A chemiresistive sensor was fabricated by the chemical modification of multi-walled carbon nanotubes (MWNTs) and chemical oxidation of polyaniline (PANI). The resistances of the sensing film samples against 100, 250, 500, 1000 ppm explosives (picric acid (PA), 2,6-dinitrotoluene (2,6-DNT) and 2,4,6-trinitrotoluene(TNT)) agents were investigated. The MWNTs with various wt. % PANI agents were characterized by TGA, SEM, FTIR and Raman spectroscopy, respectively. The experimental results showed that 1wt. % MWNTs and 10, 5, 1wt. % PANI sensor samples provided high sensitivity, excellent selectivity and good reproducibility to PA and 2,6-DNT vapours. In addition, principal component analysis (PCA) was applied to distinguish the performance of PA, 2,6-DNT and TNT agents. Our results indicate that the electric detection of explosive agents is possible with simply fabricated MWNTs-PANI devices.
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Hypoxia is regarded as an important physiological factor that controls nephrogenesis. We investigated whether the renin-angiotensin-aldosterone system (RAAS) affects hypoxia-related target genes in developing kidneys. Newborn rat pups were treated with enalapril (30 mg/kg/d) or spironolactone (200 mg/kg/d) for 7 days. Tissue hypoxia was assessed by the uptake of a hypoxyprobe-1, pimonidazole (200 mg/kg), and the expression of hypoxia-responsive genes. In the enalapril group, hypoxia-inducible factor (HIF)-1, HIF-2, and Ets-1 protein expression were not changed, compared to the control group. In the spironolactone group, HIF-1 and Ets-1 protein expression were significantly increased by immunoblots and immunohistochemistry, whereas HIF-2 protein expression was not changed, compared to the control group. In the enalapril group, the immunoactivity of pimonidazole was not significantly different from that of the controls. However, in the spironolactone group, pimonidazole staining demonstrated that the cortex and medulla underwent severe hypoxia. In summary, our data showed that aldosterone inhibition in the developing kidney augmented the hypoxic responses, and up-regulated the expression of key mediators of hypoxia including HIF-1 and Ets-1. Angiotensin II inhibition did not affect hypoxia-related alterations in the developing kidney. The components of RAAS may differentially modulate renal hypoxia and its related target genes in the developing rat kidney.
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