ライフサイエンスコーパス: rebound

1 Sleep deprivation results in a sleep rebound.

2 ab after transplantation to prevent antibody rebound.

3 on almost invariably results in robust viral rebound.

4 ing of the wake period enhancing firing rate rebound.

5 double-blind treatment to assess withdrawal/rebound.

6 reatment interruption results in rapid viral rebound.

7 s and correlated directly with time to viral rebound.

8 No patient had confirmed HIV-1 virologic rebound.

9 w numbers of activated CD4+ T cells at viral rebound.

10 late motion and/or induce abrupt continental rebound.

11 al therapy can be discontinued without virus rebound.

12 d, with few neurons combining both pause and rebound.

13 g natural killer cells, recovered with virus rebound.

14 ion of CD8(+) cells failed to induce a viral rebound.

15 response following cART withdrawal and viral rebound.

16 KO and OE mice exhibited a homeostatic sleep rebound.

17 ut an unchanged viral set point during viral rebound.

18 ase inspiratory frequency via postinhibitory rebound.

19 onal NRTI mutation accumulated over 2 years' rebound.

20 V RNA levels initially, but the levels later rebounded.

21 eturn to combination treatment if viral load rebounded.

22 after the first year P. aeruginosa densities rebounded.

23 Of the 4519 viral rebounds, 3105 (69%) were defined by measurement of a si

24 n initial drop of correlations followed by a rebound, a time course that was mimicked by the instanta

25 However, B and T cells rebounded above baseline 24 hours after HC infusion, whi

26 lts were used to calculate the rate of viral rebound according to several key factors, including age,

27 Once the inhibition is removed, rebound activation of MET-driven cell proliferative path

28 We demonstrate that blockade of this rebound activation with MEK (mitogen-activated protein k

29 Overall, only two dropouts (one rebound activity and one gastrointestinal side effect) w

30 hat circulating Ang-2 levels in GBM patients rebound after an initial decrease following cediranib (a

31 e HIV reservoir, and caused a delay in viral rebound after ART interruption.

32 There was a myopic rebound after atropine was stopped, and it was greater i

33 rvoirs in lymphoid tissues and delayed HIV-1 rebound after cART cessation in the HIV-1-infected hu-mi

34 ive patients were identified who experienced rebound after ceasing fingolimod treatment.

35 Occurrence of rebound after ceasing fingolimod treatment.

36 myeloid cells, which are the source of viral rebound after cessation of antiretroviral therapy.

37 an important cause of death, whereas immune rebound after disease remission can exacerbate underlyin

38 tem's systemic resilience and its ability to rebound after large-scale population loss.

39 logical biomarkers can predict time to viral rebound after stopping ART by analysing data from a rand

40 n 48 weeks or the probability of virological rebound after successful virological suppression.

41 te, can safely prevent or delay plasma viral rebound after the discontinuation of antiretroviral ther

42 atropine with regard to myopic progression, rebound after treatment cessation, and minimization of s

43 Although there are reports of myopic rebound after treatment is discontinued, this seems to b

44 ing platelet counts markedly inhibited tumor rebound after withdrawal of antiangiogenic therapy.

45 TMC dropped after implementation of DHR but rebounded after a transition period (949 vs 946 cases, P

46 Although total operative volume rebounded after implementation of DHR, diversity of oper

47 Virus rebounds after stopping treatment from the stable HBV co

48 sizes of the reservoirs from which infection rebounds after treatment interruption.

49 finalizing the reaction through rapid oxygen rebound, alkene synthesis proceeds through the formation

50 tion of antiretroviral therapy without viral rebound and any associated complications.

51 ) and up to 76 weeks (patients with no viral rebound and excluding those who were randomised to the p

52 10beta inhibitor to BYL719 prevents the PIP3 rebound and induces greater antitumor efficacy in HER2-a

53 age range, 18-84 years) were divided into a rebound and lymphoid hyperplasia group (group A, 30 pati

54 lecular biology of the post-IL-12 regulatory rebound and provide insight into how feedback inhibitory

55 We estimated probability of rebound and resistance with Kaplan-Meier analysis.

56 imited numbers of activated T cells at viral rebound and subsequent development of broadly reactive c

57 of patients to interrupt ART for 1 y without rebound and that rebound may occur suddenly after multip

58 vity, and then, following the CS, a pause, a rebound, and finally a late inhibition of SS activity fo

59 s recovered following post-deprivation sleep rebound, and occurs regardless of the approach to achiev

60 f spike frequency adaptation, postinhibitory rebound, and post-stimulation recovery.

