined from pretreatment to posttreatment (6 months) and change in HAZ score was ass

36 lume decreased (pretreatment, 1,118.7 cm(3); posttreatment, 870.7 cm(3); P = 0.003), whereas the nont

37 estimates of absorbed doses calculated from posttreatment (90)Y TOF PET/CT for tumor and nontumor ti

38 (7 glass spheres, 20 resin spheres) and the posttreatment (90)Y TOF PET/CT results.

39 One patient who died before week 12 posttreatment achieved a response at posttreatment week

40 symptoms significantly improved from pre- to posttreatment across all conditions and were maintained

41 In CD participants, increased posttreatment activity in dopamine-innervated regions su

42 ADC ratio (mean posttreatment ADC/mean pretreatment ADC) was calculated.

43 Active surveillance for posttreatment adverse events was performed daily for 6 d

44 Posttreatment adverse events were similar following DEC

45 Posttreatment AE rates and severity did not differ signi

46 662; SMD = -0.35, 95% CI -0.56 to -0.14) at posttreatment and also compared with inactive control at

47 m severity than those assigned to placebo at posttreatment and at follow-up.

48 ve rate in patients who became sIFE-negative posttreatment and evaluate rates of minimal residual dis

49 rs displayed limited changes in ctDNA levels posttreatment and experienced significantly shorter prog

50 DCS group but not the placebo group, at both posttreatment and follow-up (clinician-rated Y-BOCS: t62

51 n increase in hydrogen peroxide is sustained posttreatment and potential mechanisms involved in this

52 serum at diagnosis who became sIFE-negative posttreatment and who had uIFE available, the uIFE-posit

53 llected at baseline, each treatment session, posttreatment, and 1-month follow-up.

54 Baseline, posttreatment, and 6-month follow-up assessments were ma

55 f social anxiety were acquired pretreatment, posttreatment, and at 3-month follow-up.

56 ive quantitative measurement of baseline and posttreatment aromatase availability in primary tumors a

57 nhibition of MAPK and PI3K/AKT activation in posttreatment as compared with pretreatment tumor specim

58 d not change with treatment, and strength at posttreatment assessment also significantly predicted ab

59 a reduction of >=30% in YBOCS score) at the posttreatment assessment and after another month of foll

60 eek after the HRT session, youth completed a posttreatment assessment to evaluate change in the sever

61 having neither responded nor remitted at the posttreatment assessment).

62 easing importance in the detection, staging, posttreatment assessment, and detection of recurrence of

63 int was the change in score from baseline to posttreatment assessment.

64 Posttreatment assessments took place 1 hour, 1 week, and

65 e diagnosis, pretreatment, on treatment, and posttreatment assessments, and management of chronic HCV

66 ia at week 12 (SVR12) and at week 24 (SVR24) posttreatment, at which time all had a clinical response

67 Our data suggest that pre- and posttreatment Bcl-2/IgH levels from PB have significant

68 A positive posttreatment Bcl-2/IgH status was associated with short

69 Posttreatment biopsies demonstrated stable or improved g

70 Posttreatment biopsies were obtained in 15 patients and

71 At 6 months, 28 of 30 participants underwent posttreatment biopsy.

72 How baseline and posttreatment body composition affects outcome is unknow

73 direct Sanger sequencing of samples pre- and posttreatment, but not on more sensitive deep sequencing

74 Minimal residual disease (MRD) was assessed posttreatment by a polymerase chain reaction-based ligas

75 Sleep quality was significantly improved at posttreatment by psychological interventions compared wi

76 On multivariable logistic regression, low posttreatment CA 19-9 level, RECIST partial response, an

77 anges in tumor size and anatomic extent, and posttreatment CA 19-9 levels were compared between patie

78 Relative to pretreatment, at posttreatment CD participants demonstrated increased ant

79 Posttreatment cell culture and enzyme-linked immunosorbe

80 symptom score across days 2 to 4 of a 4-day posttreatment challenge (PTC) in the EEU after the grass

81 oconjunctivitis symptom scores (TRSSs) after posttreatment challenge (PTC) to rye grass in an environ

82 renchymal enhancement (BPE) (n = 91, 20.9%), posttreatment changes (n = 16, 3.8%), and other findings

83 Posttreatment changes on conventional imaging can confou

84 In this study, posttreatment clinical and immunologic reactions were co

85 elationship between pretreatment binding and posttreatment clinical status was examined.

86 y gene-modified hepatocytes observed 4 weeks posttreatment compared to traditional rAAV gene delivery

87 -1.03, 95% CI -1.44 to -0.61; p = 0.000) at posttreatment compared with inactive control.

