68 research outputs found

    Magnetization reversal of ferromagnetic nanodisc placed above a superconductor

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    Using numerical simulation we have studied a magnetization distribution and a process of magnetization reversal in nanoscale magnets placed above a superconductor plane. In order to consider an influence of superconductor on magnetization distribution in the nanomagnet we have used London approximation. We have found that for usual values of London penetration depth the ground state magnetization is mostly unchanged. But at the same time the fields of vortex nucleation and annihilation change significantly: the interval where vortex is stable enlarges on 100-200 Oe for the particle above the superconductor. Such fields are experimentally observable so there is a possibility of some practical applications of this effect.Comment: 8 pages, 9 figure

    INTERLEUKIN 33 AND FIBROSIS: PATHOGENESIS UPDATED

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    Interleukin 33 (IL-33) is a member of the IL-1 family, which is widely expressed on all types of cells. IL-33 was identified as a functional ligand for the plasma membrane receptor complex, which is a heterodimer consisting of a membrane bound ST2 receptor (growth stimulating factor). IL-33 is involved in the development of immune response with predominant release of pro-inflammatory T helper type 2 cytokines. IL-33 is widely expressed on various structure-forming cells, such as epithelial, endothelial and smooth muscle cells. Increased expression of IL-33 is observed during necrosis of these cells (after tissue or cell damage), and it is released into extracellular space, and acts as an endogenous danger signal, sending a sort of warnings to neighboring cells and tissues. Recently, many studies have shown that IL-33 can participate in development and progression of fibrosis in various organs. However, it exerts anti-inflammatory effects upon development of other diseases. This review will discuss biological characteristics of IL-33 and a role of the IL-33/ST2 signaling pathway in the development of fibrosis

    A New Chapter in the Treatment of Patients with Heart Failure. The Role of Sodium-Glucose Co-transporter Type 2 Inhibitors

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    Heart failure (HF) remains one of the major social and medical public health problems worldwide. Despite new advances in the treatment of patients with HF, the prognosis is still poor. According to the European Cardiology Society guidelines for the diagnosis and treatment of acute and chronic heart failure (CHF) 2021, a new class of drugs related to hypoglycemic has been confirmed to be effective in influencing the survival of patients with heart failure with low ejection fraction (HFpEF), regardless of the presence of disorders of carbohydrate metabolism. We are talking about inhibitors of the sodium-glucose co-transporter type 2 (iSGLT-2) or gliflozins. The article presents the results of the latest large clinical trials on the effective use of SGLT-2 in patients with HF, not only with low, but also with intact ejection fraction (HFpEF), for which there is no evidence base at the present stage. The review article presents the results of experimental studies that explored the potential mechanisms of action of gliflozins with an emphasis on new ones that are of fundamental importance for patients with heart failure, and also describes controversial and little-studied issues. Currently, there is no therapy that improves outcomes in patients with acute heart failure. The article presents the results of small analyzes of the use of iSGLT-2 in this category of patients, which are the basis for the hypothesis of their potentially effective and safe use in the case of acute decompensation of CHF, however, the role of gliflozins in this category of patients requires further in-depth study

    Clinical Efficacy and Safety of Empagliflozin in Patients with Acute Heart Failure from the First Day of Hospitalization

