Optical Intensities of Different Compartments of Subretinal Fluid in Acute Vogt-Koyanagi-Harada Disease

<div><p>Purpose</p><p>To investigate the optical intensity in different compartments of subretinal fluid in acute Vogt-Koyanagi-Harada (VKH) disease by using spectral domain optical coherence tomography (SD-OCT).</p><p>Methods</p><p>Fifty acute VKH eyes and 25 cases with acute central serous chorioretinopathy (CSCR) were included in this retrospective comparative study. The optical intensities of subretinal fluid, vitreous humour and the entire scanned region displayed by SD-OCT were measured with Image J by three independent readers. In the VKH eyes with subretinal septa, the subretinal fluid was segmented into two types of compartments, supra-septa space and sub-septa space. Optical intensity ratios of different compartments of subretinal fluids divided by vitreous humour or the entire scanned region were compared.</p><p>Results</p><p>The measurement of optical intensity was highly reproducible (intraclass correlation coefficient> 0.9). The optical intensity of the supra-septa space divided by the vitreous humour was significantly higher compared to that of sub-septa space in VKH (mean difference = 4.27 ± 5.15, p <0.001). The optical intensity ratio of the supra-septa space (1.14 ± 0.12), but not subsepta space (1.05 ± 0.05) in VKH, was significantly higher compared to that of the subretinal space in VKH without the subretinal septa (1.07 ± 0.08), and the subretinal fluid in CSCR (1.08 ± 0.09). Similar results were found for the optical intensity ratios divided by the entire scan region.</p><p>Conclusion</p><p>The optical intensity in the supra-septa space of VKH is higher compared to the sub-septa space in VKH, subretinal space in VKH and CSCR, suggesting that the components in these spaces are different.</p></div

Repeatability and reproducibility of optical intensity measurements.

<p>Repeatability and reproducibility of optical intensity measurements.</p

Scatterplot of the optical intensities of the supra-septa space and sub-septa in the same eyes with acute Vogt-Koyanagi-Harada disease.

<p>Most of the spots were above the 45-degree lines, indicating that the optical intensity of the supra-septa space was higher than that of the sub-septa space.</p

Demographic and clinical data of included subjects.

<p>Demographic and clinical data of included subjects.</p

Comparison of optical intensity ratio in different compartments of subretinal fluids.

<p>A. optical intensity ratio of subretinal fluid divided by vitreous humour; B. optical intensity of subretinal fluid divided by the entire scanned region. The <i>p</i> value was calculated using one-way analysis of variance. VKH: Vogt-Koyanagi-Harada disease. CSCR: central serous chorioretinopathy.</p

Selection of regions of interest on the optical coherence tomography images of Vogt-Koyanagi-Harada (VKH) disease and central serous chorioretinopathy (CSCR).

<p>A. selection of vitreous and subretinal space in CSCR; B. selection of vitreous, supra-septa space and sub-septa space in VKH with subretinal septa; C. selection of vitreous and subretinal space in VKH without subretinal septa; D. selection of entire region.</p

Cell Signaling Pathway in 12-O-Tetradecanoylphorbol-13-acetate-Induced LCN2 Gene Transcription in Esophageal Squamous Cell Carcinoma

LCN2 is involved in various cellular functions, including transport of small hydrophobic molecules, protection of MMP9 from proteolytic degradation, and regulating innate immunity. LCN2 is elevated in multiple human cancers, frequently being associated with tumor size, stage, and invasiveness. Our previous studies have shown that LCN2 expression could be induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in esophageal squamous cell carcinoma (ESCC) by the binding of five nucleoproteins (MISP, KLF10, KLF15, PPP1R18, and RXRβ) at a novel TPA-responsive element (TRE), at −152~−60 bp of the 5′ flanking region of the LCN2 promoter. However, much is unknown about whether these proteins can respond to TPA stimulation to regulate LCN2 transactivation and which cell signaling pathways mediate this process. In this study, expression plasmids encoding these five nucleoproteins were stably transfected into EC109 cells. Then, stable transfectant was characterized by a Dual-Luciferase Reporter Assay System. RT-PCR, real-time PCR, western blotting, specific kinase inhibitor treatment, and bioinformatics analyses were applied in this study. We found that MISP, KLF10, KLF15, PPP1R18, and RXRβ proteins could strongly respond to TPA stimulation and activate LCN2 transcriptional expression. MEK, ERK, JNK, and P38 kinases were involved in the LCN2 transactivation. Furthermore, the MEK-ERK signal pathway plays a major role in this biological process but does not involve PKCα signaling