ライフサイエンスコーパス: ALE

1 ALE across diagnoses and patterns of patient hyper- and

2 ALE across disorders but considering directionality demo

3 ALE meta-analysis reported convergence of hypoactivation

4 ALE not only represents a controllable experimental appr

5 ALE pinpoints synthetic errors in both single and metage

6 ALE-1, a homologue of lysostaphin, is a peptidoglycan hy

7 ALE-1-targeting domain binding studies employing various

8 ohort of 148 ALE patients (33 ALE(extra), 12 ALE(intra), 28 ALE-GAD65, 37 ALE(abneg)) in comparison t

9 pinal fluid (CSF) from a large cohort of 148 ALE patients (33 ALE(extra), 12 ALE(intra), 28 ALE-GAD65

10 E patients (33 ALE(extra), 12 ALE(intra), 28 ALE-GAD65, 37 ALE(abneg)) in comparison to paradigmatic

11 from a large cohort of 148 ALE patients (33 ALE(extra), 12 ALE(intra), 28 ALE-GAD65, 37 ALE(abneg))

12 ALE(extra), 12 ALE(intra), 28 ALE-GAD65, 37 ALE(abneg)) in comparison to paradigmatic examples for n

13 Unlike AGEs, very little is known about ALE effects in vitro.

14 , and accumulation of the immunoreactive AGE/ALE N( epsilon )-(carboxymethyl)lysine (CML).

15 st in part, by trapping intermediates in AGE/ALE formation and propose a mechanism for PM inhibition

16 trap reactive carbonyl intermediates in AGE/ALE formation, thereby inhibiting the chemical modificat

17 rded evidence of the key role of heme in AGE/ALE formation.

18 propose a mechanism for PM inhibition of AGE/ALE formation involving cleavage of alpha-dicarbonyl int

19 These results indicate that the AGE/ALE inhibitor PM protected against a range of pathologic

20 Our data suggest that the AGE/ALE inhibitory activity and the therapeutic effects of P

21 O and GLA and inhibited formation of the AGE/ALE N(epsilon)-(carboxymethyl)lysine during reaction of

22 uch's membrane, which is associated with AGE/ALE formation.

23 Levels of AGE/ALEs are increased in diseases like diabetes.

24 ced glycation/lipoxidation end products (AGE/ALEs).

25 ced glycation/lipoxidation endproducts (AGEs/ALEs) in 63 postmortem human donors.

26 pes, anti-glutamic acid decarboxylase65 ALE (ALE(GAD65)), and ALE without detectable antibodies (ALE(

27 t regimens in ALE(GAD65) and presumably also ALE(abneg).

28 PM, as a potent inhibitor of both AGE and ALE formation, may prove useful for limiting the increas

29 Moreover, ALE(GAD65) and ALE(abneg) lacked hallmarks of inflammation.

30 c acid decarboxylase65 ALE (ALE(GAD65)), and ALE without detectable antibodies (ALE(abneg)).

31 Raman spectra from a broad range of AGEs and ALEs, each with a characteristic fingerprint.

32 65)), and ALE without detectable antibodies (ALE(abneg)).

33 llular bases of multiple tissue-specific APA/ALE programs, such as 3' UTR lengthening in differentiat

34 odies of a stable epitope of the EKODE-based ALE and used these antibodies to investigate an approach

35 Pooling of results by ALE meta-analyses was stratified for population (mood di

36 ygdala of patients suspected with CD8 T cell ALE, which correlates with FLAIR-MRI and EEG alterations

37 Finally, a SiO(2) cryo-ALE process was proposed at a temperature of - 90 C resu

38 Cryogenic Atomic Layer Etching (cryo-ALE) of SiO(2) based on alternating a C(4)F(8) molecule

39 essfully fabricated after one- and two-cycle ALE of the trilayer graphene, respectively.

40 Using real Pacific Biosciences data, ALE identifies 12 of 12 synthetic errors in a Lambda Pha

41 At the single-base level with Illumina data, ALE recovers 215 of 222 (97%) single nucleotide variants

42 At the genome level with real-world data, ALE identifies three large misassemblies from the Spiroc

43 epitopes, anti-glutamic acid decarboxylase65 ALE (ALE(GAD65)), and ALE without detectable antibodies

44 Surprisingly, gene-distal ALE isoforms were four times more often localized to neu

45 imbalanced metabolism that is rewired during ALE.

46 have developed the Boulder ALignment Editor (ALE), which is a web-based RNA alignment editor, designe

47 as analyzed using Accumulated Local Effects (ALE) plot.

48 ctive lead (antibacterial ligand efficiency (ALE)>0.4).

49 ations that have been discovered from eleven ALE publications.

50 Autoimmune limbic encephalitis (ALE) presents with new-onset mesial temporal lobe seizur

51 Autoimmune limbic encephalitis (ALE) represents a heterogeneous disease associated with

52 An activation likelihood estimation (ALE) analysis and a novel coordinate-based network mappi

53 oci for an activation likelihood estimation (ALE) analysis.

