Optimization of window settings for standard and advanced virtual monoenergetic imaging in abdominal dual-energy CT angiography.

Objectives: To determine the optimal window setting for displaying virtual monoenergetic reconstructions of third generation dual-source, dual-energy CT (DECT) angiography of the abdomen.

Methods: Forty-five patients were evaluated with DECT angiography (90/150 kV, 180/90 ref. mAs).

Microgravity Induction of TRAIL Expression in Preosteoclast Cells Enhances Osteoclast Differentiation.

Evidence indicates that astronauts experience significant bone loss in space. We previously showed that simulated microgravity (μXg) using the NASA developed rotary cell culture system (RCCS) enhanced bone resorbing osteoclast (OCL) differentiation. However, the mechanism by which μXg increases OCL formation is unclear.

Independent regulation of cyclo-oxygenase 2 expression by p42/44 mitogen-activated protein kinases and Ca2+/calmodulin-dependent kinase.

5-Hydroxytryptamine (5-HT, 'serotonin') is a potent inducer of the early response gene cyclo-oxygenase 2 (Cox-2; prostaglandin G/H synthase) in mesangial cells. Protein kinase C (PKC), Ca2+-dependent enzymes and mitogen-activated protein kinase (p42/44 MAPK) have previously been shown to be essential modules of the signalling pathway leading from the pertussis-insensitive 5-HT2A receptor to the induction of Cox-2 mRNA expression. In the present study, PKC activation was linked to the 5-HT-mediated phosphorylation and thus the activation of p42/44 MAPK: the inhibition of PKC by the specific inhibitor GF109203x prevented p42/44 MAPK activation.

Signaling pathways mediating induction of the early response genes prostaglandin G/H synthase-2 and egr-1 by serotonin via 5-HT2A receptors.

Signaling pathways responsible for serotonin (5-HT)-mediated induction of early response genes prostaglandin G/H synthase-2 (PGHS-2, cyclooxygenase-2) and egr-1 were investigated in rat mesangial cells. Gene induction by 5-HT was dependent on 5-HT2A receptors that were pertussis toxin insensitive indicating coupling to a G-protein of the Gq family. Binding of 5-HT to this receptor activates phosphatidylinositol-specific phospholipase C (PLC) and release of Ca2+ from internal stores, but this activation was not related to PGHS-2 mRNA expression.

Mechanisms of serotonin-induced Ca2+ responses in mesangial cells.

Smooth muscle cell-like mesangial cells play an important role in the regulation of glomerular blood flow and are involved in renal inflammatory reactions, thereby interacting with circulating cells. The platelet products serotonin (5-HT) and ATP induce similar, e.g.

Regulation of platelet-derived growth factor isoform-mediated expression of prostaglandin G/H synthase in mesangial cells.

Incubation of rat renal mesangial cells with platelet-derived growth factor (PDGF) -AB or -BB led to a transient increase in prostaglandin G/H synthase-2 (PGHS-2) mRNA expression with a maximum after two hours. Expression of PGHS-1 mRNA remained unchanged during short term incubation, but was enhanced about twofold after 8 to 12 hours incubation with PDGF-AB or -BB. Enhanced PGHS activity was still observed after 24 hours.

Synergistic induction of monocyte chemoattractant protein-1 (MCP-1) by platelet-derived growth factor and interleukin-1.

Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the recruitment of monocytic cells to the site of inflammation. Resting mesangial cells express barely detectable levels of MCP-1 mRNA. Treatment of rat mesangial cells with platelet products PDGF-AB, PDGF-BB or serotonin transiently induced MCP-1 expression with a maximum after 2 to 4 h and a decline to baseline after 6 to 8 h.

Signal transduction pathways responsible for serotonin-mediated prostaglandin G/H synthase expression in rat mesangial cells.

Prostaglandin G/H synthase (PGHS) is one of the key enzymes in prostaglandin synthesis. Regulation of the mRNA expression of the two isozymes PGHS-1 and PGHS-2 was investigated in mesangial cells. PGHS-1 was constitutively expressed and not modulated by any of the stimuli used.