Central Exclusive Di-jet Production at the Tevatron

We perform a phenomenological analysis of dijet production in double pomeron exchange at the Tevatron. We find that the CDF Run I results do not rule out the presence of an exclusive dijet component, as predicted by Khoze, Martin and Ryskin (KMR). With the high statistics CDF Run II data, we predict that an exclusive component at the level predicted by KMR may be visible, although the observation will depend on accurate modelling of the inclusive double pomeron exchange process. We also compare to the predictions of the DPEMC Monte Carlo, which contains a non-perturbative model for the central exclusive process. We show that the perturbative model of KMR gives different predictions for the di-jet ET dependence in the high di-jet mass fraction region than non-perturbative models.Comment: 17 pages, 15 figure

Computing toric degenerations of flag varieties

We compute toric degenerations arising from the tropicalization of the full flag varieties $\mathcal{F}\ell_4$ and $\mathcal{F}\ell_5$ embedded in a product of Grassmannians. For $\mathcal{F}\ell_4$ and $\mathcal{F}\ell_5$ we compare toric degenerations arising from string polytopes and the FFLV polytope with those obtained from the tropicalization of the flag varieties. We also present a general procedure to find toric degenerations in the cases where the initial ideal arising from a cone of the tropicalization of a variety is not prime.Comment: 35 pages, 6 figure

THE INHIBITORY EFFECT OF PROPOLIS AND CAFFEIC ACID PHENETHYLESTER ON CYCLOOXYGENASE ACTIVITY IN J774 MACROPHAGES.

The effect of an ethanolic extract of propolis, with and without CAPE, and some of its components on cyclooxygenase (COX-1 and COX-2) activity in J774 macrophages has been investigated. COX-1 and COX-2 activity, measaured as prostaglandin E-2 (PGE(2)) production, were concentration-dependently inhibited by propolis (C x 10(-3)-3 x 10(2) mugml(-1)) with an IC50 of 2.7 mugml(-1) and 4.8 x 10(-2) mugml(-1), respectively. Among the compounds tested pinocembrin and caffeic, ferulic, cinnamic and chlorogenic acids did not affect the activity of COX isoforms. Conversely, CAPE (2.8 x 10(-4)-28 mugml(-1); 10(-9)-10(-4) M) and galangin (2.7 x 10(-4)-27 mugml(-1); 10(-9)-10(-4) M) were effective, the last being about ten-twenty times less potent. In fact the IC50 of CAPE for COX-1 and COX-2 were 4.4 x 10(-1) mugml(-1) (1.5 x 10(-6) M) and 2 x 10(-3) mugml(-1) (6.3 x 10(-9) M), respectively. The IC50 of galangin were 3.7 mugml(-1) (15 x 10(-6) M) and 3 x 10(-2) mugml(-1) (120 x 10(-1) M), for COX-1 and COX-2 respectively. To better investigate the role of CAPE, we tested the action of the ethanolic extract of propolis deprived of CAPE, which resulted about ten times less potent than the extract with CAPE in the inhibition of both COX-1 and COX-2, with an IC50 of 30 mugml(-1) and 5.3 x 10(-1) mugml(-1), respectively. Moreover the comparison of the inhibition curves showed a significant difference (p < 0.001). These results suggest that both CAPE and galangin contribute to the overall activity of propolis, CAPE being more effective

Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production.

Inhibition of neuronal cyclooxygenase-2 (COX-2) and hence prostaglandin E2 (PGE2) synthesis by non-steroidal anti-inflammatory drugs has been suggested to protect neuronal cells in a variety of pathophysiological situations including Alzheimer's disease and ischemic stroke. Ascorbic acid (vitamin C) has also been shown to protect cerebral tissue in a variety of experimental conditions, which has been attributed to its antioxidant capacity. In the present study, we show that ascorbic acid dose-dependently inhibited interleukin-1beta (IL-1beta)-mediated PGE2 synthesis in the human neuronal cell line, SK-N-SH. Furthermore, in combination with aspirin, ascorbic acid augmented the inhibitory effect of aspirin on PGE2 synthesis. However, ascorbic acid had no synergistic effect along with other COX inhibitors (SC-58125 and indomethacin). The inhibition of IL-1beta-mediated PGE2 synthesis by ascorbic acid was not due to the inhibition of the expression of COX-2 or microsomal prostaglandin E synthase (mPGES-1). Rather, ascorbic acid dose-dependently (0.1-100 microM) produced a significant reduction in IL-1beta-mediated production of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), a reliable indicator of free radical formation, suggesting that the effects of ascorbic acid on COX-2-mediated PGE2 biosynthesis may be the result of the maintenance of the neuronal redox status since COX activity is known to be enhanced by oxidative stress. Our results provide in vitro evidence that the neuroprotective effects of ascorbic acid may depend, at least in part, on its ability to reduce neuronal COX-2 activity and PGE2 synthesis, owing to its antioxidant properties. Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment

Arzanol, a prenylated heterodimeric phloroglucinyl pyrone, inhibits eicosanoid biosynthesis and exhibits anti-inflammatory efficacy in vivo.

Based on its capacity to inhibit in vitro HIV-1 replication in T cells and the release of pro-inflammatory cytokines in monocytes, the prenylated heterodimeric phloroglucinyl α-pyrone arzanol was identified as the major anti-inflammatory and anti-viral constituent from Helichrysum italicum. We have now investigated the activity of arzanol on the biosynthesis of pro-inflammatory eicosanoids, evaluating its anti-inflammatory efficacy in vitro and in vivo. Arzanol inhibited 5-lipoxygenase (EC 7.13.11.34) activity and related leukotriene formation in neutrophils, as well as the activity of cyclooxygenase (COX)-1 (EC 1.14.99.1) and the formation of COX-2-derived prostaglandin (PG)E(2)in vitro (IC(50)=2.3-9μM). Detailed studies revealed that arzanol primarily inhibits microsomal PGE(2) synthase (mPGES)-1 (EC 5.3.99.3, IC(50)=0.4μM) rather than COX-2. In fact, arzanol could block COX-2/mPGES-1-mediated PGE(2) biosynthesis in lipopolysaccharide-stimulated human monocytes and human whole blood, but not the concomitant COX-2-derived biosynthesis of thromboxane B(2) or of 6-keto PGF(1α), and the expression of COX-2 or mPGES-1 protein was not affected. Arzanol potently suppressed the inflammatory response of the carrageenan-induced pleurisy in rats (3.6mg/kg, i.p.), with significantly reduced levels of PGE(2) in the pleural exudates. Taken together, our data show that arzanol potently inhibits the biosynthesis of pro-inflammatory lipid mediators like PGE(2)in vitro and in vivo, providing a mechanistic rationale for the anti-inflammatory activity of H. italicum, and a rationale for further pre-clinical evaluation of this novel anti-inflammatory lead