61 , to determine factors associated with viral rebound, and to use these estimates to predict long-term

62 al in sensitized patients, and in abrogating rebound antibody response in patients undergoing desensi

63 en accounting for the fact that 29% of viral rebounds are temporary elevations.

64 e treated on day 3 exhibited a delayed viral rebound as compared with those treated on days 7, 10 and

65 hodium, and stepwise radical C-H abstraction/rebound, as observed with chemoselective base metals suc

66 to result in suppressed populations rapidly rebounding, as homing-resistant alleles have a significa

67 3weeks) resulted in complete cures (no tumor rebound at 120 days) of HMLER-Snail xenografts.

68 Viral rebound at or before week 12 was associated with the app

69 1.6%, SE = 2.3%, range 10.0%-48.2%, n = 37), rebounding at day 2 and increasing to frequencies above

70 Thus the beta-rebound attenuation might relate to neural processes inv

71 on of ART almost invariably results in viral rebound, attributed to a pool of long-lived, latently in

72 cit acetone solvent (SMD) because the oxygen rebound becomes barrierless in solution.

73 r cells were dramatically elevated, favoring rebound bursting and seizure generation.

74 current densities by 22% or more eliminates rebound bursting in model thalamic reticular nucleus (TR

75 aV3.3 channel-dependent functions, including rebound bursting in TRN neurons, with potential implicat

76 y of thalamic neurons to fire postinhibitory rebound bursts mediated by low-threshold calcium spikes

77 The Kaplan-Meier probability of viral rebound by 48 weeks was 0.176 (n = 26) in the efavirenz

78 proportion of participants with virological rebound (confirmed viral load >/=50 copies per mL or pre

79 non-inferior to the control for virological rebound cumulative through week 48 (19 [2.5%] of 763 pat

80 e phase delay of ON UBCs is caused by a late rebound current resulting from AMPAR recovery from desen

81 The rate of first viral rebound declined substantially over time until 7 years f

82 macological block of IA completely abolished rebound delays and, importantly, shortened synaptically

83 at controls either the Cl(-) or the OH(-) to rebound depending on the relative pi-overlap with the su

84 n and revealed no evidence of postinhibitory rebound depolarization inherent to coincidence models of

85 -arrestin2(-/-) mice with the exception of a rebound depolarization, and non-mGluR-mediated long-term

86 atment DLCOc decreased significantly, with a rebound during follow-up.

87 The rebound during the continuation phase of the SCT suggest

88 during the synchronization phase, to finally rebound during the continuation phase.

89 and well tolerated but did not prevent viral rebound during treatment interruption.

90 ed species, and levels of G. vaginalis often rebounded during treatment.

91 g bevacizumab, we did not observe a negative rebound effect (ie, shorter survival after bevacizumab i

92 choices related to environmental modeling in rebound effect assessments.

93 se displayed at steady-state and generates a rebound effect pushing quiescent cancer cells back into

94 al cost of ownership, which describe notable rebound effect sizes-from 26 to 59% and from 18 to 28%,

95 progression after cessation of treatment, a rebound effect was noted.

96 Post-NTZ rebound effect was observed only in one patient.

97 yopic progression after the study period and rebound effect were considered.

98 the cell surface substantially prevents this rebound effect, providing a rationale to combine or alte

99 x, P < 0.01) owing to a previously described rebound effect.

100 Calculations of the size of rebound effects are subject to various types of bias, am

101 The results describe moderate rebound effects for both technologies in the short term.

102 rce efficiency often underperform because of rebound effects.

103 to the pain of all protagonists followed by rebound/enhancement to ingroup pain only.

