Application value of T2 fluid-attenuated inversion recovery sequence based on deep learning in static lacunar infarction.

BACKGROUND: Regular monitoring of static lacunar infarction (SLI) lesions plays an important role in preventing disease development and managing prognosis. Magnetic resonance imaging is one method used to monitor SLI lesions. PURPOSE: To evaluate the image quality of the T2 fluid-attenuated inversion recovery (T2-FLAIR) sequence using artificial intelligence-assisted compressed sensing (ACS) in detecting SLI lesions and assess its clinical applicability. METHODS: A total of 42 patients were prospectively enrolled and scanned by T2-FLAIR. Two independent readers reviewed the images acquired with accelerated modes 1D (acceleration factor 2) and ACS (acceleration factors 2, 3, and 4). The overall image quality and lesion image quality were analyzed, as were signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and number of lesions between groups. RESULTS: The subjective assessment of overall brain image quality and lesion image quality was consistent between the two readers. The lesion display quality and the overall image quality were better with the traditional 1D acceleration method than with the ACS accelerated method. There was no significant difference in the SNR of the lacunar infarction in the images between the groups. The CNR of the images with the 1D acceleration mode was significantly lower than that of images with the ACS acceleration mode. Images with the 1D, ACS2, and ACS3 acceleration modes showed no significant differences in terms of detecting lesions but scan time can be reduced by 40% (1D vs. ACS3). CONCLUSION: ACS acceleration mode can greatly reduce the scan time. In addition, the images have good SNR, high CNR, and strong SLI lesion detection ability.

2-(2-nitrobenzylidene) indolin-3-one compound inhibits transmembrane prostate androgen-induced protein (TMEPAI) expression and cancer cell proliferation.

OBJECTIVES: The transmembrane prostate androgen-induced protein (TMEPAI) is aberrantly expressed in many cancer and plays a crucial role in tumourigenesis, which makes it a potential cancer therapeutic target for drug discovery. MATERIALS AND METHODS: Here, we employed a firefly luciferase reporter driven by the TMEPAI gene promoter to screen for compound capable of inhibiting the expression of TMEPAI, and the effects of TMEPAI inhibitor on cancer cell proliferation were evaluated using the colony formation assay, cell cycle analysis, Ki-67 immunofluorescence assay and EdU incorporation assay. RESULTS: 2-(2-nitrobenzylidene) indolin-3-one (JHY-A007-50) was identified and shown to effectively inhibit the TMEPAI promoter activity. Further studies revealed that JHY-A007-50 specifically inhibited the expression of TMEPAI at both the mRNA and protein levels. Moreover, we found that JHY-A007-50 could inhibit cell proliferation and induce cell cycle arrest at the G1 phase. Our results showed that overexpression of TMEPAI decreased the inhibitory effects of JHY-A007-50 on cancer cell proliferation, and JHY-A007-50 did not affect the cell viability of HeLa cells knocked down of TMEPAI. CONCLUSIONS: Taken together, these results suggest that compound JHY-A007-50 mediates the downregulation of TMEPAI expression and inhibits cell proliferation in cancer cells.