Publications by authors named "F E Filippov"

Background: The search for effective biomarkers for ovarian cancer (OC) early diagnosis is an urgent task of modern oncogynecology. Metabolic profiling by ultra-high performance liquid chromatography and mass spectrometry (UHPLC-MS) provides information on the totality of all low molecular weight metabolites of patient's biological fluids sample, reflecting the processes occurring in the body. The aim of the study was to research blood plasma and urine metabolomic profile of patients with serous ovarian adenocarcinoma by UHPLC-MS.

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We studied the intensity of age-specific changes in the dermis (number and proliferative activity of fibroblasts) in mice with normal and experimentally changed level of thyroid hormones. Receptors of thyroid hormones, TR-α and TR-β, in mouse dermal fibroblasts were identified by immunohistochemical methods. The relative expression of Thra, Thrb, and Dio2 genes was assessed by real-time PCR analysis.

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The goal of our work was to examine content of sirtuin 1 in human skin at different ages to uncover a role of sirtuin 1 in aging of human skin. Sirtuin 1, proliferating cells nuclear antigen (PCNA) were detected by indirect immunohistochemistry in sections of the skin of human fetuses died antenatally from 22 to 40 weeks of pregnancy and humans from birth to 85 years old, died from various causes. Our results showed that the level of sirtuin 1 in dermal fibroblasts was decreased from prenatal period to 85 years old.

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The aim of this work was to study lamin B receptors in human skin at different ages. Lamin B receptors, proliferating cells nuclear antigen (PCNA) were detected in sections of the skin by indirect immunohistochemistry. Our results showed that both portion of dermal fibroblasts with positive staining for lamin B receptors and intensity of staining of fibroblasts for lamin B receptors were maximal from birth to 20 years as compared to all other examined age-periods (from 20 weeks of pregnancy to 85 years old).

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At present time, relationships between lamins and processes leading to aging are established. Mutations of genes of lamins lead to diseases, one of them is progeria. This disease is caused by violation of splaysing of lamin A gene and accumulation the farnezylated prelamin A (progerin) in the nucleus.

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