1,599 research outputs found
Spatial and temporal phylogeny of border disease virus in pyrenean chamois (Rupicapra p. Pyrenaica)
Border disease virus (BDV) affects a wide range of ruminants worldwide, mainly domestic sheep and goat. Since 2001 several outbreaks of disease associated to BDV infection have been described in Pyrenean chamois (Rupicapra pyrenaica pyrenaica) in Spain, France and Andorra. In order to reconstruct the most probable places of origin and pathways of dispersion of BDV among Pyrenean chamois, a phylogenetic analysis of 95 BDV 5'untranslated sequences has been performed on chamois and domestic ungulates, including novel sequences and retrieved from public databases, using a Bayesian Markov Chain Monte Carlo method. Discrete and continuous space phylogeography have been applied on chamois sequences dataset, using centroid positions and latitude and longitude coordinates of the animals, respectively.
The estimated mean evolutionary rate of BDV sequences was 2.9x10(-3) subs/site/year (95% HPD: 1.5-4.6x10(-3)). All the Pyrenean chamois isolates clustered in a unique highly significant clade, that originated from BDV-4a ovine clade. The introduction from sheep (dated back to the early 90s) generated a founder effect on the chamois population and the most probable place of origin of Pyrenean chamois BDV was estimated at coordinates 42.42 N and 1.9 E. The pathways of virus dispersion showed two main routes: the first started on the early 90s of the past century with a westward direction and the second arise in Central Pyrenees. The virus spread westward for more than 125 km and southward for about 50km and the estimated epidemic diffusion rate was about 13.1 km/year (95% HPD 5.2-21.4 km/year). The strong spatial structure, with strains from a single locality segregating together in homogeneous groups, and the significant pathways of viral dispersion among the areas, allowed to reconstruct both events of infection in a single area and of migrations, occurring between neighboring areas
Recommended from our members
Structural and Functional Studies of Biotin-Dependent Carboxylases
A persisting question in biology concerns the exceptional diversity of metabolic enzymes and how they respond to their ligands and dynamic environments with remarkable precision. In humans, the family of biotin-dependent carboxylases holds important roles in intermediary metabolism. Recent years have witnessed significant progress toward understanding these enzymes' roles in homeostatic regulation. However, due to a lack of structural information, their catalytic mechanisms, as well as the macromolecular consequences of their genetic mutations, are still not well understood. This dissertation describes the characterization of two biotin-dependent carboxylases that catalyze essential metabolic transformations in humans and bacteria, using X-ray crystallography to elucidate their structures and biochemical assays to verify their activities. We engineer a novel chimeric variant of propionyl-CoA carboxylase (PCC) and produce the first crystal structure of its 750-kDa Ξ±6Ξ²6 holoenzyme. This structure reveals the architecture of PCC's twelve catalytic domains and allows the mapping of its disease-associated gene mutations to predict their effects on enzyme stability and catalysis. We also identify and describe a new domain that is integral to maintaining inter-subunit contacts within PCC. Following this, we extend our studies to methylcrotonyl-CoA carboxylase (MCC), another 750-kDa Ξ±6Ξ²6 holoenzyme that differs from