Electrode Strip Deposition for the CMS Barrel Drift Tube System

The full production ideation, design, set up and realization of the Electrode Strip Deposition for the entire construction of the CMS Barrel Drift Tube System are described in detail

Variation of the ozonosphere in the southern hemisphere in spring 2014 and 2015 based on satellite data

Satellite data were used to study changes in the Antarctic ozone hole (AOH) in 2014 and 2015. The formation of AOH is probably caused by the ozone mass transport from the polar areas to the mid-latitudes of the Southern Hemisphere. In November-December, the AOH is filled with the ozone moving from the midlatitudes. In 2014, the ozone masses moving from the Polar region to the mid-latitudes and back were equal to each other, reaching over 70 million tons. No signs of ozone destruction were found in September – December 2014. In 2015, the difference between the ozone masses reached 70.9%. The most likely reason for this was the destruction of the stratospheric ozone by the products of the eruption of Calbuco Volcano in Chile

ANTARCTIC OZONE HOLE AS A NATURAL GEOPHYSICAL OBJECT

Satellite data on total ozone content for 1985-2015 have been used. Methods of evaluating ozone deficit in the polar region and its excess in middle latitudes of the Southern Hemisphere have been developed. In early spring the ozone molecules outflow and the ozone anomaly forms. Ozone inflows the middle latitudes, its total content increases and a ring with elevated TO forms. In October-November the dynamic process reverses, from the ring the ozone molecules transfer to the polar latitudes. The amount of ozone leaving the ring into the polar regions and filling the ozone anomaly is virtually the same. The results produces indicate that the Antarctic ozone hole is a natural geophysical formation

Circular RNAs Variously Participate in Coronary Atherogenesis

Over the past decade, numerous studies have shown that circular RNAs (circRNAs) play a significant role in coronary artery atherogenesis and other cardiovascular diseases. They belong to the class of non-coding RNAs and arise as a result of non-canonical splicing of premature RNA, which results in the formation of closed single-stranded circRNA molecules that lack 5′-end caps and 3′-end poly(A) tails. circRNAs have broad post-transcriptional regulatory activity. Acting as a sponge for miRNAs, circRNAs compete with mRNAs for binding to miRNAs, acting as competing endogenous RNAs. Numerous circRNAs are involved in the circRNA–miRNA–mRNA regulatory axes associated with the pathogenesis of cardiomyopathy, chronic heart failure, hypertension, atherosclerosis, and coronary artery disease. Recent studies have shown that сirc_0001445, circ_0000345, circ_0093887, сircSmoc1-2, and circ_0003423 are involved in the pathogenesis of coronary artery disease (CAD) with an atheroprotective effect, while circ_0002984, circ_0029589, circ_0124644, circ_0091822, and circ_0050486 possess a proatherogenic effect. With their high resistance to endonucleases, circRNAs are promising diagnostic biomarkers and therapeutic targets. This review aims to provide updated information on the involvement of atherogenesis-related circRNAs in the pathogenesis of CAD. We also discuss the main modern approaches to detecting and studying circRNA–miRNA–mRNA interactions, as well as the prospects for using circRNAs as biomarkers and therapeutic targets for the treatment of cardiovascular diseases

Differential Expression of Subsets of Genes Related to HDL Metabolism and Atherogenesis in the Peripheral Blood in Coronary Artery Disease

Differential expression of genes (DEGs) in coronary artery disease (CAD) and the association between transcript level and high-density lipoprotein cholesterol (HDL-C) were studied with 76 male patients with CAD and 63 control patients. The transcript level of genes related to HDL metabolism (24 genes) and atherosclerosis-prone (41 genes) in RNA isolated from peripheral blood mononuclear cells was measured by real-time RT-PCR. Twenty-eight DEGs were identified. The expression of cholesterol transporters, ALB, APOA1, and LCAT was down-regulated, while the expression of AMN, APOE, LDLR, LPL, PLTP, PRKACA, and CETP was up-regulated. The systemic inflammation in CAD is evidenced by the up-regulation of IL1B, TLR8, CXCL5, and TNFRSF1A. For the controls, TLR8 and SOAT1 were negative predictors of the HDL-C level. For CAD patients, PRKACG, PRKCQ, and SREBF1 were positive predictors, while PRKACB, LCAT, and S100A8 were negative predictors. For CAD patients, the efficiency of reverse cholesterol transport is 73–79%, and intracellular free cholesterol seems to accumulate at hyperalphalipoproteinemia. Both atheroprotective (via S100A8) and proatherogenic (via SREBF1, LCAT, PRKACG, PRKACB, and PRKCQ) associations of gene expression with HDL-C determine HDL functionality in CAD patients. The selected key genes and involved pathways may represent HDL-specific targets for the diagnosis and treatment of CAD and atherosclerosis