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This paper addresses two fundamental issues in the peak deconvolution method of cellulose XRD data analysis: there is no standard model for amorphous cellulose and common peak functions such as Gauss, Lorentz and Voigt functions do not fit the amorphous profile well. It first examines the effects of ball milling on three types of cellulose and results show that ball milling transforms all samples into a highly amorphous phase exhibiting nearly identical powder X-ray diffraction (XRD) profiles. It is hypothesized that short range order within a glucose unit and between adjacent units survives ball milling and generates the characteristic amorphous XRD profiles. This agrees well with cellulose I d-spacing measurements and oligosaccharide XRD analysis. The amorphous XRD profile is modeled using a Fourier series equation where the coefficients are determined using the nonlinear least squares method. A new peak deconvolution method then is proposed to analyze cellulose XRD data with the amorphous Fourier model function in conjunction with standard Voigt functions representing the crystalline peaks. The impact of background subtraction method has also been assessed. Analysis of several cellulose samples was then performed and compared to the conventional peak deconvolution methods with common peak fitting functions and background subtraction approach. Results suggest that prior peak deconvolution methods overestimate cellulose crystallinity. [ABSTRACT FROM AUTHOR]

The structural characteristics of the nascent fibril produced by Gluconacetobacter xylinum (G. xylinum) have been studied under the influence of the cellulose binding dye brilliant yellow (BY) by wide angle X-ray diffraction (WAXD), Fourier transform infrared spectroscopy (FTIR) and 13C solid-state nuclear magnetic resonance. BY is found to be more effective at reducing crystallinity than fluorescent brightener 28 (FB28), pontamine fast scarlet 4 (S4B) and other dyes previously studied. Under static cultivation conditions, increasing concentrations of brilliant yellow in the growth media from 20, 50, 100 to 250 μM, result in decreasing cellulose crystallinity from 73 to 18%, respectively, as compared to 82% exhibited by the control. FTIR data indicate that the presence of BY is most effective at suppressing intra-molecular hydrogen bonding. After boiling in 70 vol% aqueous EtOH solution for 12 h, the extracted dye-altered cellulose becomes more ordered, which may be due to the extraction of BY from the BY-cellulose complex. FTIR data indicate that compared to control cellulose, the reclaimed brilliant yellow-altered cellulose contains more cellulose Iβ, where the FB28 and S4B altered cellulose remains principally Iα. Based on WAXD and NMR data we propose a dye-cellulose complex structure associated with BY. This model supports the hypothesis that microfibrils assemble through the hydrogen bonding of formed mini-sheets that consist of stacked glucan chains linked by van der Waals forces. [ABSTRACT FROM AUTHOR]

Background and Aim: Silybin is the major biologically active compound of silymarin, the standardized extract of the milk thistle (Silybum marianum). Increasing numbers of studies have shown that silybin can improve nonalcoholic steatohepatitis (NASH) in animal models and patients; however, the mechanisms underlying silybin's actions remain unclear.Methods: Male C57BL/6 mice were fed a methionine-choline deficient (MCD) diet for 8 weeks to induce the NASH model, and silybin was orally administered to the NASH mice. The effects of silybin on lipid accumulation, hepatic fibrosis, oxidative stress, inflammation-related gene expression and nuclear factor kappa B (NF-κB) activities were evaluated by biochemical analysis, immunohistochemistry, immunofluorescence, quantitative real-time PCR and western blot.Results: Silybin treatment significantly alleviated hepatic steatosis, fibrosis and inflammation in MCD-induced NASH mice. Moreover, silybin inhibited HSC activation and hepatic apoptosis and prevented the formation of MDBs in the NASH liver. Additionally, silybin partly reversed the abnormal expression of lipid metabolism-related genes in NASH. Further study showed that the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway played important roles in the silybin-derived antioxidant effect, as evidenced by the upregulation of Nrf2 target genes in the silybin treatment group. In addition, silybin significantly downregulated the expression of inflammation-related genes and suppressed the activity of NF-κB signaling.Conclusions: Silybin was effective in preventing the MCD-induced increases in hepatic steatosis, fibrosis and inflammation. The effect was related to alteration of lipid metabolism-related gene expression, activation of the Nrf2 pathway and inhibition of the NF-κB signaling pathway in the NASH liver. [ABSTRACT FROM AUTHOR]