Ultrasonic treatment was employed to improve the dispersibility of the Fe 3 O 4 nanoparticles dispersed in aqueous solutions. Electrophoresis and XPS spectra indicate that the ultrasonic treatment can induce the generation of chemisorbed hydroxyl groups and the oxidation of Fe 2+ ions on the surface of the magnetic nanoparticles, thus resulting in improved dispersibility of the magnetic nanoparticles. After growth of silica protection layers on the Fe 3 O 4 nanoparticles with different times of ultrasonic treatment, Fe 3 O 4 /SiO 2 core/shell nanoparticles with different amounts of the magnetic cores were successfully prepared.

Tobacco-specific N-nitrosamines (TSNAs), including N'-nitrosonornicotine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, N'-nitrosoanatabine, and N'-nitrosoanabasine, have been implicated as a source of carcinogenicity in tobacco and cigarette smoke. We present a rapid and effective method comprising SPE based on tetraazacalix[2]arene[2]triazine-modified silica as sorbent and analysis with HPLC-MS/MS for the determination of TSNAs and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, in rabbit plasma. The linear dynamic ranges were 10-2000 pg/mL for NNAL and 4-2000 pg/mL for the four TSNAs with good correlation coefficients (>0.9965). The LODs were in the range of 0.9-3.7 pg/mL, and the LOQs were between 2.9 and 12.3 pg/mL. The accuracies of the method were also evaluated and found to be in the range of 90.1-113.3%. This method is promising to be applied to the preconcentration and determination of TSNAs and NNAL in smoke and human body fluids.

ischemia/reperfusion (i/r) injury is a serious clinical condition characterized by high morbidity and mortality rates. donepezil plays a neuroprotective role in i/r-associated diseases. The aim of the present study was to investigate the role and the potential mechanism of action of donepezil in i/r-induced myocardial microvascular endothelial cell dysfunction. an i/r model was simulated using oxygen-glucose deprivation/reoxygenation (oGd/r) injury in human cardiac microvascular endothelial cells (cMecs). cell viability and lactate dehydrogenase release were examined following treatment with donepezil. commercial kits were used to evaluate cell apoptosis, cell permeability and caspase-3 activity. The expression levels of apoptosis-associated proteins, as well as proteins found in tight junctions or involved in the poly(adP-ribose) polymerase 1 (ParP1)/nF-κB pathway, were measured using western blotting. These parameters were also examined following ParP1 overexpression. The results demonstrated that donepezil increased cell viability and reduced toxicity in oGd/r-treated cMecs. The apoptotic rate, caspase-3 activity and protein expression levels of Bax and cleaved caspase-3 were significantly reduced following donepezil treatment, which was accompanied by Bcl-2 upregulation. Moreover, cell permeability was notably reduced, coupled with a marked increase in the expression of tight junction-associated proteins. The expression levels of proteins related to ParP1/nF-κB signaling were significantly downregulated in cMecs following donepezil treatment. However, the protective effects of donepezil on oGd/r-induced cMec injury were reversed following ParP1 overexpression. in conclusion, donepezil suppressed oGd/r-induced cMec dysfunction via ParP1/nF-κB signaling. This finding provided insight into the mechanism underlying myocardial i/r injury.

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