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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 bal warming is robustly expected to decrease MLD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 o severe mathematical learning disabilities (MLD).

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

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

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

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

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

51 72 represent a membrane localization domain (MLD), which targets ExoS to perinuclear vesicles within

52 is a conserved membrane localization domain (MLD).

53 s constitute a membrane localization domain (MLD).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Change in MLD contributed significantly to the prediction of clini

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

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

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

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

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

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

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

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

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

83 ter, nontransplanted patients) with juvenile MLD.

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

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

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

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

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

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

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

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

92 2 to 18% better than the overall accuracy of MLD and as much as 36% better than the accuracy of the H

93 rovide a structural template for analysis of MLD function.

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

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

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

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

98 anscripts associated with the progression of MLD.

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

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

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

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

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

104 s selected for by strong sinking and shallow MLD.

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

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

107 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+/

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

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

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

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

112 The MLD-containing disintegrins showed differential activiti

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

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

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

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

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

118 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;

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

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

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

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

123 e for the membrane binding properties of the MLD.

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

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

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

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

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

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

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

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

132 4beta7, and alpha9beta1, and act through the MLD motif present in one of their subunits.

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

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

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

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

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

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

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

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

141 at there is functional overlap between these MLDs.

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

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

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

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

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

147 of fifteen unrelated patients affected with MLD.

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

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

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

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

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

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

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

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

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