Publications by authors named "Sandra I Zittermann"

Detection of Listeria monocytogenes in food is currently based on enrichment methods. When L. monocytogenes is present with other Listeria species in food, the species compete during the enrichment process.

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The heterogeneity of the molecular pathology of HCC poses a formidable obstacle to the development of non-cytotoxic therapies. Several pro-tumorigenic signaling pathways can be aberrantly activated in HCC, including those triggered by Wnts. Glypican-3 (GPC3), a membrane-bound heparan sulfate proteoglycan that is overexpressed in most HCCs, promotes the growth of these tumors by stimulating Wnt signaling.

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Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are produced at sites of inflammation. Previously, we demonstrated that bFGF enhances leukocyte recruitment and endothelial cell adhesion molecule (CAM) expression during inflammation. Here, we investigated the influence of VEGF during acute inflammation and whether VEGF and bFGF cooperate to modulate leukocyte recruitment.

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CD31 (PECAM-1) is a 130-kDa member of the immunoglobulin gene superfamily expressed on endothelial cells, platelets, and most leukocytes. This report demonstrates by Western Blot and immunofluorescence that some human melanoma and adenocarcinoma cell lines express CD31 on the cell surface. The surface expression of CD31 was regulated by cell-cell contact, being higher on sparse and spontaneously detached cells.

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Basic fibroblast growth factor (bFGF, FGF-2) is a potent angiogenic factor and endothelial cell mitogen. Although bFGF levels are increased in chronically inflamed tissue, its role in inflammation is unclear. We investigated the effect of bFGF on acute dermal inflammation and the recruitment of monocytes, T cells, and neutrophils.

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Dendritic cells (DCs) are the most potent antigen-presenting cells and populate many tissues where they may participate in inflammatory reactions. The infiltration of polymorphonuclear leucocytes (PMNLs) into tissues is a prominent feature of inflammation. The mechanisms of PMNL recruitment depend on chemotactic factors and adhesion molecules expressed on endothelial cells.

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