Magnified x ray ghost imaging with tapered polycapillary optics free of the penumbra effect.

X ray ghost imaging (XGI) offers both radiation dose-reduction potential and cost-effective benefits owing to the utilization of a single-pixel detector. Most XGI schemes with laboratory x ray sources require a mechanically moving mask for either structured illumination or structured detection. In either configuration, however, its resolution remains limited by the source size and the unit size of the mask. Upon propagation, the details of the object can actually be magnified by the divergence of x rays, but at the same time, the penumbra effect produced by the finite source size is dramatically intensified, which ultimately leads to a degradation of image quality in XGI. To address these limitations, this work proposes a magnified XGI scheme using structured detection equipped with tapered polycapillary optics, which can efficiently suppress the object's penumbra as well as resolve the magnified details of the object. In general, the resolution of this scheme is no longer affected by the source size but by the microcapillary size of polycapillary. Our work fundamentally achieves cancellation of penumbra effect-induced aberration, thus paving the way for high-resolution magnified XGI.

MiR-718 mediates the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.

It has been reported that SEMA3B-AS1 is a tumor-suppressive lncRNA in gastric cardia adenocarcinoma. We explored the possible involvement of SEMA3B-AS1 in hepatocellular carcinoma (HCC). We found that SEMA3B-AS1 was downregulated in HCC tissues compared with noncancer tissues and was not affected by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In addition, SEMA3B-AS1 expression was not affect by cancer development, and low SEMA3B-AS1 levels were closely correlated with poor survival. SEMA3B-AS1 in HCC tissues was inversely correlated with microRNA (miR)-718 and positively correlated with PTEN. In HCC cells, SEMA3B-AS1 overexpression resulted in upregulated, while miR-718 overexpression resulted in downregulated phosphatase and tensin homolog (PTEN) expression. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. SEMA3B-AS1 and PTEN overexpression resulted in a reduced proliferation rate of HCC cells, while miR-718 overexpression resulted in an increased rate. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. Therefore, miR-718 may mediate the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.