Changes in ocular biological parameters after cycloplegia based on dioptre, age and sex.

The effects of cycloplegia on ocular biological parameters in children have been extensively studied, but few studies have compared these parameters between different refractive states, ages, and sexes. Therefore, the purpose of this study was to investigate the changes in ocular biometry before and after cycloplegia in different groups based on dioptre, age and sex. We examined a total of 2049 participants in this cross-sectional study. A comprehensive eye examination was conducted before cycloplegia. Cycloplegia was implemented with the application of atropine or tropicamide. Ocular biological parameters were evaluated after cycloplegia, including axial length (AL), mean keratometry (K), flat keratometry (K1), steep keratometry (K2), central corneal thickness (CCT), anterior chamber depth (ACD) and white-to-white (WTW) distance. All the participants were categorized based on dioptre, age and sex. Statistical analysis was performed with paired t tests and Wilcoxon signed-rank tests. Regarding dioptre, AL was found to be increased significantly in the Fs, Ast and FA (p < 0.05) postcycloplegia groups. We observed significant increases in K, K1, K2 and ACD in the Fs group (p < 0.05) after cycloplegia. Regarding age, we found significant increases in AL, CCT and ACD in group 1 (p < 0.05), but AL decreased significantly in groups 2 and 3 (p < 0.05) postcycloplegia. There were no significant changes found in K, K1 and K2 in the three groups after cycloplegia (p > 0.05). Regarding sex, AL and WTW were found to decrease significantly among males and increase significantly among females (p < 0.05) postcycloplegia, while K, K1 and K2 showed the opposite trends. This study showed that there were differences in some ocular biological parameters after cycloplegia across different groups; in particular, there were significant differences in AL, CCT and ACD. Attention should be devoted to the influence of cycloplegia in clinical work.

MiR-181a reduces radiosensitivity of non-small-cell lung cancer via inhibiting PTEN.

BACKGROUND: The aim of this study is to explore the effect of micro ribonucleic acid (miR)-181a on the radiosensitivity of non-small cell lung cancer (NSCLC) and its potential mechanism of action. METHODS: The differentially expressed miRNAs were screened in lung cancer tissues of radiotherapy-resistant and non-radiotherapy-resistant NSCLC patients, and verified via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Next, the effects of different miRNA expressions on patients' survival time were discussed, and target genes of miR-181a were predicted. The effect of miR-181a expression on radiosensitivity was determined using cell counting kit-8 (CCK-8) assay and flow cytometry. The direct target of miR-181a was verified via luciferase reporter assay. Phosphatase and tensin homolog deleted on chromosome ten (PTEN) was overexpressed using lentiviruses, and then whether miR-181a reduces radiosensitivity via targeting PTEN was detected via CCK-8 assay and flow cytometry. Finally, Western blotting was performed to detect the protein expression of PTEN. RESULTS: The screening results of microarray expression profile assay revealed that 15 miRNAs had significant differences in lung cancer tissues of radiotherapy-resistant NSCLC patients compared with those in non-radiotherapy-resistant NSCLC patients. The results of RT-qPCR showed that hsa-miR-181a, hsa-miR-199b, hsa-miR-489 and hsa-miR-589 were significantly up-regulated in the lung cancer tissues of radiotherapy-resistant NSCLC patients compared with those in non-radiotherapy-resistant NSCLC patients. In addition, it was found that the survival time of NSCLC patients was obviously prolonged in hsa-miR-181a low-expression group and hsa-miR-589 high-expression group, but hsa-miR-489 and hsa-miR-199b had no significant influence on the survival time of NSCLC patients. According to KEGG enrichment analysis, the target genes of miR-181a were evidently enriched in the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (AKT) signaling pathway, NSCLC signaling pathway and other cancer signaling pathways. Under the radiation dose of 2, 4, 6 and 8 Gy, the survival rate of A549 cells rose in miR-181a mimic group, but declined in miR-181a inhibitor group. Moreover, compared with that in model group, the radiotherapy-induced apoptosis was markedly inhibited in miR-181a mimic group, but markedly promoted in miR-181a inhibitor group. It was also observed that the response of cells to radiotherapy-induced apoptosis was remarkably weakened in miR-181a mimic + PTEN overexpression group compared with that in miR-181a mimic group. Finally, miR-181a mimic group had a significantly lower protein expression of PTEN and significantly higher protein expressions of CXC chemokine receptor 4 (CXCR4), phosphorylated signal transducer and activator of transcription 3 (p-STAT3), p-AKT1 and p-mammalian target of rapamycin (mTOR) than model group, while miR-181a inhibitor group had the opposite protein expressions. The protein expressions of CXCR4, p-STAT3, p-AKT1 and p-mTOR were obviously lower in miR-181a mimic + PTEN overexpression group than those in miR-181a mimic group. CONCLUSIONS: MiR-181a reduces the radiosensitivity of NSCLC via inhibiting PTEN expression.