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    Aim. Evaluation of the safety, clinical and hemodynamic effects of empagliflozin in patients with acute decompensated heart failure (ADHF) from the first day of hospitalization in the absence of signs of hemodynamic instability.Material and methods. A prospective, comparative, randomized study included 46 patients admitted to the hospital in connection with ADHF in the absence of signs of hemodynamic instability. Inclusion in the study and randomization to receive empagliflozin was carried out in the first 24 hours from the moment of admission to the hospital. The main group (n=23) from the first day of hospitalization and the entire subsequent follow-up period took empagliflozin at a daily dose of 10 and 25 mg (for patients with type 2 diabetes mellitus) in addition to basic therapy, the control group (n=23) received standard therapy without gliflozines. The observation period was 3 months and included 3 control points: 1st day of hospitalization, 7th-12th day, 3rd month of observation. Clinical, anamnestic and instrumental data were evaluated at all control points.Results. In the hospital period, by the 7th-12th day, only in the main group there was an improvement in all clinical indicators (p<0.01), an increase in the rate of diuresis (p><0.01), a decrease in the daily dose of the parenteral diuretic furosemide from 54 mg to 26 mg (p><0.01). A decrease in systolic blood pressure (SBP) occurred in both groups (p><0.01), but it was more pronounced in the comparison group [from 141 (110; 160) to 110 (90; 120) mm Hg) compared to the main group [from 140 (120; 160) to 120 (110; 130) mm Hg]. According to echocardiography data in the main group, there was a decrease in the indexed volume of the right atrium, the end-systolic volume of the left ventricle (LV ESV) and systolic pressure in the pulmonary artery, an increase in the LV ejection fraction (LV EF) (p><0.05). In the comparison group, only an increase in LV ESV was noted (p=0.04). The index of the indexed volume of the left atrium did not show significant dynamics in the main group (p=0.79), but showed a significant decrease>Λ‚0.01), a decrease in the daily dose of the parenteral diuretic furosemide from 54 mg to 26 mg (p<0.01). A decrease in systolic blood pressure (SBP) occurred in both groups (p>Λ‚0.01), but it was more pronounced in the comparison group [from 141 (110; 160) to 110 (90; 120) mm Hg) compared to the main group [from 140 (120; 160) to 120 (110; 130) mm Hg]. According to echocardiography data in the main group, there was a decrease in the indexed volume of the right atrium, the end-systolic volume of the left ventricle (LV ESV) and systolic pressure in the pulmonary artery, an increase in the LV ejection fraction (LV EF) (pΛ‚0.05). In the comparison group, only an increase in LV ESV was noted (p=0.04). The index of the indexed volume of the left atrium did not show significant dynamics in the main group (p=0.79), but showed a significant decrease in the 2nd and 3rd control points compared to the control group (p=0.01 and p=0.02). Complications, against the background of taking empagliflozin, were not noted: there were no episodes of hypotension (SBPΛ‚90 mm Hg), hypoglycemia, acute kidney injury.Conclusion. The results obtained indicate the safety of empagliflozin in patients with ADHF, regardless of the status of carbohydrate metabolism and LV EF, as well as taking into account the clinical (more intense positive dynamics of clinical symptoms of ADHF) and hemodynamic (smooth decrease in SBP, increased diuretic effect) effects of empagliflozin, this drug should be considered as an effective and safe supplement to the main therapy from the first day of hospitalization in patients with stable hemodynamic parameters

    New biological markers for a prognostic model for assessing the risk of cardiac fibrosis in patients with ST-segment elevation myocardial infarction

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    HighlightsThe developed prognostic model for assessing the risk of cardiac fibrosis in patients with STEMI with HFmrEF and HFpEF is promising from the point of view of scientific and clinical potential because similar models for predicting the risk of cardiac fibrosis in patients with index MI are not currently validated. The developed scale includes such parameters as age, LVEF, COL-1, BMI, MMP-2. The scale can be used in patients with HFmrEF and HFpEF phenotypes. Identification of patients at high risk of myocardial fibrosis will allow choosing the appropriate treatment method.Β Aim. To develop a prognostic model for assessing the risk of cardiac fibrosis (CF) in patients with preserved left ventricular ejection fraction (HFpEF) and mildly reduced ejection fraction (HFmrEF) a year after ST-segment elevation myocardial infarction (STEMI) based on clinical, instrumental and biochemical data.Methods. The prospective cohort study included 100 STEMI patients with HFmrEF (LVEF 40–49%) and with HFpEF (50% or more). Echo was performed in all patients on the 1st, 10–12th day and a year after onset of STEMI. Upon admission to the hospital and on the 10–12th day after the onset of the disease, the following serum biomarker levels were determined: those associated with changes in the extracellular matrix; with remodeling and fibrosis; with inflammation, and with neurohormonal activation. At the 1-year follow-up visit, 84 patients underwent contrast-enhanced MRI to assess fibrotic tissue percentage relative to healthy myocardium.Results. The distribution of patients by HFmrEF and HFpEF phenotypes during follow-up was as follows: HFmrEF on the 1st day – 27%, 10th day – 12%, after a year – 11%; HFpEF on the 1st day – 73%, 10th day – 88%, after a year – 89%. According to cardiac MRI at the follow-up visit (n = 84), the median distribution of fibrotic tissue percentage was 5 [1.5; 14]%. Subsequently, the threshold value of 5% was chosen for analysis: CFβ‰₯5% was found in 38 patients (the 1st group), whereas CF<5% was noted in 46 patients (the 2nd group). When analyzing the intergroup differences in biological marker concentrations in the in-patient setting and at the annual follow-up, it was determined that the most significant differences were associated with β€œST-2” (1st day) that in the β€œCFβ‰₯5%” group was 11.4 ng/mL higher on average compared to the β€œCF<5%” group (p = 0.0422); β€œCOL-1” (1st day) that in the β€œCFβ‰₯5%” group was 28112.3 pg/mL higher on average compared to the β€œCF<5%” group (p = 0.0020), and β€œNT-proBNP” (12th day) that in the β€œCF<5 %” group was 1.9 fmol/mL higher on average compared to the β€œCFβ‰₯5%” group (p = 0.0339). Certain factors (age, LVEF (12th day), collagen-1 (1st and 12th day), body mass index, matrix metalloproteinase-2 (12th day) were determined and included in the prognostic model for assessing the risk of CF a year after the STEMI (AUC ROC 0.90, Chi-square test <0.0001).Conclusion. Prognostic model (scale) based on factors such as age, left ventricular ejection fraction (12th day), collagen-1 (1st and 12th day), body mass index, matrix metalloproteinase-2 (12th day) shows high prognostic power and enables identification of patients with HFmrEF and HFpEF phenotypes and at high risk of cardiac fibrosis a year after STEMI

