Mid-infrared supercontinuum-based Fourier transform spectroscopy for plasma analysis.

Broadband mid-infrared (MIR) spectroscopy is a well-established and valuable diagnostic technique for reactive plasmas. Plasmas are complex systems and consist of numerous (reactive) types of molecules; it is challenging to measure and control reaction specificity with a good sensitivity. Here, we demonstrate the first use of a novel MIR supercontinuum (SC) source for quantitative plasma spectroscopy. The SC source has a wide spectral coverage of 1300-2700 cm-1 (wavelength range 3.7-7.7 µm), thus enabling broadband multispecies detection. The high spatial coherence of the MIR SC source provides long interaction path lengths, thereby increasing the sensitivity for molecular species. The combination of such a SC source with a custom-built FTIR spectrometer (0.1 cm-1 spectral resolution) allows detection of various gases with high spectral resolution. We demonstrate its potential in plasma applications by accurate identification and quantification of a variety of reaction products (e.g. nitrogen oxides and carbon oxides) under low-pressure conditions, including the molecular species with overlapping absorbance features (e.g. acetone, acetaldehyde, formaldehyde, etc.).

Fourier transform spectrometer based on high-repetition-rate mid-infrared supercontinuum sources for trace gas detection.

We present a fast-scanning Fourier transform spectrometer (FTS) in combination with high-repetition-rate mid-infrared supercontinuum sources, covering a wavelength range of 2-10.5 µm. We demonstrate the performance of the spectrometer for trace gas detection and compare various detection methods: baseband detection with a single photodetector, baseband balanced detection, and synchronous demodulation at the repetition rate of the supercontinuum source. The FTS uses off-the-shelf optical components and provides a minimum spectral resolution of 750 MHz. It achieves a noise equivalent absorption sensitivity of ∼10-6 cm-1 Hz-1/2 per spectral element, by using a 31.2 m multipass absorption cell.

Increased circulating cytokine receptors and ex vivo interleukin-1 receptor antagonist and interleukin-1beta production but decreased tumour necrosis factor-alpha production after a 5-km run.

BACKGROUND: The purpose of this study was to examine the effect of a 5-km run on blood leucocytes, acute-phase proteins and cytokines. In addition, cytokines were measured in the supernatants from whole-blood cell cultures incubated with lipolysaccharide (LPS). METHODS: Ten healthy, recreational trained, athletes (three women, seven men) volunteered for this investigation. Samples were drawn just before, immediately after and at 3 h, at 24 h and at 48 h after the race. RESULTS: Exercise induced a transient leucocytosis (P = 0. 0002) and a mild acute-phase reaction with increase in plasma C-reactive protein (CRP) (P = 0.0115) but not in serum amyloid A (SAA) concentrations. Although plasma interleukin 6 (IL-6) was undetectable and soluble interleukin-1 receptor type II (IL-1sRII) remained unchanged, interleukin-1 receptor antagonist (IL-1ra) concentrations were elevated directly after the race with a further increase at 3 h (P < 0.0001). Soluble tumour necrosis factor (TNF) receptors were increased immediately after the run, but the effect was more marked for sTNFr p55 (two-fold increase; P < 0.0001) than for sTNFr p75 (1.16-fold increase; P = 00007). In cell cultures, the LPS-induced release of the inflammatory cytokines doubled for IL-1beta (P < 0.0001) and for IL-1ra (P < 0.0001). In contrast, TNF-alpha production decreased after the run, and a nadir was reached at 24 h (P < 0.0001). CONCLUSION: These results suggest that a 5-km run elicits both the production of acute-phase mediators (leucocytosis and elevation of CRP) and anti-inflammatory counter-regulation as judged by the increase in circulating concentrations of IL-1ra, sTNFr p55, and sTNFrp75 and down-regulation of LPS-stimulated TNF-alpha production.

Verocytotoxin inhibits mitogenesis and protein synthesis in purified human glomerular mesangial cells without affecting cell viability: evidence for two distinct mechanisms.

Acute renal failure is one of the hallmarks of the hemolytic uremic syndrome (HUS). Infection with a verocytotoxin (VT)- or Shiga-like toxin (SLT)-producing Escherichia coli has been strongly implicated in the etiology of the epidemic form of HUS. The functional receptor for these closely related toxins appears to be a glycosphingolipid, globotriaosylceramide (Gb3). Endothelial damage in the glomeruli and arterioles of the kidney induced by VT is believed to play a crucial role in the pathogenesis of HUS. However, little information is available regarding the effects of VT on mesangial cells, which also play an important role in glomerular function. In this study, the effects of VT on human mesangial cells in vitro were investigated. Mesangial cells were enriched by collecting hillock-shaped outgrowths derived from adult human glomeruli and subsequently purified by elimination of contaminating epithelial cells by immunoseparation with ulex europaeus lectin-I (UEA-I)-coated dynabeads. The obtained and subcultured mesangial cell populations were >98% pure. Their mesangial nature was established by the presence of a-smooth muscle cell actin in highly confluent cultures and the absence of cytokeratin or platelet/endothelial cell adhesion molecule-1. Mesangial cells bound VT to bands of Gb3 and a closely related glycolipid, which is similar to a glycolipid involved in the VT-dependent cytokine production in monocytes. VT did not induce the release of cytokines or chemokines in mesangial cells. In VT-susceptible cells, binding of VT to Gb3 causes cell death by the inhibition of protein synthesis. Although protein synthesis was inhibited in mesangial cells, all cells remained viable, both under basal and tumor necrosis factor-alpha-stimulated conditions. However, the marked reduction in protein synthesis may impair a proper response of the cells in conditions of increased demand of newly synthesized proteins. Furthermore, VT markedly inhibited DNA synthesis and proliferation of mesangial cells. The inhibition of mitogenesis was also found with the B-subunit of VT-1 alone, albeit to a lesser extent, without a significant effect on protein synthesis. Because the inhibition of protein synthesis involves the A-subunit, this suggests that two distinct mechanisms contribute to the effects of VT on protein synthesis and mitogenesis. Intracellular routing of VT (A- and B-subunits) may vary between cell types and result in differential effects on human mesangial cells when compared with other cell types.