High-energy parametric oscillator and amplifier pulsed light source at 2-µm.

A laser system generating high-energy pulses at 2-µm wavelength with pulse widths tunable from 10-24 ns is described. It comprises an optical parametric oscillator that generates mJ-level signal seed radiation and an optical parametric amplifier that boosts the output to 800 mJ of combined signal and idler when pumped with 2 J pulses of 1064-nm laser light. The system operated with KTP crystals and running at 10 Hz repetition rate is characterized in the spatial, temporal, and spectral domains. The effect of saturation leads to an output pulse approaching flat-top spatial and box-shaped temporal profiles, as desired in various applications. The amplified pulses can be imaged down to sub-100 µm diameters, making this laser system a suitable driver for plasma sources of extreme ultraviolet light.

Platelet factor 4/CXCL4 induces phagocytosis and the generation of reactive oxygen metabolites in mononuclear phagocytes independently of Gi protein activation or intracellular calcium transients.

Platelet factor 4 (PF-4), a platelet-derived CXC chemokine, is known to prevent human monocytes from apoptosis and to promote differentiation of these cells into HLA-DR(-) macrophages. In this study, we investigated the role of PF-4 in the control of acute monocyte proinflammatory responses involved in the direct combat of microbial invaders. We show that PF-4 increases monocyte phagocytosis and provokes a strong formation of oxygen radicals but lacks a chemotactic activity in these cells. Compared with FMLP, PF-4-induced oxidative burst was later in its onset but was remarkably longer in its duration (lasting for up to 60 min). Furthermore, in PF-4-prestimulated cells, FMLP- as well as RANTES-induced burst responses became synergistically enhanced. As we could show, PF-4-mediated oxidative burst in monocytes does not involve Gi proteins, elevation of intracellular free calcium concentrations, or binding to CXCR3B, a novel PF-4 receptor recently discovered on endothelial cells. Moreover, we found that PF-4 acts on macrophages in a dual manner. On the one hand, very similar to GM-CSF or M-CSF, PF-4 treatment of monocytes generates macrophages with a high capacity for unspecific phagocytosis. On the other hand, short term priming of GM-CSF-induced human macrophages with PF-4 substantially increases their capability for particle ingestion and oxidative burst. A comparable effect was also observed in murine bone marrow-derived macrophages, indicating cross-reactivity of human PF-4 between both species. Taken together, PF-4 may play a crucial role in the induction and maintenance of an unspecific immune response.