88 interval [CI] 42% to 143%, P < 0.001) at 2 d posttreatment compared with pretreatment concentrations.

89 Pretreatment and posttreatment computed tomography scans of consecutive p

90 d potent anti-influenza virus activity under posttreatment conditions [median 50% effective concentra

91 Such posttreatment confounding cannot be dealt with using sta

92 ctors associated with the ability to achieve posttreatment control.

93 cted rhesus macaques that mirrored the human posttreatment controller phenotype and performed immunol

94 ented in a subset of individuals, defined as posttreatment controllers (PTCs).

95 Posttreatment controllers represent a small subset of in

96 ents were not different from the age-matched posttreatment controls.

97 Excluding posttreatment data, vitreous findings were compared with

98 gh 7 days after treatment) and in follow-up (posttreatment days 8-210), after adjustment for sociodem

99 mRNA expression, pre- and posttreatment, demonstrated significant downregulation o

100 Remission was defined as a posttreatment depression score of less than 10 as well a

101 ip between pretreatment amygdala binding and posttreatment depression score, and were unable to predi

102 depression score, and were unable to predict posttreatment depression severity using both pretreatmen

103 By 1 year posttreatment, depression measures decreased (1.5, 6.7%,

104 upfront bortezomib and explore the impact of posttreatment dFLC < 10 mg/L ("stringent dFLC response")

105 ther brain region, GABA levels at 4 weeks or posttreatment did not differ between patients with FEP a

106 Posttreatment dorsolateral prefrontal cortex activation

107 ictive dosimetry of (99m)Tc-MAA SPECT/CT and posttreatment dosimetry based on (90)Y time-of-flight (T

108 ng on intent-to-treat outcomes, within-group posttreatment effect sizes for CPT and prolonged exposur

109 A statistically significant pre- versus posttreatment effect was observed for MCCB speed of proc

110 ter than 10 to 300 mg were responders if the posttreatment eliciting dose was 1000 mg or more.

111 dose of 10 mg or less were responders if the posttreatment eliciting dose was 300 mg or more; partici

112 Posttreatment EMVI status (yEMVI) was reevaluated for bo

113 ndpoint and clinical stability relative to a posttreatment evaluation (PTE) of clinical success.

114 sion:(18)F-FDG PET/CT shows good accuracy in posttreatment evaluation of anal cancer and has a releva

115 Posttreatment evaluation was conducted with contrast mat

116 vestigator-assessed clinical response at the posttreatment evaluation.

117 Pretreatment and posttreatment examinations and treatments were completed

118 o 1.0 for baseline and from 0.48 to 0.76 for posttreatment examinations.

119 Pre- and posttreatment expression of EGFR and HER3 was compared u

120 While the posttreatment fall in hemoglobin level was greater in se

121 l-regional therapy for HCC, and the expected posttreatment findings for each form of therapy.

122 matologic response was associated with lower posttreatment FMD.

123 Posttreatment fMRI data were used to assess network chan

124 In RCTs with posttreatment follow-up >/=12 months, antiviral therapy

125 In RCTs with posttreatment follow-up <12 months, antiviral therapy co

126 mmediately after treatment, and at a 12-week posttreatment follow-up assessment.

127 DG PET/CT may play a significant role during posttreatment follow-up of anal cancer.

128 Mean posttreatment follow-up or total follow-up of untreated

129 Posttreatment follow-up ranged from 35 to 124 months (me

130 s ratio = 0.66, P < .036), during the 2-year posttreatment follow-up, and during the entire 5-year tr

131 se in all patients who completed 12 weeks of posttreatment follow-up.

132 interventions and inactive control group at posttreatment for quality of life (k = 6; n = 401; SMD =

133 of follow-up across all included studies at posttreatment for the primary outcome was 11.5 weeks.

134 ation transfer images were obtained pre- and posttreatment from veterans with (n=39) and without PTSD

135 Networks were applied to posttreatment functional MRI data to assess changes over

136 comparison conditions for target symptoms at posttreatment (g=-0.153, 90% equivalence CI=-0.227 to -0

137 vioral therapy for insomnia (CBT-I) improved posttreatment global and most sleep outcomes, often comp

138 nalysis to determine mean slopes of pre- and posttreatment growth curves on a per-tumor basis and wer

139 growth curves was used to determine pre- and posttreatment growth curves on a per-tumor basis.

