In this paper, we propose a layered decoding algorithm for protograph-based low-density parity-check Hadamard codes (PLDPC-HCs), which have been shown to be ultimate-Shannon-limit approaching. Compared with the standard decoding algorithm, the layered decoding algorithm improves the convergence rate by about two times. At a bit error rate of 2.0 × 10 −5 , the layered decoder using 20 decoding iterations shows a very small degradation of 0.03 dB compared with the standard decoder using 40 decoding iterations. Moreover, the layered decoder using 21 decoding iterations shows the same error performance as the standard decoder using 41 decoding iterations.

An efficient and convenient approach to the condensation reaction of aromatic aldehydes and diethyl phosphite using Na2CO3 as catalyst with grinding at room temperature (without any solvent) is described. This method provides several advantages such as neutral condition, simple work-up procedure, high yields and reduced environmental impact.

New bufadienolides with inhibitory activity against breast cancer cells were isolated from the eggs of toad Bufo bufo gargarizans.

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Hepatocellular carcinoma (HCC) accounts for one of the leading causes of cancer-related death, and is attributed to the dysregulation of genes involved in genome stability. DDX11, a DNA helicase, has been implicated in rare genetic disease and human cancers. Yet, its clinical value, biological function, and the underlying mechanism in HCC progression are not fully understood. Here, we show that DDX11 is upregulated in HCC and exhibits oncogenic activity via EZH2/p21 signaling. High expression of DDX11 is significantly correlated with poor outcomes of HCC patients in two independent cohorts. DDX11 overexpression increases HCC cell viabilities and colony formation, whereas DDX11 knockdown arrests cells at G1 phase without alteration of p53 expression. Ectopic expression of DDX11 reduces, while depletion of DDX11 induces the expression of p21. Treatment of p21 siRNA markedly attenuates the cell growth suppression caused by DDX11 silence. Further studies reveal that DDX11 interacts with EZH2 in HCC cells to protect it from ubiquitination-mediated protein degradation, consequently resulting in the downregulation of p21. In addition, E2F1 is identified as one of the upstream regulators of DDX11, and forms a positive feedback loop with EZH2 to upregulate DDX11 and facilitate cell proliferation. Collectively, our data suggest DDX11 as a promising prognostic factor and an oncogene in HCC via a E2F1/DDX11/EZH2 positive feedback loop.