A mendelian randomization study investigates the causal relationship between immune cell phenotypes and cerebral aneurysm

Background: Cerebral aneurysms (CAs) are a significant cerebrovascular ailment with a multifaceted etiology influenced by various factors including heredity and environment. This study aimed to explore the possible link between different types of immune cells and the occurrence of CAs.Methods: We analyzed the connection between 731 immune cell signatures and the risk of CAs by using publicly available genetic data. The analysis included four immune features, specifically median brightness levels (MBL), proportionate cell (PC), definite cell (DC), and morphological attributes (MA). Mendelian randomization (MR) analysis was conducted using the instrumental variables (IVs) derived from the genetic variation linked to CAs.Results: After multiple test adjustment based on the FDR method, the inverse variance weighted (IVW) method revealed that 3 immune cell phenotypes were linked to the risk of CAs. These included CD45 on HLA DR+NK (odds ratio (OR), 1.116; 95% confidence interval (CI), 1.001–1.244; p = 0.0489), CX3CR1 on CD14− CD16− (OR, 0.973; 95% CI, 0.948–0.999; p = 0.0447). An immune cell phenotype CD16− CD56 on NK was found to have a significant association with the risk of CAs in reverse MR study (OR, 0.950; 95% CI, 0.911–0.990; p = 0.0156).Conclusion: Our investigation has yielded findings that support a substantial genetic link between immune cells and CAs, thereby suggesting possible implications for future clinical interventions

Effect of Xinyue capsules on patients with coronary heart disease after percutaneous coronary intervention: study protocol for a randomized controlled trial

Case report form 2014.3.4R2. (PDF 1119 kb

Ground State and Excitations of Spin Chain with Orbital Degeneracy

The one dimensional Heisenberg model in the presence of orbital degeneracy is studied at the SU(4) symmetric viewpoint by means of Bethe ansatz. Following Sutherland's previous work on an equivalent model, we discuss the ground state and the low-lying excitations more extensively in connection to the spin systems with orbital degeneracy. We show explicitly that the ground state is a SU(4) singlet. We study the degeneracies of the elementary excitations and the spectra of the generalized magnons consisting of these excitations. We also discuss the complex 2-strings in the context of the Bethe ansatz solutions.Comment: Revtex, 9 pages, 3 figures; typos correcte

Emergent Schr\"{o}dinger cat states during superradiant phase transitions

Superradiant phase transitions (SPTs) are important for understanding light-matter interactions at the quantum level [1, 2], and play a central role in criticality-enhanced quantum sensing [3]. So far, SPTs have been observed in driven-dissipative systems [4-9], but the emergent light fields did not show any nonclassical characteristic due to the presence of strong dissipation. Here we report an experimental demonstration of the SPT featuring the emergence of a highly nonclassical photonic field, realized with a resonator coupled to a superconducting qubit, implementing the quantum Rabi model [10, 11]. We fully characterize the light-matter state by Wigner matrix tomography. The measured matrix elements exhibit quantum interference intrinsic of a photonic Schr\"{o}dinger cat state [12], and reveal light-matter entanglement. Besides their fundamental importance, these hitherto unobserved emergent quantum phenomena are useful for quantum metrology and fault-tolerant quantum computation.Comment: 19 pages, 14 figures, 2 table

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

Background/Aims: With increased understanding of sepsis, mortality is decreasing. However, there is still a lack of effective therapeutic strategy. The inflammatory response of macrophages is critical during sepsis. Methods: Macrophages were stimulated with LPS. Western blotting and qRT-PCR were used to detect inflammatory responses. Then, the inhibitor of microRNA-138 was transfected and Western blotting, qRT-PCR, H&E staining and ELISA were used to verify the role of microRNA-138 in inflammation. Then target gene prediction databases were used to predict the potential target of microRNA-138. Both animal and cell models under LPS challenges were established to verify the regulation of SIRT1 and microRNA-138 during inflammation. Results: The present study showed that microRNA-138 was increased in macrophages stimulated with LPS. Additionally, the NF-κB and AKT pathways were both activated. The pre-treatment of microRNA-138 inhibitor decreased inflammatory factors, downregulated the NF-κB pathway, activated the AKT pathway and protected against organ damage in mice challenged with LPS. SIRT1 was demonstrated as a potential target of microRNA-138In macrophages stimulated with LPS, the inhibition effect of microRNA-138 inhibitor on inflammation was lost by SIRT1 siRNA pre-treatment. In the animal model, the protective effect of microRNA-138 antagomir disappeared in SIRT1 knockout mice. Conclusion: We demonstrated that miR-138 participated in the inflammatory process by inhibiting SIRT1 and activating the NF-κB pathway

Mapping the Binding between the Tetraspanin Molecule (Sjc23) of Schistosoma japonicum and Human Non-Immune IgG

BACKGROUND: Schistosomal parasites can establish parasitization in a human host for decades; evasion of host immunorecognition including surface masking by acquisition of host serum components is one of the strategies explored by the parasites. Parasite molecules anchored on the membrane are the main elements in the interaction. Sjc23, a member of the tetraspanin (TSP) family of Schistosoma japonicum, was previously found to be highly immunogenic and regarded as a vaccine candidate against schistosomiasis. However, studies indicated that immunization with Sjc23 generated rapid antibody responses which were less protective than that with other antigens. The biological function of this membrane-anchored molecule has not been defined after decades of vaccination studies. METHODOLOGY AND PRINCIPAL FINDINGS: In this study, we explored affinity pull-down and peptide competition assays to investigate the potential binding between Sjc23 molecule and human non-immune IgG. We determined that Sjc23 could bind human non-immune IgG and the binding was through the interaction of the large extra-cellular domain (LED) of Sjc23 (named Sjc23-LED) with the Fc domain of human IgG. Sjc23 had no affinity to other immunoglobulin types. Affinity precipitation (pull-down assay) in the presence of overlapping peptides further pinpointed to a 9-amino acid motif within Sjc23-LED that mediated the binding to human IgG. CONCLUSION AND SIGNIFICANCE: S. japonicum parasites cloak themselves through interaction with human non-immune IgG, and a member of the tetraspanin family, Sjc23, mediated the acquisition of human IgG via the interaction of a motif of 9 amino acids with the Fc domain of the IgG molecule. The consequence of this interaction will likely benefit parasitism of S. japonicum by evasion of host immune recognition or immunoresponses. This is the first report that an epitope of schistosomal ligand and its immunoglobulin receptor are defined, which provides further evidence of immune evasion strategy adopted by S. japonicum