Oxygen solubility in ionic liquids based on 1-alkyl-3-methylimidazolium cations

This work presents the results of oxygen solubility in ionic liquids based on 1-alkyl-3-methylimidazolium cations. Solubility measurements have been carried out in gasometric apparatus at 22, 50 and 90 degrees C under atmospheric pressure. We report the Henry's constants. In general the occurrence of carbon-fluorine bonds and carbon-hydrogen bonds in ionic liquids (ILs) which can create hydrogen bonds with dissolved oxygen, significantly affects the growth of value of solubility constant K-H. Additionally, the stability of ILs towards molecular oxygen was tested. All ILs used in this study were stable in the presence of oxygen and free-radical initiator.

Exigências nutricionais de caprinos da raça Alpina em crescimento: 1. Exigência nutricional de fósforo para mantença: perdas endógenas e abate comparativo

O objetivo deste trabalho foi determinar a exigência dietética de fósforo (P) para mantença de caprinos da raça Alpina em crescimento pelo método das perdas endógenas e pela técnica do abate comparativo. Foram usados 21 animais, machos, castrados, com idade média de quatro a seis meses e 18 kg PV. Destes, três foram abatidos no início do experimento, como referência, e os 18 restantes, distribuídos em tratamentos com dietas isoenergéticas e isoprotéicas, em um delineamento inteiramente casualizado com arranjo fatorial 3x2 (nível de P na dieta [0,12; 0,21; e 0,29% MN] e forma de fornecimento da dieta [restrito ou à vontade]). O período experimental foi de 37 dias, com 30 dias para adaptação e sete dias para coleta total de fezes e urina. No final do período de coleta, três animais de cada tratamento foram abatidos. As exigências dietéticas de P para mantença foram então estimadas por meio das perdas endógenas fecal e urinária (perdas endógenas) e da retenção de P no corpo animal em relação à sua ingestão e aquele retido nos animais referência (abate comparativo). Os valores médios foram coeficiente de absorção aparente e real de P, -157+30, 98+10, 43+24, e 65+33; 235+09, 145+24%, respectivamente; perda diária endógena fecal e urinária de P, 8,84 e 4,84 mg/kg PV, respectivamente; e balanço de P, 187,62+153,87; 14,0+160,59; 85,96+337,85 mg/d; e -11,42+10,98; 1,04+9,14; -2,33+11,69 mg/kg PV, respectivamente. A exigência líquida diária estimada de P para a mantença foi de 13,68 mg/kg PV. As exigências dietéticas diárias de P para mantença foram estimadas em 72 e 58,46 mg/kg PV, pelo método das perdas endógenas e pelo abate comparativo, respectivamente.

Functional and Topological Studies with Trp-Containing Analogs of the Peptide StII(1-30) Derived From the N-Terminus of the Pore Forming Toxin Sticholysin II: Contribution to Understand its Orientation in Membrane

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Mirabegron relaxes urethral smooth muscle by a dual mechanism involving β3-adrenoceptor activation and α1-adrenoceptor blockade

Mirabegron is the first β3-adrenoceptor (AR) agonist approved for treatment of overactive bladder syndrome (OAB). This study aimed to investigate the effects of β3-adrenoceptor (AR) agonist mirabegron in mouse urethra. The possibility that mirabegron exerts α1-AR antagonism was also tested in rat smooth muscle preparations presenting α1A- (vas deferens and prostate), α1D- (aorta) and α1B-AR (spleen). Functional assays were carried out in mouse and rat isolated tissues. Competition assays for the specific binding of [(3) H]Prazosin to membrane preparations of HEK 293 cells expressing each of the human α1-ARs, as well as β-AR mRNA expression and cyclic AMP measurements in mouse urethra were performed. Mirabegron produced concentration-dependent urethral relaxations that were right shifted by the selective β3-AR antagonist L 748,337, but unaffected by β1- and β2-AR antagonists (atenolol and ICI 118,551, respectively). Mirabegron-induced relaxations were enhanced by the phosphodiesterase-4 inhibitor rolipram, and this agonist stimulated cAMP synthesis. Mirabegron also produced rightward shifts in urethral contractions induced by the α1-AR agonist phenylephrine. Schild regression analysis revealed that mirabegron behaves as a competitive antagonist of α1-AR in urethra, vas deferens and prostate (α1A-AR, pA2  ≅ 5.6) and aorta (α1D-AR, pA2  ≅ 5.4), but not in spleen (α1B-AR). The affinities estimated for mirabegron in functional assays were consistent with those estimated in radioligand binding with human recombinant α1A- and α1D-ARs (pKi ≅ 6.0). The effects of mirabegron in urethral smooth muscle are the result of β3-AR agonism together with α1A / α1D-AR antagonism.

β2 integrin-mediated crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed blood-brain barrier

In acute neuroinflammatory states such as meningitis, neutrophils cross the blood-brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated BBB endothelium supports neutrophil arrest, crawling, and diapedesis under physiological flow in vitro. Investigating the interactions of neutrophils from wild-type, CD11a(-/-), CD11b(-/-), and CD18(null) mice with wild-type, junctional adhesion molecule-A(-/-), ICAM-1(null), ICAM-2(-/-), or ICAM-1(null)/ICAM-2(-/-) primary mouse brain microvascular endothelial cells, we demonstrate that neutrophil arrest, polarization, and crawling required G-protein-coupled receptor-dependent activation of β2 integrins and binding to endothelial ICAM-1. LFA-1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in vitro. Neutrophil crawling was mediated by endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1. In the absence of crawling, few neutrophils maintained adhesive interactions with the BBB endothelium by remaining either stationary on endothelial junctions or displaying transient adhesive interactions characterized by a fast displacement on the endothelium along the direction of flow. Diapedesis of stationary neutrophils was unchanged by the lack of endothelial ICAM-1 and ICAM-2 and occurred exclusively via the paracellular pathway. Crawling neutrophils, although preferentially crossing the BBB through the endothelial junctions, could additionally breach the BBB via the transcellular route. Thus, β2 integrin-mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed BBB.