ライフサイエンスコーパス: GON

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

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

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

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

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

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

7 334; GON, 217) and 1022 eyes (non-GON, 568; GON, 454) of 611 ED patients (non-GON, 334; GON, 277) we

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

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

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

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

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

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

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

15 ipulations involving cervical input, such as GON injection.

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

17 inhibiting exocytosis of vesicles that carry GON-2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 2 years) with glaucomatous optic neuropathy (GON) and 45 eyes of 45 controls (48.0 +/- 12.6 years) wi

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

40 156 eyes with glaucomatous optic neuropathy (GON) determined by masked review with stereoscopic optic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 2, 22 had field loss at baseline, 7 had only GON, 3 were OHTs and 12 were from the 39 eyes (31%) with

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

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

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

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

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

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

66 The GON was exposed in the neck and stimulated.

67 responded to stimulation of the dura and the GON.

68 t input from the supratentorial dura and the GON.

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

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

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

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

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

74 analysed before and after stimulation of the GON.

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

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

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

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

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

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

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

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

83 tes of visual field progression in eyes with GON.

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

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

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

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

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

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