Publications by authors named "E I Mikhaĭlova"

Aplastic anemia (AA) is characterized by bone marrow (BM) aplasia and pancytopenia. BM stromal microenvironment is closely intertwined with hematopoietic cells by reciprocal regulation. It is still unclear how hematopoietic deficiency affects the bone marrow stroma of the AA patients.

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In an experiment on Wistar rats, a Heymann's active nephritis model was reproduced. After the chronic course of the disease was confirmed, we compared the effectiveness of single systemic and local transplantation of allogeneic cultured stromal cells of the mononuclear fraction of the bone marrow. Both methods of cell therapy reduced clinical manifestations of active Heymann's nephritis: proteinuria decreased and glomerular filtration rate increased 30 days after cell administration.

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The transition of β-barrel proteins from a soluble to an amyloid form is biologically significant in some cases but may lead to functional activity loss. In particular, odorant-binding proteins' (OBPs) fibrils are unable to bind odorant molecules potentially contributing to olfactory dysfunction. As shown previously, OBPs' fibrillogenesis is initiated by uncoupling of protein C-terminal fragment from the β-barrel and exposing amyloidogenic sites.

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Article Synopsis
  • Over the past decade, research has focused on developing treatments for severe systemic and neurodegenerative diseases by targeting and degrading harmful amyloid deposits without significant side effects.
  • This study investigates the impact of the immune enzyme MMP9 on various amyloids linked to Alzheimer's, Parkinson's, and other diseases, revealing that its effectiveness is influenced by the size of amyloid clusters.
  • MMP9 degrades amyloids by disrupting their internal structures rather than just breaking hydrogen bonds, which helps avoid potential side effects from other anti-amyloid therapies while promoting the breakdown and safe handling of amyloid aggregates.
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Marinobufagenin (MBG) is implicated in chronic kidney disease, where it removes Fli1-induced inhibition of the collagen-1. We hypothesized that (i) in nephrectomized rats, aortic fibrosis develops due to elevated plasma MBG and inhibited Fli1, and (ii) that the antibody to MBG reduces collagen-1 and improves vasodilatation. A partial nephrectomy was performed in male Sprague-Dawley rats.

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