[New findings on pathogenetic mechanisms in the development of age-related macular degeneration]. / Novye dannye o patogeneticheskikh mekhanizmakh razvitiya vozrastnoi makulyarnoi degeneratsii.

Age-related macular degeneration (AMD) is a complex multifactorial disease that occurs due to disfunction and degeneration of retinal pigment epithelium (RPE) and choriocapillaris, as well as death of photoreceptors. The exact pathogenetic mechanism remains uncertain. The aging process is the main and the clearest risk factor of AMD. In the development of this condition, a special role belongs to the secretory phenotype of aging spreading from one cell to another and mediated by the secretion and release of growth factors, cytokines, chemokines, proteases, and other molecules. Another major contributor is oxidative stress caused by violations in the recirculation of vitamin A in the vision cycle and accompanied by accumulation of lipofuscin, which mediates the formation of iron-based oxidants that are toxic for mitochondria. Furthermore, prolonged oxidative stress and constant light exposure induce the development of inflammation in the retina. Accumulation of metabolic products and cellular defects with age can induce an inflammatory reaction that amplifies the damage. The inflammatory processes including innate immune response, activation of microglia and parainflammation that occur locally in the vascular membrane, pigment epithelium and neuroretina are very significant contributors to the age-related changes, their progression, and the development of advanced stages of AMD. Various growth factors play a special role in the development of choroidal neovascularization (CNV). Vascular endothelial growth factor A (VEGF-A) has traditionally been considered the main factor of neoangiogenesis and, consequently, the main therapeutic target, but in recent years various studies have determined the role of other factors - VEGF-B, C, D, PGF, Gal-1, angiopoietins. This article describes the main underlying mechanisms in the development of choroidal neovascularization including retinal aging, impaired metabolic activity, mitochondrial dysfunction, inflammatory reactions and genetic variations, as well as the role of various growth factors.

[Anti-angiogenesis therapy of diabetic macular edema in patients with primary open-angle glaucoma]. / Antiangiogennaya terapiya diabeticheskogo makulyarnogo oteka u patsientov s pervichnoi otkrytougol'noi glaukomoi.

Despite the high clinical effectiveness and widespread introduction of anti-angiogenesis (anti-VEGF) therapy into practice, its long-term effect on the development of structural changes in the treatment of primary open-angle glaucoma (POAG) patients with diabetic macular edema (DME) hasn't been studied sufficiently and so presents certain interest. PURPOSE: To study the effect of anti-VEGF therapy on the structural and functional state of the retina and optic nerve in patients with DME and POAG. MATERIAL AND METHODS: The study included 72 patients (132 eyes): the 1st group - 22 patients (40 eyes) with stage I POAG and DME, the 2nd group - 25 patients (46 eyes) with DME receiving anti-VEGF therapy. The 3rd group (control) consisted of 25 patients (46 eyes) with stage I POAG. The observation period lasted 24 months. The average number of injections was 8.48±3.65. The indicators for evaluation were: visual acuity, tonometry, perimetry, optical coherence tomography (OCT) of the optic nerve and macular region. RESULTS: By the end of the observation period, the increase in IOP in the groups was +0.82 (4.4%), 0.41 (2.4%), 0.65 (3.6%) mm Hg. In the group of comorbid patients, a small-scale increase trend of BCVA was noted: +0.05 (6.6%), a decrease in MD by -2.48 Db (92.1%), an increase in excavation volume by 0.16 (43.2%) mm3, decrease in the area of RA by 0.3 mm2 (12.7%). A decrease in retinal nerve fibers layer (RNFL) thickness of 6.55 µm (7.8%), mainly the superior (9.2%), inferior (7.3%) and nasal sectors (7.9%). Loss of GCL+IPL 8.68 µm (12.7%) in the superior (19%), superonasal (20.2%) and inferonasal (20.7%) sectors. CONCLUSION: The combined course of POAG and DME is accompanied by a decrease in the functional and structural parameters of the retina and optic nerve, and a higher rate of progression of glaucomatous optic neuropathy. Long-term results did not reveal a significant deterioration in the structural parameters of the optic disc and retina against the background of anti-VEGF therapy when comparing the study groups.

Oxidative destruction of phenol on Fe/SiO2 catalysts.

In the present study, the sol-gel technique helped to obtain Fe-containing samples with a base of amorphous silicon dioxide from rice husks RH-Fe and RH-Fe-300. These materials are characterized by IR spectroscopy, X-ray phase and X-ray spectral analysis. It was shown that the samples contain silicate structures Si-O-Si(Fe) and are in an amorphous state. Structure of the surface layers of RH-Fe-300 catalyst particles was established for the first time using X-ray photoelectron spectroscopy (XPS) and energy-dispersive spectra (EDX) methods. It was shown that the surface layers of the synthesized particles are oxygen depleted due to oxygen vacancies and silanol groups, therefore defects can form in its structure. Photocatalytic activity of the samples in the phenol oxidation reaction under ultraviolet and solar irradiation in the presence of hydrogen peroxide was studied. It was shown that the degree of phenol decomposition in the presence of RH-Fe for 24 hours under solar irradiation was 92%, in the presence of RH-Fe - 17%. Under two-stage irradiation (ultraviolet and solar), the percentage of phenol decomposition using both catalysts after a day amounted to more than 80%. It was established that RH-Fe-300 catalyst increases oxidation of phenolic compounds in alkaline rice husk hydrolysates under solar irradiation in the presence of hydrogen peroxide.