Publications by authors named "A A Velmiskina"

Article Synopsis
  • tRNA-derived fragments (tRFs) serve both as biomarkers and signaling molecules in various disorders, with their expression patterns differing among blood cell types and changing with physiological conditions, such as during COVID-19.
  • The research compared tRF expression in different blood cells (erythrocytes, monocytes, lymphocytes, etc.) from both healthy donors and severe COVID-19 patients using fluorescence sorting and next-generation sequencing.
  • The study found significant changes in tRF patterns in multiple cell types during severe COVID-19, indicating that distinct blood cells respond differently to cytokine storms, which may involve regulation through nucleotide modifications and RNA enzyme activity alterations.
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Non-coding RNA expression has shown to have cell type-specificity. The regulatory characteristics of these molecules are impacted by changes in their expression levels. We performed next-generation sequencing and examined small RNA-seq data obtained from 6 different types of blood cells separated by fluorescence-activated cell sorting of severe COVID-19 patients and healthy control donors.

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Severe course of COVID-19 is largely determined by hyperactivation of the immune system, or cytokine storm, in which immune cells (lymphocytes, monocytes, etc.) play a major role. Using low-voltage scanning electron microscopy, we studied the morphology of lymphocytes and monocytes during cytokine storm.

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Severe COVID-19 alters the biochemical and morphological characteristics of blood cells in a wide variety of ways. To date, however, the vast majority of research has been devoted to the study of leukocytes, while erythrocyte morphological changes have received significantly less attention. The aim of this research was to identify erythrocyte morphology abnormalities that occur in COVID-19, compare the number of different poikilocyte types, and measure erythrocyte sizes to provide data on size dispersion.

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Fragile X syndrome (FXS) is the most common form of intellectual disability and autism spectrum disorder and is caused by CGG repeat expansion in the promoter region of the FMR1 gene, which encodes fragile X mental retardation protein. This event leads to gene silencing and the loss of gene products through DNA methylation and chromatin remodeling. Due to the pathogenesis of FXS, targeted, symptomatic, and etiological approaches have been developed for its treatment.

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