    Interacting circular nanomagnets

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    Regular 2D rectangular lattices of permalloy nanoparticles (40 nm in diameter) were prepared by the method of the electron lithography. The magnetization curves were studied by Hall magnetometry with the compensation technique for different external field orientations at 4.2K and 77K. The shape of hysteresis curves indicates that there is magnetostatic interaction between the particles. The main peculiarity is the existence of remanent magnetization perpendicular to easy plain. By numerical simulation it is shown, that the character of the magnetization reversal is a result of the interplay of the interparticle interaction and the magnetization distribution within the particles (vortex or uniform).Comment: 16 pages, 8 figure

    A hysteresis model with dipole interaction: one more devil-staircase

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    Magnetic properties of 2D systems of magnetic nanoobjects (2D regular lattices of the magnetic nanoparticles or magnetic nanostripes) are considered. The analytical calculation of the hysteresis curve of the system with interaction between nanoobjects is provided. It is shown that during the magnetization reversal system passes through a number of metastable states. The kinetic problem of the magnetization reversal was solved for three models. The following results have been obtained. 1) For 1D system (T=0) with the long-range interaction with the energy proportional to rβˆ’pr^{-p}, the staircase-like shape of the magnetization curve has self-similar character. The nature of the steps is determined by interplay of the interparticle interaction and coercivity of the single nanoparticle. 2) The influence of the thermal fluctuations on the kinetic process was examined in the framework of the nearest-neighbor interaction model. The thermal fluctuations lead to the additional splitting of the steps on the magnetization curve. 3) The magnetization curve for system with interaction and coercivity dispersion was calculated in mean field approximation. The simple method to experimentally distinguish the influence of interaction and coercivity dispersion on the magnetization curve is suggested.Comment: 22 pages, 8 figure

    Two novel mutations associated with ataxia-telangiectasia identified using an ion ampliSeq inherited disease panel

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    Β© 2017 Kuznetsova, Trofimov, Shubina, Kochetkova, Karetnikova, Barkov, Bakharev, Gusev and Sukhikh. Ataxia-telangiectasia (A-T), or Louis-Bar syndrome, is a rare neurodegenerative disorder associated with immunodeficiency. For families with at least one affected child, timely A-T genotyping during any subsequent pregnancy allows the parents to make an informed decision about whether to continue to term when the fetus is affected. Mutations in the ATM gene, which is 150 kb long, give rise to A-T; more than 600 pathogenic variants in ATM have been characterized since 1990 and new mutations continue to be discovered annually. Therefore, limiting genetic screening to previously known SNPs by PCR or hybridization with microarrays may not identify the specific pathog enic genotype in ATM for a given A-T family. However, recent developments in next-generation sequencing technology offer prompt high-throughput full-length sequencing of genomic fragments of interest. This allows the identification of the whole spectrum of mutations in a gene, including any novel ones. We report two A-T families with affected children and current pregnancies. Both families are consanguineous and originate from Caucasian regions of Russia and Azerbaijan. Before our study, no ATM mutations had been identified in the older children of these families. We used ion semiconductor sequencing and an Ion AmpliSeq β„’ Inherited Disease Panel to perform complete ATM gene sequencing in a single member of each family. Then we compared the experimentally determined genotype with the affected/normal phenotype distribution in the whole family to provide unambiguous evidence of pathogenic mutations responsible for A-T. A single novel SNP was allocated to each family. In the first case, we found a mononucleotide deletion, and in the second, a mononucleotide insertion. Both mutations lead to truncation of the ATM protein product. Identification of the pathogenic mutation in each family was performed in a timely fashion, allowing the fetuses to be tested and diagnosed. The parents chose to continue with both pregnancies as both fetuses had a healthy genotype and thus were not at risk of A-T

