Background: Diffuse macular edema (DME) and/or aberrant neovascularization (NV) can cause vision loss in diabetic retinopathy (DR) and may be modulated by growth factors and chemokines. The chemokine stromal-derived factor 1 (SDF-1) is a potent stimulator of vascular endothelial growth factor (VEGF) expression, the main effector of NV, and the key inducer of vascular permeability associated with DME. Circulating endothelial cell precursors migrating in response to SDF-1 participate in NV. Objective: To investigate the relationship between SDF-1 and (VEGF) in vitreous of patients with varying degrees of DR and DME before and after intraocular injection of triamcinolone acetonide, used to treat refractory DME. Methods: In this prospective study, 36 patients were included and observed for 6 months. Vitreous VEGF and SDF-1 levels were measured by enzyme-linked immunosorbent assay in samples obtained immediately before and 1 month after injection of triamcinolone. Results: Both VEGF and SDF-1 were significantly higher (PϽ.01) in patients with proliferative DR than in patients with nonproliferative DR. Levels of SDF-1 were markedly increased in patients with DME compared with those without DME. Vascular endothelial growth factor correlated with SDF-1 levels and disease severity (r 2 =0.88). Conclusions: Triamcinolone administration resulted in dramatic reductions of VEGF and SDF-1 to nearly undetectable levels, eliminated DME, and caused regression of active NV. Our results support a role for SDF-1 and VEGF in the pathogenesis of the adverse visual consequences of DR and suggest that the elimination of DME with regression and/or initiation of fibrosis of NV after triamcinolone injection may be due to the suppression of VEGF and SDF-1.
Herpetic stromal keratitis (SK), a frequent cause of visual impairment, is considered to represent an immune-mediated inflammatory response to persistent herpes simplex virus virions or subcomponents within the corneal stroma. The experimental disease in mice involves the essential participation of T lymphocytes, but the role of T-lymphocyte subsets in either mediating or controlling the disease is uncertain. In this report, rat monoclonal antibodies were used to selectively deplete mice in vivo of CD4+ (helper-inducer) and CD8+ (cytotoxic-suppressor) T-cell populations and the effect on herpetic SK was evaluated. As measured by flow cytometry, mice treated with anti-CD4 monoclonal antibody (GK 1.5) were >95% depleted of CD4+ T lymphocytes and mice treated with anti-CD8 monoclonal antibody (2.43) were 90% depleted of CD8+ T lymphocytes. Depleted and nonspecific mouse ascites-treated control mice were infected topically on the corneas with herpes simplex virus type 1, and the induction of various immune parameters during the acute infection was evaluated. CD4+-depleted mice failed to produce either a significant antiviral antibody or delayed-type hypersensitivity response but were capable of producing normal cytotoxic T-lymphocyte responses. In contrast, CD8+-depleted mice produced antiviral antibody and delayed-type hypersensitivity responses comparable with those in control animals, but cytotoxic T-lymphocyte responses were markedly reduced. Clinical observations of the corneas revealed that SK in CD4+-depleted mice was significantly reduced, whereas in CD8+-depleted mice SK developed more rapidly, was more severe, and involved a greater percentage of mice. These observations implicate the CD4+ T-lymphocyte subset as the principal mediators of SK and CD8+ T lymphocytes as possible regulators that control the severity of SK.
Twenty unilateral trans-femoral amputees fitted with either the Contoured Adducted Trochanteric-Controlled Alignment Method (CAT-CAM) socket (n=10) or the quadrilateral (QUAD) socket (n=10), and a “non-amputee” control group (n=10) participated in the study. Subjects meeting the following criteria were studied: healthy males between the ages of 18 and 55 years, amputation due to non-vascular pathology, an unaffected sound limb, at least six months use of the test prosthesis, and a minimal stump length of 15 cm. Subjects ambulated in two randomized trials separated by 20 minutes of rest at 2 assigned speeds: a pace reflecting normal walking speed (97 m/min=2.5 mph) or a slower speed (48.5 m/min=1.25 mph). Heart rate (HR) and Oxygen uptake (VO2) measured during steady state walking were analyzed via two-way ANOVA. Differences among means were further analyzed using Tukey post hoc and simple effects tests. Significant differences were observed between the control group and CAT-CAM subjects with respect to VO2 (p < 0.05) and HR (p < 0.01) at the slower speed. The control group and subjects using the QUAD socket also differed with respect to VO2 (p < 0.01) and HR (p < 0.01) at the slower pace. Faster pace required more energy expenditure (p < 0.01) and produced higher HR (p < 0.01) than slower speeds. At faster pace, a significantly higher energy expenditure in the QUAD than the CAT-CAM group was observed (p<0.01). It is concluded that ambulating at normal pace using the CAT-CAM socket design uses less energy than when using a QUAD socket design.
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