PCC primarily in its substrate preference. The crystal structure of MCC assumes a markedly different configuration from PCC despite the high sequence identity between the two. Theorizing that these enzymes may represent unique lineages in the evolution of the biotin-dependent carboxylases, we apply similar approaches to the study of a third biotin-dependent carboxylase. Our efforts have produced the first two holoenzyme structures of CoA-recognizing biotin-dependent carboxylases, and provide valuable insight for understanding the functions of these vital enzymes
Factors shaping the evolution of electronic documentation systems
The main goal is to prepare the space station technical and managerial structure for likely changes in the creation, capture, transfer, and utilization of knowledge. By anticipating advances, the design of Space Station Project (SSP) information systems can be tailored to facilitate a progression of increasingly sophisticated strategies as the space station evolves. Future generations of advanced information systems will use increases in power to deliver environmentally meaningful, contextually targeted, interconnected data (knowledge). The concept of a Knowledge Base Management System is emerging when the problem is focused on how information systems can perform such a conversion of raw data. Such a system would include traditional management functions for large space databases. Added artificial intelligence features might encompass co-existing knowledge representation schemes; effective control structures for deductive, plausible, and inductive reasoning; means for knowledge acquisition, refinement, and validation; explanation facilities; and dynamic human intervention. The major areas covered include: alternative knowledge representation approaches; advanced user interface capabilities; computer-supported cooperative work; the evolution of information system hardware; standardization, compatibility, and connectivity; and organizational impacts of information intensive environments
Real-time human ambulation, activity, and physiological monitoring:taxonomy of issues, techniques, applications, challenges and limitations
Automated methods of real-time, unobtrusive, human ambulation, activity, and wellness monitoring and data analysis using various algorithmic techniques have been subjects of intense research. The general aim is to devise effective means of addressing the demands of assisted living, rehabilitation, and clinical observation and assessment through sensor-based monitoring. The research studies have resulted in a large amount of literature. This paper presents a holistic articulation of the research studies and offers comprehensive insights along four main axes: distribution of existing studies; monitoring device framework and sensor types; data collection, processing and analysis; and applications, limitations and challenges. The aim is to present a systematic and most complete study of literature in the area in order to identify research gaps and prioritize future research directions
Investigating gene methylation signatures for fetal intolerance prediction
