[Effect of refractive surgery on Maklakov tonometry results]. / Vliyanie keratorefraktsionnoi khirurgii na rezul'taty tonometrii po Maklakovu.

PURPOSE: The study investigates the influence of changes in keratometric parameters after refractive surgery on the results of Maklakov tonometry. MATERIAL AND METHODS: The study examined a total of 61 people (121 eyes). The patients were divided into a control group with no history of surgery (16 people, 31 eyes), a LASIK group (13 people, 26 eyes), a femtosecond-assisted LASIK (FS-LASIK) group (16 people, 32 eyes), and a photorefractive keratectomy (PRK) group (16 people, 32 eyes). The patients underwent standard examination, keratometry (Km), Maklakov tonometry with a 10 g weight, and elastotonometry with 5, 7.5, and 15 g weights. RESULTS: In the LASIK group, the indentation diameter with 5 and 7.5 g weights correlated with Km in the central and near-paracentral zone (r=0.3-0.5). Tonometry with a 10 g weight did not correlate with anything. Tonometry with a 15 g weight inversely correlated with Km in the paracentral points (4 mm) of the strong meridian (r= -0.5 ... -0.7). In the FS-LASIK group, a significant inverse correlation with Km was observed only for the indentation diameter with a 10 g weight in the paracentral (3-4 mm) zone (r= -0.4 ... -0.5). In the PRK group, weak (r<0.4) correlations were found between Km and the indentation diameter of the 7.5 and 10 g weights for the central zone (1-2 mm). No significant correlations were found for 5 and 15 g weights.In the control group, there were practically no correlations for 5 and 7.5 g weights. The indentation diameter of the 10 g weight evenly correlated with Km at all points (r= -0.38 ... -0.60), the indentation of the 15 g weight correlated mainly with the curvature of the horizontal meridian (r= -0.37 ... -0.49). CONCLUSION: Tonometry readings with the 10 g weight are the most dependent on Km in different groups, and the readings with the 5 g weight are the least dependent. LASIK is characterized by the largest scatter of dependencies for weights of different masses, FS-LASIK - by the smallest. Tonometry readings with the 5 g weight correlated with Km only in the LASIK group, and this was the only direct correlation. Considering the inverse nature of most correlations, higher Km may be associated with an overestimation of tonometry results, and lower Km - with its underestimation.

[Modern achievements in the diagnosis and treatment of glaucoma]. / Sovremennye dostizheniya v diagnostike i lechenii glaukomy.

Glaucoma is one of the most difficult and significant ocular conditions. The chronic asymptomatic course of glaucoma progression leads to irreversible deterioration of visual functions. Many aspects of its pathogenesis, the features of its clinical presentation, diagnosis and treatment have been identified in recent years. The results of diagnostic methods: tonometry, perimetry, optical coherence tomography - with glaucoma do not have high specificity due to the large diversity of the population. When determining the target intraocular pressure (IOP), we look at the indicators of the choroidal blood flow and biomechanical stress of the cornea and sclera (fibrous membrane of the eye). Studying visual functions is important in the diagnosis and monitoring of glaucoma. The creation of a modern portable device based on a virtual reality helmet allows examination of patients with low central vision. Structural changes in glaucoma affect the optic disc and the inner retinal layers. The proposed classification of atypical discs allows determining the earliest characteristic changes in the neuroretinal rim for glaucoma in cases of difficult diagnosis. The complexity of the diagnosis of glaucoma is also associated with concomitant pathologies in elderly patients. In cases with comorbidity of primary glaucoma and Alzheimer's disease the structural and functional changes revealed by modern research methods for glaucoma are explained by both the process of secondary transsynaptic degeneration and the death of neurons as a result of an increased IOP. The starting treatment is and its type are fundamentally important for preserving visual functions. Drug therapy with prostaglandin analogues contributes to a significant and persistent decrease in the level of IOP, and mainly by utilizing the uveoscleral outflow pathway. Surgical treatment of glaucoma is an effective way to achieve the target IOP values. However, postoperative hypotension affects the bloodstream both in the central and peripapillary retina. Optical coherence tomography angiography helped establishe that the strongest factor that determines postoperative changes is the difference in IOP, not its absolute level.

