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The reaction between N 2 O and CH 4 over an Fe ion-exchanged BEA zeolite (Fe-BEA) catalyst was studied by using a pulse reaction technique, temperature-programmed desorption (TPD) and infrared (IR) spectroscopy. N 2 O readily reacted with CH 4 in the presence of an N 2 O + CH 4 mixture above 200 C, while both the O 2 + CH 4 reaction and the catalytic decomposition of N 2 O over the Fe-BEA catalyst required higher temperatures (above 400 C). In the O 2 -TPD studies, a desorption peak of O 2 was observed above 600 C after O 2 treatment at 250 C, while a new O 2 desorption peak appeared at the lower temperatures after N 2 O treatment at 250 C. However, the new O(a) species resulting from the N 2 O treatment hardly reacted with CH 4 even at 350 C, which was confirmed by the CH 4 -pulsed experiments. On the other hand, a new IR band at 3683 cm À1 , which can be assigned to the OH group on Fe ion species, was observed after O 2 or N 2 O treatment. The peak intensity at 3683 cm À1 was not changed in the exposure of CH 4 only, but decreased in the exposure of N 2 O + CH 4 mixture above 150 C. At the same time, the CH x O y (a) species such as Fe-OCH 3 were formed, which were observed by IR measurements. The adsorbed surface species showed a high reactivity with N 2 O even at low temperatures ($200 C). A possible mechanism is discussed in terms of active oxygen species such as nascent oxygen transients (O*(a)), which are formed in the exposure of N 2 O + CH 4 mixture, and may play an important role in the activation/oxidation of CH 4 at initial steps to form CH x O y (a) species.

P ulmonary arterial hypertension (PAH) is a fatal disease characterized by increased pulmonary vascular resistance, leading to right heart failure and death.1,2 Increased pulmonary vascular resistance is caused by distal pulmonary vascular remodeling, including prolonged vasoconstriction, proliferation and migration of vascular smooth muscle cells (VSMCs), and endothelial injury.3 Although multiple pharmacological agents, such as vasodilators and anticoagulants, have been developed for the treatment of PAH, long-term prognosis of patients with severe PAH remains poor because of progressive right heart failure. 3 Thus, more effective treatments need to be urgently developed.Rho-kinase (ROCK) belongs to the serine/threonine kinases family and is an important downstream effector of the small GTP-binding protein RhoA. It has been demonstrated that Rho/ROCK pathway plays an important role in various fundamental cellular functions, including contraction, motility, proliferation, and migration, leading to the development of cardiovascular diseases, including PAH. 4,5 There are 2 isoforms of ROCK: ROCK1 (Rho-kinase β) and ROCK2 (Rho-kinase α).6 ROCK1 and ROCK2 are highly homologous, sharing 65% homology in amino acid sequence and 92% homology in their kinase domains. 6 Both isoforms are ubiquitously expressed in invertebrates and vertebrates with ROCK1 expressed mainly in circulating inflammatory cells and ROCK2 in VSMC. 7,8 Homozygous ROCK1-deficient mice show open eyelids at birth and omphalocele, whereas homozygous ROCK2-deficient mice die embryonically because of placental dysfunction, 9,10 suggesting that ROCK1 and ROCK2 mediate different functions in different types of cells.We have previously reported that a long-term treatment with an isoform-nonspecific ROCK inhibitor, fasudil, suppresses the development of monocrotaline-induced and hypoxia-induced pulmonary hypertension (PH) in animal models.11,12 Furthermore, we have recently obtained a direct evidence for increased ROCK activation in patients with idiopathic PAH (IPAH). 13 However, although isoform-nonspecific ROCK inhibitors were effective in previous studies of PAH in both animals and humans, 14 the particular isoform of ROCK responsible for the effect has not been evaluated.It was previously reported that heterozygous ROCK1-deficient mice had decreased neointima formation after carotid artery ligation associated with reduced leukocytemediated inflammation. 15 Thus, ROCK1 seems to play an important role in circulating inflammatory cells in the pathogenesis of vascular diseases. 7,8 In contrast, Rho/ROCK2 pathway plays a central role in VSMC-mediated vasoconstriction © 2013 American Heart Association, Inc. Objective-Rho/Rho-kinase (ROCK) pathway in vascular smooth muscle cells (VSMCs) plays an important role in the pathogenesis of cardiovascular diseases, including pulmonary arterial hypertension (PAH). Rho-kinase has 2 isoforms, ROCK1 and ROCK2, with different functions in different cells; ROCK1 for circulating inflammatory cells and ROCK2 for the vas...

This paper extends the work of the first four parts of this series to apply the image analysis methods we have developed to characterize the fiber orientation of real non woven fabrics. The "real" fabrics chosen as typical are a carded crimped fiber web, two relatively dense overall or area bonded fabrics, a pattern or point bonded spun bonded-meltblown-spunbonded fabric, and a lightweight spunbonded nonwoven. In order to deal with real webs, it is necessary to develop a lighting system to give images with sufficient contrast along with an appropriate thresholding method to yield data suitable for analysis. The results indicate that the chord tracking method can charac terize orientation reliably when a direct measure is needed, and the information can be used to characterize and compare nonwoven laydown processes.

Objective The pleiotropic effects of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) independent of cholesterol-lowering effects are thought to be mediated through inhibition of the Rho/Rho-kinase pathway. However, we have previously demonstrated that the pleiotropic effects of regular-dose statins are mediated mainly through inhibition of the Rac1 signaling pathway rather than the Rho/Rho-kinase pathway, although the molecular mechanisms of the selective inhibition of the Rac1 signaling pathway by regular-dose statins remain to be elucidated. In this study, we tested our hypothesis that small GTP-binding protein GDP dissociation stimulator (SmgGDS) plays a crucial role in the molecular mechanisms of the Rac1 signaling pathway inhibition by statins in endothelial cells. Approach and Results In cultured human umbilical venous endothelial cells, statins concentration-dependently increased SmgGDS expression and decreased nuclear Rac1. Statins also enhanced SmgGDS expression in mouse aorta. In control mice, the protective effects of statins against angiotensin II–induced medial thickening of coronary arteries and fibrosis were noted, whereas in SmgGDS-deficient mice, the protective effects of statins were absent. When SmgGDS was knocked down by its small interfering RNA in human umbilical venous endothelial cells, statins were no longer able to induce Rac1 degradation or inhibit angiotensin II–induced production of reactive oxygen species. Finally, in normal healthy volunteers, statins significantly increased SmgGDS expression with a significant negative correlation between SmgGDS expression and oxidative stress markers, whereas no correlation was noted with total or low-density lipoprotein-cholesterol. Conclusions These results indicate that statins exert their pleiotropic effects through SmgGDS upregulation with a resultant Rac1 degradation and reduced oxidative stress in animals and humans.