Purpose: To investigate changes in subfoveal choroidal thickness (SFChT) during orthokeratology (Ortho-K) lens wear and after its cessation and the association of short-term change in SFChT with the long-term eye elongation in Ortho-K subjects. Design: A prospective clinical trial. Methods: Fifty myopic children aged between 9 and 14 years were enrolled. Twenty-nine subjects continuously wore Ortho-K lens for 12 months and discontinued for 1 month. Twenty-one subjects wearing single vision distance spectacles for 12 months were included as the control group. SFChT was assessed using optical coherence tomography. Ocular parameters, including axial length (AL), central corneal thickness (CCT), anterior chamber depth (ACD), lens thickness (LT) and apical corneal power (ACP), were also measured. Results: After 12 months of follow-up, AL elongation was larger and SFChT change was smaller in the control group compared to the Ortho-K group (both p < 0.001). In the Ortho-K group, SFChT increased by 16 lm from baseline at the 1-month visit (p < 0.001), and the magnitude of choroidal thickening remained unchanged at the 6-and 12-month visit (p = 0.289). One month after discontinuation of Ortho-K lens, SFChT and ocular parameters of the anterior segment, including ACP, CCT and ACD recovered to baseline level (All p > 0.05), and AL increased by 0.23 AE 0.18 mm compared to baseline (p = 0.018). SFChT change at 1-month was negatively associated with AL change at 13-month (standard b, À0.581, p = 0.001) after adjusting for other influencing factors, including baseline age and the ocular parameters. Conclusion: Subfoveal ChT (SFChT) significantly increased after short-term Ortho-K lens treatment and the increase maintained throughout the period of treatment. One month after Ortho-K lens cessation, SFChT, ACP, CCT and ACD returned to baseline. Short-term response in SFChT is associated with long-term change in AL in children undergoing Ortho-K lens and may be a predictor for the effectiveness of the treatment.
To evaluate the features of the choroidal structures in the eyes of myopic children obtained by enhanced depth imaging optical coherence tomography (EDI-OCT). METHODS. Ninety-six myopic children with low to moderate myopia (spherical equivalent refractive error [SER],-5.75 to-1.00 diopter) were included in this cross-sectional study. Ocular biometrics were measured using an optical low-coherence reflectometry device. Data of the choroidal structures extracted from a 7500-μm cross-sectional arc of the choroid extending from the temporal optic disc margin, including the total choroidal area, luminal area, stromal area, and choroidal vascularity index, were determined by image binarization of the EDI-OCT. Associations between demographic factors, ocular parameters, and choroidal structures were evaluated using univariate and multiple linear regression analyses. RESULTS. The study participants (mean age, 11.02 ± 1.70 years) had a mean axial length (AL) of 24.94 ± 0.70 mm. The mean total choroidal area was 2.64 ± 0.49 mm 2 (luminal area, 1.68 ± 0.32 mm 2 ; stromal area, 0.95 ± 0.19 mm 2), and the choroidal vascularity index was 0.64 ± 0.03. Multiple regression analysis showed that the luminal area was significantly associated with the AL (standard β =-0.24, P = 0.022) after adjusting for sex and corneal radius (CR), whereas the stromal area (standard β =-0.30, P = 0.003) and choroidal vascularity index (standard β = 0.36, P = 0.001) were significantly associated with age after adjusting for sex, CR, and lens thickness (LT). Sex, CR, LT, and SER showed no significant association with choroidal structures after adjusting for age and AL (all P > 0.05). CONCLUSIONS. The luminal area of the choroid tends to decrease with a longer AL, whereas the stromal area tends to decrease with increasing age in myopic children. These findings require further exploration in a longitudinal study.
Background: Long noncoding RNAs (lncRNAs) have been shown to participate in multiple biological processes and confer drug resistance. However, it remains unclear whether lncRNAs are involved in conferring cetuximab resistance in colorectal cancer (CRC) cells.Methods: Cell Counting Kit-8 (CCK-8) assays were performed to assess the sensitivity of CRC cell lines to cetuximab treatment. -2 cells were stably transduced with cetuximab resistance-associated RNA transcript 16 (CRART16) or an empty vector using lentiviral infection; the cells were designated Caco-2-CRART16 and Caco-2-NC, respectively, and were analyzed with RNA sequencing (RNA-seq). Quantitative real-time PCR (qRT-PCR) was performed to investigate RNA expression. Flow cytometry and TUNEL assays were used to assess apoptosis levels induced by cetuximab. The cell cycle, stemness biomarkers and membrane proteins of CRC cells were assessed via flow cytometry. RNA fluorescence in situ hybridization (FISH) was used to examine CRART16 localization and expression. Bioinformatics analysis was performed to predict the potential mechanism of CRART16, which was further validated by a dual-luciferase reporter assay. Differences in measurement data were compared using Student's t test, one-way ANOVA followed by Dunnett's test and two-way ANOVA.
1 Extracellular ATP is a potent signaling molecule that modulates a myriad of cellular functions through the activation of P2 purinergic receptors and is cytotoxic to a variety of cells at higher concentrations. The mechanism of ATP-elicited cytotoxicity is not fully understood. In this study, we investigated the effect of extracellular ATP on the human hepatoma Li-7A cells. 2 We observed a time-and dose-dependent growth inhibition of Li-7A cells by ATP, which is accompanied by an increase in the active form of caspase-3 as well as increased cleavage of its substrate, poly (ADP-ribose) polymerase. The cytotoxic effect of extracellular ATP was not mediated by the P2X 7 receptor, since (1) the effect was not abolished by the P2X 7 receptor antagonists oxidized ATP and KN-62, and (2) extracellular ADP, AMP, and adenosine were also cytotoxic. 3 We found that ATP and ADP were degraded to adenosine by Li-7A cells and that treatment of Li-7A cells by adenosine resulted in growth inhibition and caspase-3 activation, indicating that adenosine is the apoptotic agent. Using adenosine receptor agonists and antagonists, as well as inhibitors of adenosine transport and deamination, we showed that the cytotoxic effect of adenosine is specifically mediated by the A3 receptor even though transcripts of A1, A2 A , A2 B , and a splice variant of the P2X 7 receptors were detected in Li-7A cells by RT -PCR. 4 Cytotoxicity caused by exogenous ATP and adenosine was completely abolished by the caspase-3 inhibitor Z-DEVD-FMK, demonstrating the central role of caspase-3 in apoptosis of Li-7A cells.
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