Publications by authors named "A P Perevozchikov"

The authors describe the developmental process of intravenous anti-COVID-19 hyperimmune immunoglobulin from anti-SARS-CoV-2 neutralizing antibody-containing plasma. Furthermore, the authors investigated its safety and protective activity in animal models. The manufacturing process included standard ethanol fractionation, chromatographic purification steps and virus removal or inactivation.

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Reactive oxygen species damage various cell components including DNA, proteins, and lipids, and these impairments could be a reason for severe human diseases including atherosclerosis. Forkhead box O1 (FOXO1), an important metabolic transcription factor, upregulates antioxidant and proapoptotic genes during oxidative stress. Apolipoprotein A-I (ApoA-I) forms high density lipoprotein (HDL) particles that are responsible for cholesterol transfer from peripheral tissues to liver for removal in bile in vertebrates.

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Apolipoprotein A-I (ApoA-I) is a key component of high density lipoproteins which possess anti-atherosclerotic and anti-inflammatory properties. Insulin is a crucial mediator of the glucose and lipid metabolism that has been implicated in atherosclerotic and inflammatory processes. Important mediators of insulin signaling such as Liver X Receptors (LXRs) and Forkhead Box A2 (FOXA2) are known to regulate apoA-I expression in liver.

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Article Synopsis
  • ApoA-I is a key part of good cholesterol that helps prevent heart disease.
  • The study shows that a chemical called GW1929 can lower levels of ApoA-I by affecting how certain genes work in liver cells.
  • PPARγ, the gene affected by GW1929, plays a complicated role in controlling ApoA-I production and secretion in cells related to digestion and the liver.
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Article Synopsis
  • Complement C3 helps protect our immune system and is controlled by special proteins called nuclear receptors.
  • One important nuclear receptor, HNF4α, boosts the production of the C3 gene by sticking to certain parts of its DNA in liver cells.
  • During inflammation, a protein called TNFα reduces HNF4α levels, but both TNFα and HNF4α work together to increase C3 gene activity in a unique way.
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