Owing to its simplicity, high throughput, and ultrasensitivity, single-particle collision electrochemistry (SPCE) has attracted great attention in biosensing, especially labeled SPCE. However, the low signal conversion efficiency and much interference from complex samples limit its wide application. Here, a new and robust SPCE immunosensor was proposed for ultrasensitive cardiac troponin I (cTnI) detection by combining target-driven rolling circle amplification (RCA) with magnetic beads (MBs). Antibody-modified MBs have good stability, dispersity, and magnetic response capacity in complex samples, enabling efficient capture and separation of cTnI with high specificity and anti-interference ability. The presence of cTnI could specifically drive the formation of magnetic immunocomplexes followed by triggering RCA and enzyme digestion reaction. By using Pt nanoparticles (Pt NPs)-modified ssDNA as signal probes, one cTnI molecule could induce the release of 4.5 × 10 4 Pt NPs for collision experiments, greatly enhancing signal conversion efficiency and detection sensitivity. Based on the integration of MBs with RCA, the SPCE immunosensor realized 0.57 fg/mL cTnI detection with a wide linear range of 1 fg/mL to 50 ng/mL. Furthermore, cTnI detection in serum samples of myocardial infarction patients was successfully performed, demonstrating great application prospect of the SPCE immunosensor in clinical diagnosis.

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Objective. From the pathogenic mechanism point of view, systemic lupus erythematosus (SLE) features prominently in T lymphocyte apoptosis. Yet the regulatory mechanism underlying SLE cell apoptosis remains to be explored. This research intends to clarify the role played by miR-137 in SLE and the underlying mechanisms. Methods. Twenty SLE patients (SLE group) and twenty healthy controls (control group) were selected, from whom peripheral blood CD4+ T cells were isolated via magnetic-activated cell sorting. Reverse transcription-polymerase chain reaction (RT-PCR) quantified miR-137 and AMP-activated protein kinase (AMPK) in CD4+ T cells. Further, transfection of miR-137 mimics and inhibitors into CD4+ T cells was carried out to alter miR levels. Levels of pyroptosis, apoptosis, and inflammatory- and pyroptosis-related proteins were determined through PI staining, flow cytometry, and Western blotting, respectively. A luciferase reporter gene assay identified the targeting relation between miR-137 and AMPK. Results. SLE patients showed downregulated miR-137 and upregulated AMPK in CD4+ T cells than controls. miR-137 upregulation by miR-137 mimic transfection inhibited Jurkat cell pyroptosis and apoptosis at both mRNA and protein levels and suppressed NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome activity and pyroptosis-related protein gasdermin D (GSDMD), while miR-137 inhibitor transfection contributed to completely opposite effects. miR-137 directly targeted AMPK, as indicated by the luciferase reporter gene assay. Furthermore, miR-137 inhibitor intervention induced healthy CD4+ T cell pyroptosis and apoptosis via mediating AMPK, whereas miR-137 mimic transfection into CD4+ T cells of SLE patients leads to opposite results. Conclusion. Upregulating miR-137 inhibits CD4+ T cell pyroptosis in SLE patients by modulating the AMPK pathway, suggesting the potential diagnostic and therapeutic role of miR-137 in SLE.