Energy stability and decarbonization in developing countries: Random Forest approach for forecasting of crude oil trade flows and macro indicators

The paper observes the dependence of the main macroeconomic indicators in developing countries from the change in world prices for crude oil. We analyzed a system of simultaneous equations, which makes it possible to verify some of these hypotheses, and developed the model to forecast the impact of oil prices on budget revenues. The practical significance of this work lies in the structuring of existing knowledge on the impact of oil crisis. The results of this work can be considered confirmation of the hypothesis of the sensitivity of U.S. macroeconomic indicators to the dynamics of oil prices. Outcomes assume stable growth even in the period of shock prices for oil, which is confirmed by the statistics that were used in the model. Deep decarbonization modeling is a trend in industrial facilities that are used by developing countries. The major challenge is the issue of availability that is applicable to the countries that want to utilize this facility in their communities. Industrial modeling toward decarbonization is now a developing mechanism to curb the growing issue of atmospheric pollution. This paper proves the relevance of promoting deep decarbonization applied by the developing countries. Copyright 2022 Nyangarika, Mikhaylov, Muyeen, Yadykin, Mottaeva, Pryadko, Barykin, Fomenko, Rykov and Shvandar.The research of SB and VY is partially funded by the Ministry of Science and Higher Education of the Russian Federation under the strategic academic leadership program "Priority 2030" (Agreement 075-15-2021-1333 dated 30.09.2021).Scopu

Distinct Effects of Beta-Amyloid, Its Isomerized and Phosphorylated Forms on the Redox Status and Mitochondrial Functioning of the Blood–Brain Barrier Endothelium

The Alzheimer’s disease (AD)-associated breakdown of the blood–brain barrier (BBB) promotes the accumulation of beta-amyloid peptide (Aβ) in the brain as the BBB cells provide Aβ transport from the brain parenchyma to the blood, and vice versa. The breakdown of the BBB during AD may be caused by the emergence of blood-borne Aβ pathogenic forms, such as structurally and chemically modified Aβ species; their effect on the BBB cells has not yet been studied. Here, we report that the effects of Aβ42, Aβ42, containing isomerized Asp7 residue (iso-Aβ42) or phosphorylated Ser8 residue (p-Aβ42) on the mitochondrial potential and respiration are closely related to the redox status changes in the mouse brain endothelial cells bEnd.3. Aβ42 and iso-Aβ42 cause a significant increase in nitric oxide, reactive oxygen species, glutathione, cytosolic calcium and the mitochondrial potential after 4 h of incubation. P-Aβ42 either does not affect or its effect develops after 24 h of incubation. Aβ42 and iso-Aβ42 activate mitochondrial respiration compared to p-Aβ42. The isomerized form promotes a greater cytotoxicity and mitochondrial dysfunction, causing maximum oxidative stress. Thus, Aβ42, p-Aβ42 and iso-Aβ42 isoforms differently affect the BBBs’ cell redox parameters, significantly modulating the functioning of the mitochondria. The changes in the level of modified Aβ forms can contribute to the BBBs’ breakdown during AD