ライフサイエンスコーパス: MPR

1 MPR accumulation on the tumor cell surface during chemot

2 MPR index showed a stepwise reduction with increasing ex

3 MPR was calculated in the remaining 68 patients >151.7 p

4 MPR was greater in diastole than systole in all segment

5 MPR(CMR) and MPR(PET) for the 2 lowest scoring segments

6 MPR-R has no advantage over MPT-T concerning efficacy.

7 MPR-R significantly prolonged progression-free survival

8 Strikingly, 4-HPR but not 4-MPR restricted infection in peripheral blood mononuclear

9 4-HPR but not 4-MPR was found to specifically upregulate the protein kin

10 4-Oxo-N-(4-methoxyphenyl)retinamide (4-oxo-4-MPR) had minimal effects on DES activity.

11 N-(4-Methoxyphenyl)retinamide (4-MPR) and 4-Oxo-N-(4-methoxyphenyl)retinamide (4-oxo-4-MP

12 ly related N-(4-methoxyphenyl) retinamide (4-MPR) could reduce viral RNA levels and titers when appli

13 crovascular coronary artery disease (n=783), MPR remained independently associated with death and MAC

14 Overall, the percentage of patients with a MPR of 80% or greater at 12 months was 27.7%, while pers

15 P-1, and cells depleted of GCC185 accumulate MPRs in transport vesicles that are AP-1 decorated.

16 Suboptimal adherence (MPR<0.8) was recorded in 35 (51%).

17 DC <=1.25), 51 (4.23%) were partly adherent (MPR >=70% and PDC = 1.50) and 176 (14.60%) were switcher

18 and thirty-six (11.28%) users were adherent (MPR >=70% and PDC <=1.25), 51 (4.23%) were partly adhere

19 no difference in outcome was detected among MPR, CPR, and Rd.

20 An MPR cutoff of 2.04 was 85.1% (95% CI 71.1 to 99.2) sensi

21 An MPR cutoff of 2.04 was 92.9% (95% CI 77.9 to 100.0) sens

22 An MPR(PET) </=1.44 predicted significant CAD with 82% sens

23 Nonadherence to HT was defined as an MPR less than 80% between the first and last prescriptio

24 Adequate adherence was characterized by an MPR >/=0.8 and ideal as MPR=1.0.

25 Subjects with an MPR >80% were considered adherent.

26 Patients with an MPR of at least 0.80 were classified as adherent.

27 s 1.00 +/- 0.04, respectively; P < .001) and MPR (normal vs ischemic, 2.7 +/- 0.08 vs 1.7 +/- 1.1, re

28 MPR(CMR) and MPR(PET) for the 2 lowest scoring segments in each coron

29 ere is good correlation between MPR(CMR) and MPR(PET.) For the detection of significant CAD, MPR(PET)

30 as simulated with adenosine for both FFR and MPR.

31 Area under the ROC curve with stress MBF and MPR as the outcome measures, respectively, was 0.86 and

32 ted coronary artery disease, reduced MBF and MPR measured automatically inline using artificial intel

33 ial perfusion MR estimates of stress MBF and MPR were greater in diastole than systole in patients wi

34 Stress MBF and MPR were independently associated with both death and MA

35 meters sought associations of stress MBF and MPR with death and major adverse cardiovascular events (

36 between any of the models or between MBF and MPR, except that the Fermi model outperformed the one-co

37 global and regional stress and rest MBF and MPR.

38 the effects of eliminating the MR on MR- and MPR-mediated plasma clearance and tissue distribution of

39 e quantification of myocardial perfusion and MPR with PET have proven diagnostic and prognostic roles

40 e detection of significant CAD, MPR(PET) and MPR(CMR) seem comparable and very accurate.

41 0.7-2.6% of participants in any quarter and MPR of less than 95% for 3.3-11.1%.

42 Response rates were superior with MPR-R and MPR (77% and 68%, respectively, vs. 50% with MP; P<0.001

43 ith 82% sensitivity and 87% specificity, and MPR(CMR) </=1.45 predicted significant CAD with 82% sens

44 the remaining 141 patients by using CBRs and MPRs together, and the other half by using MPRs only.

