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<p><b>(A)</b> Light microscopy image of Jurkat cell. The straights line reveals the contrast due to the nucleus. <b>(B)</b> Cluster average spectra from HCA results. <b>(C)</b> Chemical image of Jurkat cell building from the HCA results. The colors correspond to the Raman spectra generated by HCA methods (see B) and characteristic of the different cell compartments (see description in the text). Arrows allow to highlight the differences between cells treated and untreated by the peptides.</p

Effect of various concentrations of WRK, Warn G20D and WarnF14V on Jurkat cells.

<p>Results are expressed as the percentage of cell permeabilization in comparison to the negative (PBS buffer) and positive (0.1% Triton X-100) controls. Experiments were performed in triplicates, and the results are expressed as means. Bar scales indicate standard deviations.</p

Median lethal dose (LD₅₀) of WRK on cancer cell lines tested.

<p>Median lethal dose (LD₅₀) of WRK on cancer cell lines tested.</p

Chemical images of MNC cells before the peptide injection noted (MNC) and 1 hour after injection of the different peptides (notified by + peptide name).

<p>Scale bars are notified in each image. The colors correspond to the Raman spectra generated by HCA methods and characteristic of the different cell compartments.</p

Effect of various concentrations of WRK on leukemia cell lines Jurkat, KG1 and K562.

<p>Results are expressed as the percentage of cell permeabilization in comparison to the negative (PBS buffer) and positive (0.1% Triton X-100) controls. Experiments were performed in triplicates, and the results are expressed as means. Bar scales indicate standard deviations.</p

Primary sequences and biological activities of WRK and analogs WarnG20D and WarnF14V.

<p>Primary sequences and biological activities of WRK and analogs WarnG20D and WarnF14V.</p

Skin and liver expression of A-SAA in a mouse model of psoriasiform dermatitis.

<p>C57BL/6 mice were treated daily during six days with imiquimod 5% cream (IMQ), with Vaseline (VAS) or were not treated (NT). (A) SAA1/2 and (B) SAA3 mRNA expression was determined by RT-qPCR. All data represent mean ± SEM relative expression to <i>GAPDH</i>. Statistical comparisons were performed using t test (*p<0.05; **p<0.01; ns, non-significant).</p

A-SAA mRNA expression in the skin and the serum of psoriatic and control patients.

<p>A-SAA mRNA expression in (A) the skin and (B) the serum of psoriatic patients is compared to healthy controls. Positive correlations of (C) serum A-SAA and CRP protein levels and (D) A-SAA mRNA expression in the skin and A-SAA protein concentrations in the serum of psoriatic patients. A-SAA mRNA levels from psoriatic skins are increased with (E) psoriasis severity, as evaluated by PASI, (F) disease duration, (G) cigarette smoking and (H) metabolic syndrome, respectively. A-SAA mRNA expression from 37 psoriatic skins was compared to 28 healthy skins and quantified by RT-qPCR. A-SAA protein concentrations in 17 psoriatic sera were determined by immunonephelemetry and compared to those of 11 healthy sera. Values are expressed as mean ± SEM. Statistical comparisons were performed using t test or Spearman rank correlation test (*p<0.05; **p<0.01; ***p<0.0001; ns, non-significant).</p

A-SAA production by NHEK stimulated with human IL-1α, IL-17A, IL-22, OSM, TNF-α, alone or in combination.

<p>(A) A-SAA mRNA expression and (B) protein secretion by NHEK stimulated with M5 were analyzed at different time-periods. (C) A-SAA mRNA expression and (D) protein secretion were determined 40 hours after cytokine activation. (E) A-SAA mRNA expression and (F) protein secretion by NHEK 40 hours after stimulation with four cytokines by sequentially subtracting either recombinant IL-1α, IL-17A, IL-22, OSM or TNF-α from M5. A-SAA mRNA and protein were quantified by RT-qPCR in NHEK and ELISA in supernatants, respectively. Data represent the mean ± SEM of three experiments with duplicates. Statistical comparisons were performed using 2way ANOVA test or t test (*p<0.05; **p<0.01; ***p<0.001). (G) Compared to resting control, (H) intracellular A-SAA staining was detected by immunofluorescence in the cytoplasm of NHEK stimulated with M5 in the presence of brefeldin A.</p

Expression of proinflammatory mediators by A-SAA-stimulated NHEK and in synergy with IL-17A.

<p>(A) NHEK were incubated with A-SAA (10 μg/ml) for 24 hours and the expression of TNF-α, S100A7, S100A8, hBD2, CCL20 and A-SAA was determined by RT-qPCR. (B) IL-17A (10 ng/ml) had a synergistic effect with rA-SAA. After A-SAA and IL-17A costimulation, mRNA expression of S100A7, hBD2 and A-SAA were further increased compared to A-SAA or IL-17A alone. Three independent experiments with duplicates were performed. Values are expressed as mean ± SEM fold change above unstimulated NHEK. Statistical comparisons were performed using t test (*p<0.05; **p<0.01; ***p<0.001).</p