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[Display omitted] • Adding caffeic and rosmarinic acids before the alcoholic fermentation of red wine. • The evolution of colors and polyphenolics was figured out by CIELAB and HPLC-MS. • The addition enhanced chromatic quality and copigmentation effect. • The addition can be applied as an alternative strategy for making premium red wines. Although phenolic copigments are rarely colored, they can still influence color expression in red wine copigmentation. Here, prefermentative agents, such as caffeic and rosmarinic acids, were added as copigments during Cabernet Sauvignon red winemaking. The evolution of colors and polyphenols was analyzed by tristimulus colorimetry and high-performance liquid chromatography-tandem mass spectrometry during brewing and aging periods. The results showed that the addition of caffeic and rosmarinic copigments was beneficial to obtain more saturated and vivid hue of wines. The changes in color were correlated with a significant increase in anthocyanins concentration. Moreover, the results demonstrated that the addition of the two phenolic copigments increased the concentration of total phenols and enhanced the copigmentation effect, indicating improved chromatic intensity and color stability of wines. Therefore, the addition of caffeic and rosmarinic acids is a simple and useful enological technique to obtain red wines with high color quality and aging potential. [ABSTRACT FROM AUTHOR]

Abstract: Angiogenesis, the process of new blood vessel formation from preexisting capillaries, is a multistep process. The principle cell type in this process is endothelial cells which are required to undergo proliferation, migration, differentiation, and coalescence into cord-like structures with a central lumen. However, the molecular and cellular mechanisms that regulate this process require further investigation. In this study, we have used the fibrin/fibrinogen-based three-dimensional culture to enrich for primary cultured mouse aortic endothelial cells, and to induce endothelial cell capillary morphogenesis. We found among all the cell surface markers examined that only TEM7 expression was up-regulated upon endothelial cells capillary morphogenesis. In addition, inhibition of capillary morphogenesis by serum stimulation completely blocked TEM7 expression. In contrast, stimulation of endothelial cell capillary morphogenesis with PMA enhanced TEM7 expression. Furthermore, incubation of endothelial cells with a recombinant extracellular domain of TEM7 blocked capillary morphogenesis in three-dimensional cultures. These results suggest that TEM7 is a novel protein whose cell surface expression is essential during endothelial cell capillary morphogenesis. [Copyright &y& Elsevier]

The rat aortic ring model is well utilized for evaluation of angiogenesis. We report here an alternative assay employing an ex vivo mouse aorta angiogenesis model that can be extensively manipulated and serially evaluated using digital-assisted image analysis. Mouse aortas were harvested, cut into 2-mm disks, and cultured in fibrin matrix with growth media. Radial vascular outgrowths arose from the cut edge of the aortic disk and were digitally photographed and serially quantified. A variety of culture conditions were evaluated to determine their ability to alter angiogenesis in this model. Vessel outgrowth became apparent on day 3 and continued through day 10 with linear growth occurring between days 3 and 6. Increasing concentrations of serum from 0% to 40% resulted in stimulation of angiogenesis after day 3. Suramin and endostatin dramatically inhibited angiogenesis, which was more profound when applied at day 0 than when linear growth could be identified (day 3). Cells isolated from vessel outgrowths were predominantly endothelial in origin by immunocytochemistry and FACS analysis. We demonstrate that angiogenesis in an ex vivo murine model can be easily quantified using digital image analysis, responds appropriately to stimulation and inhibition, and exhibits differential results based on time of inhibitor administration. Antiangiogenic agents may be most effective if administered before development of accelerated vessel growth. [Copyright &y& Elsevier]

Histone deacetylase (HDAC) inhibitors have been demonstrated to regulate myeloid cell differentiation. In the present study the effects of the HDAC inhibitor trichostatin A (TSA) on the tetraspanin cell surface antigen CD9 were determined in primary murine macrophages. TSA inhibited CD9 protein and message expression and was optimal by 48 h. TSA did not induce similar effects on other surface markers and resulted in a modest increase or no effect on CD54 and CD11b, respectively. These effects were concentration dependent and concomitant with increased histone H4 acetylation. While interferon-γ (IFN-γ) and TSA had similar effects on CD9 expression, transcriptional profiling demonstrated significant differences in the genes activated by these stimuli. Notably CD14 message was down-regulated by IFN-γ while increased by TSA. These results demonstrate that HDAC inhibition may modulate macrophage function in part through changes in the expression of membrane proteins associated with matrix interactions. [Copyright &y& Elsevier]

CD9, a member of the tetraspanin family is a cell surface marker expressed on myeloid and nonmyeloid as well as on neoplastic cells. The present study has focused on the role of inflammation and macrophage activation in the regulation of CD9 expression. We report that the expression of CD9 on primary cultures of murine peritoneal macrophages was down regulated by Interferon-γ, IFN-γ. This down regulation was concentration-dependent and maximal by 48 h. The changes in surface expression were consistent with similar reductions in CD9 protein and message levels by Western and Northern blot analyses. The mechanism by which IFN-γ decreases CD9 expression appears to be through the Stat1 signaling pathway as Stat1 knockout mice did not demonstrate any reduction in CD9 expression by IFN-γ treatment. These results represent the first evidence for the down regulation of CD9 expression with macrophage activation. [Copyright &y& Elsevier]