45 for MPRs and 74% (520 of 698) when CBRs and MPRs were used together, which was significantly higher

46 creasing risk of virological breakthrough as MPR fell.

47 characterized by an MPR >/=0.8 and ideal as MPR=1.0.

48 All images included axial, MPR, MIP, and VRT and were interpreted in one session.

49 The association between MPR and unfavourable outcomes was assessed according to

50 There is good correlation between MPR(CMR) and MPR(PET.) For the detection of significant

51 attached to residue N325, and that it binds MPR, via mannose 6-phosphate, with a similar affinity to

52 (PET.) For the detection of significant CAD, MPR(PET) and MPR(CMR) seem comparable and very accurate.

53 In addition, CD-MPR binding affinities are modulated by divalent cations

54 mannose 6-phosphate receptors (CI-MPR and CD-MPR) for high mannose-type N-glycans of defined structur

55 A detailed comparison of the available CD-MPR structures reveals the positional invariability of s

56 ligands is pH-dependent; the homodimeric CD-MPR binds lysosomal enzymes optimally in the pH environm

57 MPR) and the 46 kDa cation-dependent MPR (CD-MPR) are key components of the lysosomal enzyme targetin

58 n-dependent mannose 6-phosphate receptor (CD-MPR) is a key component of the lysosomal enzyme targetin

59 n-dependent mannose 6-phosphate receptor (CD-MPR) plays a key role in the delivery of lysosomal enzym

60 h different concentrations of recombinant CD-MPR or soluble CI-MPR.

61 d as essential for Man-6-P binding by the CD-MPR and domains 1-3 and 9 of the CI-MPR.

62 n(alpha1,2)Man-O-(CH(2))(8)COOMe), 2) the CD-MPR at pH 4.8 in an unbound state (i.e. endosome), and 3

63 unbound state (i.e. endosome), and 3) the CD-MPR at pH 7.4 (i.e. cell surface).

64 untered by the receptor including: 1) the CD-MPR bound at pH 6.5 (i.e. trans Golgi network) to a high

65 ic studies have shown that at pH 6.5, the CD-MPR bound to Man-6-P adopts a significantly different qu

66 The CD-MPR bound weakly or undetectably to the phosphodiester d

67 -MPR, residues 1-154) have shown that the CD-MPR exists as a homodimer and exhibits two distinct conf

68 ifferent quaternary conformation than the CD-MPR in a ligand-unbound state, a feature unique among kn

69 odified GAAs demonstrate that, unlike the CD-MPR or domain 9 of the CI-MPR, domain 5 exhibits a 14-18

70 pho-mono- or -diesters although, like the CD-MPR, it differentially recognized isomers of phosphoryla

71 s in the structure and functioning of the CD-MPR.

72 of phosphorylated glycans by the CI- and CD-MPRs has implications for understanding the biosynthesis

73 xpressing cells were fractionated using a CI-MPR affinity column, 35-45% of the total LIF molecules w

74 MPR interaction, suggesting that IncE and CI-MPR are dependent on the same binding surface on SNX5.

75 red that the binding between SNX-BARs and CI-MPR or IGF1R is mediated by the phox-homology (PX) domai

76 summary, beta2-agonist treatment enhanced CI-MPR-mediated uptake and trafficking of GAA in mice with

77 Finally, CI-MPR-KO/GAA-KO mice did not respond to combination therap

78 forming a multimeric complex required for CI-MPR sorting.

79 GGA3 phosphorylation, releasing GGA3 from CI-MPR and early endosomes.

80 proteins leads to a pronounced defect in CI-MPR endosome-to-TGN transport.

81 this study reappraise retromer's role in CI-MPR transport.

82 e quadriceps biopsies suggested increased CI-MPR at wk 12 (P=0.08), compared with baseline.

83 unctive beta2-agonist treatment increased CI-MPR expression and enhanced efficacy from gene therapy i

84 ated beta2-agonist drugs, which increased CI-MPR expression in GAA knockout (KO) mice.

