Correlation coefficient r and p value estimated with Spearman’s correlation between frequency of peribulbar steroid injections or intravitreal steroid injections and relevant Clinical parameters.

<p>Correlation coefficient r and p value estimated with Spearman’s correlation between frequency of peribulbar steroid injections or intravitreal steroid injections and relevant Clinical parameters.</p

Vitreous hyper-reflective dots in pseudophakic cystoid macular edema assessed with optical coherence tomography - Fig 1

<p>(Upper, Middle) Arrows indicate vitreous hyper-reflective dots (VHDs) in an eye with pseudophakic CME. (Lower) The rectangle displays a magnified VHD with bars measuring its vertical and horizontal diameter. The bar measuring the horizontal diameter appears shorter since the OCT scan is displayed with full vertical resolution (1:1 pixel) instead of the vertical scale adjusted to the horizontal scale (1:1 μm).</p

Preoperative and postoperative data of the eyes of enrolled subjects.

<p>Preoperative and postoperative data of the eyes of enrolled subjects.</p

2-Chlorohexadecanoic acid induces ER stress and mitochondrial dysfunction in brain microvascular endothelial cells

Peripheral leukocytes induce blood-brain barrier (BBB) dysfunction through the release of cytotoxic mediators. These include hypochlorous acid (HOCl) that is formed via the myeloperoxidase-H2O2-chloride system of activated phagocytes. HOCl targets the endogenous pool of ether phospholipids (plasmalogens) generating chlorinated inflammatory mediators like e.g. 2-chlorohexadecanal and its conversion product 2-chlorohexadecanoic acid (2-ClHA). In the cerebrovasculature these compounds inflict damage to brain microvascular endothelial cells (BMVEC) that form the morphological basis of the BBB. To follow subcellular trafficking of 2-ClHA we synthesized a ‘clickable’ alkyne derivative (2-ClHyA) that phenocopied the biological activity of the parent compound. Confocal and superresolution structured illumination microscopy revealed accumulation of 2-ClHyA in the endoplasmic reticulum (ER) and mitochondria of human BMVEC (hCMEC/D3 cell line). 2-ClHA and its alkyne analogue interfered with protein palmitoylation, induced ER-stress markers, reduced the ER ATP content, and activated transcription and secretion of interleukin (IL)−6 as well as IL-8. 2-ClHA disrupted the mitochondrial membrane potential and induced procaspase-3 and PARP cleavage. The protein kinase R-like ER kinase (PERK) inhibitor GSK2606414 suppressed 2-ClHA-mediated activating transcription factor 4 synthesis and IL-6/8 secretion, but showed no effect on endothelial barrier dysfunction and cleavage of procaspase-3. Our data indicate that 2-ClHA induces potent lipotoxic responses in brain endothelial cells and could have implications in inflammation-induced BBB dysfunction