Gilded: Contemporary Artists Explore Value and Worth

Across time and cultures, gold has served as a metaphor for what we value most. Symbolically, it stands in for goodness, excellence, brilliance, and wealth. He has a heart of gold. She is going for gold. It shone like gold. They struck gold. Found in crowns and regalia that bestow power, rings that signal matrimony, and currency traded among peoples, the metal has profound social significance. Across the arts, craftspeople have long pounded gold into thin sheets called leaves, which are applied in a process called gilding. In realms of the spiritual, gilding illuminates sacred texts, gives otherworldly luster to holy spaces, and allows religious sculptures to shine. While we most frequently associate gold leaf with historic traditions, the material appears frequently in the work of contemporary artists. Gilded: Contemporary Artists Explore Value and Worth is an exhibition curated by Emily Stamey and organized by the Weatherspoon Art Museum at UNC Greensboro. The project presents the work of seventeen present-day artists who turn to gilding as a means to reconsider our value systems. Gilding images of graffiti and sidewalks, cardboard boxes and architectural fragments, they ask us to see the beauty in what we so often overlook and honor that which we so often throw away. Gilding images of people—often those who have been disempowered or forgotten—they ask us to hold up our collective humanity. If, as the saying goes, “all that glitters is not gold,” the artists represented here offer an inverse proposition: perhaps that which does not always shine is most worthy of our attention. Gilded features the work of Radcliffe Bailey, Larissa Bates, william cordova, Angela Fraleigh, Gajin Fujita, Nicholas Galanin, Liz Glynn, Shan Goshorn, Sherin Guirguis, Titus Kaphar, Hung Liu, James Nares, Ronny Quevedo, Shinji Turner-Yamamoto, Danh Vo, Stacy Lynn Waddell, and Summer Wheat. This scholarly catalogue accompanying the show includes contributions by art historian Rebecca Zorach and poet Joshua Bennett

Activated leukocyte cell adhesion molecule (ALCAM/CD166): signaling at the divide of melanoma cell clustering and cell migration?

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Identification of degradome components associated with prostate cancer progression by expression analysis of human prostatic tissues

Extracellular proteases of the matrix metalloproteinase (MMP) and serine protease families participate in many aspects of tumour growth and metastasis. Using quantitative real-time RT–PCR analysis, we have undertaken a comprehensive survey of the expression of these enzymes and of their natural inhibitors in 44 cases of human prostate cancer and 23 benign prostate specimens. We found increased expression of MMP10, 15, 24, 25 and 26, urokinase plasminogen activator-receptor (uPAR) and plasminogen activator inhibitor-1 (PAI1), and the newly characterised serine proteases hepsin and matriptase-1 (MTSP1) in malignant tissue compared to benign prostate tissue. In contrast, there was significantly decreased expression of MMP2 and MMP23, maspin, and the protease inhibitors tissue inhibitor of metalloproteinase 3 (TIMP3), TIMP4 and RECK (reversion-inducing cysteine-rich protein with Kazal motifs) in the cancer specimens. The expression of MMP15 and MMP26 correlated positively with Gleason score, whereas TIMP3, TIMP4 and RECK expression correlated negatively with Gleason score. The cellular localisation of the expression of the deregulated genes was evaluated using primary malignant epithelial and stromal cell cultures derived from radical prostatectomy specimens. MMP10 and 25, hepsin, MTSP1 and maspin showed predominantly epithelial expression, whereas TIMP 3 and 4, RECK, MMP2 and 23, uPAR and PAI1 were produced primarily by stromal cells. These data provide the first comprehensive and quantitative analysis of the expression and localisation of MMPs and their inhibitors in human prostate cancer, leading to the identification of several genes involved in proteolysis as potential prognostic indicators, in particular hepsin, MTSP1, MMP26, PAI1, uPAR, MMP15, TIMP3, TIMP4, maspin and RECK