Colloidal AuNPs show potential as a blood-pool agent for x-ray CT imaging.

No abstract

Papillary tumors of the bile ducts are intraductal tumors with numerous minute frondlike papillary projections. Some intraductal papillary tumors of the bile ducts produce a large amount of mucin that disturbs bile flow and causes severe biliary dilatation. In the presence of a tumor of this subgroup, the entire biliary tree is dilated; segmental or lobar bile ducts are dilated disproportionately, and aneurysmal dilatation may occur. Mucin is depicted at cholangiography as multiple elongated or cordlike filling defects, and the tumor is depicted on cross-sectional images as a castlike, polypoid, or fungating mass in the dilated biliary tree. Based on these characteristic imaging features-dilatation, mucin, and tumor-correct diagnosis of intraductal papillary mucinous tumor of the bile ducts may be made.

Competition for cellular iron (Fe) is a vital component of the interaction between host and pathogen. Most bacteria have an obligate requirement for Fe to sustain infection, growth, and survival in host. To obtain iron required for growth, many bacteria secrete iron chelators (siderophores). This study was undertaken to test whether a bacterial siderophore, deferoxamine (DFO), could trigger inflammatory signals in human intestinal epithelial cells as a single stimulus. Incubation of human intestinal epithelial HT-29 cells with DFO increased the expression of IL-8 mRNA, as well as the release of IL-8 protein. The signal transduction study revealed that both p38 and extracellular signal-regulated kinase-1/2 were significantly activated in response to DFO. Accordingly, the selective inhibitors for both kinases, either alone or in combination, completely abolished DFO-induced IL-8 secretion, indicating an importance of mitogen-activated protein kinases pathway. These proinflammatory effects of DFO were, in large part, mediated by activation of Na+/H+ exchangers, because selective blockade of Na+/H+ exchangers prevented the DFO-induced IL-8 production. Interestingly, however, DFO neither induced NF-κB activation by itself nor affected IL-1β- or TNF-α-mediated NF-κB activation, suggesting a NF-κB-independent mechanism in DFO-induced IL-8 production. Global gene expression profiling revealed that DFO significantly up-regulates inflammation-related genes including proinflammatory genes, and that many of those genes are down-modulated by the selective mitogen-activated protein kinase inhibitors. Collectively, these results demonstrate that, in addition to bacterial products or cell wall components, direct chelation of host Fe by infected bacteria may also contribute to the evocation of host inflammatory responses.

What a contrast! Agents for both magnetic resonance imaging (MRI) and near‐infrared (NIR) fluorescence imaging are synthesized by encapsulating iron oxide nanoparticles and indocyanine green in a poly(lactide‐co‐glycolide) matrix. The migration of dendritic cells (DCs) via lymphatic drainage is monitored by real‐time NIR fluorescence imaging, and the tracking of DCs into lymph nodes is achieved through noninvasive MRI (see picture).