PURPOSE: The purpose of this study was to investigate the effects of leg length discrepancy on kinematic changes of the pelvis and hip during gait. METHODS: A total of ten healthy women with no history of neurological, musculoskeletal surgery or injuries, or pain in the lower limbs were recruited. They were assigned to two groups; the experimental group (LLD) consisting of five subjects leg length discrepancy of 10mm to 18mm and the control group (CON) consisting of five subjects leg length discrepancy of<10 mm. All participants were instructed to perform three walking trials for further analysis by using the Cortex 3.0 software program. Independent T-test and Mann-Whitney test were used to examine the effects of mild LLD on kinematic changes of the pelvis and hip during gait. RESULTS: Angles of hip flexion, hip abduction, pelvic obliquity, and pelvic tilt in the experimental group were not significantly different compared to those of the control group. CONCLUSION Mild leg length discrepancy induces kinematic changes in the lower limbs, including decreased hip flexion, increased hip abduction, and increased pelvic obliquity in the shorter limb, and increased hip adduction and increased pelvic obliquity in the longer limb. However, those changes were not significant.

Vascular endothelial growth factor (VEGF) plays a pivotal role in pathologic ocular neovascularization and vascular leakage via activation of VEGF receptor 2 (VEGFR2). This study was undertaken to evaluate the therapeutic mechanisms and effects of the tetrapeptide Arg-Leu-Tyr-Glu (RLYE), a VEGFR2 inhibitor, in the development of vascular permeability and choroidal neovascularization (CNV). In cultured human retinal microvascular endothelial cells (HRMECs), treatment with RLYE blocked VEGF-A-induced phosphorylation of VEGFR2, Akt, ERK, and endothelial nitric oxide synthase (eNOS), leading to suppression of VEGF-A-mediated hyper-production of NO. Treatment with RLYE also inhibited VEGF-A-stimulated angiogenic processes (migration, proliferation, and tube formation) and the hyperpermeability of HRMECs, in addition to attenuating VEGF-A-induced angiogenesis and vascular permeability in mice. The anti-vascular permeability activity of RLYE was correlated with enhanced stability and positioning of the junction proteins VE-cadherin, β-catenin, claudin-5, and ZO-1, critical components of the cortical actin ring structure and retinal endothelial barrier, at the boundary between HRMECs stimulated with VEGF-A. Furthermore, intravitreally injected RLYE bound to retinal microvascular endothelium and inhibited laser-induced CNV in mice. These findings suggest that RLYE has potential as a therapeutic drug for the treatment of CNV by preventing VEGFR2-mediated vascular leakage and angiogenesis.
Actins ; Animals ; Capillary Permeability ; Choroid ; Choroidal Neovascularization ; Claudin-5 ; Endothelial Cells ; Endothelium ; Humans ; Macular Degeneration ; Mice ; Nitric Oxide Synthase Type III ; Permeability ; Phosphorylation ; Receptors, Vascular Endothelial Growth Factor ; Retinaldehyde ; Vascular Endothelial Growth Factor A