Our study for the first time provides evidence that PLR and NLR may be useful for predicting the prognosis of PEX patients and progression to PXG.

Autophagy is biological mechanism allowing recycling of long-lived proteins, abnormal protein aggregates, and damaged organelles under cellular stress conditions. Following sequestration in double-or multimembrane autophagic vesicles, the cargo is delivered to lysosomes for degradation. ATG5 is a key component of an E3-like ATG12-ATG5-ATG16 protein complex that catalyzes conjugation of the MAP1LC3 protein to lipids, thus controlling autophagic vesicle formation and expansion. Accumulating data indicate that ATG5 is a convergence point for autophagy regulation. Here, we describe the scaffold protein RACK1 (receptor activated C-kinase 1, GNB2L1) as a novel ATG5 interactor and an autophagy protein. Using several independent techniques, we showed that RACK1 interacted with ATG5. Importantly, classical autophagy inducers (starvation or mammalian target of rapamycin blockage) stimulated RACK1-ATG5 interaction. Knockdown of RACK1 or prevention of its binding to ATG5 using mutagenesis blocked autophagy activation. Therefore, the scaffold protein RACK1 is a new ATG5-interacting protein and an important and novel component of the autophagy pathways.Autophagy is a highly conserved biological mechanism that is responsible for lysosome-dependent recycling of long-lived abnormal or misfolded proteins as well as dysfunctional or unnecessary organelles (such as depolarized mitochondria) (1). Under normal conditions, basal autophagy help maintain cellular homeostasis. Autophagy is rapidly up-regulated following stress, including nutrient deprivation, accumulation of misfolded proteins, mitochondrial depolarization, or exposure to toxic chemicals (2). Autophagy malfunctions were shown to contribute to several pathologies, such as neurodegenerative diseases, lysosomal storage disorders, and cancer (3).The process starts with the nucleation and elongation of double-membrane structures called "autophagosomes" or "autophagic vesicles." As they mature through fusion with late endosomes or lysosomes, vesicles give rise to "autolysosomes," a hybrid compartment in which vesicle contents are degraded by the action of lysosomal hydrolases (4). So far, around 33 different core autophagy proteins (ATGs) were described (5). Among them, two ubiquitination-like reactions are key to autophagic vesicle membrane elongation as follows: ATG12-ATG5-ATG16L1 and ATG8 (MAP1LC3 or shortly LC3 in mammals). The first ubiquitination-like reaction results in the covalent conjugation of a Lys-130 residue of the ATG5 protein to a ubiquitin-like protein, ATG12. Following addition of ATG16L1 to the ATG12-conjugated ATG5, a larger complex of around 669 -800 kDa forms (6). The ATG12-ATG5-ATG16L1 complex serves as an E3-like enzyme for the second ubiquitylation-like reaction. Here, the LC3 protein is covalently attached to a lipid molecule, generally to a phosphatidylethanolamine contributing to the elongation of autophagic membranes (7,8). Conversion of the free cytosolic form of LC3 (LC3-I) to the lipid-conjugated form (LC3-II) leads to its localization to dot-li...

Post-traumatic endophthalmitis comprises 25-30% of all endophthalmitis cases. Post-traumatic endophthalmitis is an important clinical condition that may have serious anatomical and functional consequences. The type of pathogenic microorganism, nature of the injury, the presence of a foreign body, and the geographical region in which the trauma occurred are all important factors influencing both treatment and prognosis. Unlike postoperative endophthalmitis, there is not a confirmed treatment protocol recommended by the Endophthalmitis-Vitrectomy Study Group in traumatic cases. In this study, we examine the incidence, risk factors, diagnosis, microbiological features, and treatment principles of post-traumatic endophthalmitis in order to guide clinicians who often encounter eye trauma related to this potential complication.

Our study results suggest that conjunctival autografting with fibrin glue has favorable visual and refractive results for patients, and is associated with lower complication rates, compared with use of the traditional 8.0 vicryl suturing technique. We suggest that fibrin tissue glue provides adequate adhesion and that graft loss will not be a problem if protective shields are used in patients postoperatively. The appropriate surgery technique should be selected by considering the advantages and disadvantages of each procedure.

Corneal thickness measurements differ depending on the device used. Corneal thicknesses that have been calculated with Pentacam were lower than the values obtained with Stratus OCT. Both devices used for CCT measurement are easily applied, noninvasive, and effective. However, the devices are not interchangeable. Stratus OCT is not optimal for CCT measurement because of the important limitations of using manual measurements, but it can be used if other measurement devices designed for the purpose are not available.