Uveal melanoma is the most common intraocular malignancy in adults, representing approximately 3% of all melanoma cases. Despite progress in chemotherapy, radiation and surgical treatment options, the prognosis and survival rates remain poor. Acetylation of histone proteins causes transcription of genes involved in cell growth, DNA replication and progression of cell cycle. Overexpression of histone deacetylases occurs in a wide spectrum of malignancies. Histone deacetylase inhibitors block the action of histone deacetylases, leading to inhibition of tumor cell proliferation. This article reviewed the potential therapeutic effects of histone deacetylase inhibitors on uveal melanoma. MEDLINE database was used under the key words/phrases: histone deacetylase, inhibitors, uveal melanoma and targeted therapies for uveal melanoma. A total of 47, English articles, not only referring to uveal melanoma, published up to February 2018 were used. Valproic acid, trichostatin A, tenovin-6, depsipeptide, panobinostat (LBH-589), vorinostat (suberanilohydroxamic acid) entinostat (MS-275), quisinostat, NaB, JSL-1, MC1568 and MC1575 are histone deacetylase inhibitors that have demonstrated promising antitumor effects against uveal melanoma. Histone deacetylase inhibitors represent a promising therapeutic approach for the treatment of uveal melanoma.

The purpose of this study was to describe the incidence, clinical characteristics, and outcome of eccentric macular holes presenting after vitrectomy and internal limiting membrane (ILM) peeling for the treatment of macular pathology and discuss the pathogenesis of holes formation. A retrospective, noncomparative, interventional case-series study of five patients who developed eccentric macular holes postoperatively following vitrectomy in 198 consecutive patients who underwent ILM peeling for idiopathic macular hole and epiretinal membrane formation between 2008 and 2015. Five patients (2.5 %) developed full-thickness eccentric macular holes postoperatively. Three patients presented with a single eccentric macular hole, one patient had an eccentric hole after a failed idiopathic macular hole surgery and one patient developed four eccentric macular holes. The mean diameter of the holes was 584 μm (range 206-1317 μm) and the average time of holes formation after vitrectomy was 27.7 weeks (range 1-140 weeks). Postoperative best-corrected visual acuity ranged from "counting fingers" to 20/25. The eyes with the holes distant from the fovea had the best final visual acuity. No further intervention was attempted and no complications occurred. The mean follow-up time was 26.8 months. The postoperative macular holes after vitrectomy and ILM peeling were variable in number, size, and time of appearance but remained stable and were not associated with any complications. The pathogenesis of macular holes is most consistent with contraction of the residual ILM or secondary epimacular proliferation probably stimulated by ILM peeling.

Patients with Stargardt disease exhibited more depressive symptoms compared to healthy individuals according mainly to PHQ-9 scores. Moderate depression was significantly correlated visual function decline.

Patients with CM having undergone proton beam therapy seem to be more depressed compared to a sample of healthy individuals, and the level of depression is correlated with their visual acuity.

Abstract. Background/Aim: Acute allergic rhinoconjuctivitis is the most common form of ocular allergies. The pathogenetic mechanisms are based on an immunoglobulin E (IgEAcute allergic rhinoconjuctivitis is the most common form of ocular allergies, affecting at least 15-20% of the population. It is divided into seasonal (hay fever), which is released by pollen in the spring and summer, and perennial, which appears throughout the year and is induced by dust mites, animal dander and mold allergens (1, 2). The pathogenetic mechanisms of acute allergic conjunctivitis are based on an immunoglobulin E (IgE)-mediated hypersensitivity reaction, where IgE binds initially to highaffinity receptors on mast cells and basophils and then to the aforementioned allergens. The subsequent activation of mast cells results in the release of inflammatory mediators, including histamine, tryptase, prostaglandins, chemokines and leukotrienes (1). Monocytes, eosinophils and platelets also afford low-affinity IgE receptors (2). Subjects experience acute episodes of redness, tearing, ocular and nasal itching, sneezing, congestion and rhinorrhoea. Slit lamp examination usually reveals bilateral eyelid edema along with conjunctival swelling, chemosis and papillary reaction (1, 2). 403