104 O](2+) occurs by an electron transfer-oxygen rebound (ET-OT) mechanism leading to aryl 1-methyl-1-phe

105 The cases presented herein highlight that rebound events after ceasing fingolimod treatment may ha

106 ereby inhibitory coupling via postinhibitory rebound excitation actually generates fast modes of insp

107 ediated increases in frequency are caused by rebound excitation following an inhibitory synaptic voll

108 l fast Ca(2+) transients were noted in SMCs (rebound excitation).

109 uished by their dendritic calcium signaling, rebound excitation, and physiological responses to dopam

110 y response and a slower G-protein-coupled DA rebound excitation.

111 dal neurons also exhibited weaker driven and rebound firing compared with prototypic neurons.

112 tinct temporal evolution in AC, with quicker rebound firing in infragranular layers.

113 to achieve HIV-1 remission and prevent viral rebound following analytical treatment interruption (ATI

114 Rates, quantity, and timing of parasitemia rebound following CTX remain undefined.

115 improved virologic control and delayed viral rebound following discontinuation of antiretroviral ther

116 improves virologic control and delays viral rebound following discontinuation of antiretroviral ther

117 Spine BMD tended to rebound following discontinuation of FTC/TDF.

118 which can reactivate and contribute to viral rebound following treatment interruption.

119 ite ART, indicated two important sources for rebound following treatment interruption.

120 Minimal estimates of the number of rebounding/founder (R/F) variants were determined by sin

121 s, and efforts were made to help the species rebound from the brink of extinction, which occurred as

122 ulations of Orbicella species are capable of rebounding from reductions in population size under suit

123 carbene mediates homolytic C-H cleavage and rebounds from the resulting organoiron intermediate to f

124 Children experiencing rebound >/=5,000 copies/ml were much less likely to resu

125 iraemia (80-5,000 copies/ml) and 10% with VL rebound >/=5,000 copies/ml.

126 esuppressed <80 copies/ml after confirmed VL rebound >/=5,000 copies/ml.

127 Although the adiposity rebound has been in focus because of a shown association

128 Risk difference between groups in (1) viral rebound (ie, >/=1 HIV RNA measurement of >50 copies/mL)

129 ansmission from 2006-2010 with a significant rebound in 2012-2013.

130 hat ART interruption resulted in rapid viral rebound in all SIV-infected SMs, indicating that the vir

131 in ADCC-competent antibodies, despite viral rebound in all subjects who underwent the short ATI.

132 There was no rebound in bAs related to cessation of FA supplementatio

133 malaria vectors could presage a catastrophic rebound in disease incidence and mortality.

134 nd thus causes activation of PI3Kalpha and a rebound in downstream signaling.

135 n) and AUY922, which durably prevented viral rebound in HIV-infected humanized NOD scid IL-2Rgamma(-/

136 nical malaria, but this result was offset by rebound in later years in areas with higher-than-average

137 ed the spatio-temporal trends of decline and rebound in malaria prevalence in 2012-13 at the village

138 aimed to investigate the rate of first viral rebound in people that have achieved initial suppression

139 llular reservoirs that would typically cause rebound in plasma viremia after antiretroviral therapy c

140 se of continental ice sheets induced crustal rebound in tectonically stable regions of North America

141 However, a rebound in the cell number was observed after the prolon

142 l load (p=0.0003) were associated with viral rebound in the multivariate analysis only.

143 VRC01 slightly delayed plasma viral rebound in the trial participants, as compared with hist

144 ed people discontinuing therapy experience a rebound in the virus level (hereafter, "rebound virus")

145 ers of clinical progression, including viral rebound in those interrupting therapy.

146 om the above circumstances, HIV unexpectedly rebounded in 3 patients on 2 days per week treatment and

147 24 weeks of fully suppressive therapy, virus rebounded in all animals, although the monkeys that were

148 virological non-suppression, and virological rebound, in HIV-positive people on ART in the UK.

149 annot eradicate the HIV reservoir, and viral rebound is generally rapid after treatment interruption.

150 This rebound is suppressed and tumor growth inhibition enhanc

151 be able to continue before developing viral rebound is unknown.

152 a movement above sensorimotor regions (beta-rebound) is attenuated when movement-execution errors ar

153 formation, which does not result from oxygen rebound, is similar to that widely suggested for P450 mo

154 sleep (SWS) EEG delta (1.0 to 4.0 Hz) power rebound like WT littermates, spontaneous waking fails to

155 on, supporting an emerging notion that rapid rebound may not necessarily occur in non-heme oxoiron(IV

156 terrupt ART for 1 y without rebound and that rebound may occur suddenly after multiple years.

