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EN
INTRODUCTION: Primary open-angle glaucoma (POAG) is an eye disease, which characterized by impairment of retinal neurons resulted in a changes in optic nerve head, damage and death retinal ganglion cells by apoptosis, which lead to loss of vision. Therefore, the scientists were pointed out some resemblance of pathomechanism of neurodegenerative diseases and glaucoma. The number of animal studies have been conducted to examine the role of sirtuins in ocular aging. Upregulation of SIRT1 has been shown to have an important protective effect against various ocular diseases, such as cataract, retinal degeneration, optic neuritis and uveitis. AIM(S): Assessment of the relationship between SIRT1 gene expression level in patients with POAG and the control group. Additionally, analyze the effect of SIRT1 expression level on the progression of POAG depending on clinical parameters. METHOD(S): The study included 34 patients of POAG and 31 control subjects. RNA was extracted from peripheral blood, digested with DNase and converted to cDNA. The SIRT1 expression levels were measured by QPCR method. The non‑parametric Mann‑Whitney U test was applied to determine the levels of mRNA expression in blood of POAG patients and healthy subjects. The non-parametrical statistical tests (ANOVA with post hoc Tukey’s HSD test) were applied to compare level of mRNA expression with clinical parameters of POAG patients. RESULTS: The results shown no statistically significant differences between SIRT1 mRNA levels of POAG patients and controls (p>0.05). However, there was significant association of the SIRT1 expression level with progression of POAG based on RA value (Rim Area), p=0.012. We observed increase of SIRT1 expression level with the early stage of glaucoma, which confirms the protective role of sirtuin in the development of glaucoma. CONCLUSIONS: In conclusion, our study showed a statistically significant association of SIRT1 genes with progression of POAG in a Polish population. FINANCIAL SUPPORT: This work was supported by Umed in Lodz Grants no 500/5-108-05/500-41.
EN
 Keratoconus (KC) is a corneal disease associated with structural abnormalities in the corneal epithelium, Bowman's layer and stroma and altered concentration of tear components. KC corneas show a different pattern of collagen lamellae than their normal counterparts. Also, a reduction of several collagen types in KC epithelium and stroma was observed. Altered expression and/or activity of lysyl oxidase, a critical enzyme of the biogenesis of connective tissue detected in KC corneas, may weaken covalent bonds between collagen and elastin fibrils, what may lead to biomechanical deterioration of the cornea. Increased activity of matrix metalloproteinases observed in KC may induce the degradation of the extracellular matrix causing damage to the cornea. Oxidative and nitrative stress play an important role in KC pathogenesis and KC corneas are characterized by the disturbed lipid peroxidation and nitric oxide pathways. Malfunctioning of these pathways may lead to accumulation of their toxic by-products inducing several detrimental effects, along with apoptosis of the corneal cells, which may result from the loss of β-actin or increased levels of cytokines, including interleukin-1 and -6. Change in the expression of genes associated with wound healing, including the nerve growth factor and the visual system homeobox 1, may contribute to increased susceptibility of KC corneas to injury. Consequently, biochemical changes may play an important role in KC pathophysiology and, therefore, can be considered in prevention, diagnosis, prognosis and in the therapy of this disease as well.
EN
Diabetic retinopathy is the leading cause of adult vision loss and blindness. The most important contributors to the development of diabetic retinopathy are hyperglycemia and hypoxemia that lead to increased vasopermeability, endothelial cell proliferation, and pathological neovascularization. In our previous studies, close relationship between proangiogenic activity of sera from type 2 diabetes mellitus patients (DM2) with background retinopathy, assessed in the in vivo serum-induced mouse cutaneous test (SIA), and VEGF and IL-18 serum concentration were observed. Moreover, it was clearly shown that IGF-1 might play an important role in the negative regulation of neoangiogenesis induced by DM2 patients' sera by diminishing the VEGF stimulatory effect. To confirm the observed phenomenon we evaluated the effect of DM2 patients' sera on the in vitro proliferative activity of human endothelial cells, which is critical for the sprouting and generation of new blood capillaries. Endothelial proliferative activity was significantly higher in the presence of sera from DM2 patients than from healthy controls (P<0.001), as estimated by the MTT test. Moreover, the examined sera from DM2 patients were characterized by increased IL-18 (P<0.05), diminished IGF-1 (P<0.02), and unchanged VEGF levels compared with those in controls. In conclusion, the present study showed a strong stimulatory effect of DM2 patients' sera on the proliferation of endothelial cells, which, along with the findings of our previous studies, proves that the described phenomenon is universal and valid for both animal and human endothelium.
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