Repeatability and Agreement of Central Vault for Implantable Collamer Lens Obtained by the Tomey OA-2000 Biometer and Spectralis OCT.

Objective: To assess repeatability and agreement of central vault for implantable collamer lens (ICL) measured by the Tomey OA-2000 biometry and Spectralis optical coherence tomography (OCT). Methods: In this prospective study, the central vault was measured by the Tomey OA-2000 biometer and Spectralis OCT in 84 eyes (43 patients) after ICL implantation at six month follow-up. Three consecutive scans were obtained by one experienced technician using Tomey OA-2000 and the Spectralis OCT in the same day. The coefficient of variation (CoV), intraclass correlation coefficient (ICC), within-subject standard deviation (Sw), and 2.77 Sw were calculated to assess the repeatability and reproducibility. The paired t-test and Bland-Altman plots were used to analyze the differences and agreements of central vault measured by two devices. Results: Repeatability of the central vault measured by Tomey OA-2000 biometer and Spectralis OCT showed that the CoV was 2.71% and 1.66%, respectively. The ICC for both devices was 0.996 and 0.999, respectively. The paired t-test showed that central vault measured by Tomey OA-2000 biometer was -7.25 ± 23.57 microns lower than that measured by Spectralis OCT (P = 0.006). The mean difference between measurements for Tomey OA-2000 and ASM-OCT with 95% limits of agreement (LoAs) was -38.94 to 53.44 µm. Conclusion: Both Tomey OA-2000 biometer and Spectralis OCT displayed good repeatability for the measurement of central vault of ICL. Good reliability and agreement were observed between Tomey OA-2000 biometer and Spectralis OCT. Both instruments are useful but not replaced each other for central vault measurements.

The efficacy and safety of 0.01% atropine alone or combined with orthokeratology for children with myopia: A meta-analysis.

OBJECTIVE: To evaluate the efficacy and safety of 0.01% atropine alone and in combination with orthokeratology for myopia control using a meta-analysis. METHODS: PubMed, Cochrane Library, and EMBASE were searched. We included eligible randomized controlled trials (RCTs), non-RCTs, and retrospective cohort studies, published up to August 1, 2022. We calculated the weighted mean difference (WMD) and 95% confidence interval (CI) for all outcomes and plotted them in forest plots. RESULTS: Fourteen studies were included; 4 and 11 in the 0.01% atropine monotherapy and atropine-orthokeratology (AOK) groups, respectively. Compared with orthokeratology (OK) alone, 0.01% atropine alone had similar effects on slowing the axial elongation (WMD: -0.00 mm; 95% CI: -0.05-0.04, p<0.31), while AOK significantly lowered axial growth. Moreover, the baseline myopic degree and duration of treatment were influential for the change in axial elongation (WMD: -0.12 mm; 95% CI: -0.17--0.07, p = 0.00001 and WMD: -0.11 mm; 95% CI: -0.15--0.108, p<0.00001, respectively). Additionally, the AOK may reduce the change rate of the spherical equivalent refraction and the accommodation amplitude (WMD: -0.13 D; 95% CI: 0.07-0.19, p<0.001 and WMD: -1.08 mm; 95% CI: -1.73--0.43, p<0.0001, respectively), and cause a slight increase in the diameter of the pupil (WMD: 0.56 mm; 95% CI: 0.43-0.70, p = 0.007). No significant differences in the uncorrected distant visual acuity, best corrected visual acuity, intraocular pressure, tear film break-up time, lipid layer thickness, and corneal endothelial cell density were found between the OK and AOK groups. CONCLUSION: In slowing the axial elongation, 0.01% atropine alone and OK alone have similar effects, while AOK is more effective than OK alone in slowing down the axial elongation. Furthermore, the baseline degree of myopia and treatment duration may affect changes in axial elongation.

Posterior corneal elevation changes during 12 month of overnight orthokeratology.

Aims: the aim of this study to investigate the elevation changes in posterior corneal surface after 12 months of orthokeratology (ortho-k) treatment. Methods: In this retrospective chart review, medical records of 37 Chinese children who wore ortho-k lenses over 12 months were reviewed. The data of only right eye were analyzed. Variables including the flat and steep keratometry of anterior and posterior corneal principal meridians, central corneal thickness (CCT), posterior thinnest elevation of cornea (PTE), posterior central elevation of cornea (PCE) and posterior mean elevation of cornea (PME) were measured by Pentacam. Variables including anterior chamber depth (ACD), lens thickness (CLT) and ocular axis length (AL) were measured by optical biometry. All variables differences between baseline and 12 months after ortho-k treatment were assessed by statistical analyses. Results: The average age of all subjects was 10.70 ± 1.75 years (range 8-15 years old). The baseline spherical equivalent (SE) was -3.26 ± 1.52 D (-0.50D to -5.00D). Both flat and steep keratometry of anterior corneal surface and CCT were significantly decreased after 12 month follow up during ortho-k treatment (both P < 0.000). Both flat and steep keratometry of posterior corneal surface were not significantly different after 12 month follow up compared with that of baseline (P = 0.426, 0.134 respectively). PCE, PTE and PME were not significantly changed over 12 months of ortho-k treatment (P = 0.051, 0.952 and 0.197 respectively). The ACD was significantly decreased in 12 month follow up during ortho-k treatment (P = 0.001). The CLT and the AL were significantly increased during this period (both P < 0.000). Conclusion: Although the anterior corneal surface was significantly changed by ortho-k lens, the posterior corneal surface did not show any changes during 12 months follow up. Simultaneously, The ACD, CLT and AL were significantly changed during this period.

