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1 t in primary open angle glaucoma influencing aqueous outflow.
2 us, Bves may be a key regulatory molecule in aqueous outflow.
3 nship between collagen type I metabolism and aqueous outflow.
4 in the morphology of the tissues involved in aqueous outflow.
5 cular meshwork stiffer and more resistant to aqueous outflow.
6  degrades extracellular matrix and increases aqueous outflow.
7 regulate the production of MMP-3 and improve aqueous outflow.
8  a probable mechanism for IL-1alpha-enhanced aqueous outflow.
9 rk leading to a reduction in the facility of aqueous outflow.
10 rticipation of SC cells in the regulation of aqueous outflow.
11  (LAT), a prostaglandin analogue, to enhance aqueous outflow.
12 on, has been found to increase resistance to aqueous outflow across the TM.
13  target therapeutic interventions to improve aqueous outflow and further advance our understanding of
14 regulation will likely contribute to altered aqueous outflow and intraocular pressure.
15 ous eyes may contribute to the resistance of aqueous outflow and the development of primary open-angl
16  data show a correlation between morphology, aqueous outflow, and IOP, indicating a modulatory role o
17 the physiology of TM cells in the context of aqueous outflow, and the viral anterior uveitis.
18 s to demonstrate noninvasive measurements of aqueous outflow (AO) structures in the human eye, examin
19 res allowed visualization of large and small aqueous outflow channel networks that could not be appre
20 to the concept of the cellular regulation of aqueous outflow, current methods used for its study, and
21  are promising for studying other aspects of aqueous outflow dynamics.
22 low and further advance our understanding of aqueous outflow dysregulation in the pathogenesis of gla
23  a significant increase (P < 0.01, n = 7) in aqueous outflow facility (53% and 64%, respectively) fro
24             Phenoxyacetic acids can increase aqueous outflow facility and alter HTM cell shape and at
25 The present study was undertaken to evaluate aqueous outflow facility and its age dependence in these
26 a risk factors of elevated IOP and decreased aqueous outflow facility and may potentially serve as a
27                                 At peak IOP, aqueous outflow facility and total TGFbeta2 levels in aq
28 res in the inner wall of Schlemm's canal and aqueous outflow facility has been reported previously in
29 digm that the stiffer the ECM, the lower the aqueous outflow facility through the TM.
30                                              Aqueous outflow facility was increased significantly in
31 ous humor outflow pathway leads to increased aqueous outflow facility, suggesting a critical role for
32 x metabolism and have been shown to increase aqueous outflow facility.
33 canal (SC) provide the bulk of resistance to aqueous outflow from the anterior chamber.
34  can be experimentally induced by disturbing aqueous outflow from the eye, resulting in intraocular p
35 roteinases (MMPs) contribute to conventional aqueous outflow homeostasis in their capacity to remodel
36 robeads into the anterior chamber to occlude aqueous outflow in rats (2.5-7 microL) and mice (1 micro
37  a detailed assessment and quantification of aqueous outflow in real time.
38 acellular matrix and increased resistance to aqueous outflow in the absence of PrP(C).
39  play crucial roles in the regulation of the aqueous outflow in the eyes and are closely associated w
40  results indicate that at least a portion of aqueous outflow in the mouse eye is through the uveoscle
41 which are presumed to increase resistance to aqueous outflow in viral anterior uveitis and POAG.
42 glaucoma therapy because it acts to increase aqueous outflow in vivo and in vitro.
43                                 In glaucoma, aqueous outflow into the Schlemm's canal (SC) is obstruc
44 ocular pressure due to a reduction in normal aqueous outflow is a major causal risk factor.
45 etailed measurement of the dynamics of human aqueous outflow is difficult to achieve with currently a
46                   We hypothesized that mouse aqueous outflow is segmental, and that transgenic deleti
47 lar meshwork (TM) plays an important role in aqueous outflow, its anatomy in relation to at-risk popu
48 elop a technique to image and quantify human aqueous outflow noninvasively and in real time.
49                      This is consistent with aqueous outflow obstruction superimposed on a circadian
50 n indicates that increased resistance in the aqueous outflow pathway contributes to ocular hypertensi
51             Evaluation of HA staining in the aqueous outflow pathway in comparison to that in other o
52 l for noninvasively imaging the conventional aqueous outflow pathway in mouse models of glaucoma.
53 ranyl isoprenylation of CaaX proteins in the aqueous outflow pathway increases aqueous humor outflow,
54 ar pressure, possible changes in Cx43 in the aqueous outflow pathway may provide an additional contri
55 uction in the collector channel-intrascleral aqueous outflow pathway, preventing flow to the visible
56 ajor ANGPT ligands in the development of the aqueous outflow pathway.
57  Hyaluronan (HA) is a major component of the aqueous outflow pathway.
58  into extracellular matrix remodeling in the aqueous outflow pathway.
59 SCE and TM cells lining tissues of the major aqueous outflow pathway.
60 ective stress response specific to the eye's aqueous outflow pathways and provide the first known dia
61 canal and for ultrastructural studies of the aqueous outflow pathways within the juxtacanalicular tis
62 s are enriched in specific cell types in the aqueous outflow pathways, retina, optic nerve head, peri
63 musculature is not essential for maintaining aqueous outflow pathways.
64 mum, 0.002% vol/vol) was perfused to outline aqueous outflow patterns, followed by perfusion-fixation
65                          However, effects on aqueous outflow physiology have not been determined, and
66 nts reduce intraocular pressure by enhancing aqueous outflow, probably by stimulating ciliary muscle
67 urnover, an event linked to modifications of aqueous outflow resistance and intraocular pressure home
68 lular matrices, which has a direct impact on aqueous outflow resistance and IOP.
69 licular tissue (JCT) is the probable site of aqueous outflow resistance in normal eyes and of the inc
70 ulation of chondroitin sulfates may increase aqueous outflow resistance in the POAG TM.
71 and excess ECM has been proposed to increase aqueous outflow resistance in the trabecular meshwork (T
72 lycan in the regulation of the physiological aqueous outflow resistance or in the maintenance of the
73 f elevated intraocular pressure is increased aqueous outflow resistance owing to an accumulation of e
74 ers conventional outflow facility (increases aqueous outflow resistance) of rat eyes.
75  extracellular matrix, a likely site for the aqueous outflow resistance, and thus restores normal out
76 ously, that pores contribute only 10% of the aqueous outflow resistance, may require reevaluation.
77 ctile mechanisms are important to modulating aqueous outflow resistance, mirroring mechanisms in prim
78 he potential role of HA in the regulation of aqueous outflow resistance.
79                                              Aqueous outflow structures, including SC and CCs, can be
80                   We sought to visualize the aqueous outflow system in 3 dimensions (3D) in living hu
81 helial cells, whereas VEGF-A obliterated the aqueous outflow system.
82 AGs) contribute to the filtration barrier of aqueous outflow through the trabecular meshwork (TM).
83 caca fascicularis, using laser injury to the aqueous outflow tissue at the anterior chamber angle.
84 ts and modulated the trabecular component of aqueous outflow whereas another channel, TRPV4, mediated
85 medications that increase pressure-sensitive aqueous outflow will dampen intraocular pressure spikes