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Since two decades, corneal crosslinking (CXL) has been proposed as the sole therapeutic option to halt progression of keratoconus or other ectatic diseases. CXL aims at stiffening the cornea using a combination of ultraviolet-A light and a chromophore (vitamin B2, riboflavin), and has been proposed in various indications, from progressive ectatic diseases to corneal infection. Despite being in clinical use for many years, many controversies and discrepancies exist towards CXL procedure and its exact role is still under debate. We report an up-to-date review of the state of the art of CXL and describe the basic principles, the different existing CXL techniques reporting basic and clinical evidence, as well as the new perspectives and the possible future developments of the procedure.<br /><br /> To evaluate postoperative change in choroidal thickness (CT) in patients with anisometropic amblyopia undergoing keratorefractive surgery.<br /><br /> Anisometropic amblyopic patients and nonamblyopic patients who underwent keratorefractive surgery were included in the study. The eyes were divided into three groups. Group 1 consisted of eyes with anisometropic amblyopia, group 2 were the nonamblyopic fellow eyes, and group 3 (control group) were nonamblyopic eyes which had undergone keratorefractive surgery. At the third postoperative month, the CT of these eyes were measured by Enhanced Depth Imaging OCT (EDI-OCT). The choroidal thickness (CT) was measured in the subfoveal area and at 500 micron intervals nasally and temporally.<br /><br /> Twenty-three anisometropic amblyopia patients with amblyopic and fellow eyes and 23 control eyes were enrolled. The mean subfoveal choroidal thickness (CT) was 387.3±168.8μm in group 1, 412.2±88.8μm in group 2 and 337.3±99μm in group 3 (P 0.019). Group 1 and group 2 showed higher choroidal thickness (CT) in the nasal and temporal quadrants than group 3 (P 0.03, P 0.04). At the third postoperative month, central foveal choroidal thickness was 356.6±115.5μm in group 1, 375.1±112.5μm in group 2 and 284.4±98.9μm in group 3 (P 0.071). Choroidal thickness (CT) in the nasal and temporal quadrants at the third postoperative month was also similar (P 0.210, P 0.103).<br /><br /> The macular choroid is thicker in amblyopic eyes and non-amblyopic fellow eyes than in the nonamblyopic controls. Improved fixation after refractive surgery may normalize CT.<br /><br />The macular choroid is thicker in amblyopic eyes and non-amblyopic fellow eyes than in the nonamblyopic controls. Improved fixation after refractive surgery may normalize CT.<br /><br /> To evaluate and to compare the phacoemulsification machine parameters in eyes with and without XFS, requiring cataract surgery.<br /><br /> Patients who underwent phacoemulsification and in-the-bag IOL implantation for cataract were included in this retrospective study. All surgeries were performed by the same experienced surgeon using the stop &amp; chop technique with the same phacoemulsification device (Infiniti Vision System, Alcon Laboratories, Inc., USA). Patients were divided into two groups according to the presence of exfoliation material (XFM). Each group consisted of consecutive patients. Their characteristics and intraoperative phacoemulsification parameters were compared.<br /><br /> Sixty-eight eyes of 68 patients [29 in the exfoliation syndrome (XFS) (-) group, 39 in XFS (+)] were enrolled. There were no statistical differences regarding preoperative patient characteristics. There was a statistically significant difference in total U/S time, phaco time, aspiration time and estimated fluid used between the XFS (+ongation does not result in additional complications.The interplay between nutrient scarcity and signal transduction circuits is an important aspect of tumorigenesis that regulates many aspects of cancer progression. Glutamine is a critical nutrient for cancer cells, as it contributes to biosynthetic reactions that sustain cancer proliferation and growth. In tumors, because nutrient utilization can often outpace supply, glutamine levels can become limiting and oncogene-mediated metabolic rewiring triggers signaling cascades that support nutrient stress survival. Recently, we identified that in pancreatic ductal adenocarcinoma (PDAC) cells, glutamine depletion can trigger p21-activated kinase (Pak) activation through EGFR signaling as a means to circumvent metabolic stress. Here, we elucidate that glutamine starvation, as well EGF stimulation, can enhance the presence of many different Pak phosphoforms, and that this activation only occurs in a subset of PDAC cells. [https://www.selleckchem.com/products/ex229-compound-991.html ex229 chemical structure] Pak is a well-established effector of Rac1, and while Rac1 mutant variants can modulate the metabolic induction of Pak phosphorylation, Rac1 inhibition only partially attenuates Pak activation upon glutamine depletion. We decipher that in order to efficiently suppress metabolic activation of Pak, both EGFR and Rac1 signaling must be inhibited. These results provide a mechanistic understanding of how glutamine-regulated signal transduction can control Pak activation in PDAC cells.Podocyte injury has been considered as a major contributor to the progression of diabetic nephropathy (DN). Long non-coding RNAs (lncRNAs) are being found to be involved in DN pathogenesis. The current research was designed to elucidate the potential role and latent molecular mechanism of long non-coding RNA MIAT in HG-induced podocyte injury. Our data demonstrated that MIAT expression was substantially elevated but miR-130a-3p was diminished in HG-challenged podocytes. Additionally, lack of MIAT mitigated HG-evoked inflammatory reaction in podocytes as evidenced by the diminished the release of inflammatory mediators TNF-α, IL-6 and IL-1β. Moreover, depletion of MIAT evidently amplified cell viability and alleviated HG-triggered apoptosis, reflected as the downregulation of Bax expression concomitant with the enhancement of Bcl-2 expression in HG-exposed podocytes. Mechanistically, MIAT effectively modulated TLR4 expression through acting as a competing endogenous sponge of miR-130a-3p, and TLR4 was confirmed as a specific target gene of miR-130a-3p. More importantly, the miR-130a-3p/TLR4 crosstalk contributed to the protective effect of MIAT knockdown on HG-provoked podocyte damage. Collectively, these findings highlighted that blocking MIAT/miR-130a-3p/TLR4 network play vital regulatory roles in mitigating HG-induced inflammation damage and apoptosis, thereby protecting podocyte from HG-stimulated injury, implying that MIAT might be a promising therapeutic strategy for developing effective treatments against DN progression.