ライフサイエンスコーパス: MLD

1 MLD is predicted to be a multiple membrane-spanning prot

2 MLD is widely expressed in human tissues and is localize

3 MLD overexpression inhibited biosynthesis of the EGF rec

4 MLD(+) patients differed from MLD(-) patients only by lo

5 0.001), area stenosis (NRI 0.63, p = 0.002), MLD (NRI 0.62, p = 0.001), and MLA (NRI 0.43, p = 0.01).

6 ngle dose of drug to mice infected with 100x MLD(50) virus is shown to eradicate advanced infections

7 against pneumonic plague challenge with 250 MLD Y. pestis CO92, immunization with recombinant F1 did

8 meter stenosis (0.68), area stenosis (0.66), MLD (0.75), or MLA (0.78).

9 rved in primary and SV40t fibroblasts from a MLD patient (ASA-I179S) cultured in multi-well plates.

10 y for proper localization of one but not all MLDs.

11 cy of 97.9%, 89.9%, and 99.1% with the AMFM, MLD, and HIST methods, respectively.

12 This revealed an MLD-related progressive increase in distinct classes of

13 Compared with FFR as the "gold standard," an MLD of 2.8 mm had the highest sensitivity and specificit

14 Similarly, treating an MLD mouse model decreased sulfatides and lysosulfatide l

15 and MH diameter at the base (CC = +0.35) and MLD (CC = +0.42) (all P < 0.05).

16 the development and achievements of ALD and MLD and their applications for energy storage and conver

17 irections for new material design by ALD and MLD and untapped opportunities in energy storage and con

18 ificant emphasis is dedicated to the ALD and MLD designed materials, their crucial role in enhancing

19 In the past few decades, ALD and MLD have been intensively studied for energy storage and

20 ermore, the large-scale potential of ALD and MLD techniques is discussed and predicted.

21 Herein, this review focuses on ALD and MLD's role in fabricating materials for electro-, photo-

22 ummary, challenges and prospects for ALD and MLD-designed materials for CO(2) transformation.

23 nstrated strong correlations between FFR and MLD (r=0.79, P<0.0001) as well as between FFR and MLA (r

24 benefits observed in murine models of KD and MLD, chronic CGT inhibition negatively impacted both the

25 not differ significantly between MLD(+) and MLD(-) patients.

26 on family of disintegrin, displaying RGD and MLD motifs are reported.

27 P = 0.002) explained 13% of variability and MLD (B = 0.29; P = 0.002), and idiopathic MH duration (B

28 P = 0.002) explained 13% of variability and MLD (beta = 0.29; P = 0.002), and idiopathic MH duration

29 leotides, and that their R(g) values vary as MLD(0.5) in an ideal solvent, and hence as N(0.34).

30 More generally, we predict the average MLD values of large nonviral ssRNAs scale as N(0.67+/-0.

31 urvival did not differ significantly between MLD(+) and MLD(-) patients.

32 tegory were related to overall survival, but MLD was not.

33 Outcomes were summarized descriptively by MLD strata.

34 The combined MLD and SUV(P90) model generalized in the validation sub

35 Further, the CT694 MLD is able to complement ExoS DeltaMLD when ectopically

36 bal warming is robustly expected to decrease MLD.

37 d computer-based methods: mean lung density (MLD) and the histogram analysis (HIST).

38 ublished methods, namely, mean lung density (MLD) and the lowest fifth percentile of the histogram (H

39 metal anodes via molecular-layer deposition (MLD) is reported.

40 sition (ALD) and molecular layer deposition (MLD) methods utilize various strategies, including ultra

41 sition (ALD) and molecular layer deposition (MLD) techniques, the gas-phase thin film deposition proc

42 through a shoaling of the mixed layer depth (MLD) and a consequent increase of the SRD and DMS concen

43 m), that affects both the mixed layer depth (MLD) and the strength and duration of internal waves.

