Scleral Fixated Secondary IOLs: An Outcomes Comparison Between the Yamane and Gore-Tex-Sutured Techniques.

BACKGROUND AND OBJECTIVE: Among secondary intraocular lens (IOL) techniques, scleral fixated IOLs (SFIOLs) offer advantages in cases without capsular support. In this article, we compare outcomes between two types of Gore-Tex scleral sutured IOLs with the Yamane technique. PATIENTS AND METHODS: This study was a retrospective chart review of patients who underwent SFIOL implantation. RESULTS: Analysis revealed a statistically significant improvement in final postoperative visual acuity (VA) for sutured SFIOLs (P < 0.001, Envista (n = 29) 95% CI 0.47 to 1.04, Akreos (n = 23) 95% CI 0.32 to 0.81) with no statistical improvement in the Yamane group (P = 0.44, n = 15, 95% CI -0.33 to 0.71). Outcomes analysis revealed greater incidences of cystoid macular edema (CME) in the Yamane cohort (P < 0.05) and a higher rate of reoperations in the Akreos cohort (P < 0.02). All complications related to suture material (n = 4) and IOL decentration (n = 2) occurred in the sutured SFIOL group. CONCLUSIONS: The sutureless Yamane technique offered fewer subsequent surgeries and suture-specific complications while revealing diminished VA improvement in long-term follow-up compared to the sutured SFIOLs. [Ophthalmic Surg Lasers Imaging Retina 2024;55:384-390.].

A novel manganese-dependent ATM-p53 signaling pathway is selectively impaired in patient-based neuroprogenitor and murine striatal models of Huntington's disease.

The essential micronutrient manganese is enriched in brain, especially in the basal ganglia. We sought to identify neuronal signaling pathways responsive to neurologically relevant manganese levels, as previous data suggested that alterations in striatal manganese handling occur in Huntington's disease (HD) models. We found that p53 phosphorylation at serine 15 is the most responsive cell signaling event to manganese exposure (of 18 tested) in human neuroprogenitors and a mouse striatal cell line. Manganese-dependent activation of p53 was severely diminished in HD cells. Inhibitors of ataxia telangiectasia mutated (ATM) kinase decreased manganese-dependent phosphorylation of p53. Likewise, analysis of ATM autophosphorylation and additional ATM kinase targets, H2AX and CHK2, support a role for ATM in the activation of p53 by manganese and that a defect in this process occurs in HD. Furthermore, the deficit in Mn-dependent activation of ATM kinase in HD neuroprogenitors was highly selective, as DNA damage and oxidative injury, canonical activators of ATM, did not show similar deficits. We assessed cellular manganese handling to test for correlations with the ATM-p53 pathway, and we observed reduced Mn accumulation in HD human neuroprogenitors and HD mouse striatal cells at manganese exposures associated with altered p53 activation. To determine if this phenotype contributes to the deficit in manganese-dependent ATM activation, we used pharmacological manipulation to equalize manganese levels between HD and control mouse striatal cells and rescued the ATM-p53 signaling deficit. Collectively, our data demonstrate selective alterations in manganese biology in cellular models of HD manifest in ATM-p53 signaling.