ライフサイエンスコーパス: GON

1 GON blockade is safe and effective for CH prevention.

2 GON-14 also contains a putative THAP DNA-binding domain.

3 uperior hemifield defects, and cluster 3 (10 GON) held deep inferior hemifield defects only or in com

4 A rescuing gon-14::GON-14::VENUS reporter is broadly expressed during devel

5 at lymphatic filariasis and activates TRP-2, GON-2 & CED-11 TRP channels in Brugia malayi muscle cell

6 Cluster 2 (26 GON) exhibited primarily deep superior hemifield defects

7 Eight-three eyes (24 healthy, 30 OHT, and 29 GON) of 65 patients who underwent at least 3 visits were

8 GON, 347) of 551 AD patients (non-GON, 334; GON, 217) and 1022 eyes (non-GON, 568; GON, 454) of 611

9 GON, 454) of 611 ED patients (non-GON, 334; GON, 277) were included.

10 334; GON, 217) and 1022 eyes (non-GON, 568; GON, 454) of 611 ED patients (non-GON, 334; GON, 277) we

11 A total of 928 eyes (non-GON, 581; GON, 347) of 551 AD patients (non-GON, 334; GON, 217) an

12 Cluster 4 (6 GON) showed deep defects in both hemifields.

13 Cluster 1 (71 GON + 3 normal optic discs) included early, localized de

14 A GON-4::GFP fusion protein, which rescues a gon-4 mutant

15 Alternatively, GEM-4 could affect GON-2 activity levels by either promoting endocytosis or

16 and/or the presence of adverse effects after GON blockade.

17 he OHT group (-0.59 mum/year; P = 0.025) and GON group (-0.79 mum/year; P = 0.058) were faster than t

18 the OHT group (-0.59 um/year; P = 0.025) and GON group (-0.79 um/year; P = 0.058) were faster than th

19 CC thinning in the OHT group (P = 0.065) and GON groups (P = 0.015), but was not associated with the

20 FOLR-1 and GON-2 are required for the activation of the NSM neurons

21 FOLR-1 and GON-2 physically interact in a heterologous system, and

22 HSN neurons and egg laying in an FOLR-1- and GON-2-dependent manner.

23 It is also possible that GEM-4 and GON-2 act in parallel to each other.

24 ssel density loss were detectable in OHT and GON groups.

25 ll, our data indicate that GEM-4 antagonizes GON-2.

26 Suspected PACG (sPACG) was defined as GON without PACS or PAC but with evidence of prior laser

27 ipulations involving cervical input, such as GON injection.

28 The AUC to discriminate between GON and normal was 0.92 with sensitivity of 77% at 95% s

29 We suggest that control of organ shape by GON-1 and fibulin in C. elegans may provide a model for

30 inhibiting exocytosis of vesicles that carry GON-2.

31 ostasis and Mg2+ uptake by intestinal cells; GON-2 is also required for gonad development.

32 gon-2 encodes a predicted cation channel (GON-2) of the TRPM subfamily of TRP proteins and is like

33 The TRPM channels GON-2 and GTL-2 regulate Mg2+ homeostasis and Mg2+ uptak

34 ceptor potential melastatin (TRPM) channels, GON-2 and GTL-2, mediate this newly described rapid path

35 or a more objective approach to characterize GON that could facilitate replication and comparability

36 input from the ipsilateral and contralateral GON (n = 5).

37 The sensitivity of SAP-OHTS to detect GON (using the disc photograph as diagnostic standard) w

38 itivities of both functional tests to detect GON increased to 42%.

39 A DL algorithm was trained to detect GON on fundus photos, using the proposed objective defin

40 standard to develop a DL algorithm to detect GON on fundus photos.

41 Sensitivity of the mfVEP to detect GON, for cluster criteria with disc structure specificit

42 ecificity of our network for differentiating GON from NGON were 85.53% and 89.02%, respectively.

43 he utility of the MRW-BMO in differentiating GON from NGON was assessed using the area under the curv

44 photos had high performance to discriminate GON from normal.

45 he non-symptomatic contralateral side, early GON branching with rejoining at a distal point, and a co

46 This proposed electrochemical GON-based enantiomeric bio-sensor becomes a highly promi

47 an ADAMTS 9 and ADAMTS 20, and of C. elegans GON-1, is required for cell migration during embryogenes

48 lidated against intra-operative examination: GON entanglement by the occipital artery, increased nerv

49 meters for defining a reference standard for GON have been proposed.