157 ding the origin of HIV variants during viral rebound may provide insight into the composition of the

158 hat the error-related modulation of the beta-rebound may reflect salience processing, independent of

159 intermediate energy, a previously unexpected rebound mechanism contributes significantly to the react

160 The rebound mechanism for alkane hydroxylation was invoked o

161 tly hydroxylates the substrate via an oxygen-rebound mechanism.

162 e reaction proceeds through a novel "reverse-rebound" mechanism with diradical intermediates.

163 This feature, combined with the "fluoride-rebound" mechanism, was translated into a protocol for t

164 erves as a constitutional component for the "rebound model" of memory T cell maturation.

165 e atom without bond rupture; and second, the rebounding molecule abstracts a surface D atom to form N

166 2 years, but they were associated with less rebound myopic progression (for atropine 0.01%, mean myo

167 Viral rebound occurred despite plasma VRC01 concentrations gre

168 No HIV rebound occurred during the study.

169 Viral rebound occurred in the majority of suppressed animals a

170 RT interruption in 95%, with a rate of viral rebound of 5% per year in the first 3 months, and a 50%

171 py until ATI day 288, when a low-level virus rebound of 60 HIV-1 copies/ml occurred, which increased

172 immunosuppressive therapy without inducing a rebound of antibody titer or an increase in proteinuria.

173 Then, a rebound of Fe(IV) (O) with (.) NO2 affords [(TAML)Fe(III

174 Rebound of hepatitis B virus DNA and hepatitis B core-re

175 ized rats induced an apparent time-dependent rebound of the MAOB protein level to about 200% over con

176 ence of latent viral reservoirs allows for a rebound of viral load upon cessation of therapy.

177 g antiretroviral therapy (ART) that leads to rebound of virus if treatment is stopped.

178 suppression during movement and postmovement rebounds of up to 3 s as viewed in data averaged across

179 reach errors attenuate the postmovement beta-rebound, only the kinematic errors that trigger trial-to

180 imulation, showed no signs of postinhibitory rebound or post-stimulation recovery, and no depolarizin

181 ent using search terms fingolimod and either rebound or reactivation.

182 or to PGT121 alone in delaying time to viral rebound or reducing peripheral blood mononuclear cell (P

183 Within this small trial, no viral rebound or resistance was identified.

184 episodes of cerebrospinal fluid (CSF) viral rebound or sustained plasma and CSF viremia during treat

185 esult in significantly higher rates of viral rebound or viral failure.

186 ults did not suggest the emergence of marked rebound or withdrawal signs or symptoms when suvorexant

187 cortex-and, to a lesser extent, the midbrain-rebounded or surpassed control levels.

188 oencephalopathy (PML), and the occurrence of rebounds or disease activity after its discontinuation.

189 etroviral therapy [ART] and at risk of viral rebound) or treatment-naive patients initiating their fi

190 101 people included, 4519 had a first viral rebound over 58 038 person-years (7.8 per 100 person-yea

191 r, the "Berlin patient" remained free of HIV rebound over a decade after stopping cART.

192 portion of people on ART will not have viral rebound over their lifetime, which has implications for

193 The rebound pathway, as seen by the induction of phosphoryla

194 the reactive trajectories undergo the oxygen rebound pathway, but this increases to 90% in simulation

195 state, and trajectories branch to the oxygen rebound pathway, which gives tert-butanol and acetone, o

196 and other catalysts that operate via radical rebound pathways.

197 based study would be helpful to confirm this rebound phenomenon and to determine contributing factors

198 ibit class 2 excitability and postinhibitory rebound (PIR), for the integrators that are typically us

199 Rebound plasma HIV sequences were identical to those obt

200 day 3 after infection, experienced sustained rebound plasma viraemia when treatment was interrupted.