Pregnancy is a complicated and long procedure during one or more offspring development inside a woman. A short period of oxygen shortage after birth is quite normal for most babies and does not threaten their health. However, if babies have to suffer from a long period of oxygen shortage, then this condition is an indication of pathological fetal intolerance, which probably causes their death. The identification of the pathological fetal intolerance from the physical oxygen shortage is one of the important clinical problems in obstetrics for a long time. The clinical syndromes typically manifest five symptoms that indicate that the baby may suffer from fetal intolerance. At present, liquid biopsy combined with high-throughput sequencing or mass spectrum techniques provides a quick approach to detect real-time alteration in the peripheral blood at multiple levels with the rapid development of molecule sequencing technologies. Gene methylation is functionally correlated with gene expression; thus, the combination of gene methylation and expression information would help in screening out the key regulators for the pathogenesis of fetal intolerance. We combined gene methylation and expression features together and screened out the optimal features, including gene expression or methylation signatures, for fetal intolerance prediction for the first time. In addition, we applied various computational methods to construct a comprehensive computational pipeline to identify the potential biomarkers for fetal intolerance dependent on the liquid biopsy samples. We set up qualitative and quantitative computational models for the prediction for fetal intolerance during pregnancy. Moreover, we provided a new prospective for the detailed pathological mechanism of fetal intolerance. This work can provide a solid foundation for further experimental research and contribute to the application of liquid biopsy in antenatal care
A multimedia educational module for the restoration of single-tooth implants
Item does not contain fulltex
Inferring pandemic growth rates from sequence data
Using sequence data to infer population dynamics is playing an increasing role in the analysis of outbreaks. The most common methods in use, based on coalescent inference, have been widely used but not extensively tested against simulated epidemics. Here, we use simulated data to test the ability of both parametric and non-parametric methods for inference of effective population size (coded in the popular BEAST package) to reconstruct epidemic dynamics. We consider a range of simulations centred on scenarios considered plausible for pandemic influenza, but our conclusions are generic for any exponentially growing epidemic. We highlight systematic biases in non-parametric effective population size estimation. The most prominent such bias leads to the false inference of slowing of epidemic spread in the recent past even when the real epidemic is growing exponentially. We suggest some sampling strategies that could reduce (but not eliminate) some of the biases. Parametric methods can correct for these biases if the infected population size is large. We also explore how some poor sampling strategies (e.g. that over-represent epidemiologically linked clusters of cases) could dramatically exacerbate bias in an uncontrolled manner. Finally, we present a simple diagnostic indicator, based on coalescent density and which can easily be applied to reconstructed phylogenies, that identifies time-periods for which effective population size estimates are less likely to be biased. We illustrate this with an application to the 2009 H1N1 pandemic
Accelerated evolution of SARS-CoV-2 in free-ranging white-tailed deer