85 sly demonstrated the benefit of increased CI-MPR-mediated uptake of recombinant human acid-alpha-gluc

86 om clenbuterol in GAA-KO mice that lacked CI-MPR in muscle, where it failed to reverse the high glyco

87 ade controlling PACS-1- and GGA3-mediated CI-MPR sorting.

88 ivity, as measured by decreased levels of CI-MPR and lower activities of cellular lysosomal hydrolase

89 Cycling of CI-MPR between the TGN and early endosomes is mediated by G

90 that mediate the retrograde transport of CI-MPR from endosomes to the TGN independently of the core

91 lenbuterol, which increases expression of CI-MPR in muscle, was administered with the AAV vector.

92 The integral role of CI-MPR was demonstrated by the lack of effectiveness from c

93 IncE peptide inhibits the interaction of CI-MPR with SNX5.

94 addition of clenbuterol in the absence of CI-MPR, as was lysosomal vacuolation, which correlated with

95 ing that clenbuterol's effect depended on CI-MPR expression.

96 s, GGA3 and PACS-1 bind to an overlapping CI-MPR trafficking motif and their sorting activity is cont

97 or knockout of retromer does not perturb CI-MPR transport, the targeting of the retromer-linked sort

98 independent mannose 6-phosphate receptor (CI-MPR) and Insulin-like growth factor 1 receptor (IGF1R);

99 independent mannose-6-phosphate receptor (CI-MPR) and sortilin.

100 independent mannose 6-phosphate receptor (CI-MPR) and the 46 kDa cation-dependent MPR (CD-MPR) are ke

101 independent mannose-6-phosphate receptor (CI-MPR) follows a highly regulated sorting itinerary to del

102 independent mannose 6-phosphate receptor (CI-MPR) from endosomes to the trans-Golgi network (TGN), is

103 independent mannose-6-phosphate receptor (CI-MPR) in skeletal muscle.

104 independent mannose 6-phosphate receptor (CI-MPR) is a multifunctional protein that binds diverse int

105 independent mannose-6-phosphate receptor (CI-MPR) mediated uptake.

106 -kDa cation-independent Man-6-P receptor (CI-MPR) that transports newly synthesized acid hydrolases f

107 independent mannose-6-phosphate receptor (CI-MPR), a receptor for lysosomal hydrolases, and other end

108 independent mannose 6-phosphate receptor (CI-MPR), and we analyzed the effects of this modification o

109 independent mannose 6-phosphate receptor (CI-MPR), which contains multiple mannose 6-phosphate (Man-6

110 independent mannose-6-phosphate receptor (CI-MPR)-mediated uptake and intracellular trafficking of GA

111 independent mannose 6-phosphate receptor (CI-MPR).

112 independent mannose-6-phosphate receptor (CI-MPR).

113 t for a high-affinity binding to receptor CI-MPR, while the presence of a M6P moiety at the alpha-1,6

114 -dependent mannose 6-phosphate receptors (CI-MPR and CD-MPR) for high mannose-type N-glycans of defin

115 ndependent mannose-6-phosphate receptors (CI-MPR) in the soma is disrupted in mutant hAPP neurons, ca

116 did regulate retromer-mediated retrograde CI-MPR trafficking, which required its association with end

117 omatis infection interferes with the SNX5:CI-MPR interaction, suggesting that IncE and CI-MPR are dep

118 trations of recombinant CD-MPR or soluble CI-MPR.

119 oding the N-terminal three domains of the CI-MPR (Dom1-3His) which contains both a mannose 6-phosphat

120 The CI-MPR also recognizes lysosomal enzymes that elude UCE mat

121 re performed using truncated forms of the CI-MPR and plasminogen.

122 e loop connecting domains 1 and 2) of the CI-MPR are key determinants for plasminogen binding but are

123 By contrast, the CI-MPR bound with high affinity to glycans containing eithe

124 ysis of LIF glycopeptides enriched on the CI-MPR column revealed that all six N-glycan sites could be

125 ts show that the N-terminal region of the CI-MPR containing domains 1 and 2, but not domain 1 alone,

126 From validating the CI-MPR dependency of SNX1/2-SNX5/6 tubular profile formatio

127 The CI-MPR is a receptor for plasminogen, and this interaction

128 The extracellular region of the CI-MPR is comprised of 15 repetitive domains and contains t

129 critical to achieve high affinity for the CI-MPR receptor.

