BackgroundSeveral studies reported the efficacy of orthokeratology for myopia control. Somehow, there is limited publication with follow-up longer than 3 years. This study aims to research whether overnight orthokeratology influences the progression rate of the manifest refractive error of myopic children in a longer follow-up period (up to 12 years). And if changes in progression rate are found, to investigate the relationship between refractive changes and different baseline factors, including refraction error, wearing age and lens replacement frequency. In addition, this study collects long-term safety profile of overnight orthokeratology.MethodsThis is a retrospective study of sixty-six school-age children who received overnight orthokeratology correction between January 1998 and December 2013. Thirty-six subjects whose baseline age and refractive error matched with those in the orthokeratology group were selected to form control group. These subjects were followed up at least for 12 months. Manifest refractions, cycloplegic refractions, uncorrected and best-corrected visual acuities, power vector of astigmatism, corneal curvature, and lens replacement frequency were obtained for analysis.ResultsData of 203 eyes were derived from 66 orthokeratology subjects (31 males and 35 females) and 36 control subjects (22 males and 14 females) enrolled in this study. Their wearing ages ranged from 7 years to 16 years (mean ± SE, 11.72 ± 0.18 years). The follow-up time ranged from 1 year to 13 years (mean ± SE, 6.32 ± 0.15 years). At baseline, their myopia ranged from −0.5 D to −8.0 D (mean ± SE, −3.70 ± 0.12 D), and astigmatism ranged from 0 D to −3.0 D (mean ± SE, −0.55 ± 0.05 D). Comparing with control group, orthokeratology group had a significantly (p < 0.001) lower trend of refractive error change during the follow-up periods. According to the analysis results of GEE model, greater power of astigmatism was found to be associated with increased change of refractive error during follow-up years.ConclusionsOvernight orthokeratology was effective in slowing myopia progression over a twelve-year follow-up period and demonstrated a clinically acceptable safety profile. Initial higher astigmatism power was found to be associated with increased change of refractive error during follow-up years.

Lymph node ratio significantly decreases the stage migration caused by inadequate examined lymph nodes. The advantage of TNrM was validated with a patient cohort from the Eastern medical center.

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Mesenchymal stem cell (MSC) therapy has been investigated intensively for many years. However, there is a potential risk related to MSC applications in various cell niches. Methods: The safety of intravitreal MSC application and the efficacy of MSC-derived conditioned medium (MDCM) were evaluated in the normal eye and the diseased eye, respectively. For safety evaluation, the fundus morphology, visual function, retinal function, and histological changes of the retina were examined. For efficacy evaluation, the MDCM was intravitreally administrated in a rodent model of anterior ischemic optic neuropathy (rAION). The visual function, retinal ganglion cell (RGC) density, and neuroinflammation were evaluated at day 28 post-optic nerve (ON) infarct. Results: The fundus imaging showed that MSC transplantation induced retinal distortion and venous congestion. The visual function, retinal function, and RGC density were significantly decreased in MSC-treated eyes. MSC transplantation induced astrogliosis, microgliosis, and macrophage infiltration in the retina due to an increase in the HLA-DR-positive MSC proportion in vitreous. Treatment with the MDCM preserved the visual function and RGC density in rAION via inhibition of macrophage infiltration and RGC apoptosis. Conclusions: The vitreous induced the HLA-DR expression in the MSCs to cause retinal inflammation and retina injury. However, the MDCM provided the neuroprotective effects in rAION.