9 research outputs found

    Cell composition in BALF of PBS-, LPS-, PLN- and heat inactivated PLN-treated mice.

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    <p>Macrophage and neutrophil counts in BALF from WT mice, 6 hours after inoculation of PBS, LPS (2 pg/mouse), heat inactivated PLN (HIPLN 500 ng/mouse) or PLN (500 ng/mouse). Data are plotted in Box&Whiskers graph (median+interquartile range N = 5 per group). * P<0.05 versus PBS.</p

    PLN activates HEK cells via TLR4.

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    <p>IL-8 production in HEK-293 cells transfected with CD14 and either TLR2 or TLR4 were incubated with medium (control), LPS (100 ng/ml), LTA (5 µg/ml) or PLN (1 µg/ml) for 6 hours. In some experiments polymyxin B (P) was used at 10 µg/ml. Data are mean±SEM (N = 4 per group). * P<0.01 versus control, † P<0.001 versus control, ‡P<0.001 versus LPS.</p

    Acute RHPS4 exposure is associated with telomerase inhibition in brain tumor cells <i>in vitro</i>.

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    <p>(A) TRAP assay using ethanol-precipitated telomere extended DNA products after 30 minutes extension in non-drug treated brain tumor cells. High levels of telomerase activity are observed in each cell line. (B–D) TRAP assays in RHPS4-treated brain tumor lysates reveals complete telomerase inhibition in all cell lines at each drug concentration. 0.1 µg of total protein lysate was loaded per well in each TRAP assay. <i>CHAPS, CHAPS buffer only no lysate control; TS, telomere substrate internal control 61-bp oligonucleotide.</i></p

    c-Myc activation is not associated with degree of RHPS4 sensitivity.

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    <p>(A) c-Myc transcription factor assay. Jurkat cell nuclear extracts show activation and specificity of c-Myc proportional to concentration of extract analyzed and in the presence of wild-type or mutant competitor. (B–C) No significant difference in c-Myc activation was observed between untreated PFSK-1 or C6 cells and RHPS4-treated cells. Asterisk denotes significant reduction in c-Myc levels when either PFSK-1 or C6 untreated cells were exposed to a wild-type oligonucleotide competitor (p≤0.05). (D–E) c-Myc quantitative reverse transcriptase PCR. No difference in PFSK-1 or C6 c-Myc gene expression was observed between representative RHPS4-treated cells and untreated cells.</p

    Acute RHPS4 exposure inhibits proliferation of high grade brain tumor cells <i>in vitro</i>.

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    <p>Proliferation of tumor cells was impaired in malignant brain tumor cells after acute 72 hours exposure to RHPS4. (A–C) PFSK-1, DAOY, U87 and (E) Res196 cells exhibited IC<sub>50</sub> values of 2.7, 2.2, 1.1, and 1.6 µM respectively when 0.5–5.0 µM RHPS4 was used, representing a significant inhibition of cell proliferation (p≤0.05 for each drug concentration versus untreated). (D, F–G) Within this concentration range, KNS42, C6 and GB-1 cells were resistant to RHPS4. (H–I) At higher concentrations of RHPS4 exposure C6 and GB-1 cells exhibited IC<sub>50</sub> values of 26 µM and 32 µM respectively, representing a significant inhibition of cell proliferation (p≤0.05 for each drug concentration versus untreated). Error bars indicate standard error from three independent experiments. (J–M) Light microscopy of PFSK-1, DAOY, C6 and GB-1 cells showing a marked reduction in cellular density after RHPS4 exposure. <i>Magnifications, x20; Scale bar = 25 </i><i>µm</i>.</p

    TEM results in subjects with and without PCD.

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    <p>Key: TEM =  transmission electron microscopy analysis; OAD =  outer dynein arm defect; IAD =  inner dynein arm defect; MD =  microtubular disorganization defect; ALI = culture at air-liquid interface; PCD =  primary ciliary dyskinesia.</p