44 limitations in simulating mixed layer depth (MLD) in the North Pacific, global warming is robustly ex

45 nt sinking interacts with mixed layer depth (MLD) to further modulate optimal sizes, with smaller siz

46 rmocline and ascended to mixed layer depths (MLD) during nighttime.

47 The method limits of detection (MLDs) in yoghurt extracts were found to be 0.5 and 0.25n

48 ported here will be important for diagnosing MLD and MSD patients and for monitoring the efficacy of

49 ly found within the minimum linear diameter (MLD) (104 of 139 deposits, 74%).

50 Minimum linear diameter (MLD) and base diameter (BD) defined idiopathic MH size.

51 zontal and vertical minimum linear diameter (MLD), horizontal and vertical basal hole diameter (BHD),

52 The lesion site minimum lumen diameter (MLD) (2.26 +/- 0.82 mm) by QCA correlated less well with

53 greater loss in mean minimum lumen diameter (MLD) (TT: -0.15+/-0.15; CT: -0.17+/-0.26; and CC: -0.03+

54 easurements included minimum lumen diameter (MLD) and diameter stenosis (DS).

55 ssessed by comparing minimal lumen diameter (MLD) between simulations and post-stenting OCT measureme

56 very high agreement for mean lumen diameter (MLD) between stent simulations and post-stenting uCT in

57 o differences in the minimal lumen diameter (MLD) between the two zones before treatment; an increase

58 meter, smaller final minimal lumen diameter (MLD) by angiography and smaller stent lumen cross-sectio

59 mean (SD) change in minimum lumen diameter (MLD) from baseline to concluding angiogram of all qualif

60 or in reconstructing minimum lumen diameter (MLD) was 0.05 ( 0.03 mm) which was < 1% (95% CI 0.13-1.6

61 ed of 2018 patients, minimal lumen diameter (MLD) was measured by quantitative coronary angiography.

62 lumen CSA and stent minimum lumen diameter (MLD) were measured by IVUS imaging.

63 easurements included minimum lumen diameter (MLD), interpolated reference diameter and diameter steno

64 osis, area stenosis, minimal lumen diameter (MLD), minimal lumen area (MLA) and %APV.

65 IVUS minimum lumen diameter (MLD), minimum lumen area (MLA), cross-sectional narrowin

66 mean blood pressure, minimum lumen diameter (MLD), number of coronary lesions and total occlusions we

67 Smaller pretreatment minimum lumen diameter (MLD), smaller final MLD, longer stent length, diabetes m

68 er stenosis [%S] and minimum lumen diameter [MLD).

69 s [DS] and follow-up minimal lumen diameter [MLD]) were determined.

70 d lesion lumen area, maximum lumen diameter, MLD, plaque area and area stenosis.

71 determined prePTCA minimal lumen diameters (MLD) were similar in vehicle and RPR101511A-treated pigs

72 ren with mathematical learning disabilities (MLD) during arithmetic training compared to those who re

73 o severe mathematical learning disabilities (MLD).

74 e (thermal) average maximum ladder distance (MLD) and use it as a measure of the "extendedness" of th

75 Ebola virus glycoprotein mucin-like domain (MLD) is implicated in Ebola virus cell entry and immune

76 ein (GP) 2 portion of the mucin-like domain (MLD) of MARV GP, termed the wing region.

77 The mucin-like domain (MLD) of the EBOV GP may enhance virus immune system evas

78 n resembling a membrane localization domain (MLD) found in anti-host proteins from Yersinia, Pseudomo

79 tivity nor the membrane localization domain (MLD) of ExoS, was required to elicit this phenotype.

80 irmed that the membrane localization domain (MLD) of ExoU had a direct affinity for PI(4,5)P2, and we

81 72 represent a membrane localization domain (MLD), which targets ExoS to perinuclear vesicles within

82 is a conserved membrane localization domain (MLD).

83 s constitute a membrane localization domain (MLD).

