ライフサイエンスコーパス: chorioretinal

1 , such vessels would typically be defined as chorioretinal anastomoses (CRAs); however, continuing st

2 h a highly disorganised retinal vasculature, chorioretinal anastomoses and the persistence of embryon

3 ed restoring venous outflow by 1) creating a chorioretinal anastomosis, 2) administering recombinant

4 eating a laser-induced or surgically induced chorioretinal anastomosis, 2) administering recombinant

5 igh myopia was staphyloma (23%), followed by chorioretinal atrophy (19.3%).

6 ttled foveal changes (3 patients), extensive chorioretinal atrophy (2 patients), or small yellowish s

7 ithin the PXE subgroups, eyes without CNV or chorioretinal atrophy (Group 1) showed the least reducti

8 ithout choroidal neovascularization (CNV) or chorioretinal atrophy (Group 1); eyes with active or fib

9 macular degeneration and progressive bifocal chorioretinal atrophy (MCDR1/PBCRA; telomeric).

10 the congenital ocular defects of Sveinsson's chorioretinal atrophy and congenital retinal coloboma.

11 d with concurrent development of progressive chorioretinal atrophy and hyperpigmented deposits in the

12 Most common reported toxicities were chorioretinal atrophy and vascular occlusions.

13 racterized by a childhood-onset, progressive chorioretinal atrophy confined to the posterior pole.

14 ed to decrease in size, and moderate macular chorioretinal atrophy developed.

15 ere focal pigment mottling of the retina and chorioretinal atrophy in 11 of the 17 eyes with abnormal

16 Staphyloma and chorioretinal atrophy increased in prevalence with incre

17 Staphyloma and chorioretinal atrophy lesions were the most common fundu

18 Fundus examination revealed chorioretinal atrophy of the posterior pole contiguous w

19 ive or fibrotic CNV (Group 2); and eyes with chorioretinal atrophy only (Group 3).

20 FP vs 545 eyes [6.9%] by UWFI; P < .001) and chorioretinal atrophy or scarring by 116% (50 eyes [0.6%

21 We report a case in which diffuse chorioretinal atrophy was developed at the injection sit

22 (21%) had grade 3 disease in which profound chorioretinal atrophy was present outside the fovea.

23 ary atrophy were common while staphyloma and chorioretinal atrophy were rare, pathologic myopia appea

24 In 4 eyes, well-delineated macular chorioretinal atrophy with a hyperpigmented ring develop

25 indings were focal macular pigment mottling, chorioretinal atrophy with a predilection for the macula

26 Funduscopy revealed circular areas of chorioretinal atrophy, and FAF imaging showed sharply de

27 aphyloma, lacquer cracks, Fuchs spot, myopic chorioretinal atrophy, and myopic choroidal neovasculari

28 were older than 50 years and showed profound chorioretinal atrophy, as well as coarse hyperpigmented

29 nd group 2 consisted of 33 eyes with diffuse chorioretinal atrophy, but not to the extent of patchy c

30 Peripapillary chorioretinal atrophy, central retinal thickness, and su

31 This later evolved to chorioretinal atrophy, most marked in the mid-peripheral

32 All eyes presented with diffuse chorioretinal atrophy, which resembles pathologic myopic

33 There was no evidence of chorioretinal atrophy.

34 retinal degeneration, resulting in profound chorioretinal atrophy.

35 s, which progressed to the eventual profound chorioretinal atrophy.

36 nal atrophy, but not to the extent of patchy chorioretinal atrophy.

37 ding 1 case diagnosed through histology from chorioretinal biopsy and another case associated with a

38 Chorioretinal biopsy confirmed the diagnosis of ECD in 1

39 dertaken of all patients that have undergone chorioretinal biopsy for suspected lymphoma at Moorfield

40 Chorioretinal biopsy provided a definitive diagnosis of

41 production of neurotrophic agents, improved chorioretinal blood circulation, and inhibition of proin

42 segment and lens dysgenesis, retinal folds, chorioretinal coloboma, and Peters anomaly.

43 with bilateral microphthalmia and bilateral chorioretinal coloboma.

44 ercentage of lesions demonstrating excessive chorioretinal damage without CNV formation.

45 The most common colobomatous anomaly was a chorioretinal defect present in 109 eyes (71.2%).

46 (GA) of the choroid and retina is a blinding chorioretinal degeneration caused by deficiency of ornit

47 by ornithine accumulation and a progressive chorioretinal degeneration of unknown pathogenesis.

