Institute of Experimental Cardiology

Low-density lipoprotein cholesterol (LDL-C) is a major cardiovascular risk factor and an indicator of hypolipidemic therapy effectiveness. However, direct and calculated methods for determining "LDL-C" present the sum of the cholesterol in all apoB-containing lipoproteins, including lipoprotein(a) [Lp(a)]. There has been an ongoing debate about the correctness of LDL-C in patients with elevated Lp(a) concentrations up to now. The aim of this study was to evaluate the effect of Lp(a) concentration on the LDL-C calculated by different equations. The study included the results of fasting lipids and Lp(a) concentration of 566 measurements from 283 patients (before and after lipid-lowering therapy prescribing, after exclusion of 17 patients with incomplete data). LDL-C and LDL-C corrected for Lp(a)-cholesterol (LDL-Ccorr) were calculated by Friedewald, Martin-Hopkins, and Sampson equations. We assessed 566 measurements of lipids and Lp(a). The number of values reclassified to a higher risk category was 10% and 13% with Martin-Hopkins and Sampson equations compared to the Friedewald formula. The percentage of Lp(a)-cholesterol (Lp(a)-C) in the LDL-C calculated by three formulas was up to 90% or more depending on the concentration of LDL-C and Lp(a). When stratified by clinically significant LDL-C thresholds, the proportion of values LDL-Ccorr reclassified to a lower risk category ranged from 30 to 59%. Comparison of LDL-C concentrations calculated by Friedewald, Martin-Hopkins, and Sampson equations showed high consistency in patients without elevated triglycerides. The LDLcorr is reasonable to use in patients with Lp(a) concentration ≥ 30 and ≥41 mg/dL when using the Martin-Hopkins and Sampson equations, respectively. These data may help clinicians interpret LDL-C goal attainment in patients with elevated Lp(a) and avoid misclassification driven by the Lp(a)-cholesterol component.

A three-dimensional reconstruction of the microstructure of the defects associated with the formation of fatigue cracks in samples destroyed during low-cycle fatigued tests has been performed by serial-section focused ion beam tomography. The geometric parameters of defects containing Hf, Nb, Ti, Al, and Ni, identified during 3D reconstruction, were determined. The morphology of individual particles is presented by a set of shapes that form flat (carpet-like) conglomerates up to several tens of microns in size, which cannot be detected by nondestructive testing methods. The revealed morphological features make it possible to propose a complex of measures aimed at increasing the service life of parts made of granulated heat-resistant nickel alloy EP741NP; this is an important practical result.

Atherosclerosis is a complex cardiovascular disease characterised by the accumulation of lipids, inflammatory cells, and fibrous elements within arterial walls, leading to plaque formation and increased risk of cardiovascular events. Recent evidence highlights the pivotal roles of purinergic receptors in mediating the inflammatory and cellular processes associated with atherosclerosis. This review examines the roles of purinergic receptors in the pathophysiology of atherosclerosis, with a particular focus on the P1 subtype (A2A and A3 receptors), the P2X subtype (P2X4 and P2X7 receptors), and the P2Y subtype (P2Y2, P2Y11, and P2Y12 receptors). The A2A and A3 receptors are involved in modulating vascular inflammation, endothelial cell function, and vascular smooth muscle cell calcification. P2X4 has been implicated in the production of pro-inflammatory cytokines and the promotion of plaque inflammation, whereas P2X7 contributes to vascular inflammation, plaque progression, and rupture. The P2Y2 receptor plays critical roles in regulating vascular inflammation and calcification, smooth muscle cell migration, and plaque growth. Furthermore, the P2Y11 receptor has been shown to modulate endothelial cell inflammation, while P2Y12 is associated with lipid accumulation, foam cell formation, vascular smooth muscle cell migration, and plaque development. By synthesising current knowledge on the involvement of purinergic signalling in atherosclerosis, this review discusses potential therapeutic targets for intervention. Specifically, P2Y receptor antagonists present promising avenues for reducing inflammation and improving vascular function in atherosclerotic patients. However, despite the advancements in understanding purinergic receptor functions, challenges remain in translating this knowledge into clinical practice. Further research is essential to unravel the intricate signalling pathways of these receptors and to develop effective biomarker strategies and therapeutic interventions aimed at combatting atherosclerosis and its associated complications.

are registered for Thailand for the fi rst time.This increases the number of Plateros species in Indochina to 95, and the number of species registered in Thailand, with the discovery of another three species previously known only from southwestern China and Vietnam, to 25.An annotated checklist of Plateros species of Thailand is also provided.