84 second (middle), lumenally oriented domain (MLD) and transfers cholesterol to NPC1's N-terminal doma

85 in (termed the membrane localization domain [MLD]) targets ExoS to the Golgi-endoplasmic reticulum (G

86 oS (termed the membrane localization domain, MLD) were necessary and sufficient for membrane localiza

87 onses upon equivalent 50% mouse lethal dose (MLD(50)) challenges with influenza virus.

88 While ZIKV-RGN has a 50% mouse lethal dose (MLD(50)) of ~10(5) focus forming units (FFUs), ZIKV-Para

89 The mean lethal dose (MLD) for pneumonic plague in guinea pigs was estimated t

90 riments showed that the minimum lethal dose (MLD) of 40 Gy led to the specific ablation of hematolymp

91 Here, we used multiple low-dose (MLD) streptozotocin (STZ) injections and the NOD mouse m

92 RP models that included the mean lung dose (MLD) and patient characteristics were examined.

93 s unclear whether manual lymphatic drainage (MLD) following primary total knee arthroplasty (TKA) is

94 BPA-mutated AML with multilineage dysplasia (MLD; >/= 50% dysplastic cells in 2-3 lineages) remains t

95 Each MLD contains a four-helical bundle, with the conserved a

96 e YopE MLD functionally complements the ExoS MLD for intracellular targeting in mammalian cells.

97 e fatty acid (lipid) desaturase gene family, MLD.

98 imensions (whether final lumen area or final MLD).

99 r reference lumen diameter and smaller final MLD were strong predictors of in-stent restenosis.

100 minimum lumen diameter (MLD), smaller final MLD, longer stent length, diabetes mellitus, unstable an

101 FMRFamide, MLD/pedal peptide, allatotropin, RNamide, excitatory pep

102 Similarly, there was a high agreement for MLD between stent simulation and OCT in clinical trainin

103 MLD(+) patients differed from MLD(-) patients only by lower mean WBC counts, not by bi

104 placebo group, which was not different from MLD in the tranilast groups (1.72 to 1.78+/-0.76 to 80 m

105 scale HTS, primary cultured fibroblasts from MLD patients were transformed using SV40 large T antigen

106 For any given MLD, the event rate was exaggerated in the presence of d

107 We treated patients who had MLD with atidarsagene autotemcel (arsa-cel), a hematopoi

108 The baseline horizontal MLD was 591.7 +/- 219.4 mum and the vertical MLD was 552

109 - 0.28 logMAR), only in eyes with horizontal MLD of > 650 mum, but not when other MLD cut-offs were u

110 the N-linked fatty acid, also accumulates in MLD and is considered a key driver of pathology although

111 Change in MLD contributed significantly to the prediction of clini

112 orced vital capacity and greater % change in MLD(e/I) (respectively) throughout methacholine testing,

113 ponsiveness (as represented by the change in MLD(e/i) ) during methacholine challenge is greater in o

114 cits (Gross Motor Function Classification in MLD level 0 or 1) and an IQ of at least 85, when age at

115 tion (Gross Motor Function Classification in MLD), loss of any language function, and magnetic resona

116 inicians to anticipate the disease course in MLD patients, identifying individuals at high risk of se

117 n preventing inflammation-mediated damage in MLD-STZ and in preventing and reversing diabetes in NOD

118 mall airways as estimated via differences in MLD(e/i) slopes (groupxln(1 + % PD20 interaction; p = 0.

119 clude that FAAH has a protective function in MLD and may represent a novel therapeutic target for tre

120 ficant for both patients with late-infantile MLD (66% [95% CI 48.9-82.3]) and early-juvenile MLD (42%

121 patients with presymptomatic late-infantile MLD (P<0.001), those with presymptomatic early-juvenile

122 among untreated patients with late-infantile MLD and 100% (95% CI, 100 to 100) among treated patients

123 patients with presymptomatic late-infantile MLD.

124 We conclude that (1) an IVUS MLD and MLA of 2.8 mm and 5.9 mm2, respectively, strongl

125 untreated vessel (with a DS > 50%) and IVUS MLD were independent predictors of cardiac events.

