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Prenatal exposure to perfluoroalkyl substances (PFAS) has been reported to affect body weight from birth to childhood, but the results remain inconclusive. We investigated whether umbilical cord blood concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are associated with children’s risk trajectory for obesity. 600 children were randomly selected from the Hamamatsu Birth Cohort for Mothers and Children (HBC study) and their umbilical cord serum PFAS concentrations were quantified. Participants underwent BMI measurements at ages 1, 4, 10, 18, 24, 32, 40, 50, and 66 months. Growth curve modeling with random intercept was performed with standardized BMI as outcome variable. PFOS was negatively associated with standardized BMI (β = − 0.34; p = 0.01), with a marginally significant interaction with the child’s age (β = 0.0038; p = 0.08). PFOA was negatively associated with standardized BMI (β = − 0.26, 95% CI − 0.51, 0; p = 0.05), with a significant interaction with the child’s age (β = 0.005; p = 0.01). Stratified analysis by sex revealed that these effects were significant only among girls. Prenatal exposure to PFAS initially was associated with lower standardized BMI during infancy, but this effect dissipated over time and reversed in direction during later childhood. The effects of prenatal PFAS on higher standardized BMI is stronger in girls.

We investigated the anatomical differences in the choroidal structure between pregnant women in the first trimester of pregnancy and age-matched healthy nonpregnant women using enhanced depth imaging optical coherence tomography (EDI-OCT) and choroidal binarization analysis. The main parameters measured in the two study groups, namely, pregnant women in the first trimester and healthy nonpregnant women, were choroidal thickness and the choroidal luminal area. Binarization of the EDI-OCT images from each patient was performed, and the choroidal vascularity index (CVI) was calculated. The correlations between the baseline characteristics of the subjects and the CVI were investigated using linear mixed model analysis. As a result, there was no statistically significant difference in the mean age, best-corrected visual acuity, axial length, central retinal thickness, subfoveal choroidal thickness, systolic blood pressure (BP), or diastolic BP between the two study groups. Conversely, a significant difference was observed in the CVI (P = 0.012) between the two groups. The multivariate analysis identified a significant correlation between the CVI and the systolic BP (P = 0.0044, linear mixed test). Taken together, a larger choroidal luminal area was associated with a higher systolic BP, especially in the first trimester of pregnancy. Our findings may provide further insight into the choroidal changes that occur during pregnancy.

This study aimed to compare blue-on-yellow (B/Y) perimetry with white-on-white (W/W) perimetry in eyes with branch retinal vein occlusion (BRVO). The following measurements were performed in 29 eyes of 29 patients with resolved BRVO: W/W and B/Y perimetries using 10-2 test grid, retinal volume (RV) using optical coherence tomography (OCT), and vessel densities (VD) of the superficial capillary layer (VDs) and deep capillary layer (VDd) using OCT angiography (OCTA). First, the difference in the retinal sensitivity (RS) between BRVO-affected and unaffected areas was compared between RS_B/Y and RS_W/W in the parafoveal and extrafoveal areas. Moreover, the structure–function relationship between vessel density and RS was compared between B/Y and W/W perimetries (RS_B/Y and RS_W/W, respectively). The difference in RS between BRVO-affected and unaffected areas was significantly larger with RS_B/Y than with RS_W/W in both the parafoveal and extrafoveal areas. In the parafoveal area, VDs, VDd, and RV were significantly correlated with both RS_W/W and RS_B/Y. In contrast, in the extrafoveal area, only VDd was included in the optimal models. Our findings suggest that RS_B/Y more strongly reflects the anatomical structure and BRVO-affected area.

We investigated long-term treatment responses in patients with treatment-naïve polypoidal choroidal vasculopathy (PCV) undergoing photodynamic therapy (PDT) with intravitreal ranibizumab (IVR). The medical charts of 14 patients with treatment-naïve PCV who underwent PDT with IVR were retrospectively reviewed. Patients were followed up and treated with additional IVR for ≥3 years. Best-corrected visual acuity (BCVA), central foveal thickness (CFT), greatest linear dimension (GLD) on angiography, polyp regression and central choroidal thickness (CCT) were assessed. Associations between these functional or anatomic outcomes with age, baseline CCT, baseline GLD or choroidal vascular hyperpermeability (CVH) were investigated using univariate and multivariate analysis. Mean logMAR BCVA improved significantly at 3 years (0.34 ± 0.24 to 0.12 ± 0.29, p = 0.003). Greater BCVA improvement and longer time to first recurrence was significantly associated with CVH. Fewer number of IVR retreatment within 3 years was associated with thicker baseline CCT. Mean CCT significantly decreased at 3 years (217 ± 33 µm to 197 ± 48 µm, p = 0.003). Greater decrease of CCT was significantly associated both with greater number of IVR retreatment within 3 years and absence of CVH. These results showed that pachychoroid characteristics at baseline was associated long-term functional and anatomic outcomes in patients with treatment-naïve PCV who had undergone combination PDT and IVR.

Tributyltin (TBT), one of the organotin compounds, is a well-known environmental pollutant. In our recent study, we reported that TBT induces mitochondrial dysfunction, in human-induced pluripotent stem cells (iPSCs) through the degradation of mitofusin1 (Mfn1), which is a mitochondrial fusion factor. However, the effect of TBT toxicity on the developmental process of iPSCs was not clear. The present study examined the effect of TBT on the differentiation of iPSCs into the ectodermal, mesodermal, and endodermal germ layers. We found that exposure to nanomolar concentration of TBT (50 nM) selectively inhibited the induction of iPSCs into the ectoderm, which is the first step in neurogenesis. We further assessed the effect of TBT on neural differentiation and found that it reduced the expression of several neural differentiation marker genes, which were also downregulated by Mfn1 knockdown in iPSCs. Taken together, these results indicate that TBT induces developmental neurotoxicity via Mfn1-mediated mitochondrial dysfunction in iPSCs.

Smoking is a major cause of respiratory conditions. To date, the genetic pleiotropy between smoking behavior and lung function/chronic obstructive pulmonary disease (COPD) have not been systematically explored. We leverage large data sets of smoking behavior, lung function and COPD, and addressed two questions, (1) whether the genetic predisposition of nicotine dependence influence COPD risk and lung function; and (2) the genetic pleiotropy follow causal or independent model. We found the genetic predisposition of nicotine dependence was associated with COPD risk, even after adjusting for smoking behavior, indicating genetic pleiotropy and independent model. Two known nicotine dependent loci (15q25.1 and 19q13.2) were associated with smoking adjusted lung function, and 15q25.1 reached genome-wide significance. At various suggestive p-value thresholds, the smoking adjusted lung function traits share association signals with cigarettes per day and former smoking, substantially greater than random chance. Empirical data showed the genetic pleiotropy between nicotine dependence and COPD or lung function. The basis of pleiotropic effect is rather complex, attributable to a large number of genetic variants, and many variants functions through independent model, where the pleiotropic variants directly affect lung function, not mediated by influencing subjects’ smoking behavior.