994 resultados para extracellular fluid


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The importance of the frying oil as a heat-transfer medium and as a source of flavor precursors for the formation of potato chip flavor was investigated. Potato slices were fried in palmolein or silicone fluid, and the volatile flavor compounds of the resulting chips were isolated onto Tenax and analyzed by gas chromatography-mass spectrometry. Although the heat-transfer coefficients of the oils did not differ significantly, their temperature profiles during frying were different, probably due to greater turbulence on placing potato slices in palmolein, leading to more efficient heat transfer. Levels of Strecker aldehydes and sulfides in chips fried in the two media were not significantly different, but levels of pyrazines were significantly higher in palmolein-fried chips. Amounts of 2,4-decadienal were also significantly higher in palmolein-fried chips, but there was no significant difference in hexanal levels between the samples.

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Comparisons of 2D fluid simulations with experimental measurements of Ar/Cl-2 plasmas in a low-pressure inductively coupled reactor are reported. Simulations show that the wall recombination coefficient of Cl atom (gamma) is a crucial parameter of the model and that neutral densities are very sensitive to its variations. The best agreement between model and experiment is obtained for gamma = 0.02, which is much lower than the value predicted for stainless steel walls (gamma = 0.6). This is consistent with reactor wall contaminations classically observed in such discharges. The electron density, negative ion fraction and Cl atom density have been investigated under various conditions of chlorine and argon concentrations, gas pressure and applied rf input power. The plasma electronegativity decreases with rf power and increases with chlorine concentration. At high pressure, the power absorption and distribution of charged particles become more localized below the quartz window. Although the experimental trends are well reproduced by the simulations, the calculated charged particle densities are systematically overestimated by a factor of 3-5. The reasons for this discrepancy are discussed in the paper.

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Transcriptome analysis using microarray technology represents a powerful unbiased approach for delineating pathogenic mechanisms in disease. Here molecular mechanisms of renal tubulointerstitial fibrosis (TIF) were probed by monitoring changes in the renal transcriptome in a glomerular disease-dependent model of TIF ( adriamycin nephropathy) using Affymetrix (mu74av2) microarray coupled with sequential primary biological function-focused and secondary

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Synovial fluid is a potential source of novel biomarkers for many arthritic disorders involving joint inflammation, including juvenile idiopathic arthritis. We first compared the distinctive protein ‘fingerprints’ of local inflammation in synovial fluid with systemic profiles within matched plasma samples. The synovial fluid proteome at the time of joint inflammation was then evaluated across clinical subgroups to identify early disease associated proteins. We measured the synovial fluid and plasma proteomes using the two-dimensional fluorescence difference gel electrophoresis approach. Image analysis software was used to highlight the expression levels of joint and subgroup associated proteins across the study cohort (n = 32). A defined subset of 30 proteins had statistically significant differences (p < 0.05) between sample types such that synovial fluid could be differentiated from plasma. Furthermore distinctive synovial proteome expression patterns segregate patient subgroups. Protein expression patterns localized in the chronically inflamed joint therefore have the potential to identify patients more likely to suffer disease which will spread from a single joint to multiple joints. The proteins identified could act as criteria to prevent disease extension by more aggressive therapeutic intervention directed at an earlier stage than is currently possible.

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This review aims to summarise our knowledge to date on the protein complement of the synovial fluid (S F). The tissues, structure and pathophysiology of the synovial joint are briefly described. The salient features of the S F proteome, how it is composed and the influence of arthritic disease are highlighted and discussed. The concentrations of proteins that have been detected and quantified in SF are drawn together from the literature on osteoarthritis, rheumatoid arthritis and juvenile idiopathic arthritis. The measurements are plotted to give a perspective on the dynamic range of protein levels within the SF. Approaches to proteomic analysis of SF to date are discussed along with their findings. From the recent literature reviewed within, it is becoming increasingly clear that analysis of the SF proteome as a whole, could deliver the most valuable differential diagnostic fingerprints of a number of arthritic disorders. Further development of proteomic platforms could characterise prognostic profiles to improve the cliniciads ability to resolve unremitting disease by existing and novel therapeutics.

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Background: Neutrophil elastase (NE) activity is increased in lung diseases such as a1-antitrypsin (A1AT) deficiency and pneumonia. It has recently been shown to induce expression of cathepsin B and matrix metalloprotease 2 (MMP-2) in vitro and in a mouse model. It is postulated that increased cathepsin B and MMP-2 in acute and chronic lung diseases result from high levels of extracellular NE and that expression of these proteases could be inhibited by A1AT augmentation therapy.

Methods: Cathepsin and MMP activities were assessed in bronchoalveolar lavage (BAL) fluid from patients with A1AT deficiency, pneumonia and control subjects. Macrophages were exposed to BAL fluid rich in free NE from patients with pneumonia following pretreatment with A1AT. MMP-2, cathepsin B, secretory leucoprotease inhibitor (SLPI) and lactoferrin levels were determined in BAL fluid from A1AT-deficient patients before and after aerosolisation of A1AT.

Results: BAL fluid from both patients with pneumonia and those with A1AT deficiency containing free NE had increased cathepsin B and MMP-2 activities compared with BAL fluid from healthy volunteers. The addition of A1AT to BAL fluid from patients with pneumonia greatly reduced NE-induced cathepsin B and MMP-2 expression in macrophages in vitro. A1AT augmentation therapy to A1AT-deficient individuals also reduced cathepsin B and MMP-2 activity in BAL fluid in vivo. Furthermore, A1AT-deficient patients had higher levels of SLPI and lactoferrin after A1AT augmentation therapy.

Conclusion: These findings suggest a novel role for A1AT inhibition of NE-induced upregulation of MMP and cathepsin expression both in vitro and in vivo.