126 (66% [95% CI 48.9-82.3]) and early-juvenile MLD (42% [12.3-71.8]).

127 1), those with presymptomatic early-juvenile MLD (P = 0.04), and those with early-symptomatic early-j

128 those with early-symptomatic early-juvenile MLD (P<0.001).

129 among untreated patients with early-juvenile MLD and 87.5% (95% CI, 38.7 to 98.1) and 80.0% (95% CI,

130 symptomatic late-infantile or early-juvenile MLD and those with early-symptomatic early-juvenile MLD,

131 tomatic and early-symptomatic early-juvenile MLD, respectively.

132 those with early-symptomatic early-juvenile MLD, the risk of severe motor impairment or death was si

133 matic or early symptomatic stage of juvenile MLD is associated with a reasonable chance for disease s

134 ) and nontransplanted patients with juvenile MLD born between 1967 and 2007 were included in this cas

135 Patients with juvenile MLD born between 1975 and 2009 and who received HSCT at

136 Among patients with juvenile MLD, patients who underwent HSCT had a better gross moto

137 ter, nontransplanted patients) with juvenile MLD.

138 Patients with metachromatic leukodystrophy (MLD) and multiple sulfatase deficiency (MSD) displayed a

139 sease (KD) and metachromatic leukodystrophy (MLD) are caused by accumulation of the glycolipids galac

140 torage disease metachromatic leukodystrophy (MLD) characterized by massive intralysosomal storage of

141 Metachromatic leukodystrophy (MLD) is a lysosomal storage disorder caused by mutations

142 Metachromatic leukodystrophy (MLD) is a lysosomal storage disorder caused mainly by mu

143 Metachromatic leukodystrophy (MLD) is a rare, inherited, demyelinating lysosomal stora

144 Metachromatic leukodystrophy (MLD) is an ultrarare, severe lysosomal storage disorder

145 treatment for metachromatic leukodystrophy (MLD) remains a substantial unmet medical need.

146 d resulting in metachromatic leukodystrophy (MLD), a neurodegenerative lysosomal storage disease.

147 patients with metachromatic leukodystrophy (MLD), a progressive neurodegenerative LSD.

148 s for juvenile metachromatic leukodystrophy (MLD), reported with variable outcome and without compari

149 mouse model of metachromatic leukodystrophy (MLD).

150 d on pre-symptomatic patients affected by LI-MLD treated with ex vivo autologous haematopoietic stem

151 e-infantile metachromatic leukodystrophy (LI-MLD).

152 Changes in the mean MLD and lesion-specific MLD also followed the same trend

153 The mean MLD by IVUS was 72 +/- 8% of the expected stent diameter

154 which we used an attenuated VSV-EBOV with no MLD that expressed green fluorescent protein (GFP) (VSV-

155 NPC1-MLD uses two protruding loops to bind NPC2, analogous to

156 crystal structure of a complex of human NPC1-MLD and NPC2 bearing bound cholesterol-3-O-sulfate.

157 2 to 18% better than the overall accuracy of MLD and as much as 36% better than the accuracy of the H

158 rovide a structural template for analysis of MLD function.

159 Cotransfection of MLD with the epidermal growth factor (EGF) receptor resu

160 However, 11 died of MLD progression, resulting in similar overall survival w

161 e present study investigated the efficacy of MLD after TKA.

162 ed DMS diagnostic models to global fields of MLD and chlorophyll simulated with an Ocean General Circ

163 CEBPA-mutated AML patients for the impact of MLD, karyotype, and additional mutations.

164 ed lyso-sulfatide levels in a mouse model of MLD.

165 rather exacerbated the disease phenotype of MLD mice.

166 anscripts associated with the progression of MLD.

167 measurement in DBS for newborn screening of MLD.