50 based on an objective reference standard for GON, was significantly associated with worse Rasch-adjus

51 uman ADAMTS-4 or ADAMTS-9 can substitute for GON-1 in transgenic worms, suggesting functional conserv

52 The reference test for GON was specialist evaluation of fundus photographs or O

53 ansient receptor potential melastatin) gene, GON-2, which may sense the intestinal distension caused

54 visual field abnormalities: early glaucoma (GON and abnormal visual field, mean deviation >-6 decibe

55 Both eyes were graded GON in 71 (38%) of the 185 subjects.

56 isc photographs from 50% of eyes were graded GON.

57 improve the detection of macular defects in GON modestly without loss of specificity when appropriat

58 seems to be a marker for disease severity in GON related to decreased RNFL thickness and may thus rep

59 using disposable graphene oxide nanoribbon (GON) screen printed electrodes.

60 Greater occipital nerve (GON) blockade is a short-term preventive therapy for clu

61 MRI) in identifying greater occipital nerve (GON) pathologies in chronic headache patients.

62 , innervated by the greater occipital nerve (GON) that is a branch of the C(2) spinal root.

63 stimulation of the greater occipital nerve (GON) were studied before and after dural stimulation.

64 OP>=21 mmHg without glaucomatous neuropathy (GON).

65 ss related to glaucomatous optic neuropathy (GON) along maximally independent axes.

66 patients with glaucomatous optic neuropathy (GON) and 189 eyes of healthy subjects were clustered wit

67 e presence of glaucomatous optic neuropathy (GON) and 24-2 visual field abnormalities: early glaucoma

68 patients with glaucomatous optic neuropathy (GON) and 289 age-matched participants without GON from t

69 2 years) with glaucomatous optic neuropathy (GON) and 45 eyes of 45 controls (48.0 +/- 12.6 years) wi

70 patients with glaucomatous optic neuropathy (GON) and pathologic optic nerve DIR hypersignal, signifi

71 om those with glaucomatous optic neuropathy (GON) can be optimized by training with clustered data.

72 156 eyes with glaucomatous optic neuropathy (GON) determined by masked review with stereoscopic optic

73 h and without glaucomatous optic neuropathy (GON) followed during the first 13 years of the ADAGES un

74 hanges due to glaucomatous optic neuropathy (GON) from non-glaucomatous optic disc changes due to non

75 ith glaucomatous-appearing optic neuropathy (GON) from the Diagnostic Innovations in Glaucoma Study (

76 ded as either glaucomatous optic neuropathy (GON) or normal by two independent masked experts, and di

77 diagnosis of glaucomatous optic neuropathy (GON) or ocular hypertension (OHT) and at least 2 disc st

78 definition of glaucomatous optic neuropathy (GON) using clearly defined parameters from optical coher

79 f identifying glaucomatous optic neuropathy (GON) using IOP corrected and uncorrected for corneal bio

80 patients with glaucomatous optic neuropathy (GON) were tested with a fundus tracked perimeter (CMP; C

81 ven eyes with glaucomatous optic neuropathy (GON), 31 with progressive optic neuropathy (PGON) 53 wit

82 standard for glaucomatous optic neuropathy (GON).

83 nsistent with glaucomatous optic neuropathy (GON).

84 80 eyes with glaucomatous optic neuropathy (GON).

85 bability of glaucomatous optical neuropathy (GON), and estimates of cup-to-disc (C/D) ratios.

86 lash hexons together to form group-of-nine (GON) tiles and bind GONs to GONs.

87 (non-GON, 334; GON, 217) and 1022 eyes (non-GON, 568; GON, 454) of 611 ED patients (non-GON, 334; GO

88 A total of 928 eyes (non-GON, 581; GON, 347) of 551 AD patients (non-GON, 334; GO

89 -GON, 581; GON, 347) of 551 AD patients (non-GON, 334; GON, 217) and 1022 eyes (non-GON, 568; GON, 45

90 -GON, 568; GON, 454) of 611 ED patients (non-GON, 334; GON, 277) were included.

91 ly tested to classify optic discs as normal, GON, or NGON, using 2183 digital color fundus photograph

92 Presence or absence of GON was determined based on morphology of the optic disc

93 and discussions related to the definition of GON in AI applications as presented by the Glaucoma Work

94 The newly proposed objective definition of GON used as reference standard may increase the comparab

95 se from the use of subjective definitions of GON and highlighted the need for a more objective approa

96 sensitivity and specificity for detection of GON occurred at 20.9 mm Hg for GAT (59%, 90%) and 18.4 m

97 roposed algorithm for the differentiation of GON from NGON yields results that have a higher sensitiv

98 The facilitatory effect of GON stimulation on dural stimulation suggests a central

99 22 images (660 images of NGON, 676 images of GON, and 486 images of normal optic discs) was used for

100 could be mediated by a direct inhibition of GON-2 by GEM-4, since both proteins are predicted to be

101 DAMTS-20 (1911 amino acids) are orthologs of GON-1, an ADAMTS protease required for gonadal morphogen

102 fVEP or SAP was defined as the percentage of GON eyes that had an abnormality on the functional test.