The zoonotic origin of the COVID-19 pandemic virus highlights the need to fill the vast gaps in our knowledge of SARS-CoV-2 ecology and evolution in non-human hosts. Here, we detected that SARS-CoV-2 was introduced from humans into white-tailed deer more than 30 times in Ohio, USA during November 2021-March 2022. Subsequently, deer-to-deer transmission persisted for 2β8 months, disseminating across hundreds of kilometers. Newly developed Bayesian phylogenetic methods quantified how SARS-CoV-2 evolution is not only three-times faster in white-tailed deer compared to the rate observed in humans but also driven by different mutational biases and selection pressures. The long-term effect of this accelerated evolutionary rate remains to be seen as no critical phenotypic changes were observed in our animal models using white-tailed deer origin viruses. Still, SARS-CoV-2 has transmitted in white-tailed deer populations for a relatively short duration, and the risk of future changes may have serious consequences for humans and livestock
ΠΠ°ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π° β ΡΠ½ΠΈΠ²Π΅ΡΡΠ°Π»ΡΠ½ΡΠΉ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠ°ΠΊΡΠΎΡ Π² ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠΈ ΠΎΡΠ³Π°Π½ΠΎΠ² ΠΈ ΡΠΈΡΡΠ΅ΠΌ ΠΏΡΠΈ COVID-19
Relevance. The pathogenesis of COVID-19 remains one of the most pressing. The literature discusses the role of iron as a factor supporting inflammatory processes, hypercoagulability and microcirculation crisis in severe COVID-19.The aim of study. was to identify changes in iron metabolism in patients with severe COVID-19 and hyperferritinemia.Material and methods. In this study, we used a content analysis of available scientific publications and our own observations of the peculiarities of the clinical picture and laboratory parameters in patients with a severe course of COVID-19 who had hyperferretinemia at the height of the disease. The main group consisted of 30 patients hospitalized in the Department of Anesthesiology, Resuscitation and Intensive Care of N.A. Semashko City clinical Hospital No. 38 with the diagnosis COVID-19, bilateral polysegmental pneumonia, severe course and hyperferritinemia. The diagnosis of a new coronavirus infection was confirmed by visualization of bilateral viral lung lesions with chest CT-scan, positive PCR test for SARS-CoV-2 and the presence of immunoglobulins to SARS-CoV-2. The control group consisted of 20 healthy volunteers. The study evaluated the biochemical parameters of iron metabolism, fibrinolysis and markers of inflammation. Changes associated with impaired iron metabolism were assessed by the level of serum iron, transferrin, daily and induced iron excretion in the urine. Statistical processing was carried out using nonparametric methods.Results. All patients with severe COVID-19 and hyperferritinemia showed signs of impaired iron metabolism, inflammation and fibrinolysis β a decrease in the level of transferrin (p<0.001), serum iron (p><0.005), albumin (p><0.001), lymphocytes (p><0.001) and an increase in leukocytes (p><0.001), neutrophils (p><0.001), CRP (p><0.005), IL-6 (p><0.001), D-dimer (p><0.005), daily urinary iron excretion (p><0.005) and induced urinary iron excretion (p><0.001). Conclusions The study showed that in the pathogenesis of the severe course of COVID-19, there is a violation of iron metabolism and the presence of a free iron fraction. The appearance of free iron can be caused by damage to cells with the βreleaseβ of iron from cytochromes, myoglobin, hemoglobin, or violation of the binding of iron to transferrin, which may be the result of a change in the protein structure or violation of the oxidation of iron to the trivalent state. When assessing the degree of viral effect on the body, one should take into account the