168 The derived amino acid sequence of MLD contains three consensus motifs, HX3H, HX2HH, and HX

169 A-mediated gene therapy for the treatment of MLD.SIGNIFICANCE STATEMENT Herein, we describe the metho

170 towards the development and understanding of MLD thin films for high performance next-generation batt

171 el I of evidence does not support the use of MLD in primary TKA.

172 levant benefits in children with early-onset MLD by preserving cognitive function and motor developme

173 symptomatic or early-symptomatic early-onset MLD with biochemical and molecular confirmation of diagn

174 (NHx) cohort of 31 patients with early-onset MLD, matched by age and disease subtype.

175 izontal MLD of > 650 mum, but not when other MLD cut-offs were used.

176 to develop a phenotype matrix that predicts MLD phenotype given ARSA alleles in a patient's genotype

177 MLD (QCA lesion length and preinterventional MLD and DS and IVUS preinterventional lumen and arterial

178 nts indicated improvement over the published MLD-alone model (AUC, 0.77 vs. 0.72; P = 0.0001 vs. 0.02

179 ity, and 2 additional children died of rapid MLD progression 1.5 and 8.6 years after HSCT, resulting

180 ratory:inspiratory mean lung density ratios (MLD(e/i) , as determined by computed tomography [CT]) th

181 (RCTs) comparing patients who have received MLD versus a group of patients who did not undergo MLD f

182 ition, we found that substitution of the RID MLD with the MLDs from two different effector domains fr

183 igh certainty by combining the normal lung's MLD and pretreatment (18)F-FDG PET/CT SUV(P90) This refi

184 on, together with strong sinking and shallow MLD produce size distributions with smaller range, means

185 s selected for by strong sinking and shallow MLD.

186 Likewise, each of the six MLD residues was necessary for full virulence in cell cu

187 chemic lesions, ischemic lesions had smaller MLD (1.3 vs. 1.7 mm, p = 0.01), smaller MLA (2.5 vs. 3.8

188 0.03+/-0.22 mm; P=0.006) and lesion-specific MLD (TT: -0.15+/-0.06; CT: -0.18+/-0.03; and CC: -0.06+/

189 Changes in the mean MLD and lesion-specific MLD also followed the same trend.

190 pared with diameter stenosis, area stenosis, MLD, and MLA, %APV by coronary CTA improves identificati

191 The MLD (2.5 +/- 0.5 mm) and minimum stent CSA (6.0 +/- 1.7

192 The MLD values of viral ssRNAs that package into capsids of

193 The MLD-containing disintegrins showed differential activiti

194 calized with a fusion protein containing the MLD of ExoS.

195 In contrast, VSV-EBOV containing the MLD showed substantially better targeting and eliminatio

196 ull-length EBOV GP (VSV-EBOV) containing the MLD was substantially more effective and safer than a pa

197 ipases to the plasma membrane and define the MLD of ExoU as a member of a new class of PI(4,5)P2 bind

198 o zones before treatment; an increase in the MLD in both zones after balloon angioplasty and a signif

199 umn (i.e., stratification and changes in the MLD resulting in lower nutrients and NPP).

200 position of the integrin-binding loop in the MLD-containing subunit.

201 rallel construct with an EBOV GP lacking the MLD (VSV-EBOVDeltaMLD).

202 red it to that of a glycoprotein lacking the MLD.

203 om 3.51 +/- 0.46 mm to 3.22 +/- 0.44 mm; the MLD decreased from 3.22 +/- 0.47 mm to 2.03 +/- 0.72 mm;

204 etion mutations to show that portions of the MLD are required for membrane localization and catalytic

205 Deletion of the MLD did not inhibit type III secretion of ExoS from P. a

206 add to our understanding of the role of the MLD in ExoU-mediated virulence.

207 a significant versus slight reduction of the MLD in the balloon treatment versus balloon plus laser z

208 This causes a shallowing of the MLD which prevents nutrients from reaching the euphotic

209 C slope was calculated for each third of the MLD(e/i) response and compared between groups.

210 e for the membrane binding properties of the MLD.

211 t important amino acid is that preceding the MLD motif.