    ИНЀАРКВ ΠœΠ˜ΠžΠšΠΠ Π”Π 2-Π“Πž ВИПА: Π‘ΠžΠ’Π Π•ΠœΠ•ΠΠΠ«Π™ Π’Π—Π“Π›Π―Π” НА ΠŸΠ ΠžΠ‘Π›Π•ΠœΠ£

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    HighlightsThe article describes the main differences between the types of myocardial infarction, in particular, differences between type 1 and type 2 myocardial infarction, the complexity of diagnosis and management of patients with myocardial infarction type 2, and summarizes data on the prevalence of patients with myocardial infarction type 2. The arguments supporting the need for further researches to differentiate various phenotypes of myocardial infarction are provided.Β AbstractDespite the high interest in the study of type 2 MI, many unresolved issues concerning diagnosis, criteria for diagnosis and, especially, therapeutic tactics remain unresolved. The available data regarding type 2 MI remain limited and inconsistent, and are based on sources that include the analysis of type 1 MI. According to various predictions, the prevalence of type 2 MI will increase even more. Type 2 MI management strategy should be patient-specific and in accordance with the etiology and pathogenesis, therefore, timely diagnosis, and MI differentiation according to universally accepted definitions is a relevant scientific topic and a practical necessity.Thus, summarizing all the above, we can say that type 2 myocardial infarction is a topic that encompasses many unresolved issues concerning diagnosis, patient management and further secondary prevention.ΠžΡΠ½ΠΎΠ²Π½Ρ‹Π΅ полоТСнияВ ΠΎΠ±Π·ΠΎΡ€Π΅ освСщСны основныС различия Ρ‚ΠΈΠΏΠΎΠ² ΠΈΠ½Ρ„Π°Ρ€ΠΊΡ‚Π° ΠΌΠΈΠΎΠΊΠ°Ρ€Π΄Π°, Π² частности отличия ΠΈΠ½Ρ„Π°Ρ€ΠΊΡ‚Π° 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ° ΠΎΡ‚ 1-Π³ΠΎ Ρ‚ΠΈΠΏΠ°, описаны слоТности диагностики ΠΈ вСдСния ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚ΠΎΠ² с ΠΈΠ½Ρ„Π°Ρ€ΠΊΡ‚ΠΎΠΌ ΠΌΠΈΠΎΠΊΠ°Ρ€Π΄Π° 