effect of various regulators of iron metabolism, as well as an assessment of the level of free iron not associated with transferrin. Keywords: new coronavirus infection, COVID-19, SARS-CoV-2, iron metabolism, free iron, ferritin, transferrin, NTBI, nontransferrin bound iron>Λ0.001), serum iron (pΛ0.005), albumin (pΛ0.001), lymphocytes (pΛ0.001) and an increase in leukocytes (pΛ0.001), neutrophils (pΛ0.001), CRP (pΛ0.005), IL-6 (pΛ0.001), D-dimer (pΛ0.005), daily urinary iron excretion (pΛ0.005) and induced urinary iron excretion (pΛ0.001).Conclusions. The study showed that in the pathogenesis of the severe course of COVID-19, there is a violation of iron metabolism and the presence of a free iron fraction. The appearance of free iron can be caused by damage to cells with the βreleaseβ of iron from cytochromes, myoglobin, hemoglobin, or violation of the binding of iron to transferrin, which may be the result of a change in the protein structure or violation of the oxidation of iron to the trivalent state. When assessing the degree of viral effect on the body, one should take into account the effect of various regulators of iron metabolism, as well as an assessment of the level of free iron not associated with transferrin.Β ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ. ΠΠΎΠΏΡΠΎΡ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π° COVID-19 ΠΎΡΡΠ°Π΅ΡΡΡ ΠΎΠ΄Π½ΠΈΠΌ ΠΈΠ· ΡΠ°ΠΌΡΡ
Π°ΠΊΡΡΠ°Π»ΡΠ½ΡΡ
. Π Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΠ΅ ΠΎΠ±ΡΡΠΆΠ΄Π°Π΅ΡΡΡ ΡΠΎΠ»Ρ ΠΆΠ΅Π»Π΅Π·Π° Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΡΠ°ΠΊΡΠΎΡΠ°, ΠΏΠΎΠ΄Π΄Π΅ΡΠΆΠΈΠ²Π°ΡΡΠ΅Π³ΠΎ Π²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΏΡΠΎΡΠ΅ΡΡΡ, Π³ΠΈΠΏΠ΅ΡΠΊΠΎΠ°Π³ΡΠ»ΡΡΠΈΡ ΠΈ ΠΊΡΠΈΠ·ΠΈΡ ΠΌΠΈΠΊΡΠΎΡΠΈΡΠΊΡΠ»ΡΡΠΈΠΈ ΠΏΡΠΈ ΡΡΠΆΠ΅Π»ΠΎΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠΈ COVID-19.Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ. ΠΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π° Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΡΡΠΆΠ΅Π»ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ COVID-19 ΠΈ Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΠ΅ΠΉ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π Π½Π°ΡΡΠΎΡΡΠ΅ΠΌ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Ρ ΠΊΠΎΠ½ΡΠ΅Π½Ρ-Π°Π½Π°Π»ΠΈΠ· ΠΈΠΌΠ΅ΡΡΠΈΡ
ΡΡ Π½Π°ΡΡΠ½ΡΡ
ΠΏΡΠ±Π»ΠΈΠΊΠ°ΡΠΈΠΉ ΠΈ ΡΠΎΠ±ΡΡΠ²Π΅Π½Π½ΡΠ΅ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ Π·Π° ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΡΠΌΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΡΠΈΠ½Ρ ΠΈ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΡΡ
ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΎΠ² Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΡΠΆΠ΅Π»ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ COVID-19, ΠΈΠΌΠ΅Π²ΡΠΈΡ
Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΡ Π² ΠΏΠ΅ΡΠΈΠΎΠ΄ Π½Π°ΠΈΠ±ΠΎΠ»ΡΡΠΈΡ
ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΡΠ½ΠΎΠ²Π½Π°Ρ Π³ΡΡΠΏΠΏΠ° ΡΠΎΡΡΠΎΡΠ»Π° ΠΈΠ· 30 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ², Π³ΠΎΡΠΏΠΈΡΠ°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
Π² ΠΎΡΠ΄Π΅Π»Π΅Π½ΠΈΠ΅ Π°Π½Π΅ΡΡΠ΅Π·ΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ, ΡΠ΅Π°Π½ΠΈΠΌΠ°ΡΠΈΠΈ ΠΈ ΠΈΠ½ΡΠ΅Π½ΡΠΈΠ²Π½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ Π‘ΠΠ± ΠΠΠ£Π Β«ΠΠΎΡΠΎΠ΄ΡΠΊΠ°Ρ Π±ΠΎΠ»ΡΠ½ΠΈΡΠ° β 38 ΠΈΠΌ. Π.Π. Π‘Π΅ΠΌΠ°ΡΠΊΠΎΒ» Ρ Π΄ΠΈΠ°Π³Π½ΠΎΠ·ΠΎΠΌ Β«COVID-19, Π΄Π²ΡΡΡΠΎΡΠΎΠ½Π½ΡΡ ΠΏΠΎΠ»ΠΈΡΠ΅Π³ΠΌΠ΅Π½ΡΠ°ΡΠ½Π°Ρ ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΡ, ΡΡΠΆΠ΅Π»ΠΎΠ΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅Β» ΠΈ Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΠ΅ΠΉ. ΠΠΈΠ°Π³Π½ΠΎΠ· Π½ΠΎΠ²ΠΎΠΉ ΠΊΠΎΡΠΎΠ½Π°Π²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΠΏΠΎΠ΄ΡΠ²Π΅ΡΠΆΠ΄Π°Π»ΡΡ Π²ΠΈΠ·ΡΠ°Π»ΠΈΠ·Π°ΡΠΈΠ΅ΠΉ Π΄Π²ΡΡΡΠΎΡΠΎΠ½Π½Π΅Π³ΠΎ Π²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ Π»Π΅Π³ΠΊΠΈΡ
