Next-to-leading order QCD corrections to electroweak Zjj production in the POWHEGBOX

We present an implementation of electroweak Z-boson production in association with two jets at hadron colliders in the POWHEG framework, a method that allows the interfacing of NLO-QCD calculations with parton-shower Monte Carlo programs. We focus on the leptonic decays of the weak gauge boson, and take photonic and non-resonant contributions to the matrix elements fully into account. We provide results for observables of particular importance for the suppression of QCD backgrounds to vector-boson fusion processes by means of central-jet-veto techniques. While parton-shower effects are small for most observables associated with the two hardest jets, they can be more pronounced for distributions that are employed in central-jet-veto studies.Comment: 12 pages, 5 figure

Once-daily intrapleural urokinase treatment of complicated parapneumonic effusion in pediatric patients

In this paper, we describe our experience in the treatment of childhood empyema using urokinase. Patients' ages ranged from 2 to 12 years. Urokinase (dosage: 3,100 IU/kg/day) was diluted in normal saline to produce 1000 IU/ml (maximum dosage 100,000 IU in 100 ml of normal saline). After 2 hours, the clamped catheters were released and connected to water-seal suction at a negative pressure of 10 cm H2O. Pleural irrigations were continued once a day until thoracostomy tube output decreased to less than 10 ml/day (urokinase treatment mean duration: 11.5 days). The complete resolution of the chest effusion was assessed on chest ultrasound scan and radiographs. None of the patients experienced any side effects due to urokinase. It would now seem reasonable to advocate small chest tube thoracostomy and intrapleural urokinase as first-line treatment of pleural empyema in children, with surgery indicated as a secondaryintervention

Slepton pair production in the POWHEG BOX

We present an implementation for slepton pair production at hadron colliders in the POWHEG BOX, a framework for combining next-to-leading order QCD calculations with parton-shower Monte-Carlo programs. Our code provides a SUSY Les Houches Accord interface for setting the supersymmetric input parameters. Decays of the sleptons and parton-shower effects are simulated with PYTHIA. Focussing on a representative point in the supersymmetric parameter space we show results for kinematic distributions that can be observed experimentally. While next-to-leading order QCD corrections are sizable for all distributions, the parton shower affects the color-neutral particles only marginally. Pronounced parton-shower effects are found for jet distributions.Comment: 10 pages, 4 figure

Synthesis and Biological Evaluation of New Antitubulin Agents Containing 2-(3′,4′,5′-trimethoxyanilino)-3,6-disubstituted-4,5,6,7-tetrahydrothieno[2,3-c]pyridine Scaffold

Two novel series of compounds based on the 4,5,6,7-tetrahydrothieno[2,3-c]pyridine and 4,5,6,7-tetrahydrobenzo[b]thiophene molecular skeleton, characterized by the presence of a 3′,4′,5′-trimethoxyanilino moiety and a cyano or an alkoxycarbonyl group at its 2- or 3-position, respectively, were designed, synthesized, and evaluated for antiproliferative activity on a panel of cancer cell lines and for selected highly active compounds, inhibition of tubulin polymerization, and cell cycle effects. We have identified the 2-(3′,4′,5′-trimethoxyanilino)-3-cyano-6-methoxycarbonyl-4,5,6,7-tetrahydrothieno[2,3-c]pyridine derivative 3a and its 6-ethoxycarbonyl homologue 3b as new antiproliferative agents that inhibit cancer cell growth with IC50 values ranging from 1.1 to 4.7 μM against a panel of three cancer cell lines. Their interaction with tubulin at micromolar levels leads to the accumulation of cells in the G2/M phase of the cell cycle and to an apoptotic cell death. The cell apoptosis study found that compounds 3a and 3b were very effective in the induction of apoptosis in a dose-dependent manner. These two derivatives did not induce cell death in normal human peripheral blood mononuclear cells, suggesting that they may be selective against cancer cells. Molecular docking studies confirmed that the inhibitory activity of these molecules on tubulin polymerization derived from binding to the colchicine site

5,7-Disubstituted-[1,2,4]triazolo[1,5-a][1,3,5]triazines as pharmacological tools to explore the antagonist selectivity profiles toward adenosine receptors

The structureeactivity relationship of new 5,7-disubstituted-[1,2,4]triazolo[1,5-a][1,3,5]triazines as adenosine receptors (ARs) antagonists has been explored. The introduction of a benzylamino group at C5 with a free amino group at C7 increases the affinity toward all the ARs subtypes (10: KihA1 \ubc 94.6 nM; KihA2A \ubc 1.11 nM; IC50hA2B \ubc 2214 nM; KihA3 \ubc 30.8 nM). Replacing the free amino group at C7 with a phenylureido moiety yields a potent and quite selective hA2A AR antagonist (14: hA2A AR Ki \ubc 1.44 nM; hA1/hA2A \ubc 216.0; hA3/hA2A \ubc 20.6). This trend diverges from the analysis on the pyrazolo[4,3-e][1,2,4]triazolo[1,5-c]pyrimidine series previously reported. With the help of an in silico receptor-driven approach, we have rationalized these observations and elucidated from a molecular point of view the role of the benzylamino group at C5 in determining affinity toward the hA2A AR

Pyrazolo-triazolo-pyrimidines as adenosine receptor antagonists: A complete structure–activity profile

In the last 5 years, many efforts have been conducted searching potent and selective human A3 adenosine antagonists. In this field several different classes of compounds, possessing very good affinity (nM range) and with a broad range of selectivity, have been proposed. Recently, our group synthesized a new series of pyrazolo-triazolo-pyrimidines bearing different substitutions at the N5 and N8 positions, which have been described as highly potent and selective human A3 adenosine receptor antagonists. The present review summarizes available data and provides an overview of the structure–activity relationships found for this class of human A3 adenosine receptor antagonists

Pyrazolo-triazolo-pyrimidines as adenosine receptor antagonists: Effect of the N-5 bond type on the affinity and selectivity at the four adenosine receptor subtypes

In the last few years, many efforts have been made to search for potent and selective human A3 adenosine antagonists. In particular, one of the most promising human A3 adenosine receptor antagonists is represented by the pyrazolo-triazolo-pyrimidine family. This class of compounds has been strongly investigated from the point of view of structure-activity relationships. In particular, it has been observed that fundamental requisites for having both potency and selectivity at the human A3 adenosine receptors are the presence of a small substituent at the N8 position and an unsubstitued phenyl carbamoyl moiety at the N5 position. In this study, we report the role of the N5-bond type on the affinity and selectivity at the four adenosine receptor subtypes. The observed structure-activity relationships of this class of antagonists are also exhaustively rationalized using the recently published ligand-based homology modeling approach