140 BDI decrease >/=95%), and superior response (posttreatment HAM-D or BDI score of 0) using multilevel

141 -D or >/=9 BDI points), extreme nonresponse (posttreatment HAM-D score >/=21 or BDI score >/=31), sup

142 Forty-eight weeks posttreatment, HBV DNA rebounded to baseline levels in a

143 as of uncertainty among the various types of posttreatment hematopoietic clones.

144 misinin component, as well as the absence of posttreatment hemolysis with these drugs.

145 Posttreatment high-grade gliomas are usually monitored w

146 ic bacterial frequencies were not persistent posttreatment, however, with individual taxa showing onl

147 Differences between pretreatment and posttreatment HRCT scan scores, pulmonary function test

148 t of pretreatment HVPG, changes in HVPG, and posttreatment HVPG on the development of hepatic decompe

149 Given differences in expected posttreatment imaging findings, the current radiologic t

150 Accurate interpretation of posttreatment imaging is essential for guiding further m

151 llar arterial anastomosis, were recorded and posttreatment imaging results were reviewed.

152 -specific dose conversion factors for common posttreatment imaging times are reported along with a ch

153 ratory tests, follow-up visits, and pre- and posttreatment imaging using (68)Ga-DOTATOC PET/CT from p

154 Uptake on pre- and posttreatment imaging was measured and compared.

155 posttreatment in 4 individuals, and 4 weeks posttreatment in 1 patient (14 IU/mL).

156 NA (range, 15-57 IU/mL) was measured 2 weeks posttreatment in 4 individuals, and 4 weeks posttreatmen

157 eosinophil granule proteins, were increased posttreatment in both groups.

158 n, iron absorption, and utilization pre- and posttreatment in children with afebrile malaria, hookwor

159 There was a large group difference at posttreatment, in which the DCS group exhibited lower se

160 d evidence of a previously undetected strain posttreatment; in many studies, this is interpreted as r

161 nhanced social functioning was mirrored by a posttreatment increase in their blood OXT concentrations

162 etermine the association between frailty and posttreatment infections.

163 rapy, a difference not entirely explained by posttreatment IOP elevation.

164 ient in the SLT group (2.0%) had a transient posttreatment IOP spike greater than 5 mm Hg.

165 patient survival in the 24 hours immediately posttreatment is the key objective.

166 We examined whether pretreatment and posttreatment levels of cognitive restraint, disinhibiti

167 emistry (IHC) was performed on both pre- and posttreatment liver biopsies of 59 PIVENS patients rando

168 ment was assessed by paired pretreatment and posttreatment liver biopsies, magnetic resonance elastog

169 nt had a severe adverse reaction, developing posttreatment liver failure resulting in death.

170 and three ADV-treated (14%) patients during posttreatment long-term follow-up with an overall annual

171 t least 1 subjective symptom for >=6 months (posttreatment Lyme disease symptoms [PTLDS]).

172 hase early Lyme disease, Lyme arthritis, and posttreatment Lyme disease syndrome, as well as the nece

173 ponse to this protein is not associated with posttreatment Lyme disease syndrome.

174 Primary tumor size was assessed on pre- and posttreatment magnetic resonance images according to 1D

175 nd immature gametocytes but does not prevent posttreatment malaria transmission.

176 served in healthy control mice (baseline and posttreatment mean k(PL), 0.011 and 0.017 sec(-1), respe

177 sec(-1), respectively, P = .91; baseline and posttreatment mean nLac, 0.16 and 0.21, respectively, P

178 sec(-1), respectively, P = .01; baseline and posttreatment mean nLac, 0.28 and 0.22, respectively, P

179 wed greater improvement from pretreatment to posttreatment (mean difference, -3.62; 95% CI, -0.81 to

180 0.956]) and higher for all pretreatment than posttreatment measurements (ICC, 0.761 [95% CI: 0.209, 0

181 ordance correlation coefficient for pre- and posttreatment measurements was 0.83 (95% confidence inte

182 olchicine or vehicle and subject to pre- and posttreatment mechanical testing, which consisted of a s

183 Posttreatment median systolic and diastolic BP improved

184 relationship between tumor-absorbed dose and posttreatment metabolic activity was assessed per metast

185 eport at baseline, at weeks 8 and 16, and at posttreatment months 3 and 6.

186 Absence of late enhancement at posttreatment MR imaging was significantly associated wi

187 Three radiologists assessed pre- and posttreatment MRI findings using LI-RADS version 2018 an

188 Posttreatment MRI reassessment indicated a "safe" ymrLRP

189 No effect was seen on MTORC1 activation, but posttreatment MTORC1 and VH were correlated (rho = 0.51;

190 ll as in cell lines and tissues derived from posttreatment NB tumors.