54 conducted activation likelihood estimation (ALE) meta-analyses directly comparing the voxelwise conv

55 een mixed; activation likelihood estimation (ALE) meta-analyses have failed to identify a consistent

56 Activation likelihood estimation (ALE) meta-analyses were conducted on peak voxel coordina

57 Thus, activation likelihood estimation (ALE) meta-analysis was conducted for whole-brain foci co

58 Anatomical likelihood estimation (ALE) meta-analysis was performed using extracted coordin

59 antitative Activation Likelihood Estimation (ALE) meta-analysis.

60 cluded for Activation Likelihood Estimation (ALE) meta-analysis.

61 e anatomic/activation likelihood estimation (ALE) method.

62 Activation likelihood estimation (ALE) was used to perform a quantitative meta-analysis of

63 f the graphene layers, atomic layer etching (ALE), a cyclic etching method achieved through chemical

64 ation with an Arbitrary Lagrangian-Eulerian (ALE) formulation in a deformable ventricle and includes

65 sider both an arbitrary Lagrangian-Eulerian (ALE) hydrocode and a finite discrete element method (FDE

66 e present an Assembly Likelihood Evaluation (ALE) framework that overcomes these limitations, systema

67 Using adaptive laboratory evolution (ALE) and metabolic engineering in a strain engineered to

68 Adaptive Laboratory Evolution (ALE) has emerged as an experimental approach to discover

69 re, we deploy adaptive laboratory evolution (ALE) to re-optimize growth performance of a genome-reduc

70 Following adaptive laboratory evolution (ALE), the knockouts increase their growth rate by up to

71 Using adaptive laboratory evolution (ALE), we show that Sad can substitute for the roles of e

72 optimized via adaptive laboratory evolution (ALE).

73 protein sequences via alternative last exon (ALE) isoforms.

74 lines and found that alternative last exons (ALEs) often confer isoform-specific localization.

75 forms, incorporating alternative last exons (ALEs) that are more proximal to the transcription start

76 ted with antibodies targeting extracellular (ALE(extra)) epitopes, intracellular (ALE(intra)) epitope

77 uit Sad for PLP biosynthesis and glycolysis, ALE employs various mechanisms, including active site mu

78 y of anti-inflammatory treatment regimens in ALE(GAD65) and presumably also ALE(abneg).

79 eases revealed discrete immune signatures in ALE subgroups.

80 a) exhibited features of neuro-inflammation, ALE(extra) displayed features of neuro-inflammation as w

81 llular (ALE(extra)) epitopes, intracellular (ALE(intra)) epitopes, anti-glutamic acid decarboxylase65

82 euronal antigen-specific CD8 T cell-mediated ALE allowed us to corroborate our preliminary clinical f

83 nt of innate immunity in CD8 T cell-mediated ALE.

84 Moreover, ALE(GAD65) and ALE(abneg) lacked hallmarks of inflammati

85 Numerous ALE studies have been published, providing a strong impe

86 Binding of ALE-1 to S. aureus cells through its C-terminal 92 resid

87 Identification of ALE-subtype specific markers facilitated classification

88 d 50% identity with the N-terminal region of ALE-1 from Staphylococcus capitis EPK1.

89 hibited lysine modification and formation of ALEs during copper-catalyzed oxidation of low density li

90 hich the linkage between genomic position of ALEs and subcellular localization enables coordinated in

91 sed platform that comprehensively reports on ALE acquired mutations and their conditions, (ii) report

92 en BD-youths and BD-adults identified by our ALE meta-analyses are useful as brain-based diagnostic o

93 to be an advanced lipoxidation end product (ALE).

94 AGE) and advanced lipoxidation end products (ALE) in tissue proteins during aging and in chronic dise

95 otein by advanced lipoxidation end products (ALEs) during lipid peroxidation reactions in vitro.

96 n of the advanced lipoxidation end products (ALEs) N(epsilon)-(carboxymethyl)lysine, N(epsilon)-(carb

97 oducts (AGEs) and lipoxidation end products (ALEs), to protect against diabetes-induced retinal vascu

98 dvanced lipoxidation/glycation end products (ALEs/AGEs).

99 c markers facilitated classification of rare ALE-associated tumors, which may prompt further diagnost

100 easingly revealing as the number of reported ALE experiments and identified mutations continue to exp

101 rom a protein-coding ASCC3 mRNA to a shorter ALE isoform of which the RNA, rather than an encoded pro

102 Significant ALE results confirmed previous findings implicating the

103 Synthetic ALE (malondialdehyde-lysine [MDA-Lys]) (50 micromol/l) c

104 We also conclude that ALEs derived from polyunsaturated fatty acids are increa

105 We hypothesized that ALEs can have proinflammatory effects in monocytes.

106 These new results suggest that ALEs can promote monocyte activation and vascular compli

107 The ALE-1-targeting domain belongs to the SH3b domain family

108 In this study, we demonstrated the ALE process of graphene layers without noticeably damagi

109 In summary, the ALE framework provides a comprehensive, reference-indepe

110 We believe that the ALE technique presented herein can be applicable to all

111 e false clusters better than the widely used ALE method by performing numerical experiments, and that

112 While ALE(intra) exhibited features of neuro-inflammation, ALE