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Ultrasonic guided wave non-destructive testing technology, as one of the most widely used techniques in non-destructive testing, has encountered challenges in breaking the diffraction limit to achieve finer super-resolution imaging during its development. As a type of wave accompanying ultrasonic guided wave damage detection, the transient wave has had the potential to achieve super-resolution imaging in recent years due to its high wave number and sub-wavelength characteristics. In order to overcome its spatial attenuation characteristics, this study constructs a periodic plate-column structure metamaterial. By utilizing its resonance with sub-wavelength Bloch modes at specific frequencies and the interaction with transient waves carrying sub-wavelength information, the wave carrying sub-wavelength signals is amplified, transformed, and transmitted to the far field, thereby achieving super-resolution imaging. The dispersion characteristics of the periodic plate-column structure were simulated and experimentally investigated. The super-resolution imaging effect of the periodic plate-column structure metamaterial was simulated using the time-reversal imaging method and experimentally validated, providing a basis for achieving damage super-resolution imaging with periodic plate-column structures. [ABSTRACT FROM AUTHOR]

17β‑estradiol (E2) can inhibit cardiac fibrosis in female patients with heart failure (HF) and activate cell division cycle 42 (Cdc42), however it is unknown whether 17β‑estradiol (E2) can ameliorate differentiation and collagen synthesis in TGF‑β1‑stimulated mouse cardiac fibroblasts (MCFs) by regulating cell division cycle 42 (Cdc42). The present study aimed to investigate the roles of estrogen and Cdc42 in preventing myocardial fibrosis and the underlying molecular mechanisms. An ELISA was used to measure the levels of E2 and Cdc42 in the serum of patients with heart failure (HF), and western blotting was used to measure the expression levels of Cdc42 in TGF‑β1‑stimulated immortalized MCFs. MCFs were transfected with a Cdc42 overexpression (OE) lentivirus or small interfering RNA (siRNA), or treated with a Cdc42 inhibitor (MLS‑573151), and the function of Cdc42 was assessed by western blotting, immunofluorescence staining, reverse transcription‑quantitative PCR and dual‑luciferase reporter assays. Western blotting and immunofluorescence staining were performed to verify the protective effect of E2 on TGF‑β1‑stimulated MCFs, and the association between the protective effect and Cdc42. The results demonstrated that Cdc42 levels were increased in the serum of patients with HF and were positively correlated with the levels of E2; however, Cdc42 levels were decreased in TGF‑β1‑stimulated MCFs. Cdc42 inhibited MCF differentiation and collagen synthesis, as indicated by the protein expression of α‑smooth muscle actin, collagen I and collagen III. Mechanistically, Cdc42 inhibited the transcription of TGF‑β1 by promoting the expression of p21 (RAC1)‑activated kinase 1 (Pak1)/JNK/c‑Jun signaling pathway proteins and inhibiting the activity of the Tgfb1 gene promoter. In addition, E2 inhibited the differentiation and collagen synthesis of TGF‑β1‑stimulated MCFs, and promoted the protein expression of Pak1, JNK and c‑Jun, consistent with the effects of Cdc42, whereas the effects of E2 were abolished when Cdc42 was knocked down. The aforementioned findings suggested that E2 could inhibit differentiation and collagen synthesis in TGF‑β1‑stimulated MCFs by regulating Cdc42 and the downstream Pak1/JNK/c‑Jun signaling pathway.

The superiority of drug-coated balloon (DCB) in treating small vessels, branching lesions, and high-risk bleeding lesions in coronary heart disease patients has been confirmed. However, its safety and efficacy in large vessels are still unclear. We aimed to investigate whether the efficacy of DCB in large vessels is not inferior to that of drug-eluting stent (DES). From November 2019 to April 2022, a total of 88 patients in our hospital who underwent coronary angiography for the first time and decided to receive DCB or DES treatment were selected. Indicators including late lumen loss (LLL), major adverse cardiovascular event (MACE) rate, major bleeding and all-cause mortality were evaluated at 9 months and 1-year post percutaneous coronary intervention (PCI) therapy. The primary endpoint of 9-month LLL was -0.07 in the DCB group and 0.19 mm in the DES group (p value＜0.001). 1-year cumulative MACE rates were similar in the DCB and DES groups (3.03% vs. 7.23%, P=0.519), TLR rates were similar (3.03% vs. 7.23%, P=0.519), Major bleeding was similar (3.03% vs. 5.45%, P=0.580), and 1 case of Cardiac death in DES group. For LLL, the DCB-only strategy was non-inferior to DES in treating de novo large lesions in the coronary arteries. Furthermore, the efficacy of DCB was comparable to DES at 1 year of follow-up for secondary clinical endpoints.