Segmental Analysis of Macular Layers in Patients With Unilateral Primary Open-Angle Glaucoma.

PURPOSE: To measure the thicknesses of the inner layers of the macula in both eyes of patients with unilateral primary open-angle glaucoma (POAG) and compare them with normal control eyes. METHODS: This prospective, cross-sectional pilot study enrolled patients with unilateral POAG, who had visual field defect in only 1 eye, and controls with a normal eye examination. Horizontal and vertical B-scan images centered on the fovea were obtained using spectral domain optical coherence. Semiautomatic delineation and segmentation of the inner layers of the retina were performed to evaluate macular retinal nerve fiber layer (mRNFL), ganglion cell complex (GCC) and ganglion cell-inner plexiform layer (GC-IPL) thicknesses. Mean, superior, inferior, nasal, and temporal inner macular layer thicknesses were compared between affected eyes, fellow eyes without visual field defect, and control eyes. RESULTS: Nineteen patients with unilateral POAG and 14 normal control eyes were enrolled. In the affected POAG eyes, thinning of the mRNFL, GCC, and GC-IPL layers on horizontal and vertical scans were significant when compared with controls (P<0.05), particularly on vertical scans (P<0.001). The mean regional macular GCC and GC-IPL were most severely thinned in the inferior and temporal perifoveal regions. The unaffected eye of patients with unilateral POAG showed significant thinning of the mRNFL only in the vertical scan when compared with normal controls (P<0.05). CONCLUSIONS: Spectral domain optical coherence tomography detected significant thinning of the mRNFL, GCC, and GC-IPL in the affected eyes of patients with unilateral POAG. Fellow eyes showed early structural changes only in the vertical mRNFL scans when compared with normal controls.

Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats.

BACKGROUND: Impaired wound healing is a complication of diabetes and a serious problem in clinical practice. We previously found that whey protein (WP) was able to regulate wound healing normally in streptozotocin (STZ)-diabetic models. This subsequent study was designed to assess the effect of WP on heat shock protein-72 (Hsp72) and keratin16 (Krt16) expression during wound healing in diabetic rats. METHODS: WP at a dosage of 100 mg/kg of body weight was orally administered daily to wounded normal and STZ-diabetic rats for 8 days. RESULTS: At day 4, the WP-treated diabetic wound was significantly reduced compared to that in the corresponding control. Diabetic wounded rats developed severe inflammatory infiltration and moderate capillary dilatation and regeneration. Treated rats had mild necrotic formation, moderate infiltration, moderate to severe capillary dilatation and regeneration, in addition to moderate epidermal formation. Hsp72 and Krt16 densities showed low and dense activity in diabetic wounded and diabetic wounded treated groups, respectively. At day 8, WP-treatment of diabetic wounded animals revealed great amelioration with complete recovery and closure of the wound. Reactivity of Hsp72 and Krt16 was reversed, showing dense and low, or medium and low, activity in the diabetic wounded and diabetic wounded treated groups, respectively. Hsp72 expression in the pancreas was found to show dense reactivity with WP-treated diabetic wound rats. CONCLUSION: This data provides evidence for the potential impact of WP in the up-regulation of Hsp72 and Krt16 in T1D, resulting in an improved wound healing process in diabetic models.

Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats

BACKGROUND: Impaired wound healing is a complication of diabetes and a serious problem in clinical practice. We previously found that whey protein (WP) was able to regulate wound healing normally in streptozotocin (STZ)-dia-betic models. This subsequent study was designed to assess the effect of WP on heat shock protein-72 (Hsp72) and keratin16 (Krt16) expression during wound healing in diabetic rats. METHODS: WP at a dosage of 100 mg/kg of body weight was orally administered daily to wounded normal and STZ-diabetic rats for 8 days. RESULTS: At day 4, the WP-treated diabetic wound was significantly reduced compared to that in the corresponding control. Diabetic wounded rats developed severe inflammatory infiltration and moderate capillary dilatation and regeneration. Treated rats had mild necrotic formation, moderate infiltration, moderate to severe capillary dilatation and regeneration, in addition to moderate epidermal formation. Hsp72 and Krt16 densities showed low and dense activity in diabetic wounded and diabetic wounded treated groups, respectively. At day 8, WP-treatment of diabetic wounded animals revealed great amelioration with complete recovery and closure of the wound. Reactivity of Hsp72 and Krt16 was reversed, showing dense and low, or medium and low, activity in the diabetic wounded and diabetic wounded treated groups, respectively. Hsp72 expression in the pancreas was found to show dense reactivity with WP-treated diabetic wound rats. CONCLUSION: This data provides evidence for the potential impact of WP in the up-regulation of Hsp72 and Krt16 in T1D, resulting in an improved wound healing process in diabetic models.