CuO Nano-structures Prepared in Rosmarinus Officinalis Leaves Extract Medium: Efficient Catalysts for the Aqueous Media Preparation of Dihydropyrano[3, 2-c]chromene Derivatives.

CuO nano-structures were prepared in Rosmarinus Officinalis leaves extract medium via a green bio-chemical method and were used for the one-pot synthesis of dihydropyrano [3,2-c] chromene derivatives. This procedure is very simple and the products were synthesized in high to excellent yields.

Pentafluorophenylammonium triflate (PFPAT) catalyzed facile construction of substituted chromeno[2,3-d]pyrimidinone derivatives and their antimicrobial activity.

A new, simple thermally efficient and solvent-free condensation of 2-amino-3-cyano-6-methyl-4-phenyl-4H-pyran-5-ethylcarboxylate derivatives with coumarin-3-carboxylic acid employing pentafluorophenylammonium triflate (PFPAT) as an inexpensive organocatalyst for the synthesis of a series of ethyl 4,5-dihydro 7-methyl-2-(2-oxo-2H-chromen-3-yl)-4-oxo-5-aryl-3H-chromeno[2,3-d]pyrimidine-6-carboxylate derivatives is described. This method has the advantages of high yields, a cleaner reaction, simple methodology, short reaction times, easy workup, and greener conditions. All the compounds were evaluated for their in vitro antimicrobial activity against different bacterial and fungal strains.

Role of nicotinamide adenine dinucleotide phosphate-reduced oxidase proteins in Pseudomonas aeruginosa-induced lung inflammation and permeability.

Earlier studies indicated a role for reactive oxygen species (ROS) in host defense against Pseudomonas aeruginosa infection. However, the role of nicotinamide adenine dinucleotide phosphate-reduced (NADPH) oxidase (NOX) proteins and the mechanism of activation for NADPH oxidase in P. aeruginosa infection are not well-defined. Here, we investigated the role of NOX2 and NOX4 proteins in P. aeruginosa infection, ROS generation, and endothelial barrier function in murine lungs and in human lung microvascular endothelial cells (HLMVECs). Airway instillation of P. aeruginosa strain 103 (PA103) significantly increased ROS concentrations in bronchial alveolar lavage (BAL) fluid, along with the expression of NOX2 and NOX4, but not NOX1 and NOX3, in lung tissue. In addition, PA103-infected HLMVECs revealed elevated concentrations of ROS, NOX2, and NOX4. In murine lungs and HLMVECs, PA103 induced the NF-κB pathway, and its inhibition blocked PA103-dependent NOX2 and NOX4 expression. Barrier function analysis showed that heat-killed PA103 induced endothelial permeability in a dose-dependent manner, which was attenuated by treatment with small interfering (si)RNA specific for NOX4, but not NOX2. Furthermore, the knockdown of NOX4, but not NOX2, with siRNA reduced PA103-mediated apoptosis in HLMVECs. In vivo, the down-regulation of NOX4 with NOX4 siRNA attenuated PA103-induced lung vascular permeability. The deletion of NOX2 in mice exerted no effect on permeability, but offered significant resistance to P. aeruginosa-induced lung inflammation. These data show that P. aeruginosa lung infection up-regulates NOX2 and NOX4 expression and ROS generation, which play distinct roles in regulating lung inflammation, apoptosis, and permeability.

An investigation of nitric oxide metabolites during symptomatic myocardial ischaemia in relation to exercise tolerance test.

BACKGROUND: Nitric oxide (NO) plays a pivotal role in the pathophysiology of coronary heart disease (CHD). Low plasma concentrations of NO metabolites (nitrite and nitrate), the stable oxidation products of NO have been reported in patients with CHD but this is controversial. Plasma nitrite and nitrate concentrations during symptomatic myocardial ischaemia and in response to exercise in subjects with CHD have not been studied. We therefore measured plasma nitrite and nitrate concentrations in subjects before and after an exercise tolerance test (ETT). MATERIAL/METHODS: Plasma nitrite and nitrate concentrations were measured before and after an ETT in 24 subjects with symptomatic exercise-induced myocardial ischaemia (positive ETT) and in 27 subjects without exercise-induced myocardial ischaemia (negative ETT). RESULTS: Plasma nitrate concentrations were higher (p<0.002) before and after the ETT in subjects with a positive ETT (31.51+/-21.80 mol/L and 30.86+/-21.42 mol/L respectively) than in the subjects with a negative ETT (14.75+/-6.71 mol/L and 15.64+/-6.50 mol/L respectively). Plasma nitrite concentrations before and after the ETT were similar in both groups. Within each group, plasma nitrite and nitrate concentrations were not altered by exercise. CONCLUSIONS: Subjects with exercise-induced myocardial ischaemia have higher plasma nitrate concentration than subjects without exercise-induced myocardial ischaemia. This is consistent with either a compensatory or an inflammatory response of the vascular endothelium to endothelial damage. Symptomatic exercise-induced ischaemia is not associated with altered plasma NO metabolite concentrations.