The effects of eyelash extensions on the ocular surface.

PURPOSE: To investigate the effects of eyelash extensions on the ocular surface. METHODS: This prospective study included 32 participants with eyelash extensions in both eyes. Symptoms and clinical parameters such as conjunctival vascular density, tear meniscus height (TMH), noninvasive tear break-up time, bulbar redness, meibography, lipid layer thickness, and corneal staining were assessed in the right eyes. These measurements were taken at baseline and 1 h, 1 day, 1 week, and 1 month after eyelash extensions were applied. RESULTS: At 1 h after eyelash extensions, ocular symptoms were reported by 27 participants (84.44 %), the most common being foreign body sensation (59.38 %). However, the Ocular Surface Disease Index scores were not statistically different between baseline, 1 week, and 1 month after eyelash extension (P > 0.05). TMH increased significantly at 1 h after eyelash extensions, from 0.27 ± 0.08 mm (baseline) to 0.29 ± 0.07 mm (P = 0.02). Subsequently, TMH decreased and was the lowest at 1 week at 0.24 ± 0.08 mm. First tear break-up time and average tear break-up time decreased to the lowest at 1 week after eyelash extension, with 8.36 ± 4.6 s and 10.71 ± 4.99 s, respectively, both of which were statistically different from baseline (P < 0.05). Corneal staining score was highest at 1 h after eyelash extensions at 0.78 ± 1.34. However, there were no significant differences in the conjunctival vascular density, bulbar redness, meiboscore, or lipid layer thickness. CONCLUSION: This study demonstrates that eyelash extensions can lead to an imbalance in ocular surface homeostasis, resulting in corneal epithelial defects and short-term decreased tear film stability.

Scutellarin Reduces Cerebral Ischemia Reperfusion Injury Involving in Vascular Endothelium Protection and PKG Signal.

Flavonoid glycoside scutellarin (SCU) has been widely applied in the treatment of cerebral ischemic diseases in China. In this article, we conducted research on the working mechanisms of SCU in hypoxia reoxygenation (HR) injury of isolated cerebral basilar artery (BA) and erebral ischemia reperfusion (CIR) injury in rat models. In isolated rat BA rings, HR causes endothelial dysfunction (ED) and acetylcholine (ACh) induces endothelium-dependent vasodilation. The myography result showed that SCU (100 µM) was able to significantly improve the endothelium-dependent vasodilation induced by Ach. However, SCU did not affect the ACh-induced relaxation in normal BA. Further studies suggested that SCU (10-1000 µM) dose-dependently induced relaxation in isolated BA rings which were significantly blocked by the cGMP dependent protein kinase (PKG) inhibitor Rp-8-Br-cGMPs (PKGI-rp, 4 µM). Pre-incubation with SCU (500 µM) reversed the impairment of endothelium-dependent vasodilation induced by HR, but the reversing effect was blocked if PKGI-rp (4 µM) was added. The brain slice staining test in rats' model of middle cerebral artery occlusion (MCAO) induced CIR proved that the administration of SCU (45, 90 mg/kg, iv) significantly reduced the area of cerebral infarction. The Western blot assay result showed that SCU (45 mg/kg, iv) increased brain PKG activity and PKG protein level after CIR surgery. In conclusion, our findings suggested that SCU possesses the ability of protecting brain cells against CIR injury through vascular endothelium protection and PKG signal.