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Da-Wei Liu

Publications and source records attributed to Da-Wei Liu.

5 recordsLinked to original sources
PubMed2005

Ethoxylated bisphenol dimethacrylate-based amorphous calcium phosphate composites.

Improving the anti-demineralizing/remineralizing and mechanical properties of amorphous calcium phosphate (ACP) composites has been the focus of our recent research. In this study, an ethoxylated bisphenol A dimethacrylate (EBPADMA) was blended with triethylene glycol dimethacrylate (TEGDMA), 2-hydroxyethyl methacrylate (HEMA) and methacryloxyethyl phthalate (MEP) to form experimental resins with different EBPADMA/TEGDMA molar ratios (0.50, 0.85 and 1.35) and a constant HEMA/MEP molar ratio (8.26). Composites were prepared by admixture of either unmilled or milled zirconia-ACP filler (40% by mass) and photo-activated resin (60% by mass). One aim was to test if improved ion release can be achieved by elevating the EBPADMA/TEGDMA ratio while lowering the level of surface active methacryloxyethyl phthalate in the resin without adversely affecting the biaxial flexure strength (BFS), degree of vinyl conversion (DC) and water sorption (WS) of composites. A second aim was to assess the effect of using milled vs. unmilled ACP on these properties. Ion release of all composites was significantly above the theoretical minimum necessary for remineralization. Calcium ion release was not impeded by binding with the carboxylic acid groups of MEP. Increased supersaturation was attained with increasing EBPADMA/TEGDMA ratio in the resin. Variations in resin composition had no effect on BFS or DC of composites. The BFS of the milled ACP composites was higher than the BFS of unmilled ACP composites (56% and 79%, respectively for dry and wet specimens). DC of composites was only moderately reduced (13.6% and 7.3%, for unmilled and milled ACP, respectively) compared to unfilled resins. WS decreased in the following order: unmilled ACP composites>milled ACP composites>copolymers. Fine-tuning of the resin and utilizing milled ACP filler improved the remineralizing potential of ACP composites without impeding their DC, BFS or WS.

Adsorption↗
PubMed2003

Intrapulmonary expression of scavenger receptor and CD14 and their relation to local inflammatory responses to endotoxemia in mice.

This study was first designed to investigate systematically the kinetics of surface expression of scavenger receptors (SRs) and CD14 on alveolar macrophages in vivo and in vitro and their relation with local pro- and antiinflammatory responses in endotoxemia. The expression of SR and CD14 in lungs was down- and up-regulated, respectively, in the presence of endotoxemia, which might be due to decreased expression of SR and increased expression of CD14 on the surface of the resident macrophages. Down-regulation of SRs on alveolar macrophages not only induces decreased defensive function of the macrophages, it also enhances lipopolysaccharide (LPS)-induced activation of alveolar macrophages possibly through increasing LPS binding to CD14. Although CD14 is a key receptor responsible for LPS to activate macrophages, both phospholipase C and anti-CD14 antibody can completely inhibit activation of alveolar macrophages initiated by only LPS 1 ng/ml, as determined by tumor necrosis factor-alpha (TNFalpha) production, but it does not significantly change TNFalpha release upon cell stimulation by LPS 10 microg/ml. There was an intrinsic relation of enhanced intrapulmonary pro- and antiinflammatory responses with changes in SR and CD14 expression, which suggests that the down-regulation of SR and up-regulation of CD14 might be an important mechanism for the lung to change from a defense organ to an effector organ during sepsis.

Animals↗
PubMed2002

Induction of acute hepatic injury by endotoxin in mice.

OBJECTIVE: To investigate the changes of scavenger receptor (SR) and CD14 in Kupffer cells in endotoxemia in order to uncover the mechanism of the liver to turn a defense organ into effector one in sepsis. METHODS: Mouse models of endotoxemia of different severity were reproduced by injection of different doses of lipopolysaccharide (LPS) via the tail vein. The expression of SR and CD14 in the liver was assayed by immunohistochemistry and was subsequently analyzed with an image analysis system. The levels of TNF-alpha and IL-6 in liver tissue were determined with ELISA. RESULTS: The expression of SR in the liver in the high-dose group was markedly decreased one hour after injection of LPS, and also in the low-dose group at 3 hours. The expression of SR in the liver in the two groups was shown to be progressively decreased with the time prolonged. There was significant difference in average optical density (OD) values of SR between the two groups. The expression of CD14 in the two groups was shown to be significantly increased one hour after injection of LPS, and more significantly with the time prolonged. But there was no significant difference in OD values of CD14 between the two groups. The contents of intrahepatic proinflammatory mediators TNF-alpha, IL-6, ALT and TBIL were significantly increased after injection of LPS. Correlation analysis revealed that the changes of TNF-alpha, IL-6, ALT, and TBIL were negatively correlated with the expression of SR, and positively with the expression of CD14. CONCLUSION: The up-regulation of CD14 expression and down-regulation of SR expression on Kupffer cells might be one of the important mechanisms for the conversion of Kupffer cells from immune defensive to inflammatory response cells in acute hepatic injury.

Acute Disease↗
PubMed2002

[Rapid amplification of 3' cDNA end of Suaeda liaotungensis betaine aldehyde dehydrogenase using one-step PCR].

Based on part of a known cDNA sequence of Suaeda liaotungensis betaine aldehyde dehydrogenase, we successfully cloned the 3' cDNA end of S. lianotungensis betaine aldehyde dehydrogenase using one-step PCR with a gene-specific primer and universal primer. Compared with the typical 3' RACE, one-step PCR is rapid, simple and inexpensive. It is very rapid to amplify an unknown cDNA 3' end using this method.

Journal Article↗