201 Rebounding plasma HIV-1 sequences were phylogenetically

202 nderwent treatment interruption and compared rebounding plasma virus with that found within cells pri

203 Shifts in the viral rebound populations could be detected in some participan

204 ns.SIGNIFICANCE STATEMENT Our study examines rebound, postburst, and synaptically evoked inhibitory p

205 ng cessation of this stimulus, a significant rebound potential was seen that was sometimes sufficient

206 rates; and (v) reduced spike clustering and rebound potentials.

207 quent 2 h exposure to light produced a rapid rebound potentiation.

208 velopmental changes in inhibition and lacked rebound potentiation.

209 need to consider potential conflicts between rebounding predators or endangered predators and prey.

210 This 'rebound' prehension was only evoked in trained and food-

211 reintroduction of combination treatment for rebound, preserved future treatment options and did not

212 irst time, the rate constants for the oxygen rebound process (kOT), which are in the range of <0.8 x

213 s allows for the direct interrogation of the rebound process, providing insight into this uniformly i

214 and, soon after its formation, collapses and rebounds, producing high pressure pulses.

215 igrostriatal neurons differ substantially in rebound properties with mesoaccumbal neurons displaying

216 ssion of viral replication with ART, viremia rebounds rapidly after treatment interruption.

217 1740 individuals had subsequent virological rebound (rate=3.6/100 person-years).

218 suggest that the probability of first viral rebound reaches a plateau of 1.4% per year after 45 year

219 Efforts to model the rebound reaction in a synthetic system have been unsucce

220 Additionally, we find that the rate of rebound responses in nuclear neurons after a synchronous

221 onomic status was predictive of longitudinal rebound risk (adjusted hazard ratio [HR] for greatest fi

222 ctly participate in the characteristic pause-rebound sensory response that CINs exhibit in vivo in re

223 wal alters viral dynamics: we found a higher rebound set point but similar peak viral loads compared

224 deprivation and is necessary for homeostatic rebound sleep (i.e., the increased sleep that occurs aft

225 e, these neurons are necessary for promoting rebound sociability following an acute period of isolati

226 human (HIV) and simian (SIV); however, virus rebounds soon after ART is withdrawn.

227 ictal generation and induced postinhibitory rebound spiking in pyramidal neurons, enhancing neuronal

228 mylation step in competition with the oxygen rebound step typically used by most oxygenases for formi

229 ntermediate substrate radical in the halogen rebound step.

230 eral systolic prestretch and septal systolic rebound stretch.

231 treated and untreated mice after body weight rebound, suggesting that BChE gene transfer did not alte

232 as having severe relapses consistent with a rebound syndrome and similar features to our 5 cases.

233 hese cases provide evidence for a fingolimod rebound syndrome at a clinically relevant frequency, hig

234 Rebound syndrome was defined as new severe neurological

235 that was diffusely tender on palpation, with rebound tenderness in the right lower quadrant.

236 h faster synaptic depression and homeostatic rebound than RS cells.

237 (29%) of the 3105 people with observed viral rebound, the next viral load value after rebound was 50

238 l therapy (cART) eventually experience viral rebound, the return of viral loads to pretreatment level

239 inhibited ERK signaling, which subsequently rebounded, the MEK inhibitor CKI suppressed ERK signalin

240 et counts had a nadir at day 3 followed by a rebound thrombocytosis at day 21, with nadir values sign

241 wever, removal of cART results in plasma HIV rebound, thus highlighting its inability to entirely rid

242 Our results predict large variation in rebound times following LRA therapy, which will complica

243 s to <400 copies/mL by week 24, or confirmed rebound to >400 copies/mL at or after week 16 following

244 in both reactivation of latent virus (virus rebound to 10(3) viral RNA copies/ml plasma in the absen

245 triplet spin surface; (ii) substrate radical rebound to a Cu(II) hydroperoxide favors the proximal, n

246 month lag between the end of DO delivery and rebound to the final near-steady emissions level.

247 he unusually strong steric barrier to oxygen rebound to the neopentyl center C-1si, which is flanked

248 declined markedly after 2 doses of IPTp but rebounded to 34% (by PCR) at delivery.

249 Interestingly, c-Jun protein rebounded to normal levels 4 h following U0126 exposure

250 d [(P(Im))Fe(IV) horizontal lineO] (7); this rebounds to give [(P(Im))Fe(III)(NO3(-))] (4a).The gener

251 ocular pressure measurements using the ICare rebound tonometer (ICare, Helsinki, Finland) were obtain

252 glaucoma can perform self-tonometry using a rebound tonometer and examine patient acceptability.