130 The CI-MPR recognizes lysosomal enzymes bearing the Man-6-P mod

131 e results show the mechanism by which the CI-MPR recognizes Man-P-GlcNAc-containing ligands and provi

132 To determine how the CI-MPR recognizes phosphodiesters, the structure of domain

133 To identify the lysine residue(s) of the CI-MPR that serve(s) as an essential determinant for recogn

134 ish that SNX5 and SNX6 associate with the CI-MPR through recognition of a specific WLM endosome-to-TG

135 igh-affinity Man-6-P binding sites of the CI-MPR to domains 1-3 and 9 and one low-affinity site to do

136 que carbohydrate binding sites allows the CI-MPR to interact with the structurally diverse phosphoryl

137 This ability of the CI-MPR to target phosphodiester-containing enzymes ensures

138 e three carbohydrate binding sites of the CI-MPR, a phosphorylated glycan microarray was probed with

139 hat, unlike the CD-MPR or domain 9 of the CI-MPR, domain 5 exhibits a 14-18-fold higher affinity for

140 ngles 1-4, but not kringles 1-3, bind the CI-MPR, indicating an essential role for the LBS in kringle

141 ay was probed with truncated forms of the CI-MPR.

142 y the CD-MPR and domains 1-3 and 9 of the CI-MPR.

143 1Ser(278), promoting binding of PACS-1 to CI-MPR to retrieve the receptor to the TGN.

144 antly higher for oblique MPR than for curved MPR (P=.01), curved MIP (P=.03), and VRT (P<.001).

145 d 83% for curved MIP, 93% and 81% for curved MPR, and 91% and 73% for VRT).

146 han evaluation of prerendered images (curved MPR, curved MIP, or VRT images).

147 tions (MIPs, 5 mm thick), prerendered curved MPRs, prerendered curved MIPs, or prerendered three-dime

148 nd loss of either protein leads to defective MPR carrier biogenesis at the TGN and endosomes.

149 tor (CI-MPR) and the 46 kDa cation-dependent MPR (CD-MPR) are key components of the lysosomal enzyme

150 The CMR-derived MPR (MPR(CMR)) correlated well with PET-derived measurem

151 In case of difficulties MPR or MinIP projection was used.

152 % confidence interval: 0.73 to 0.94) and for MPR(CMR) was 0.83 (95% confidence interval: 0.74 to 0.92

153 receiver-operating characteristic curve for MPR(PET) to detect significant CAD was 0.83 (95% confide

154 s indicate that this domain is important for MPR recycling to the Golgi complex.

155 Thus, although IH is not necessary for MPR in this neuron type, it contributes indirectly by co

156 thin 4 wk, which served as the reference for MPR index assessment.

157 or all bone lesions was 35% (247 of 698) for MPRs and 74% (520 of 698) when CBRs and MPRs were used t

158 thm derives the aortic centerline, generates MPRs orthogonal to the centerline, and segments the true

159 Global MPR correlated well with number of obstructed vessels (P

160 Global MPR index was higher in patients with normal MPI (n = 51

161 By multivariable regression analysis, global MPR index was associated with global stress TPD, age, an

162 ging-Raman imaging nanoparticle (termed here MPR nanoparticle) can accurately help delineate the marg

163 PRs) and subsequent capture of the hydrolase-MPR complexes into clathrin-coated vesicles or transport

164 el outperformed the one-compartment model if MPR was used as the outcome measure (P = .02).

165 cantly higher in the MPT-T arm: 16% vs 2% in MPR-R, resulting in a significant shorter duration of ma

166 grade >/=3 toxicity was neutropenia: 64% in MPR, 29% in CPR, and 25% in Rd patients (P < .0001).

167 For each 1 U decrease in MPR, the adjusted hazard ratios for death and MACE were

168 on of maintenance therapy (5 vs 17 months in MPR-R), irrespective of age.

