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Considering the channel noise was present, we presented techniques to reconstruct the feedback polynomial as well as the initial state of a scrambler placed after a channel encoder. The previous algorithms could not keep the detection performance over the design requirements, such as a false-alarm probability. Thus, we proposed a modified scheme to improve the detection capability. With multiple output sequences of matched filter that were scrambled by the same scrambler, we reduced the number of samples required for the reconstruction of the feedback polynomial when the signal-to-noise ratio was <0 dB. Meanwhile, we proposed a scheme to restore the initial state of the scrambler in the presence of channel noise. We also developed two lemmas and two theorems to reconstruct the synchronous scrambler with block summation. Following the lemmas and the theorems, we could use the blocks to generate a new sequence with certain method such as multiplying a dual word, and detect the optimal multiple of the original scrambler's feedback polynomial, or even the correct one.Index Terms-Synchronous scrambler, linear feedback shift register, linear block codes.

The abiotic reaction products of polycyclic aromatic hydrocarbons (PAHs) with hydroxyl radicals ( • OH) and nitrate radicals ( • NO 3 ) are nitro-, oxygen-, and hydroxyl-containing PAHs (NPAHs, OPAHs, and OHPAHs). Four methods of the highest occupied molecular orbital (HOMO), Fukui function (FF), dual descriptor (DD), and population of π electrons (PP-π) are selected to predict the chemical reactivity of PAHs attacked by • OH and • NO 3 in this study. The predicted • OH-initiated and • NO 3 -initiated transformation products are compared with the main PAH transformation products (PAH-TPs) observed in the laboratory. The results indicate that PP-π and DD approaches fail to predict the transformation products of fused PAHs containing five-membered rings. By predicting the PAH-TPs of 13–14 out of the 15 parent PAHs accurately, HOMO and FF methods were shown to be suitable for predicting the transformation products formed from the abiotic reactions of fused PAHs with • OH and • NO 3 .

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The alleviating effect of Sodium butyrate (SB) on intestinal injuries incurred by glycinin in feed was investigated in common carp. The control group (without glycinin and SB), the Gly group (with glycinin), and the remaining 4 groups were added SB (0.75, 1.50, 2.25, 3.00 g/kg) respectively based on the Gly group. 6 groups of diets were isonitrogenous and isoenergetic, and fish were fed with these 6 diets for eight weeks. The findings revealed that glycinin caused apoptosis in the intestine, up-regulated JNK, caspase-3, Bax, caspase-9, p38, caspase-8 and FasL gene expression in the MI, DI and hepatopancreas, while down-regulating ERK and Bcl-2 apoptotic genes. However, no eminent effect on the PI. In contrast, SB2 and SB3 groups eminently reversed these adverse effects. Dietary glycinin eminently reduced the expression of ZO-1, Claudin3, Claudin7 and Occludin1 genes in the MI and DI. SB2 and SB3 groups eminently up-regulated the expression of ZO-1, Claudin3, Claudin7 and Occludin1 expression levels, thereby improving the function of the tightly connected barrier in the intestine. Dietary glycinin also eminently increased serum levels of D-lactate, diamine oxidase, serotonin and endothelin, leading to intestinal damage and increased intestinal permeability. SB2 and SB3 groups reduced serum levels of D-lactate, diamine oxidase, serotonin and endothelin, regulating intestinal permeability. Glycinin disrupted the morphological structure of the intestine, while the SB2 and SB3 groups increased the height and width of the folds of the intestinal villi, thus maintaining the morphological integrity of the intestine. Dietary glycinin upset the intestinal microecological balance by increasing Proteobacteria abundance while lowering Clostridium and Bacteroidetes abundance. The SB2 and SB3 groups altered the composition and number of dominant taxa while increasing the abundance of Firmicutes and Acidobacteria. In conclusion, SB could inhibit apoptosis of intestinal cells through the JNK/FasL/caspase-8 signalling pathway and up-regulate the expression of intestinal tight junction (TJ) genes, maintain intestinal physical barrier and regulate intestinal flora, thereby alleviating glycinin-induced intestinal damage.