253 On average, IOP by the rebound tonometer was 2.66 mm Hg lower than Goldmann app

254 The IOPs with the rebound tonometer were similar whether obtained by self-

255 d using Goldmann applanation tonometry and a rebound tonometer.

256 IOP measurements using Icare rebound tonometry, Tonopen, and Goldmann tonometry are i

257 MP-9 mRNA remained suppressed, although they rebounded toward pretreatment values 4 weeks after azith

258 iradical species were observed in the oxygen rebound trajectories.

259 eath ligand 2(+) dendritic cells and ILT3(+) rebounded Tregs was detected after transient Treg deplet

260 deficient platelets completely prevented the rebound tumor growth.

261 s plasma viremia to undetectable levels that rebound upon cART treatment interruption.

262 Conversely, P-S6k levels rebound upon recovery from sedation and are increased wh

263 ersists despite treatment and leads to viral rebound upon treatment discontinuation.

264 Rebounding variants were compared with those in pre-ART

265 tional analysis); and subsequent virological rebound (viral load >200 copies per mL) in those with in

266 ective antiretroviral therapy (ART) can fuel rebound viremia after ART interruption and is a central

267 se findings suggest that a source of initial rebound viremia could be populations of infected cells t

268 lications for devising strategies to prevent rebound viremia due to reactivation of rare latently inf

269 therapy regimens could conceivably suppress rebound viremia from persistent HIV reservoirs.

270 Both patients experienced rebound viremia within 2 weeks of the most recent negati

271 Despite the absence of rebound viremia, we were able to recover infectious HIV

272 ogenetic analyses suggest that the origin of rebound virus was distinct from the viruses identified p

273 ce a rebound in the virus level (hereafter, "rebound virus") from a persistent reservoir.

274 AIDS Clinical Trials Group study A5068 with rebound virus, using single-genome amplification and Pri

275 voirs are replication incompetent, and (iii) rebounding virus after CD8(+) cell depletion is replicat

276 of these clonally proliferating cells to the rebounding virus is unknown.

277 uption showed that VRC01 exerted pressure on rebounding virus, resulting in restriction of recrudesce

278 Most rebound-virus populations showed significant diversity.

279 he adaptive immune response to prevent viral rebound (VR) and control infection.

280 The risk difference for viral rebound was 0.107 (1-sided 95% CI, 0.028 to infinity) an

281 The median time to rebound was 4 weeks in the A5340 trial and 5.6 weeks in

282 ral rebound, the next viral load value after rebound was 50 copies per mL or less with no regimen cha

283 Viral rebound was defined as the first single viral load of mo

284 analysis demonstrated that the posttreatment rebound was driven by the CD4(+)CD25(+)Foxp3(+) neuropil

285 Viral rebound was measured at 28,000 copies/mL on day 13 post-

286 However, a substantial rebound was observed between sessions, with suPAR levels

287 No viral rebound was observed in the plasma of 67% of the ART-tre

288 nimals ( approximately 33%), a delayed viral rebound was observed that is consistent with the establi

289 Curiously, no EEG or behavioral sleep rebound was observed, even after 4 days of induced wakef

290 with human participants, along with the beta-rebound, we examine beta-activity during the preparation

291 orie restriction (CR) often fails because of rebound weight gain.

292 The reduced transmission and rebound were confirmed directly by incidence data from T

293 The other factors associated with viral rebound were current age at follow-up and calendar year

294 Thus, infection rebounds when treatment is interrupted by reactivation o

295 Below this range, patients will always rebound, whereas above this range, patients are predicte

296 penetration into the specimen followed by a rebound which leaves the specimen unscathed.

297 e investigated factors associated with viral rebound with Poisson regression.

298 exercise attenuated the waist circumference rebound with the greatest effect in the MED/LC(PA+) grou

299 ed ART and remained aviremic for 7.4 months, rebounding with HIV RNA of 36 copies/mL that rose to 59,

300 ctivation dropped significantly after PE but rebounded within 4 days concomitant with a rising suPAR