169 emulsification cataract surgery performed in MPRs of Kaiser Permanente Colorado from 2011 to 2014.

170 f office-based cataract surgery performed in MPRs.

171 capacity to interact with the beta3 integrin MPR (L325R) or NPLY sequence (W359A).

172 thalidomide being replaced by lenalidomide (MPR-R).

173 tion with melphalan-prednisone-lenalidomide (MPR) and compared lenalidomide maintenance therapy with

174 tion with melphalan-prednisone-lenalidomide (MPR) or cyclophosphamide-prednisone-lenalidomide (CPR) o

175 R-R) with melphalan-prednisone-lenalidomide (MPR) or melphalan-prednisone (MP) followed by placebo in

176 ved samples on a regular basis and had lower MPR than those who did not (P < 0.05).

177 l, 31 of 32 (97%) recipients accepted F-LR + MPR platelets; none developed antibodies to donor lympho

178 , platelet concentrates prepared from F-LR + MPR whole blood were also nonimmunogenic; that is, 10 of

179 uction followed by lenalidomide maintenance (MPR-R) with melphalan-prednisone-lenalidomide (MPR) or m

180 patients stop and restart medications makes MPR a robust measure of adherence over time that reflect

181 rrelated well with PET-derived measurements (MPR(PET)) (r = 0.75, p < 0.0001).

182 Median MPR was 0.79 (range, 0-1.3).

183 Median MPR was 100% in intervention participants compared to 96

184 05%) users were non-adherent to medications (MPR <70%).

185 The CMR-derived MPR (MPR(CMR)) correlated well with PET-derived measurements

186 Measurements of the PD neuron MPR at more hyperpolarized voltages resulted in a reduct

187 The PD neuron MPR is sensitive to blockers of H- (IH) and calcium-curr

188 ulation and retention by the tumors, with no MPR accumulation in the surrounding healthy tissue, allo

189 ccuracy was significantly higher for oblique MPR than for curved MPR (P=.01), curved MIP (P=.03), and

190 88% for transverse, 99% and 91% for oblique MPR, 94% and 86% for oblique MIP, 94% and 83% for curved

191 play methods, especially interactive oblique MPRs, permits higher diagnostic accuracy than evaluation

192 ribute to the generation or amplification of MPR, but how the interaction of these currents with line

193 Unlike most cases of MPR, in these optimal models, the values of resonant- (f

194 ystematically characterize the complexity of MPR space across event costs and identify events support

195 tion to receive MPR-R (nine 4-week cycles of MPR followed by lenalidomide maintenance therapy until a

196 a mechanistic explanation the dependence of MPR on the ICa gating variable time constants.

197 ombined treatment related to the kinetics of MPR upregulation and abrogation of this event abolished

198 Subsequently, a novel mechanism of MPR action was elucidated, with the development of novel

199 Multivariate linear regression models of MPR and proportional hazards models of persistence were

200 OCRL1 with pacsin 2 and promotes scission of MPR-containing carriers.

201 Decreasing the value of MPR, at which a cut-point was taken, was associated with

202 Intravenous injection of MPRs into glioblastoma-bearing mice led to MPR accumulat

203 re, SKIP regulated retrograde trafficking of MPRs in noninfected cells.

204 ted Rab9-dependent retrograde trafficking of MPRs, thereby attenuating lysosome function.

205 lecular distinction between the transport of MPRs and TGN46 to the trans-Golgi.

206 osed role of AP-1 in retrograde transport of MPRs from late endosomes to the Golgi and indicates that

207 ifA-SKIP accounted for the effect of SifA on MPR transport and lysosome function.

208 melphalan plus stem-cell transplantation or MPR consolidation therapy after induction, and 251 patie

209 The BOLD response and PET MPR were positively correlated (R = 0.67; P < .001).

210 patients (10%) never took up a prescription (MPR=0).

211 %, 32%, and 8% of the patients in the MPR-R, MPR, and MP groups, respectively.

212 Medication possession ratio (MPR) and implementation outcomes (adoption, acceptabilit

213 ng the modified Medication Possession Ratio (MPR) and the Proportion of days covered (PDC) approach.

