This is the first nationwide population-based epidemiological study of PCA. We demonstrate that PCA can be associated with other disorders, especially AD.

This study investigated the neuroprotective effects of administration of ROCK inhibitor E212 on ischemic optic neuropathy. METHODS.Rats received an intravitreal injection of either E212 or PBS immediately after optic nerve infarct. The oxidative stress in the retina was detected by performing superoxide dismutase activity and CellROX assays. The integrity of retinal pigment epithelium was determined by staining of zona occludens 1. The visual function, retinal ganglion cell (RGC) density, and RGC apoptosis were determined by using flash visual-evoked potential analysis, retrograde FluoroGold labeling, and TdT-dUTP nick end-labeling assay. Macrophage infiltration was detected by staining for ED1. The protein levels of TNF-α, p-CRMP, p-AKT1, p-STAT3, and CD206 were evaluated using Western blotting. RESULTS.Administration of E212 resulted in a 1.23-fold increase in the superoxide dismutase activity of the retina and 2.28-fold decrease in RGC-produced reactive oxygen species as compared to the levels observed upon treatment with PBS (P < 0.05). Moreover, E212 prevented the disruption of the blood-retinal barrier (BRB) in contrast to PBS. The P1-N2 amplitude and RGC density in the E212-treated group were 1.75-and 2.05-fold higher, respectively, than those in the PBS-treated group (P < 0.05). The numbers of apoptotic RGCs and macrophages were reduced by 2.93-and 2.54-fold, respectively, in the E212treated group compared with those in the PBS-treated group (P < 0.05). The levels of p-AKT1, p-STAT3, and CD206 were increased, whereas those of p-PTEN, p-CRMP2, and TNF-α were decreased after treatment with E212 (P < 0.05). CONCLUSIONS.Treatment with E212 suppresses oxidative stress, BRB disruption, and neuroinflammation to protect the visual function in ischemic optic neuropathy.

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Purpose: To evaluate the rate of and time to complete vascularization in premature infants and to explore associated factors.Methods: A monocentric, retrospective cohort study including 541 premature infants who underwent screening for retinopathy of prematurity (ROP) between July 2016 and June 2019. Patients underwent regular dilated fundus examinations with indirect ophthalmoscopy until complete vascularization. The worse eye of each patient was included for analyses. The proportion of infants with complete retinal vascularization at the last visit and the time to full vascularization was analyzed.Results: Among all infants (average gestational age 31.29 6 3.12 weeks), 490 (90.57%) had complete records of retinal vascularization outcomes, of whom 439 (89.59%) achieved complete vascularization. The average postmenstrual age for complete vascularization was 45.39 6 11.04 weeks, and 95.22% achieved completion before 64 weeks of postmenstrual age. Retinopathy of prematurity developed in 118 (22.56%) infants; 33 (6.10%) received antivascular endothelial growth factor treatment. For all infants screened for ROP, lower birth weight, presence of ROP, and antivascular endothelial growth factor therapy predicted delayed complete vascularization; for infants diagnosed with ROP, only lower birth weight predicted delayed complete vascularization. Subgroup analysis showed significant differences between patients without ROP, with untreated ROP, and with treated ROP in time to complete vascularization and its rate (99.7%, 66.2%, and 16.7%, respectively).Conclusion: Lower birth weight predicted delayed complete vascularization. Antivascular endothelial growth factor therapy and the presence of ROP, including ROP severity, may also affect time to complete vascularization. These findings should help improve the understanding and management of persistent avascular retina in preterm infants.

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