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ°, ΠΎΠ±ΠΎΠ±Ρ‰Π΅Π½Ρ‹ Π΄Π°Π½Π½Ρ‹Π΅ ΠΎ частотС выявлСния Π΄Π°Π½Π½ΠΎΠ³ΠΎ Ρ‚ΠΈΠΏΠ° заболСвания. ΠŸΡ€Π΅Π΄ΡΡ‚Π°Π²Π»Π΅Π½Ρ‹ Π°Ρ€Π³ΡƒΠΌΠ΅Π½Ρ‚Ρ‹ Π² ΠΏΠΎΠ»ΡŒΠ·Ρƒ нСобходимости Π΄Π°Π»ΡŒΠ½Π΅ΠΉΡˆΠΈΡ… исслСдований, посвящСнных ΠΈΠ·ΡƒΡ‡Π΅Π½ΠΈΡŽ Ρ€Π°Π·Π»ΠΈΡ‡Π½Ρ‹Ρ… Ρ„Π΅Π½ΠΎΡ‚ΠΈΠΏΠΎΠ² ΠΈΠ½Ρ„Π°Ρ€ΠΊΡ‚Π° ΠΌΠΈΠΎΠΊΠ°Ρ€Π΄Π°.Β Π Π΅Π·ΡŽΠΌΠ΅ΠΠ΅ΡΠΌΠΎΡ‚Ρ€Ρ Π½Π° высокий интСрСс ΠΊ ΠΈΠ·ΡƒΡ‡Π΅Π½ΠΈΡŽ ΠΈΠ½Ρ„Π°Ρ€ΠΊΡ‚Π° ΠΌΠΈΠΎΠΊΠ°Ρ€Π΄Π° (ИМ) 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ°, остаСтся мноТСство Π½Π΅Ρ€Π΅ΡˆΠ΅Π½Π½Ρ‹Ρ… вопросов, связанных с диагностикой, критСриями постановки Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π° ΠΈ, ΠΏΡ€Π΅ΠΆΠ΄Π΅ всСго, Ρ‚Π°ΠΊΡ‚ΠΈΠΊΠΎΠΉ лСчСния заболСвания. Доступная информация ΠΎΠ± ИМ 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ° основана Π½Π° Π·Π°Ρ€ΡƒΠ±Π΅ΠΆΠ½Ρ‹Ρ… источниках, Π²ΠΊΠ»ΡŽΡ‡Π°ΡŽΡ‰ΠΈΡ… Π°Π½Π°Π»ΠΈΠ· ИМ 1-Π³ΠΎ Ρ‚ΠΈΠΏΠ°, ΠΈ носит ΠΎΠ³Ρ€Π°Π½ΠΈΡ‡Π΅Π½Π½Ρ‹ΠΉ ΠΈ Ρ€Π°Π·Ρ€ΠΎΠ·Π½Π΅Π½Π½Ρ‹ΠΉ Ρ…Π°Ρ€Π°ΠΊΡ‚Π΅Ρ€. По ΠΏΡ€ΠΎΠ³Π½ΠΎΠ·Π°ΠΌ, Ρ€Π°ΡΠΏΡ€ΠΎΡΡ‚Ρ€Π°Π½Π΅Π½Π½ΠΎΡΡ‚ΡŒ ИМ 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ° Π±ΡƒΠ΄Π΅Ρ‚ Ρ‚ΠΎΠ»ΡŒΠΊΠΎ ΡƒΠ²Π΅Π»ΠΈΡ‡ΠΈΠ²Π°Ρ‚ΡŒΡΡ. Π’Π°ΠΊΡ‚ΠΈΠΊΠ° вСдСния Π±ΠΎΠ»ΡŒΠ½Ρ‹Ρ… ИМ 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ° Π΄ΠΎΠ»ΠΆΠ½Π° ΠΎΠΏΡ€Π΅Π΄Π΅Π»ΡΡ‚ΡŒΡΡ ΠΈΠ½Π΄ΠΈΠ²ΠΈΠ΄ΡƒΠ°Π»ΡŒΠ½ΠΎ Π² ΠΊΠ°ΠΆΠ΄ΠΎΠΉ ΠΊΠΎΠ½ΠΊΡ€Π΅Ρ‚Π½ΠΎΠΉ клиничСской ситуации Π² соотвСтствии с этиологиСй ΠΈ ΠΏΠ°Ρ‚ΠΎΠ³Π΅Π½Π΅Π·ΠΎΠΌ, поэтому своСврСмСнная диагностика ΠΈ конкрСтизация Ρ‚ΠΈΠΏΠ° ИМ ΠΏΠΎ Π£Π½ΠΈΠ²Π΅Ρ€ΡΠ°Π»ΡŒΠ½ΠΎΠΌΡƒ ΠΎΠΏΡ€Π΅Π΄Π΅Π»Π΅Π½ΠΈΡŽ ΠΏΡ€Π΅Π΄ΡΡ‚Π°Π²Π»ΡΡŽΡ‚ Π½Π΅ Ρ‚ΠΎΠ»ΡŒΠΊΠΎ Π½Π°ΡƒΡ‡Π½Ρ‹ΠΉ, Π½ΠΎ ΠΈ практичСский интСрСс. Π’Π°ΠΊΠΈΠΌ ΠΎΠ±Ρ€Π°Π·ΠΎΠΌ, вопросы диагностики ΠΈΠ½Ρ„Π°Ρ€ΠΊΡ‚ ΠΌΠΈΠΎΠΊΠ°Ρ€Π΄Π° 2-Π³ΠΎ Ρ‚ΠΈΠΏΠ°, вСдСния ΠΏΠ°Ρ†ΠΈΠ΅Π½Ρ‚ΠΎΠ² ΠΈ Π²Ρ‚ΠΎΡ€ΠΈΡ‡Π½ΠΎΠΉ ΠΏΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΠΊΠΈ Ρ‚Ρ€Π΅Π±ΡƒΡŽΡ‚ дальнСйшСго исслСдования
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