191 Posttreatment nodule histology showed that 15/135 (11.1%

192 duced changes were sustained over the entire posttreatment observation interval (25-78 min) and consi

193 active, and biomicroscopic findings pre- and posttreatment of observed anterior stromal necrosis (ASN

194 patients with IGHV-M achieved MRD-negativity posttreatment; of these, PFS was 79.8% at 12.8 years.

195 rol subjects) assessment and 39 pairs at the posttreatment or T2 assessment.

196 Median (range) time from earliest posttreatment oral HPV16 DNA detection to recurrence was

197 ated with curative intent, 124 had 1 or more posttreatment oral rinses available and were included in

198 although infrequent, persistent HPV16 DNA in posttreatment oral rinses is associated with poor progno

199 gies for detecting MRD and correlations with posttreatment outcomes.

200 motherapy using pretreatment clinical stage, posttreatment pathologic stage, estrogen receptor (ER) s

201 PrepN-stage and posttreatment pathological N-stage (ypN-stage) were comb

202 n 7 of the 8 appearance scales compared with posttreatment patients (exception was skin) (P < .001 to

203 Pretreatment and posttreatment patients 18 years and older who were consu

204 From April 2005 to August 2008, 783 pre- and posttreatment PB samples were quantified by quantitative

205 t 24 hours after therapy) and in the delayed posttreatment period (days 2-5 after therapy).

206 rol of both nausea and vomiting in the acute posttreatment period (first 24 hours after therapy) and

207 arterial phase hyperenhancement in the early posttreatment period is common and expected.

208 Pre- and posttreatment PET comparative scans should ideally be ob

209 Pre- and posttreatment PET scans were acquired in protocols compl

210 Posttreatment PET/CT (Deauville) predicts overall surviv

211 Posttreatment PET/CT (Deauville) showed significantly in

212 The specificity of posttreatment PET/CT (Deauville) was 95.7% versus 76.4%

213 ng after induction chemotherapy in the early posttreatment phase, chemotherapy-induced changes in tum

214 rall survival; MRD status is the single best posttreatment predictor of long-term outcomes after CIT.

215 d patient-reported outcomes in patients with posttreatment primary breast cancer.

216 a highly aggressive malignancy with a dismal posttreatment prognosis-implicate XBP1s in promoting tum

217 Monitoring posttreatment proteolysis may lead to a novel class of i

218 Pre-PET (Q1), post-PET (Q2), and posttreatment (Q3) questionnaires were sent to referring

219 peripheral blood, at a median of 12.8 years posttreatment (range, 9.5-14.7).

220 tologic and immunologic changes suggest that posttreatment reactions following DEC and IVM share a co

221 to the occurrence of immune-mediated severe posttreatment reactions following ivermectin distributio

222 bset-specific analysis demonstrated that the posttreatment rebound was driven by the CD4(+)CD25(+)Fox

223 ) are thought to drive tumor progression and posttreatment recurrence in multiple solid tumors.

224 ment failure was due to nonresponse (n = 2), posttreatment relapse (n = 9), reinfection (n = 1), and

225 ived from bone marrows of newly diagnosed or posttreatment-relapsed MM patients, in both US- and Euro

226 Network connectivity measured at posttreatment related to abstinence at 6-month follow-up

227 eatment, at week 3, and after treatment) and posttreatment remission status based on cut points.

228 d 5-HT1A binding could improve prediction of posttreatment remission status.

229 latively stable for at least 6 and 12 months posttreatment, respectively.

230 Pretherapy planning and posttreatment response assessments rely heavily on gadol

231 It also highlights the importance of posttreatment restaging.

232 sson and Cox regression to evaluate pre- and posttreatment risk factors for infection, respectively.

233 y help to educate clinicians and patients on posttreatment risk, prevention, and management of lymphe

234 previously undetected variant present in the posttreatment sample in addition to a variant that was d

235 ignificantly differ between pretreatment and posttreatment samples and serum contained predominantly

236 All 11 participants who had MRM detected in posttreatment samples failed azithromycin.

237 Pre- and posttreatment samples were assessed for macrolide resist

238 rts to enable dose computation from a single posttreatment scan in a manner that may be applied to a

239 se in binding potential between the pre- and posttreatment scans indexed enhanced synaptic dopamine a

240 abolic response rates, indicated by negative posttreatment scans.