48 ies for choroideremia, an X-linked recessive chorioretinal degeneration, demand a better understandin

49 , 80.5 years) without evidence or history of chorioretinal disease and from nine donors with AMD (age

50 Assessment of chorioretinal disease is dependent on the ability to vis

51 t1 mutant mice develop a rapidly progressing chorioretinal disease that begins with photoreceptor deg

52 central serous chorioretinopathy (cCSC) is a chorioretinal disease with unknown disease etiology.

53 armacotherapies in diagnosing and monitoring chorioretinal disease.

54 photography screening in the near future for chorioretinal disease.

55 tection of subtle microstructural changes in chorioretinal diseases by improving imaging of the choro

56 T will be added to photography screening for chorioretinal diseases in the near future.

57 es of 32 patients with or without any ocular chorioretinal diseases were enrolled prospectively.

58 ther define this new technology's utility in chorioretinal diseases.

59 the clinician's ability to assess and manage chorioretinal diseases.

60 es to be a beneficial tool for evaluation of chorioretinal diseases.

61 te-dot syndromes are a heterogenous group of chorioretinal disorders that have many common clinical f

62 may be used in the treatment of a variety of chorioretinal disorders.

63 ified to cause microcephaly, lymphedema, and chorioretinal dysplasia (MLCRD) as well as chorioretinal

64 d chorioretinal dysplasia (MLCRD) as well as chorioretinal dysplasia, microcephaly, and mental retard

65 volume and eye developmental anomalies with chorioretinal dysplasia.

66 nd lymphedema from a microcephaly-lymphedema-chorioretinal-dysplasia cohort.

67 Choroideremia (CHM) is an X-linked chorioretinal dystrophy that is caused by mutations with

68 typical RP starting in the second decade to chorioretinal dystrophy with a later age of onset.

69 Migration of the chorioretinal EC line Rf/6a and a primary culture of hum

70 hic representation and thickness database of chorioretinal layers in normal macula were generated.

71 n = 6 [12%]), optic disc edema (n = 3 [6%]), chorioretinal lesions (n = 2 [4%]), vitritis (n = 1 [2%]

72 testing and was suspected to be the cause of chorioretinal lesions after other viral and infectious c

73 In 6 weeks, the chorioretinal lesions had healed and visual acuity had i

74 lving, placoid, or multifocal nonnecrotizing chorioretinal lesions may be a feature of active Zika vi

75 virus and that share analogous features with chorioretinal lesions reported in cases of Dengue fever

76 ant imaging studies and clinical features of chorioretinal lesions that are presumably associated wit

77 ly hypofluorescence and late staining of the chorioretinal lesions.

78 bretinal, confluent, placoid, and multifocal chorioretinal lesions.

79 mmation levels, and by the size reduction in chorioretinal lesions.

80 optical sectioning of the vasculature called chorioretinal optical sectioning (CROS).

81 ndpoint encompassing new active inflammatory chorioretinal or inflammatory retinal vascular lesions,

82 Three-dimensional mapping of chorioretinal oxygen tension allowed quantitative P(O2)

83 Three-dimensional chorioretinal P(O2) maps were generated in rat eyes unde

84 ted visual acuity of 20/20 or better with no chorioretinal pathology.

85 phakic patients and may be mistaken for true chorioretinal pathology.

86 bility of SFCT measurements in patients with chorioretinal pathology.

87 en in the OCT images relate to the excavated chorioretinal scar observed clinically.

88 ritis, branch retinal artery occlusions, and chorioretinal scarring in a case of intrauterine transmi

89 Chorioretinal scarring was present in 3 patients (7%).

90 chiae (P < 0.002), vitritis (P < 0.005), and chorioretinal scars (P < 0.02).

91 Chorioretinal scars with pigment accumulations developed

92 be aware of atypical eye findings, including chorioretinal scars.

93 With a lower fraction of inspired oxygen, chorioretinal vascular P(O2) and mean arteriovenous P(O2

94 Light flicker-induced changes in the chorioretinal vasculature P(O2) and arteriovenous P(O2)

95 Measurement of changes in the chorioretinal vasculature P(O2) can potentially advance

96 d our ability to assess the integrity of the chorioretinal vasculature.

97 nsional mapping of oxygen tension (P(O2)) in chorioretinal vasculatures.

98 A recent report has suggested that chorioretinal venous anastomosis can be achieved in some