Background: Clinical guidelines currently suggest that transthoracic echocardiography (TTE) be carried out in all patients with suspected endocarditis, but the use of TTE where there is a low probability of infective endocarditis has a poor diagnostic yield. This screening approach may no longer be appropriate. Objective: To examine whether clinical criteria might aid decision making with respect to the use of TTE in possible endocarditis. Design: A retrospective review of patient records. Setting: Cardiology department of a tertiary referral centre. Patients: 500 consecutive hospital inpatients referred for TTE to exclude endocarditis. Main outcome measures: Evidence of endocardial vegetations on TTE and the presence of predetermined clinical criteria that may predispose to, or be suggestive of, endocarditis. Results: Evidence of infective endocarditis was detected on echocardiography in 43 of the 500 patients (8.6%). In 239 patients (48%), vegetations and certain prespecified clinical criteria were both absent. These criteria were: vasculitic/embolic phenomena; the presence of central venous access; a recent history of injected drug use; presence of a prosthetic valve; and positive blood cultures. The collective absence of these five criteria indicated a zero probability of TTE showing evidence of endocarditis. Conclusions: The use of simple clinical criteria during the decision making process may avoid many unnecessary TTE examinations in hospital inpatients with a low probability of endocarditis.

Background Rheumatoid arthritis (RA) is a complex autoimmune disease with multiple etiological factors, among which aberrant memory CD4 T cells activation plays a key role in the initiation and perpetuation of the disease. SIGIRR (single immunoglobulin IL-1R-related receptor), a member of the IL-1 receptor (ILR) family, acts as a negative regulator of ILR and Toll-like receptor (TLR) downstream signaling pathways and inflammation. The aim of this study was to investigate the potential roles of SIGIRR on memory CD4 T cells in RA and the underlying cellular and molecular mechanisms. Methods Single-cell transcriptomics and bulk RNA sequencing data were integrated to predict SIGIRR gene distribution on different immune cell types of human PBMCs. Flow cytometry was employed to determine the differential expression of SIGIRR on memory CD4 T cells between the healthy and RA cohorts. A Spearman correlation study was used to determine the relationship between the percentage of SIGIRR+ memory CD4 T cells and RA disease activity. An AIA mouse model (antigen-induced arthritis) and CD4 T cells transfer experiments were performed to investigate the effect of SIGIRR deficiency on the development of arthritis in vivo. Overexpression of SIGIRR in memory CD4 T cells derived from human PBMCs or mouse spleens was utilized to confirm the roles of SIGIRR in the intracellular cytokine production of memory CD4 T cells. Immunoblots and RNA interference were employed to understand the molecular mechanism by which SIGIRR regulates TNF-α production in CD4 T cells. Results SIGIRR was preferentially distributed by human memory CD4 T cells, as revealed by single-cell RNA sequencing. SIGIRR expression was substantially reduced in RA patient-derived memory CD4 T cells, which was inversely associated with RA disease activity and related to enhanced TNF-α production. SIGIRR-deficient mice were more susceptible to antigen-induced arthritis (AIA), which was attributed to unleashed TNF-α production in memory CD4 T cells, confirmed by decreased TNF-α production resulting from ectopic expression of SIGIRR. Mechanistically, SIGIRR regulates the IL-1/C/EBPβ/TNF-α signaling axis, as established by experimental evidence and cis-acting factor bioinformatics analysis. Conclusion Taken together, SIGIRR deficiency in memory CD4 T cells in RA raises the possibility that receptor induction can target key abnormalities in T cells and represents a potentially novel strategy for immunomodulatory therapy.

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Background Coronary heart disease (CHD) is causing by the aberrant aggregation of immune cells in plaque. This study aimed to identify abnormal T cell subtypes and inflammatory factors in CHD patients.Methods and results T cell subsets from 187 CHD patients were analyzed using flow cytometry. Plasma concentration of cytokines were analyzed by Luminex. Flow cytometric analysis revealed that the number of ThGM cells was higher in CHD patients. The proportion of Th17 and Th1 cells were also increased in CHD patients. levels of IL-4, IL-5, IL-6, and IL-10 were significantly higher in CHD patients (P<0.05). However, levels of GM-CSF were slightly lower in CHD patients. Conclusions ThGM can be considered as a diagnostic marker of CDH.

Background Coronary heart disease (CHD) is causing by the aberrant aggregation of immune cells in plaque. This study aimed to identify abnormal T cell subtypes and inflammatory factors in CHD patients.Methods and results T cell subsets from 187 CHD patients were analyzed using flow cytometry. Plasma concentration of cytokines were analyzed by Luminex. Flow cytometric analysis revealed that the number of ThGM cells was higher in CHD patients. The proportion of Th17 and Th1 cells were also increased in CHD patients. levels of IL-4, IL-5, IL-6, and IL-10 were significantly higher in CHD patients (P<0.05). However, levels of GM-CSF were slightly lower in CHD patients. Conclusions ThGM can be considered as a diagnostic marker of CDH.