Traditional treatments have a poor effect on alcoholic liver diseases. Linderae radix (LR), the dried root of Lindera aggregata (Sims) Kosterm., has been frequently used in traditional Chinese medicine for treating various diseases, and has been shown to exhibit a protective effect on liver injury. In the present study, LR extracts were made using various solvents, and then administrated to rats to establish a model of ethanol-induced liver injury. The study aimed to investigate the therapeutic effects and potential mechanism of LR extracts on acute alcoholic liver injury. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycercide (TG), cholesterol (TC), methane dicarboxylic aldehyde (MDA) and superoxide dismutase (SOD) were determined using an automatic biochemistry analyzer. In addition, pathological examination was performed by hematoxylin-eosin staining. The levels of MDA and SOD, and the expression levels of nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α and interleukin (IL)-1β in liver tissue were investigated immunohistochemically. The expression of cytochrome P450 2E1 (CYP2E1) mRNA was quantified by reverse transcription-quantitative polymerase chain reaction. The results indicated that LR extracts improved the histopathological status and decreased the serum levels of ALT, AST, TG, TC and MDA. Furthermore, the levels of MDA and inflammatory mediators (NF-κB, TNF-α and IL-1β) were decreased in liver tissues, and the overexpression of CYP2E1 mRNA induced by ethanol treatment. LR extracts exhibited a protective effect on alcoholic liver injury and the mechanism may be associated with the anti-inflammatory and anti-oxidative action.

Objective Activation of osteoclastogenesis at the bone site in rheumatoid arthritis (RA) is well established. The mechanisms by which circulating osteoclast precursors contribute are still unclear. Peroxisome proliferator–activated receptor γ coactivator 1β (PGC‐1β) is implicated in transcriptional regulation of osteoclastogenesis in mouse models. This study was undertaken to investigate the contribution of PGC‐1β to circulating osteoclast precursors and its link to bone destruction in RA. Methods PGC‐1β expression in RA peripheral blood CD14+ monocytes was increased and showed correlation with joint destruction shown on radiographs. Cells from RA patients or healthy controls were transfected with a lentivirus vector for PGC‐1β gene silencing or overexpression and cultured with macrophage colony‐stimulating factor and RANKL. Bone resorption activity, bone‐degrading enzymes, and signaling molecules were measured in these mature osteoclasts. Results Increased nuclear accumulation of PGC‐1β was observed in RA peripheral blood CD14+ monocytes, and these cells had stronger osteoclastogenesis than in healthy controls. PGC‐1β protein expression was positively correlated with radiographic joint destruction (r = 0.396–0.413; all P < 0.05). PGC‐1β knockdown suppressed (51–82% reduction) the expression of cathepsin K, tartrate‐resistant acid phosphatase (TRAP), and matrix metalloproteinase 9 (MMP‐9), as well as osteoclast differentiation and bone resorption activity. Conversely, PGC‐1β overexpression increased these markers (by 1.5–1.8‐fold) and osteoclastogenesis. VIVIT, an inhibitor of NFATc1 activation, inhibited the effect of overexpressed PGC‐1β by reducing cathepsin K, TRAP, and MMP‐9 expression. Chromatin immunoprecipitation assay and dual‐luciferase reporter gene assay showed PGC‐1β bound to NFATc1 promoter, leading to transcriptional activation. Conclusion Activation of the PGC‐1β/NFATc1 pathway in circulating osteoclast precursors was associated with bone destruction in RA. This may represent a new treatment target.

Furfuryl Alcohol.-MCM-41 supported Cu/La-catalyst with high metal loading level and dispersion degree is prepared via a novel preparative method. The catalyst exhibits high activity and selectivity in the hydrogenation of furfural (I) to furfuryl alcohol (II). -(HAO, X.

This article deals with the issue of asymptotic stabilization for a linear parabolic partial differential equation (PDE) with an unknown space-varying reaction coefficient and multiple local piecewise uniform control. Clearly, the unknown reaction coefficient belongs to a function space. Hence, the fundamental difficulty for such issue lies in the lack of a conceptually simple but effective parameter identification technique in a function space. By the Lyapunov technique combined with a variant of Poincaré-Wirtinger inequality, an update law is derived for estimate of the unknown reaction coefficient in a function space.Then a spatiotemporal adaptive state feedback control law is constructed such that the estimate of the unknown coefficient is bounded and the closed-loop PDE is asymptotically stable in the sense of spatial  1 norm if a sufficient condition given in terms of space-time varying linear matrix inequalities (LMIs) is fulfilled for the estimated coefficient and the control gains. Both analytical and numerical approaches are proposed to construct a feasible solution to the space-time varying LMI problem. With the aid of the semigroup theory, the well-posedness and regularity of the closed-loop PDE is also analyzed. Moreover, two extensions of the proposed adaptive control scheme are discussed: the PDE in N-D space and the PDE with unknown diffusion and reaction coefficients. Finally, numerical simulation results are presented to support the proposed spatiotemporal adaptive control design.