Institution
Kazan Federal University
Education•Kazan’, Russia•
About: Kazan Federal University is a education organization based out in Kazan’, Russia. It is known for research contribution in the topics: Population & Chemistry. The organization has 9868 authors who have published 14390 publications receiving 135726 citations. The organization is also known as: Kazan (Volga region) Federal University & Kazan State University.
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TL;DR: In this paper, serum cytokine profiles associated with HPS revealed a more proinflammatory milieu as compared to HFRS, and HPS was strictly characterized by the upregulation of cytokine levels.
Abstract: Hantavirus infection is an acute zoonosis that clinically manifests in two primary forms, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). HFRS is endemic in Europe and Russia, where the mild form of the disease, is prevalent in the Tatarstan region. HPS is endemic in Argentina, as well as other countries of North and South American. HFRS and HPS are usually acquired via the upper respiratory tract by inhalation of virus-contaminated aerosol. Although the pathogenesis of HFRS and HPS remains largely unknown, postmortem tissue studies have identified endothelial cells as the primary target of infection. Importantly, cell damage due to virus replication, or subsequent tissue repair, have not been documented. Since no single factor has been identified that explains the complexity of HFRS or HPS pathogenesis, it has been suggested that a cytokine storm may play a crucial role in the manifestation of both diseases. In order to identify potential serological markers that distinguish HFRS and HPS, serum samples collected during early and late phases of the disease were analyzed for 48 analytes using multiplex magnetic bead-based assays. Overall, serum cytokine profiles associated with HPS revealed a more proinflammatory milieu as compared to HFRS. Furthermore, HPS was strictly characterized by the upregulation of cytokine levels, in contrast to HFRS where cases were distinguished by a dichotomy in serum cytokine levels. The severe form of hantavirus zoonosis, HPS, was characterized by the upregulation of a higher number of cytokines than HFRS (40 vs. 21). In general, our analysis indicates that, although HPS and HFRS share many characteristic features, there are distinct cytokine profiles for these diseases. These profiles suggest a strong activation of an innate immune and inflammatory responses are associated with HPS, relative to HFRS, as well as a robust activation of Th1-type immune responses. Lastly, the results of our analysis suggest that serum cytokines profiles of HPS and HFRS cases are consistent with the presence of extracellular matrix degradation, increased mononuclear leukocyte proliferation and transendothelial migration.
38 citations
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TL;DR: Large-scale and long-time molecular dynamics simulations demonstrating the transformation of a single kaolin alumosilicate sheet to a halloysite nanotube are reported, which show the tendency to form twin-tube structures.
Abstract: We report large-scale and long-time molecular dynamics simulations demonstrating the transformation of a single kaolin alumosilicate sheet to a halloysite nanotube. The models we consider contain up to 5 × 105 atoms, which is two orders of magnitude larger than that used in previous theoretical works. It was found that the temperature plays a crucial role in the formation of the rolled geometry of the halloysite. For the models with periodic boundary conditions, we observe the tendency to form twin-tube structures, which is confirmed experimentally by atomic force microscopy imaging. The molecular dynamics calculations show that the rate of the rolling process is very sensitive to the choice of the winding axis and varies from 5 ns to 25 ns. The effects of the open boundary conditions and the initial form of the kaolin alumosilicate sheet are discussed. Our simulation results are consistent with experimental TEM and AFM halloysite tube imaging.
38 citations
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TL;DR: The results indicate that the pathogenic PF4-containing HIT-like immune complexes induce direct prothrombotic platelet activation via FcγRIIA receptors followed by non-apoptotic calpain-dependent death of platelets, which can be an important mechanism of thrombocytopenia during HIT development.
Abstract: Heparin-induced thrombocytopenia (HIT) is a complication of heparin therapy sometimes associated with thrombosis. The hallmark of HIT is antibodies to the heparin/platelet factor 4 (PF4) complex that cause thrombocytopenia and thrombosis through platelet activation. Despite the clinical importance, the molecular mechanisms and late consequences of immune platelet activation are not fully understood. Here, we studied immediate and delayed effects of the complexes formed by human PF4 and HIT-like monoclonal mouse anti-human-PF4/heparin IgG antibodies (named KKO) on isolated human platelets in vitro. Direct platelet-activating effect of the KKO/PF4 complexes was corroborated by the overexpression of phosphatidylserine (PS) and P-selectin on the platelet surface. The immune platelet activation was accompanied by a decrease of the mitochondrial transmembrane potential (ΔΨm), concurrent with a significant gradual reduction of the ATP content in platelets, indicating disruption of energy metabolism. A combination of PS expression and mitochondrial depolarization induced by the PF4-containing immune complexes observed in a substantial fraction of platelets was considered as a sign of ongoing platelet death, as opposed to a subpopulation of activated live platelets with PS on the plasma membrane but normal ΔΨm. Both activated and dying platelets treated with KKO/PF4 formed procoagulant extracellular microvesicles bearing PS on their surface. Scanning and transmission electron microscopy revealed dramatic morphological changes of KKO/PF4-treated platelets, including their fragmentation, another indicator of cell death. Most of the effects of KKO/PF4 were prevented by an anti-FcγRII monoclonal antibody IV.3. The adverse functional and structural changes in platelets induced by the KKO/PF4 complexes were associated with strong time-dependent activation of calpain, but only trace cleavage of caspase 3. The results indicate that the pathogenic PF4-containing HIT-like immune complexes induce direct prothrombotic platelet activation via FcγRIIA receptors followed by non-apoptotic calpain-dependent death of platelets, which can be an important mechanism of thrombocytopenia during HIT development.
38 citations
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TL;DR: In this paper, the straightforward dressing of macroscopically shaped supports (i.e., β-SiC and α-Al2O3) with a mesoporous and highly nitrogen-doped carbon-phase starting from food processing raw materials is described.
38 citations
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TL;DR: In this paper, the problem of finding the eigenvalues and eigenfunctions of an ordinary second-order differential problem with a spectral parameter nonlinearly occurring in the boundary condition at the load attachment point is reduced to finding the Eigenvalue and Eigenfunction of a bar with an elastically attached load.
Abstract: We study the problem on the eigenvibrations of a bar with an elastically attached load. The problem is reduced to finding the eigenvalues and eigenfunctions of an ordinary secondorder differential problem with a spectral parameter nonlinearly occurring in the boundary condition at the load attachment point. We prove the existence of countably many simple positive eigenvalues of the differential problem. The problem is approximated by a grid scheme of the finite element method. We study the convergence and accuracy of the approximate solutions.
38 citations
Authors
Showing all 10096 results
Name | H-index | Papers | Citations |
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Richard G. Pestell | 130 | 479 | 54210 |
Alexander Spiridonov | 126 | 1198 | 77296 |
V. Stolyarov | 119 | 238 | 79004 |
Sergei D. Odintsov | 112 | 609 | 62524 |
Hans-Uwe Simon | 96 | 461 | 51698 |
Yuri Lvov | 89 | 342 | 27397 |
Alexei A. Starobinsky | 88 | 340 | 42331 |
Yakov Kuzyakov | 87 | 667 | 37050 |
V. E. Semenov | 74 | 372 | 22577 |
John W. Weisel | 73 | 323 | 17866 |
Klaus T. Preissner | 72 | 333 | 21289 |
Alexander Tropsha | 71 | 288 | 22898 |
Roland Winter | 68 | 468 | 15193 |
Christoph Schick | 68 | 443 | 16664 |
Marat Gilfanov | 62 | 350 | 14987 |