RESUMEN
Purpose: To determine the distribution and characteristics of peripheral refraction in adults with myopia using the novel multispectral refraction topography. Method: A total of 187 adults with myopia were recruited for this study. This study was conducted in two stages. Part I: participants were divided into 6 groups based on the central refraction of the right eyes, Part II: according to the interocular differences in refractive error (IOD) of the central refraction, we divided the participants into isomyopia group (IOD<1.00 D) and anisomyopia group (IOD≥1.0 D). We surveyed the characteristics of peripheral refraction and relative peripheral refraction (RPR), as well as the correlation between RPR and central refraction, age, sex, and axial length. Result: Part I: With an increase in the degree of myopia, relative peripheral hyperopia developed from the center to the periphery. A statistically significant hyperopia shift compared to the center (P < 0.05) was first observed on the temporal side within a 40° field of view at the posterior pole of the retina. The RPR of the temporal, superior, and inferior retinas positively correlated only with age. Part II: In the isomyopic participants, there was no difference in peripheral refraction between the eyes (P < 0.05). In the anisomyopic participants, the RPR of the more myopic eyes was more hyperopic than that of the less myopic eyes in NRDV40-50, SRDV10-20, SRDV30-50, TRDV20-30, TRDV40-50, and IRDV10-40. Conclusion: With an increase in the degree of myopia, relative peripheral hyperopia developed from the center to the periphery, and peripheral refraction progressed at different rates in various retinal zones.
RESUMEN
Recent studies implicate the defects or altered expression of the orphan nuclear receptor Nurr1 gene in the substantia nigra in Parkinson's disease pathogenesis. In an attempt to corroborate the treatment-modifying disease that would replicate the effect of Nurr1, it has been found that amodiaquine and Nurr1 had the same chemical scaffolding, indicating a crucial structure-activity relationship. Interestingly, amodiaquine stimulate the transcriptional function of Nurr1 by physical interaction with its ligand-binding domain (LBD). However, the signaling route by which Nurr1 is activated by amodiaquine to cause the protective effect remains to be elucidated. We first demonstrated that amodiaquine treatment ameliorated behavioural deficits in 6-OHDA Parkinson's disease mouse model, and it promoted dopaminergic neurons protection signified by Tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA; Tyrosine hydroxylase (TH) protein expression level and the immunoreactivity in the substantia nigra compacta. Subsequently, we used inhibitors to ascertain the effect of amodiaquine on Akt and P38 Mapk as crucial signaling pathways for neuroprotection. Wortmannin (Akt Inhibitor) induced a significant reduction of Akt mRNA; however, there was no statistical difference between the amodiaquine-treated group and the control group suggesting that amodiaquine may not be the active stimulant of Akt. Western blot analysis confirmed that the phosphorylated Akt decreased significantly in the amodiaquine group compared to the control group. In the same vein, we found that amodiaquine substantially increased the level of phosphorylated P38 Mapk. When P38 Mapk inhibited by SB203580 (P38-Mapk Inhibitor), the total P38 Mapk but not the phosphorylated P38 Mapk decreased significantly, while tyrosine hydroxylase significantly increased. These results collectively suggest that amodiaquine can augment tyrosine hydroxylase expression via phosphorylated P38 Mapk while negatively regulating the phosphorylated Akt in protein expression.