[Structural and functional changes in the retina of patients with primary open-angle glaucoma and compensated intraocular pressure while undergoing retinoprotective therapy]. / Strukturno-funktsional'nye izmeneniia setchatki u patsientov s pervichnoi otkrytougol'noi glaukomoi pri kompensirovannom vnutriglaznom davlenii na fone retinoprotektornoi terapii.

PURPOSE: To evaluate the efficacy and safety of intramuscular Retinalamin for retinoprotection in patients with open-angle glaucoma and normalized intraocular pressure (IOP). MATERIAL AND METHODS: The study included 180 patients (355 eyes) randomized into the main (n=90) and control groups (n=90). The patients of the main group received intramuscular Retinalamin injections; the course was repeated 6 months later. Patient examination was performed at 1, 3, 6, 7, 9 and 12 months. RESULTS: Vision acuity did not change in the main group after the treatment courses (p=0.3732, p=0.6862), nor in the control group (p=0.7751). IOP didn't have significant changes during the whole course of the study neither in the main group (p=0.7632), nor in the control group (p=0.3921). MD index in the main group has increased from -5.52±2.76 to -4.82±2.73 dB (measurements from 6 visits: p=0.0391, p=0.0201, p=0.0302, p=0.3708, p=0.0151, p=0.0353). Control group showed negative MD trend (from -3.51±1.84 to -4.60±2.61 dB; p=0.0012). PSD index has changed from 4.63±1.60 to 4.05±1.43 dB (p=0.0081) in the main group, and from 3.73±1.19 to 4.29±1.53 dB (p=0.0027) in the control group. Average thickness of retinal nerve fiber layer (RNFL) and the volume of neuroretinal rim were stable in both the main (p=0.8039, p=0.9005) and the control groups (p=0.7448, p=0.9620). Ganglion cell complex (GCC) thickness remained stable in the main group (p=0.0377), but has decreased in the control group (p=0.0250). P50 amplitude and latency were stable in the main group (6.54±2.61-6.53±2.64 µV, p=0.0479; 48.39±3.69-50.86±4.09 ms, p=0.0271), while in the control group P50 amplitude has decreased (p=0,0031) and the latency has increased (p=0,0194). In the main group, N95 amplitude has stabilized (p=0.0141) with worsened latency (p=0.0492). N95 amplitude in the control group has worsened (p=0.0195), while latency has stabilized (p=0.3401). CONCLUSION: Systemic use of Retinalamin has significant retinoprotective effect confirmed by the dynamics of morphological and functional parameters in patients with POAG and IOP compensation.

Deregulation of signaling pathways involved in sorafenib resistance of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common neoplasms worldwide. Hepatocarcinogenesis is associated with deregulation of the cell signaling thus targeted therapy can decelerate HCC progression by specific inhibition of alternated signaling cascades. Sorafenib is the only multitarget drug approved for HCC treatment that blocks several crucial oncogenic signaling pathways thus suppressing tumor growth, metastasis and providing survival benefit for subset of patients sensitive to sorafenib. Compensatory activation of other tumorigenic mechanisms may lead to decrease of HCC sensitivity to sorafenib. HCC are heterogenic tumors of epithelial origin, and presence of low-differentiated subpopulations of cancer stem cells or dedifferentiated fibroblastoid cells, that are less sensitive to sorafenib due to resistance to growth-inhibitory action of the drug, promotes HCC resistance to sorafenib. Analysis of the expression profile of genes encoding tissue-specific proteins, components of cell junctions, stem cell and mesenchymal markers can reveal sorafenib-resistant populations in HCC and identify signaling pathways that reduce response to sorafenib. Identification of individual sorafenib resistance mechanisms may be useful for rational choice of an appropriate combination of targeted drugs for retardation of HCC progression and improving the efficacy of therapy