No abstract

We evaluated soluble interleukin-2 receptors (sIL-2R), neopterin and adenosine deaminase (ADA) in pleural effusions from 93 patients with tuberculosis, malignancies, uremia, pneumonia and other kinds of pleurisy. There were significantly elevated ADA (102.7 ± 47 U/1) and sIL-2R (8,238 ± 4,117 U/ml) values in tuberculous (TB) pleural fluids as compared with other non-TB pleural fluids (p < 0.005). The neopterin levels in pleural fluid were significantly lower in the cancer group (17.3 ± 7.8 nmol/l; p < 0.005) and most strikingly elevated (309.4 ± 112.2 nmol/l; p < 0.0001) in patients with uremic pleural effusions. Using cut-off values of 60 U/l in ADA and 5,000 U/l in sIL-2R, 92.0 and 86.9% of pleural effusions were TB in origin. Eighty-four percent of patients with malignant pleural effusions had neopterin levels less than 25 nmol/l.

No abstract

Taxol, a microtubule stabilizing agent, has been extensively investigated for its antitumor activity. The cytotoxic effect of taxol is generally attributed to its antimicrotubule activity and is believed to be cell cycle dependent. Herein, we report that taxol induces hyperphosphorylation and reorganization of the vimentin intermediate filament in 9L rat brain tumor cells, in concentration- and time-dependent manner. Phosphorylation of vimentin was maximum at 10(-6) M of taxol treatment for 8 h and diminished at higher (10(-5) M) concentration. Enhanced phosphorylation of vimentin was detectable at 2 h treatment with 10(-6) M taxol and was maximum after 12 h of treatment. Taxol-induced phosphorylation of vimentin was largely abolished in cells pretreated with staurosporine and bisindolymaleimide but was unaffected by H-89, KT-5926, SB203580, genistein, and olomoucine. Thus, protein kinase C may be involved in this process. Hyperphosphorylation of vimentin was accompanied by rounding up of cells as revealed by scanning electron microscopy. Moreover, there was a concomitant reorganization of the vimentin intermediate filament in the taxol-treated cells, whereas the microtubules and the actin microfilaments were less affected. Taken together, our data demonstrate that taxol induces hyperphosphorylation of vimentin with concomitant reorganization of the vimentin intermediate filament and that this process may be mediated via a protein kinase C signaling pathway.

Sodium sulfite has pro-inflammatory properties in vitro and can induce potent chemotactic factor IL-8 production. Possible signal transduction pathways required for IL-8 gene expression following exposure to sulfite are the NF-kappa B, ERK, and p-38-dependent pathways. Salmeterol, fluticasone, and montelukast all have inhibitory effects on sodium sulfite-induced IL-8 production in A549 cells.