ΠΏΡΠΈ ΠΊΠΎΠΌΠΏΡΡΡΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΠΌΠΎΠ³ΡΠ°ΡΠΈΠΈ Π³ΡΡΠ΄Π½ΠΎΠΉ ΠΊΠ»Π΅ΡΠΊΠΈ, ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΠΌ ΠΠ¦Π -ΡΠ΅ΡΡΠΎΠΌ Π½Π° SARS-CoV-2 ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΠ³Π»ΠΎΠ±ΡΠ»ΠΈΠ½ΠΎΠ² ΠΊ SARS-CoV-2. ΠΡΡΠΏΠΏΡ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΈ 20 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ±ΡΠΎΠ²ΠΎΠ»ΡΡΠ΅Π². Π ΡΠ°Π±ΠΎΡΠ΅ Π΄Π°Π½Π° ΠΎΡΠ΅Π½ΠΊΠ° Π±ΠΈΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Π΅ΠΉ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π°, ΡΠΈΠ±ΡΠΈΠ½ΠΎΠ»ΠΈΠ·Π° ΠΈ ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ. ΠΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ, ΡΠ²ΡΠ·Π°Π½Π½ΡΠ΅ Ρ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΎΠ±ΠΌΠ΅Π½Π° ΠΆΠ΅Π»Π΅Π·Π°, ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈ ΠΏΠΎ ΡΡΠΎΠ²Π½Ρ ΡΡΠ²ΠΎΡΠΎΡΠΎΡΠ½ΠΎΠ³ΠΎ ΠΆΠ΅Π»Π΅Π·Π°, ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½Π°, ΡΡΡΠΎΡΠ½ΠΎΠΉ ΠΈ ΠΈΠ½Π΄ΡΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΡΠΊΡΠ΅ΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΠΌΠΎΡΠΎΠΉ. Π‘ΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΡΡ ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΡ ΠΎΡΡΡΠ΅ΡΡΠ²Π»ΡΠ»ΠΈ Ρ ΠΏΠΎΠΌΠΎΡΡΡ Π½Π΅ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ².Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π£ Π²ΡΠ΅Ρ
ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΡΠΆΠ΅Π»ΡΠΌ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ΠΌ COVID-19 ΠΈ Π³ΠΈΠΏΠ΅ΡΡΠ΅ΡΡΠΈΡΠΈΠ½Π΅ΠΌΠΈΠ΅ΠΉ ΠΎΡΠΌΠ΅ΡΠ°Π»ΠΈΡΡ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΡΠ΅ ΠΏΡΠΈΠ·Π½Π°ΠΊΠΈ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π°, Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ ΠΈ ΡΠΈΠ±ΡΠΈΠ½ΠΎΠ»ΠΈΠ·Π° β ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΡΠΎΠ²Π½Ρ ΡΡΠ²ΠΎΡΠΎΡΠΎΡΠ½ΠΎΠ³ΠΎ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½Π° (p<0,001), ΠΆΠ΅Π»Π΅Π·Π° (p><0,005) ΠΈ Π°Π»ΡΠ±ΡΠΌΠΈΠ½Π° (p><0,001), Π»ΠΈΠΌΡΠΎΡΠΈΡΠΎΠ² (p><0,001) Π² ΠΊΡΠΎΠ²ΠΈ, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΡ Π² Π½Π΅ΠΉ Π»Π΅ΠΉΠΊΠΎΡΠΈΡΠΎΠ² (p><0,001), Π½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΠΎΠ² (p><0,001), Π‘Π Π (p><0,005), ΠΠ-6 (p><0,001), D-Π΄ΠΈΠΌΠ΅ΡΠ° (p><0,005), Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΡΡΠΎΡΠ½ΠΎΠΉ (p><0,005) ΠΈ ΠΈΠ½Π΄ΡΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΡΠΊΡΠ΅ΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΠΌΠΎΡΠΎΠΉ (p><0,001). Π·Π°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅ ΠΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΎ, ΡΡΠΎ Π² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ ΡΡΠΆΠ΅Π»ΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ COVID-19 ΠΈΠΌΠ΅Π΅Ρ ΠΌΠ΅ΡΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π° ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠΉ ΡΡΠ°ΠΊΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π°. ΠΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ ΠΆΠ΅Π»Π΅Π·Π° ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π²ΡΠ·Π²Π°Π½ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠ»Π΅ΡΠΎΠΊ Ρ Π²ΡΡΠ²ΠΎΠ±ΠΎΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΆΠ΅Π»Π΅Π·Π° ΠΈΠ· ΡΠΈΡΠΎΡ
