Purpose To determine clinical characteristics and identify factors associated with better visual outcomes in patients who had vitrectomy for vitreous haemorrhage (VH) associated with Terson syndrome (TS). Methods The records of 48 patients (54 corresponding eyes) who underwent vitrectomy for VH associated with TS from January 2008 to December 2017 were retrospectively reviewed. The main outcome measure was the final postoperative visual acuity.Results At the last visit, 34 eyes (63.0%) achieved a BCVA of 0.3 or better. Eyes associated with traumatic brain injury had a better visual outcome than those with primary intracerebral haemorrhage (P = 0.042). In the primary intracerebral haemorrhage group, patients with hypertension-induced intracranial haemorrhage (IH) showed poorer final visual acuities than the ruptured intracranial aneurysm group (P = 0.023). In the delayed vitrectomy group, epiretinal membrane and peripheral retina changes were more common (P < 0.05). However, the difference in final visual acuity between the early and delayed vitrectomy groups was not significant (P = 0.69). Conclusion Most of the patients obtained visual recovery after vitrectomy for TS. VH associated with ruptured intracranial aneurysm or traumatic brain injury or eyes without retinal haemorrhage are predictive of better prognosis. Although the timing of vitrectomy was not related to the final postoperative visual outcome, early vitrectomy by three months seems to suggest less epiretinal membrane formation, retinal tears, and retinal detachments.
Since DNA damage is a first incident occurred during a tumour attack, it is rational that histone H2A.X phosphorylation on tyrosine 39 (H2A.X Y39ph) may act as a tumour-relevant factor. This study was aimed to test the authenticity of the hypothesis. Uveal melanoma MP65 cells were transfected for expression of KRas mutated. H2A.X phosphorylation and ERK1/2 was measured, and transwell experiment was performed to examine the consequents of H2A.X Y39ph on MP65 cells developing and migration. Regulatory relationship between H2A.X Y39ph and ERK1/2 downstream genes were measured. Moreover, whether JMJD6 and MDM2 are involved in H2A.X phosphorylation was studied. Mutation of Ras activated ERK1/ 2 signalling and inhibited H2A.X phosphorylation at Y39. Silence of H2A.X Y39ph contributed to the regulation of MP65 cells growth, migration and transcription of ERK1/2 downstream genes, including CYR61, IGFBP3, WNT16B, NT5E, GDF15 and CARD16. The repressed H2A.X phosphorylation through Ras-ERK1/2 signalling might be through MDM2-mediated JMJD6 degradation. Our study suggested that Ras-ERK1/2 signalling inhibited H2A.X phosphorylation at Y39, which led to the uncontrolled developing and migration of uveal melanoma cells. In addition, H2A.X phosphorylation was mediated possibly through JMJD6 which could be degraded by MDM2.
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