241 However, mean posttreatment scores for CPT and prolonged exposure rema

242 1,700 patients provided individual pre- and posttreatment scores on the Hamilton Depression Rating S

243 Pretreatment and posttreatment sera were obtained from 48 women with meta

244 In 7 patients with posttreatment serum available for analysis, we observed

245 ie early therapeutic efficacy, whereas these posttreatment sex differences contribute to clinical tre

246 Immune monitoring posttreatment showed an increase in effector T cells rec

247 ion of rTMD23 in mice, both pretreatment and posttreatment, significantly increased the survival rate

248 istologic comparison of the pretreatment and posttreatment skin was performed using serial internal c

249 id not show significant changes from pre- to posttreatment states.

250 A pretreatment and posttreatment study was conducted in 51 participants (me

251 Posttreatment surrogate end points, such as progression

252 most useful test for initial staging and in posttreatment surveillance settings.

253 the ITG with unquantifiable HCV RNA 12 weeks posttreatment (sustained virological response 12 weeks a

254 was sustained virologic response at 12 weeks posttreatment (SVR12).

255 l and superior temporal gyri correlated with posttreatment symptom improvement.

256 n with urethritis, resistance mutations, and posttreatment symptom persistence.

257 omarker identifies patients at high risk for posttreatment symptomatic RP.

258 Higher PRS significantly predicted greater posttreatment symptoms in the combined replication analy

259 At 8-week posttreatment, the EA group reported a reduction of -6.6

260 VM) or fall (post-DEC) in the first 24 hours posttreatment, the eosinophil count rose significantly i

261 From pretreatment to posttreatment, the intervention increased daily energy i

262 lymphocyte counts during the first 24 hours posttreatment, the overall pattern of hematologic and im

263 At the posttreatment time point, SOL improved by 19.03 (95% CI,

264 in cocaine dependence (CD) pretreatment and posttreatment to determine whether these changes relate

265 imaging data were collected at baseline and posttreatment to examine brain reward circuitry.

266 with end points reassessed early at 2 weeks posttreatment to minimize confounding from exercise adap

267 In posttreatment tumor tissue of patients with malignant gl

268 ferentially expressed in pretreatment versus posttreatment tumors.

269 gical activity from the delivered CPT in the posttreatment tumors.

270 descriptive statistics and compared pre- and posttreatment uBPA concentrations using generalized esti

271 We hypothesized that posttreatment urinary BPA (uBPA) concentrations would be

272 of all-cause mortality or recurrence 30 days posttreatment, using multivariable unconditional logisti

273 ts receiving azathioprine (AZA) therapy, and posttreatment Vdelta2 T cell recovery correlated with ti

274 The uBPA concentrations 2 d posttreatment versus pretreatment tended to be higher (1

275 pha(4)beta(7) was reported to induce durable posttreatment viral suppression.

276 ease patients as positive at the baseline or posttreatment visit than two-tiered testing (87.5% and 6

277 77 participants (99.1%) underwent at least 1 posttreatment visit.

278 d slightly from randomization until the last posttreatment visit.

279 the study group (respective median pre- and posttreatment volume: 76.1 cm(3) and 58.4 cm(3) for read

280 he control group (respective median pre- and posttreatment volume: 79.9 cm(3) and 83.8 cm(3) for read

281 Pre- and posttreatment volumes (Wilcoxon signed rank test) and ra

282 severely impairs host immunity, resulting in posttreatment vulnerability to reinfection and reactivat

283 At the posttreatment/wait assessment, 73% of the intensive cogn

284 7.4] years), improvement in PTSD severity at posttreatment was greater when CPT was administered indi

285 measure was sustained virologic response at posttreatment week 12 (SVR12) in patients with a genotyp

286 atients with sustained virologic response at posttreatment week 12 (SVR12).

287 dpoint was sustained virological response at posttreatment week 12 (SVR12).

288 ed virologic response (HCV RNA <25 IU/mL) at posttreatment week 12 (SVR12).

289 Sustained virologic response at posttreatment week 12 (SVR12).

290 at analysis, sustained virologic response at posttreatment week 12 was achieved in 100% (6/6, 95% con

291 tudy outcome was SVR12 (HCV-RNA <25 IU/mL at posttreatment week 12) in patients naive to treatment.

292 l below the lower limit of quantification at posttreatment week 12).

293 One patient died at posttreatment week 3; this was not considered related to

294 week 12 posttreatment achieved a response at posttreatment week 4.

295 One patient relapsed at posttreatment week 4.

296 Paired sequences (pre- and posttreatment) were analyzed.

297 At 36 months posttreatment with IDA, 18/33 (55%; 95% CI, 38-72%) clea

298 However, pretreatment and posttreatment with type I and III IFNs significantly red

299 %) and in all other monkeys at 10 to 49 days posttreatment, with recurrent zoster in one treated monk

300 Posttreatment xenograft tumors had increased synthesis o