Intersite Coulomb repulsion driven quadrupole instability and magnetic ordering in the orbital frustrated Ba2_2MgReO6_6

We develop an unrestricted Hartree-Fock mean-field method including Coulomb repulsion U, V and spin-orbital coupling $\lambda$ self$-$consistently to investigate the mechanism of structural instability and magnetic ordering in Ba$_2$MgReO$_6$. A comprehensive quadrupole phase diagram versus U and V with $\lambda$=0.28eV is calculated. Our results demonstrate that, while U and $\lambda$ mainly lead to the onsite quadrupole $Q_{x^2-y^2}$ and $Q_{3z^2-r^2}$ with orbital frustration, the easy-plane anisotropy or the intersite Coulomb repulsion V can remove the frustration. Finally, the V$>$10meV would arrange $Q_{x^2-y^2}$ antiparallelly, accompanied with small parallel $Q_{3z^2-r^2}$, and stabilize Ba$_2$MgReO$_6$ into the body centered tetragonal structure. Such antiparallel $Q_{x^2-y^2}$ provides a new mechanism of Dzyaloshinskii-Moriya interaction, and gives rise to the canted antiferromagnetic (CAF) state along [110] axis. Moreover, sizable octupoles such as $O_{21}^{31}$, $O_{21}^{33}$, $O_{21}^{34}$ and $O_{21}^{36}$ are discovered for the first time in CAF states. Our study not only provides a comprehensive understanding of the nature and exotic properties in Ba$_2$MgReO$_6$, but also reveals some commonality of 5d compounds

Altered microRNA expression profile with miR-146a upregulation in CD4+ T cells from patients with rheumatoid arthritis

Introduction: Increasing evidence indicates that microRNAs (miRNAs) play a critical role in the pathogenesis of inflammatory diseases. The aim of the study was to investigate the expression pattern and function of miRNAs in CD4 + T cells from patients with rheumatoid arthritis (RA).Methods: The expression profile of miRNAs in CD4 + T cells from synovial fluid (SF) and peripheral blood of 33 RA patients was determined by microarray assay and validated by qRT-PCR analysis. The correlation between altered expression of miRNAs and cytokine levels was determined by linear regression analysis. The role of miR-146a overexpression in regulating T cell apoptosis was evaluated by flow cytometry. A genome-wide gene expression analysis was further performed to identify miR-146a-regulated genes in T cells.Results: miRNA expression profile analysis revealed that miR-146a expression was significantly upregulated while miR-363 and miR-498 were downregulated in CD4 + T cells of RA patients. The level of miR-146a expression was positively correlated with levels of tumor necrosis factor-alpha (TNF-α), and in vitro studies showed TNF-α upregulated miR-146a expression in T cells. Moreover, miR-146a overexpression was found to suppress Jurkat T cell apoptosis. Finally, transcriptome analysis of miR-146a overexpression in T cells identified Fas associated factor 1 (FAF1) as a miR-146a-regulated gene, which was critically involved in modulating T cell apoptosis.Conclusions: We have detected increased miR-146a in CD4 + T cells of RA patients and its close correlation with TNF-α levels. Our findings that miR-146a overexpression suppresses T cell apoptosis indicate a role of miR-146a in RA pathogenesis and provide potential novel therapeutic targets. © 2010 Li et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.published_or_final_versio

Antibody Responses and the Effects of Clinical Drugs in COVID-19 Patients

The coronavirus disease 2019 (COVID-19) emerged around December 2019 and have become a global epidemic disease currently. Specific antibodies against SAS-COV-2 could be detected in COVID-19 patients’ serum or plasma, but the clinical values of these antibodies as well as the effects of clinical drugs on humoral responses have not been fully demonstrated. In this study, 112 plasma samples were collected from 36 patients diagnosed with laboratory-confirmed COVID-19 in the Fifth Affiliated Hospital of Sun Yat-sen University. The IgG and IgM antibodies against receptor binding domain (RBD) and spike protein subunit 1 (S1) of SAS-COV-2 were detected by ELISA. We found that COVID-19 patients generated specific antibodies against SARS-CoV-2 after infection, and the levels of anti-RBD IgG within 2 to 3 weeks from onset were negatively associated with the time of positive-to-negative conversion of SARS-CoV-2 nucleic acid. Patients with severe symptoms had higher levels of anti-RBD IgG in 2 to 3 weeks from onset. The use of chloroquine did not significantly influence the patients’ antibody titer but reduced C-reaction protein (CRP) level. Using anti-viral drugs (lopinavir/ritonavir or arbidol) reduced antibody titer and peripheral lymphocyte count. While glucocorticoid therapy developed lower levels of peripheral lymphocyte count and higher levels of CRP, lactate dehydrogenase (LDH), α-Hydroxybutyrate dehydrogenase(α-HBDH), total bilirubin (TBIL), direct bilirubin (DBIL). From these results, we suggested that the anti-RBD IgG may provide an early protection of host humoral responses against SAS-COV-2 infection within 2 to 3 weeks from onset, and clinical treatment with different drugs displayed distinct roles in humoral and inflammatory responses