Poly(ADP-Ribose) Polymerase 1: Cellular Pluripotency, Reprogramming, and Tumorogenesis.

Poly(ADP-ribos)ylation (PARylation) is the catalytic function of the Poly(ADP-ribose) polymerases (Parps) family for post-translational modification in cellular process. Being a major member of Parps, Parp1 is a crucial nuclear factor with biological significance in modulating DNA repair, DNA replication, transcription, DNA methylation and chromatin remodeling through PARylation of downstream proteins. In addition, high expression level and activity of Parp1 are correlated with pluripotent status, reprogramming, and cancer. Furthermore, epigenetic modulation of Parp1 is explored for regulating wide variety of gene expression. Genetic and pharmaceutical disruption of Parp1 further confirmed the importance of Parp1 in cell growth, DNA repair, and reprogramming efficiency. Taken together, the proximity toward the understanding of the modulation of Parp1 including interaction and modification in different fields will provide new insight for future studies. In this review, the biological significance of Parp1 in transcription and the epigenetic modulation of Parp1 in pluripotent status, reprogramming process and cancer will be summarized.

CHD1L Regulated PARP1-Driven Pluripotency and Chromatin Remodeling During the Early-Stage Cell Reprogramming.

PARP1 and poly(ADP-ribosyl)ation (PARylation) have been shown to be essential for the initial steps of cellular reprogramming. However, the mechanism underlying PARP1/PARylation-regulated activation of pluripotency loci remains undetermined. Here, we demonstrate that CHD1L, a DNA helicase, possesses chromatin remodeling activity and interacts with PARP1/PARylation in regulating pluripotency during reprogramming. We found that this interaction is mediated through the interplay of the CHD1L macro-domain and the PAR moiety of PARylated-PARP1. Chromatin immunoprecipitation assays demonstrated the co-occupancy of CHD1L and PARP1 at Pou5f1, Nanog, and Esrrb pluripotency loci. Knockdown of CHD1L significantly blocked the binding activity of PARP1 at pluripotency loci and inhibited the efficiency of PARP1-driven reprogramming. Notably, we found that CHD1L-promoted reprogramming requires both a PARP1-interacting domain and DNA helicase activity, partly contributing to the chromatin-remodeling states of pluripotency loci. Taken together, these results identify CHD1L as a key chromatin remodeler involved in PARP1/PARylation-regulated early-stage reprogramming and pluripotency in stem cells.

Targeting autophagy enhances BO-1051-induced apoptosis in human malignant glioma cells.

PURPOSE: BO-1051 is an N-mustard derivative that is conjugated with DNA-affinic 9-anilinoacridine. Since BO-1051 was reported to have strong anticancer activity, we investigated the effect and underlying mechanism of BO-1051 in human glioma cell lines. METHODS: Human glioma cell lines U251MG and U87MG were studied with BO-1051 or the combination of BO-1051 and autophagic inhibitors. Growth inhibition was assessed by MTT assay. Apoptosis was measured by annexin V staining followed by flow cytometry and immunoblotting for apoptosis-related molecules. Induction of autophagy was detected by acridine orange labeling, electron microscopy, LC3 localization and its conversion. Transfection of shRNA was used to determine the involvement of Beclin1 in apoptotic cell death. RESULTS: MTT assay showed that BO-1051 suppressed the viability of four glioma cell lines (U251MG, U87MG, GBM-3 and DBTRG-05MG) in a dose-dependent manner. The IC(50) values of BO-1051 for the glioma cells were significantly lower than the values for primary neurons cultures and normal fibroblast cells. Moreover, BO-1051 not only induced apoptotic cell death, but also enhanced autophagic flux via inhibition of Akt/mTOR and activation of Erk1/2. Importantly, suppression of autophagy by 3-methyladenine or bafilomycin A1 significantly increased BO-1051-induced apoptotic cell death in U251MG and U87MG cells. In addition, the proportion of apoptotic cells after BO-1051 treatment was enhanced by co-treatment with shRNA against Beclin1. CONCLUSIONS: BO-1051 induced both apoptosis and autophagy, and inhibition of autophagy significantly augmented the cytotoxic effect of BO-1051. Thus, a combination of BO-1051 and autophagic inhibitors offers a potentially new therapeutic modality for the treatment of malignant glioma.