212 n the 54 lesions treated with ELCA+PTCA, the MLD increased from 0.73+/-0.38 mm before ELCA to 2.10+/-

213 showed that HCT is sufficient to rescue the MLD, that recipient hematolymphoid tissues were repopula

214 uracy was 81%, which was 21% better than the MLD and 25% better than the HIST method.

215 the AMFM performed 7 to 27% better than the MLD and 4 to 36% better than the HIST methods.

216 was significantly (p < 0.01) better than the MLD and HIST methods.

217 Deletion mapping showed that the MLD included a symmetrical leucine-rich motif within res

218 Our results, which show that the MLD is located at the apex and the sides of each glycopr

219 4beta7, and alpha9beta1, and act through the MLD motif present in one of their subunits.

220 to an accuracy of 94.7% and 97.4% using the MLD and HIST methods, respectively.

221 rain tumors in immunodeficient mice when the MLD was expressed within the EBOV glycoprotein than when

222 y, compared to an accuracy of 74.6% with the MLD and 64.4% with the HIST methods.

223 Mutations of the leucines within the MLD did not affect type III secretion or translocation i

224 Mutations of charged residues within the MLD did not affect type III secretion, delivery into HeL

225 The organization of the leucines within the MLD of ExoS is different from that of previously describ

226 A conserved arginine within the MLD was critical for interaction of each protein with PI

227 ternal leucines and an isoleucine within the MLD, but not charged or other hydrophobic residues, targ

228 nd that substitution of the RID MLD with the MLDs from two different effector domains from the Vibrio

229 at there is functional overlap between these MLDs.

230 w the thermocline and frequently ascended to MLD during daytime either to warm muscles or repay oxyge

231 Intravascular ultrasound MLD was the most important quantitative predictor of car

232 rsus a group of patients who did not undergo MLD following primary TKA were accessed.

233 -up DS (QCA lesion length); and 3) follow-up MLD (QCA lesion length and preinterventional MLD and DS

234 (binary restenosis) and secondary (follow-up MLD and follow-up DS) end points.

235 At follow-up, MLD was 1.76+/-0.77 mm in the placebo group, which was n

236 res onto a linear polymer model and by using MLD as a measure of effective contour length, we predict

237 MLD was 591.7 +/- 219.4 mum and the vertical MLD was 552.9 +/- 198.2 mum.

238 rZIKV-RGN in a virulent Paraiba-like virus (MLD(50) < 10 FFU).

239 oped RP(Early) Predictors for RP(Early) were MLD alone (AUC, 0.72; P = 0.02; pHL, 0.87), SUV(P10), SU

240 of fifteen unrelated patients affected with MLD.

241 Genes associated with MLD were identified, confirmed on a quantitative polymer

242 ying effective intervention in children with MLD and provides novel metrics for assessing response to

243 hat brain activity patterns in children with MLD are significantly discriminable from neurotypical pe

244 remediates poor performance in children with MLD, but also induces widespread changes in brain activi

245 Foveal floor width was correlated with MLD (r = 0.36; P <= 0.001) and BD (r = 0.30; P <= 0.001)

246 Foveal floor width was correlated with MLD (r = 0.36; P 0.001) and BD (r = 0.30; P 0.001), but

247 ity to ARSA genotype in 489 individuals with MLD.

248 in T lymphocytes and brain of patients with MLD and generally marked nervous tissue damage in the LS

249 in primary T lymphocytes of 24 patients with MLD compared to 24 age- and sex-matched healthy controls

250 agene autotemcel (arsa-cel) in patients with MLD.

251 k = 1/[1+e((-) (x) ())]; x = -6.08 + [0.17 x MLD] + [1.63 x SUV(P90)]).

252 These data indicate that the YopE MLD functionally complements the ExoS MLD for intracellu

253 Residues 54-75 of YopE (termed YopE-MLD) were necessary and sufficient for intracellular loc

254 The YopE-MLD localized ExoS to intracellular membranes and target