103 ntly higher than that for the probability of GON by human graders (partial AUC = 0.529 vs 0.411, resp

104 deviation (rho=0.54) than the probability of GON given by human graders (rho=0.48; P < .001).

105 An extensive region of GON-14 contains blocks of sequence similarity to transpo

106 to evaluate the effectiveness and safety of GON blockade in patients with CH.

107 2, 22 had field loss at baseline, 7 had only GON, 3 were OHTs and 12 were from the 39 eyes (31%) with

108 f collagen IV (EMB-9), whereas FBL-1 opposes GON-1 by stabilizing EMB-9.

109 y and useful for evaluating eyes with OHT or GON.

110 In addition, eyes with progressive GON (PGON) were identified (n = 39).

111 for glaucomatous ONH features and referable GON (defined as ONH appearance worrisome enough to justi

112 on fundus images alone can detect referable GON with higher sensitivity than and comparable specific

113 , sensitivity, and specificity for referable GON and glaucomatous ONH features.

114 The algorithm's AUC for referable GON was 0.945 (95% confidence interval [CI], 0.929-0.960

115 e most crucial features related to referable GON were: presence of vertical cup-to-disc ratio of 0.7

116 ation >-6 decibels [dB]), glaucoma suspects (GON and normal visual field), and ocular hypertensives (

117 We find that GON-1 and fibulin have antagonistic roles in controlling

118 We propose that GON-1 regulates a developmental switch out of an initial

119 We speculate that GON-1 controls morphogenesis by remodelling basement mem

120 The GON was exposed in the neck and stimulated.

121 requires the folate receptor FOLR-1 and the GON-2 calcium channel.

122 responded to stimulation of the dura and the GON.

123 t input from the supratentorial dura and the GON.

124 a distal point, and a connection between the GON and the lesser occipital nerve.

125 ld or suboccipital muscles innervated by the GON induced an increased excitability of dural responses

126 In C. elegans, the GON-1 ADAMTS metalloprotease regulates both elongation a

127 In the GON group, ED eyes with baseline betaPPA progressed fast

128 Supramaximal electrical stimulation of the GON (20 s to 5 min) enhanced afferent dural input in 8/2

129 Of the GON eyes, 31.0% showed both significant GCC loss and ves

130 Visualization of the GON involved generating 2-D image slices with sequential

131 xcitability to electrical stimulation of the GON was observed in C-fibre responses (P < 0.001).

132 analysed before and after stimulation of the GON.

133 Therefore, the GON-1 protease normally promotes tissue elongation and e

134 e propose that GEM-1 acts in parallel to the GON-2 channel to promote cation uptake within the develo

135 MRI possesses the ability to visualize the GON and identify suspected trigger points associated wit

136 When the normal group was compared with the GON group, the FDT pattern SD (PSD) area was larger than

137 These GON disposable platforms use just 50 muL of sample and a

138 cluster and spreading 70.5% of the eyes with GON across the other four clusters, in good agreement wi

139 vB-ICA-mm placed 68.6% of the eyes with GON in a cluster labeled G and 98.4% of the eyes with no

140 mportant patterns of field loss in eyes with GON in a manner consistent with years of clinical experi

141 A total of 80 eyes with GON were classified as mild, moderate and advanced in 15

142 tes of visual field progression in eyes with GON.

143 elds from normal eyes plus 46 from eyes with GON.

144 Adamts20 shows remarkable homology with GON-1, an ADAMTS family protease required for distal tip

145 PACG was defined as PACS or PAC with GON.

146 of AD (395 eyes) and ED (419) patients with GON and 276 eyes of AD (106) and ED (170) patients with

147 n visual field series from 200 patients with GON confirmed on two occasions by stereophoto review.

148 The holes in the RNFL seen in patients with GON were probably due to a local loss of RNFL fibers and

149 egeneration in optic nerves in patients with GON.

150 ata set (123 eyes/123 glaucoma patients with GON; 135 eyes/135 normal control subjects).

151 ON) and 289 age-matched participants without GON from the Diagnostic Innovations in Glaucoma Study (D