214 as defined as a medication possession ratio (MPR) less than 80%.

215 less than 95%, medication possession ratio (MPR) of less than 95%, and HIV viral load of 1000 copies

216 The mean medication possession ratio (MPR) was 0.64 (median 0.57) for the 13,956 subjects.

217 and calculating medication possession ratio (MPR), that is, the ratio of total days' supply of medica

218 lated using the medication possession ratio (MPR).

219 was defined as medication possession ratio (MPR): the proportion of the 365 followup days covered by

220 trajectories in medication possession ratio (MPR, a validated adherence metric based on pharmacy refi

221 ch patient, the medication possession ratio (MPR: proportion of follow-up days patients were dispense

222 ment adherence (medication possession ratio [MPR]) and persistence were evaluated over a 1-year perio

223 ence using the medication possession ration (MPR) and its relation to virological outcomes in a large

224 ssion occurred [152 patients]) or to receive MPR (153 patients) or MP (154 patients) without maintena

225 re ineligible for transplantation to receive MPR-R (nine 4-week cycles of MPR followed by lenalidomid

226 assigned to receive MPT-T, and 319 received MPR-R.

227 a paradigm for mannose 6-phosphate receptor (MPR) independent lysosomal targeting, binding to beta-gl

228 ulation of the mannose-6-phosphate receptor (MPR) on the tumor cell surface.

229 7A localize to mannose 6-phosphate receptor (MPR)-containing trafficking intermediates, and loss of e

230 and tethering mannose 6-phosphate receptor (MPR)-containing transport vesicles en route to the Golgi

231 primarily the mannose 6-phosphate receptor (MPR).

232 by binding to mannose 6-phosphate receptors (MPRs) and subsequent capture of the hydrolase-MPR comple

233 Mannose 6-phosphate receptors (MPRs) are transported from endosomes to the Golgi after

234 Mannose 6-phosphate receptors (MPRs) deliver newly synthesized lysosomal enzymes to end

235 ransmembrane, mannose 6-phosphate receptors (MPRs) that cycle between the TGN and endosomes.

236 recycling of mannose 6-phosphate receptors (MPRs) to the Golgi and for microtubule nucleation at the

237 ransported by mannose-6-phosphate receptors (MPRs).

238 inferring maximum parsimony reconciliations (MPRs) relies on user-defined costs for each type of even

239 s, free oblique multiplanar reconstructions (MPRs), free oblique maximum intensity projections (MIPs,

240 cells results from accumulation of recycling MPRs in a population of light, small vesicles downstream

241 a-I; 0 of 5) nor Mirasol pathogen reduction (MPR; 1 of 7) treatment of donor platelets prevented allo

242 d more precisely in multiplanar reformatted (MPR) and volume rendered (VR) images.

243 ween talin and the membrane-proximal region (MPR) in the beta-integrin cytoplasmic domain.

244 n with an integrin membrane-proximal region (MPR) that is critical for integrin activation.

245 Regional MPR index was associated with the same variables and wit

246 Regional MPR indices were significantly different in obstructed a

247 tigraphic estimations of global and regional MPR in multivessel patients using a cadmium zinc telluri

248 Global and regional MPR was assessed using flow difference (stress - rest) a

249 determination of Rhizomucor pusillus rennin (MPR) activity, in free and in immobilized form, along wi

250 Myocardial perfusion reserve (MPR) index was calculated as the ratio of the stress and

251 ntification of myocardial perfusion reserve (MPR) is an emerging topic in nuclear cardiology with an

252 perfusion and myocardial perfusion reserve (MPR) measurements in patients with coronary artery disea

253 stress MBF and myocardial perfusion reserve (MPR) serving as continuous measures.

254 ly (P < .001); myocardial perfusion reserve (MPR) was 2.4 +/- 0.82 (P < .001).

255 e quantitative myocardial perfusion reserve (MPR) was calculated in 720 myocardial sectors (8 sectors

256 MBF and myocardial perfusion reserve (MPR) were calculated for each segment, and mean values i

257 flow (MBF) and myocardial perfusion reserve (MPR, the ratio of stress to rest MBF).