Abstract The brachiopod mantle, which has a row of setae along its edge, plays a crucial role in environmental interactions and defence reflexes, triggering rapid valve closure. However, the organization of the muscular and nervous systems in the mantle of rhynchonelliform brachiopods, as well as the sensory mechanisms of the mantle setae, remains largely unexplored. In this study, we present a morpho‐functional analysis of the neuromuscular system of the mantle in the brachiopod Hemithiris psittacea, using transmission electron microscopy, immunocytochemistry, and in vivo video recordings of mantle movements. The mantle contains numerous thin muscles extending from its central region to the periphery, but not reaching the mantle edge. The contraction of these muscles allows the mantle with setae to retract into the mantle cavity. Additionally, the mantle is innervated by numerous radial nerves that connect to the marginal mantle nerve. We demonstrate that mantle contraction may occur independently of the central nervous system. However, the subenteric ganglion plays a role in maintaining the mantle in a pre‐contracting state during rest, thus enhancing the sensory selectivity of the setal sensory complexes.

An electrochemical method is proposed for the forming of contacts to high-temperature thermoelements with barrier layers based on refractory-metal alloys. The contacts are destined for thermoelements with operating temperatures up to 900 K. The barrier layers have specific resistance of no more than 15.3 × 10−8 Ω m and specific contact resistance of no more than 1.5 × 10−9 Ω m2. The best results were obtained for barrier layers based on Mo–Ni alloy with a Mo content of 36.5 wt %. Ag films obtained by electrochemical deposition were used as a commutation layer in the contacts. The contacts were shown to be thermally stable at the limiting operating temperatures of the thermoelements and have an adhesive strength of at least 10.3 MPa.

Background and Objectives: Atherosclerosis is one of the main reasons for cardiovascular disease development. This study aimed to analyze the association of mtDNA mutations and atherosclerotic plaques in carotid arteries of patients with atherosclerosis and conditionally healthy study participants from the Novosibirsk region. Methods: PCR fragments of DNA containing the regions of 10 investigated mtDNA mutations were pyrosequenced. The heteroplasmy levels of mtDNA mutations were analyzed using a quantitative method based on pyrosequencing technology developed by M. A. Sazonova and colleagues. Results: In the analysis of samples of patients with atherosclerotic plaques of the carotid arteries and conditionally healthy study participants from the Novosibirsk region, four proatherogenic mutations in the mitochondrial genome (m.5178C>A, m.652delG, m.12315G>A and m.3256C>T) and three antiatherogenic mutations in mtDNA (m.13513G>A, m.652insG, and m.14846G>A) were detected. A west-east gradient was found in the distribution of the mtDNA mutations m.5178C>A, m.3256C>T, m.652insG, and m.13513G>A. Conclusions: Therefore, four proatherogenic mutations in the mitochondrial genome (m.5178C>A, m.652delG, m.12315G>A, and m.3256C>T) and three antiatherogenic mutations in mtDNA (m.13513G>A, m.652insG, and m.14846G>A) were detected in patients with atherosclerotic plaques in their carotid arteries from the Novosibirsk region.

Atherosclerosis is a chronic disease characterized by the increased infiltration and retention of LDL particles in arterial walls. There are several mechanisms underlying atherogenesis, with the pro-atherogenic modifications of LDL playing a significant role. One such modification of native LDL is desialylation, which is characterized by the removal of terminal sialic acid from ApoB-100 glycans that induces critical changes in the overall functionality of the LDL particle. The aim of this study was to model the desialylation of native LDL in mice, resembling a phenomenon previously observed in atherosclerotic patients. LDL desialylation was induced in C57BL/6J mice via the injection of exogenous neuraminidase. The degree of LDL desialylation and its duration were assessed. The impact of LDL desialylation on blood lipid levels was evaluated. Furthermore, the morphological alterations in the aorta during LDL desialylation in the bloodstream were examined. The control group of C57BL/6J mice received saline injections, while the experimental group underwent a single injection of IgG-conjugated Vibrio cholerae neuraminidase. The LDL sialic acid levels were assessed 1-7 days post-injection using the Warren method and normalized to total protein content measured via the Lowry method. A similar protocol was followed for the subchronic administration of the IgG-neuraminidase conjugate over a 6-week period. The blood lipid profiles were analyzed using commercial kits. The atherosclerotic plaque burden in the mouse aorta was quantified using Oil Red O and hematoxylin-eosin staining. A single administration of 20 mU IgG-neuraminidase conjugate resulted in decreased LDL sialic acid levels for 5 days, gradually recovering by days 6-7. Subchronic administration maintained reduced LDL sialic acid levels for up to 2 months. Notably, sustained LDL desialylation was associated with elevated LDL cholesterol levels. A sustained desialylation of LDL in C57BL/6J mice was achieved through subchronic administration of IgG-conjugated neuraminidase. This study provides an approach for sustained LDL desialylation in mice. Further studies using apolipoprotein E knockout mice and LDL desialylation will reveal the role of this process in the occurrence and development of atherosclerosis.