Publications by authors named "Victor Yu Glanz"

Atherosclerosis is a complex disorder that involves several mechanisms of pathogenesis tightly related to each other: lipid accumulation, inflammation and structural changes in the arterial wall. The main source of lipids accumulating in the arterial wall is low-density lipoprotein (LDL) atherogenically modified by desialylation or oxidation. Oxidized LDL can be produced as a result of enhanced generation of reactive oxygen species by mitochondria during oxidative stress.

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Advances in genetic engineering and genomic studies facilitated the development of animal models of human diseases. To date, numerous models based on different animal species are available for the most socially significant human diseases, such as cardiovascular disorders, cancer, neurodegenerative and metabolic disorders. Modern genetic methods allow creating animals with certain genes up- or downregulated, as well as bearing specific mutations.

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Sialic acid residues are frequently located at the terminal positions of glycoconjugate chains of cellular glycocalyx. Sialidases, or neuraminidases, catalyse removal of these residues thereby modulating various normal and pathological cellular activities. Recent studies have revealed the involvement of sialidases in a wide range of human disorders, including neurodegenerative disorders, cancers, infectious diseases and cardiovascular diseases.

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The demand for novel anti-influenza drugs persists, which is highlighted by the recent pandemics of influenza affecting thousands of people across the globe. One of the approaches to block the virus spreading is inhibiting viral sialidase (neuraminidase). This enzyme cleaves the sialic acid link between the newly formed virions and the host cell surface liberating the virions from the cell and maintaining the cycle of infection.

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