Publications by authors named "Anne C Belliveau"

Purpose: To determine whether: (1) change in lamina cribrosa depth occurs more frequently than change in neuroretinal parameters in glaucoma, and (2) Bruch's membrane or anterior sclera should be used as a reference plane when measuring laminar depth.

Design: Prospective observational study.

Participants: One hundred fifty-five glaucoma patients and 35 healthy controls.

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Purpose: To determine whether structural abnormalities of the lamina cribrosa explain the presence of optic disc hemorrhages, we determined the spatial concordance between disc hemorrhages and laminar disinsertions from the sclera.

Design: Prospective noninterventional study.

Participants: From open-angle glaucoma patients followed up prospectively, we identified 52 eyes of 46 open-angle glaucoma patients with optic disc hemorrhage (ODH+ group) in at least 1 optic disc photograph during follow-up.

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Purpose: To determine whether beta and gamma peripapillary atrophy (PPA) areas measured with optical coherence tomography (OCT) enhances glaucoma diagnosis in myopic subjects.

Methods: We included 55 myopic glaucoma patients and 74 myopic nonglaucomatous controls. Beta-PPA comprised the area external to the clinical disc margin, with absence of retinal pigment epithelium and presence of Bruch's membrane.

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Purpose: Ruling out glaucoma in myopic eyes often poses a diagnostic challenge because of atypical optic disc morphology and visual field defects that can mimic glaucoma. We determined whether neuroretinal rim assessment based on Bruch's membrane opening (BMO), rather than conventional optic disc margin (DM)-based assessment or retinal nerve fiber layer (RNFL) thickness, yielded higher diagnostic accuracy in myopic patients with glaucoma.

Design: Case-control, cross-sectional study.

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Purpose: To compare the diagnostic accuracy of conventional sector-based analysis with a method devised to detect the smallest localized neuroretinal rim and retinal nerve fiber layer thickness (RNFLT) damage.

Methods: One eye of 151 glaucoma patients and 83 healthy controls (median age and MD, 71.7 and 66.

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Purpose: To describe longitudinal rates of change of neuroretinal parameters in patients with glaucoma and healthy controls, and to evaluate the influence of covariates.

Design: Prospective longitudinal study.

Participants: Treated patients with glaucoma (n = 192) and healthy controls (n = 37).

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Purpose: To investigate the rate of visual field and optic disc change in patients with distinct patterns of glaucomatous optic disc damage.

Design: Prospective longitudinal study.

Participants: A total of 131 patients with open-angle glaucoma with focal (n = 45), diffuse (n = 42), and sclerotic (n = 44) optic disc damage.

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The mechanical loading of striated muscle is thought to play an important role in shaping bones and joints. Here, we examine skeletogenesis in late embryogenesis (embryonic day 18.5) in Myf5-/-:MyoD-/- fetuses completely lacking striated muscle.

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To determine which combination of skeletal muscle-derived neurotrophic factors may be important for the survival of specific subpopulations of developing spinal cord motor neurons, we used Myf5 and MyoD (myogenic regulatory factors) knockouts, containing differentially committed myogenic precursor cells (MPCc) and immunohistochemistry against several muscle-secreted neurotrophic factors. At the peak of motor neuron cell death, skeletal muscle development is delayed in the back and body wall muscles of Myf5-/- embryos and in the limb muscles of MyoD-/- embryos. We hypothesized that, if the skeletal muscle was indeed an important source of survival factors for motor neurons, the back, the abdominal wall, and the forelimb MPCs of Myf5-/- or MyoD-/- embryos should produce at least some neurotrophic factors necessary for the survival of motor neurons.

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The aim of this study was to approach the question of neuronal dependence on neurotrophins during embryonic development in mice in a way other than gene targeting. We employed amyogenic mouse embryos and fetuses that develop without any skeletal myoblasts or skeletal muscle and consequently lose motor and proprioceptive neurons. We hypothesized that if, in spite of the complete inability to maintain motor and proprioceptive neurons, the remaining spinal and dorsal root ganglia tissues of amyogenic fetuses still contain any of the neurotrophins, that particular neurotrophin alone is not sufficient for the maintenance of motor and proprioceptive neurons.

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To further investigate the role of MyoD during skeletal myogenesis, we backcrossed mdx mutant mice (lacking dystrophin) with MyoD knock-out mice to obtain viable mice with MyoD allele on a pure mdx background. However, after nine generations of backcrossing, it was not possible to obtain a viable mdx:MyoD-/- phenotype (designated as: mdx:MyoD-/-(9th)). The compound-mutant embryos were examined just before birth.

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