258 Neuronal membrane potential resonance (MPR) is associated with subthreshold and network oscilla

259 f only the soluble extracellular region (sCD-MPR, residues 1-154) have shown that the CD-MPR exists a

260 nomer contacts in the functioning of the sCD-MPR, site-directed mutagenesis was used to generate a co

261 The mean +/- SD MPR was 0.52+/-0.31.

262 The MPR assessments were compared to FFR (n = 44 coronary se

263 The MPR index was 1.11 (IQR, 1.01-1.21) versus 1.30 (IQR, 1.

264 The MPR was 1.54 +/- 0.36 in segments with FFR < or =0.75 (n

265 The MPR was 1.54 +/- 0.49 in coronary segments with > or =50

266 The MPR was calculated from the ratio between stress and res

267 The binding sites for beta-GCase and the MPR are functionally separate, so that a stable ternary

268 nce Resonance Energy Transfer (FRET) for the MPR by employing computational simulation techniques and

269 d in 35%, 32%, and 8% of the patients in the MPR-R, MPR, and MP groups, respectively.

270 Preliminary results show that the MPR index is lower in patients with perfusion defects an

271 Lower adherence as measured using the MPR was strongly associated with unfavourable therapeuti

272 ut-point of 1.00 to a 79% reduction when the MPR cut-point was set at 0.8.

273 The MPRs were detected by all three modalities with at least

274 The interaction between the MPRs and its ligands is pH-dependent; the homodimeric CD

275 Endogenous ligands for the MPRs that contain solely phosphomonoesters (Man-6-P) or

276 re extracted and analysed to determine their MPR and identify instances of unfavourable viral outcome

277 STX16, Vti1a, and VAMP3 is required for this MPR transport but not for the STX6-dependent transport o

278 currents with linear currents contributes to MPR is not well understood.

279 Depletion of STX10 leads to MPR missorting and hypersecretion of hexosaminidase.

280 f MPRs into glioblastoma-bearing mice led to MPR accumulation and retention by the tumors, with no MP

281 progression-free survival (PFS) in triplet (MPR and CPR) vs doublet (Rd) lenalidomide-containing reg

282 opulation, the alkylator-containing triplets MPR and CPR were not superior to the alkylator-free doub

283 risingly, F-LR platelets that then underwent MPR were accepted by 21 of 22 (95%) recipients (P < .001

284 d MPRs together, and the other half by using MPRs only.

285 nd primary tumors was 7% with MPR-R, 7% with MPR, and 3% with MP.

286 ar rate of second primary tumors was 7% with MPR-R, 7% with MPR, and 3% with MP.

287 ession-free survival benefit associated with MPR-R was noted in patients 65 to 75 years of age but no

288 stem-cell transplantation, as compared with MPR, significantly prolonged progression-free and overal

289 MPR-R (hazard ratio for the comparison with MPR, 0.34; P<0.001) that was age-independent.

290 also demonstrate that LIMP-2 interacts with MPR in living cells.

291 -free survival was significantly longer with MPR-R (31 months) than with MPR (14 months; hazard ratio

292 hs) vs 23 months (95% CI, 19-27 months) with MPR-R (hazard ratio, 0.87; 95% CI, 0.72-1.04; P = .12).

293 idomide maintenance vs myelosuppression with MPR.

294 6% reduction in the rate of progression with MPR-R (hazard ratio for the comparison with MPR, 0.34; P

295 ematologic toxicity was more pronounced with MPR-R, especially grades 3 and 4 neutropenia: 64% vs 27%

296 Response rates were superior with MPR-R and MPR (77% and 68%, respectively, vs. 50% with M

297 ntly longer with MPR-R (31 months) than with MPR (14 months; hazard ratio, 0.49; P<0.001) or MP (13 m

298 frequent with high-dose melphalan than with MPR (94.3% vs. 51.5%), as were gastrointestinal adverse

299 lan plus stem-cell transplantation than with MPR (median progression-free survival, 43.0 months vs. 2

300 horter with volume-rendered images than with MPR images (reader 1: 42 vs 78 seconds, P<.001; reader 2