To establish percentile curves of refractive development for children and adolescents aged 5–18y in Hubei Province.

A cross-sectional study was conducted in 103 county-level administrative districts of Hubei Province via a multistage stratified cluster sampling strategy. Participants underwent non-cycloplegic autorefraction, and spherical equivalent refraction (SER) of the right eye was calculated. Generalized additive models for location, scale, and shape (GAMLSS) were applied to construct age-specific standard SER percentile curves stratified by gender and region. Moreover, age-related curves of annual refractive progression rate at each percentile were plotted.

A total of 1255454 participants (673341 boys and 582113 girls) aged 5–18y (mean age: 11.13±3.59y) were enrolled. An overall myopic shift trend was observed with advancing age. The median SER was +0.25 diopters (D) at 5 years of age and decreased to -0.50 D at 9 years of age. From 5 to 18 years of age, the refractive progression was -6.63 D at the 3rd percentile, while the values were -3.25 D and -1.00 D at the 50^th and 97^th percentiles, respectively. Girls and rural children presented higher myopic degrees. The annual age-dependent refractive progression rate curve showed a U-shaped pattern, with greater annual refractive changes in lower percentiles and peak refractive progression occurring at younger ages.

Children in lower SER percentiles suffer from more severe myopia and faster refractive progression. Therefore, earlier and targeted intensive myopia interventions are warranted for children with SER below the 50^th percentile.

To compare the effect of orthokeratology (OK) and defocus incorporated multiple segment (DIMS) lenses on axial length (AL) elongation in bilateral myopic anisometropic children.

This retrospective study enrolled bilateral myopic anisometropic children categorized into two groups: OK lenses and DIMS lenses. The eyes with more myopia (MM) were divided into MM eyes and the fellow eyes with less myopia (LM) into LM eyes. According to the myopia degree in MM eyes, the subjects were further assigned to -0.50 to -3.00 D subgroup and -3.25 to -6.00 D subgroup. The t-test was used to analyze the changes in AL elongation between groups and AL differences in both eyes, and the relationship between AL changes and baseline data was evaluated by Pearson linear correlation analysis.

Totally 202 children (8-14y) were divided into OK group with mean age 10.97±1.91y (46 males and 50 females) and DIMS group with mean age 11.05±2.06y (58 males and 48 females). After 1y, the changes of AL in OK-MM eyes (0.14±0.18 mm) were significantly slower than that in OK-LM eyes (0.20±0.19 mm) and DIMS-MM eyes (0.19±0.18; P<0.001, P=0.037). The OK-LM eyes and DIMS-LM eyes, DIMS-MM eyes and DIMS-LM eyes showed no statistically significant difference in AL changes (P=0.337, 0.381). In the -0.50 to -3.00 D subgroups, DIMS-LM eyes had better effect of AL control than OK-LM eyes, the changes of AL in OK-MM eyes and DIMS-MM eyes were no statistically significant. In the -3.25 to -6.00 D subgroups, the results were similar in total group. The change of AL in four subgroups was negatively correlated with age (P<0.05).

OK lens can reduce binocular anisometropia; DIMS lens has similar effect on the control of binocular myopia in children with myopic anisometropia. The OK lenses are more effective than DIMS lenses with higher degrees of myopia, while DIMS lens retard AL elongation more effectively than OK lens when the spherical equivalent refraction of MM eyes is lower than -3.00 D.

To explore the causal links among circulating inflammatory proteins (CIPs) and the varying severities of diabetic retinopathy (DR).

This research utilized a two sample Mendelian randomization (MR) approach to explore the causal relationships between 91 CIPs and various severities of DR: background DR (BDR) or non-proliferative DR (NPDR), and proliferative DR (PDR). Single-nucleotide polymorphisms (SNPs) related to the 91 CIPs as exposure factors were identified. These SNPs were selected from an extensive genome-wide association study (GWAS) analyzing large genomic datasets. Genetic variation data of various DR phenotypes provided by the FinnGen collaboration were utilized as outcomes. Inverse-variance weighting (IVW) was used as the main MR analysis. Robustness of study results was evaluated through a series of sensitivity analyses, employing the MR-pleiotropy-test and mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) to confirm the absence of pleiotropy.

In a bidirectional MR analysis, we uncovered a complex relationship between CIPs and DR. Elevated levels of tumor necrosis factor ligand superfamily member 14 (TNFSF14), latency associated peptide transforming growth factors beta-1 (LAP-TGF-beta1), interleukin-10 (IL-10), and vascular endothelial growth factor A (VEGF-A) were associated with a reduced risk of NPDR. Conversely, elevated levels of fibroblast growth factor 23 (FGF-23) were associated with an increased risk of NPDR. Concentrations of adenosine deaminase (ADA), matrix metalloproteinase-10 (MMP-10), eotaxin, and IL-10 showed elevated levels and were linked to a reduced risk of NPDR. On the other hand, the levels of oncostatin-M, beta-nerve growth factor (β-NGF), and interleukin-7 (IL-7) were elevated and associated with an increased risk of SNPDR. Elevated levels of ADA, MMP-10, and macrophage colony-stimulating factor 1 (CSF1) were linked to a lower likelihood of PDR. Conversely, elevated levels of Caspase 8 and glial cell line-derived neurotrophic factor (GDNF) were associated with an increased risk of PDR. In reverse MR analysis, DR affected the expression of these factors.

Our research demonstrates evidence supporting a potential causal link between key inflammatory factors and the risk and prognosis of various DR phenotypes. These findings emphasize the regulation of inflammatory factors responses as a strategic approach for preventing and managing DR. Altogether, our results validate the pathogenic role of inflammatory factors dysregulation in DR and support the rationale for exploring immunotherapeutic targets further.