ΡΠΎΠΌΠΎΠ², ΠΌΠΈΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π°, Π³Π΅ΠΌΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π° Π»ΠΈΠ±ΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² ΡΠ²ΡΠ·ΡΠ²Π°Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ, ΡΡΠΎ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠΌ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΡΡΡΠΊΡΡΡΡ Π±Π΅Π»ΠΊΠ° ΠΈΠ»ΠΈ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Π² ΡΡΠ΅Ρ
Π²Π°Π»Π΅Π½ΡΠ½ΠΎΠ΅ ΡΠΎΡΡΠΎΡΠ½ΠΈΠ΅. ΠΡΠΈ ΠΎΡΠ΅Π½ΠΊΠ΅ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ Π²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π½Π° ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌ ΡΠ»Π΅Π΄ΡΠ΅Ρ ΡΡΠΈΡΡΠ²Π°ΡΡ ΠΈ Π²Π»ΠΈΡΠ½ΠΈΠ΅ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠΎΠ² ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π°, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΡΠ΅Π½ΠΊΡ ΡΡΠΎΠ²Π½Ρ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ, Π½Π΅ ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠ³ΠΎ Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ ΠΆΠ΅Π»Π΅Π·Π°. ΠΠ»ΡΡΠ΅Π²ΡΠ΅ ΡΠ»ΠΎΠ²Π°: Π½ΠΎΠ²Π°Ρ ΠΊΠΎΡΠΎΠ½Π°Π²ΠΈΡΡΡΠ½Π°Ρ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡ, COVID-19, SARS-CoV-2, ΠΎΠ±ΠΌΠ΅Π½ ΠΆΠ΅Π»Π΅Π·Π°, ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ΅ ΠΆΠ΅Π»Π΅Π·ΠΎ, ΡΠ΅ΡΡΠΈΡΠΈΠ½, ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½, NTBI, nontransferrin bound iron>Λ0,001), ΠΆΠ΅Π»Π΅Π·Π° (pΛ0,005) ΠΈ Π°Π»ΡΠ±ΡΠΌΠΈΠ½Π° (pΛ0,001), Π»ΠΈΠΌΡΠΎΡΠΈΡΠΎΠ² (pΛ0,001) Π² ΠΊΡΠΎΠ²ΠΈ, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΡ Π² Π½Π΅ΠΉ Π»Π΅ΠΉΠΊΠΎΡΠΈΡΠΎΠ² (pΛ0,001), Π½Π΅ΠΉΡΡΠΎΡΠΈΠ»ΠΎΠ² (pΛ0,001), Π‘Π Π (pΛ0,005), ΠΠ-6 (pΛ0,001), D-Π΄ΠΈΠΌΠ΅ΡΠ° (pΛ0,005), Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΡΡΠΎΡΠ½ΠΎΠΉ (p0,005) ΠΈ ΠΈΠ½Π΄ΡΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΡΠΊΡΠΊΡΠ΅ΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΠΌΠΎΡΠΎΠΉ (pΛ0,001).ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΠΎΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΎ, ΡΡΠΎ Π² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ ΡΡΠΆΠ΅Π»ΠΎΠ³ΠΎ ΡΠ΅ΡΠ΅Π½ΠΈΡ COVID-19 ΠΈΠΌΠ΅Π΅Ρ ΠΌΠ΅ΡΡΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π° ΠΈ Π½Π°Π»ΠΈΡΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠΉ ΡΡΠ°ΠΊΡΠΈΠΈ ΠΆΠ΅Π»Π΅Π·Π°. ΠΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ ΠΆΠ΅Π»Π΅Π·Π° ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ Π²ΡΠ·Π²Π°Π½ΠΎ ΠΏΠΎΠ²ΡΠ΅ΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠ»Π΅ΡΠΎΠΊ Ρ Π²ΡΡΠ²ΠΎΠ±ΠΎΠΆΠ΄Π΅Π½ΠΈΠ΅ΠΌ ΠΆΠ΅Π»Π΅Π·Π° ΠΈΠ· ΡΠΈΡΠΎΡ
ΡΠΎΠΌΠΎΠ², ΠΌΠΈΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π°, Π³Π΅ΠΌΠΎΠ³Π»ΠΎΠ±ΠΈΠ½Π° Π»ΠΈΠ±ΠΎ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² ΡΠ²ΡΠ·ΡΠ²Π°Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ, ΡΡΠΎ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠΎΠΌ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΡΡΡΡΠΊΡΡΡΡ Π±Π΅Π»ΠΊΠ° ΠΈΠ»ΠΈ Π½Π°ΡΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΡ ΠΆΠ΅Π»Π΅Π·Π° Π² ΡΡΠ΅Ρ
Π²Π°Π»Π΅Π½ΡΠ½ΠΎΠ΅ ΡΠΎΡΡΠΎΡΠ½ΠΈΠ΅. ΠΡΠΈ ΠΎΡΠ΅Π½ΠΊΠ΅ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ Π²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ Π²Π»ΠΈΡΠ½ΠΈΡ Π½Π° ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌ ΡΠ»Π΅Π΄ΡΠ΅Ρ ΡΡΠΈΡΡΠ²Π°ΡΡ ΠΈ Π²Π»ΠΈΡΠ½ΠΈΠ΅ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠΎΠ² ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΆΠ΅Π»Π΅Π·Π°, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΎΡΠ΅Π½ΠΊΡ ΡΡΠΎΠ²Π½Ρ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΠ³ΠΎ, Π½Π΅ ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠ³ΠΎ Ρ ΡΡΠ°Π½ΡΡΠ΅ΡΡΠΈΠ½ΠΎΠΌ ΠΆΠ΅Π»Π΅Π·Π°.
- β¦