Synthesis of boron nitride nanotubes from ammonia and a powder mixture of boron and iron oxide

Boron nitride nanotubes (BNNTs) were synthesized from the reaction of ammonia gas with a powder mixture of boron and iron oxide in a tubular reactor connected to a mass spectrometer for the on-line chemical analysis of the reactor outlet stream at different temperatures and inlet gas compositions. XRD results showed that hexagonal and rhombohedral boron nitrides, iron, boron oxide, and iron boride were the solid phases formed in these materials depending on the reaction temperature and gas composition. It was observed that the crystallinity of the product increased with an increase in temperature. The synthesized materials exhibited Type II isotherms. The chemical analysis revealed that the only reaction taking place in the gas phase was the decomposition reaction of the ammonia gas and BNNTs were produced by the reaction of nitrogen formed from the decomposition reaction with FexBy formed from the reaction of B with Fe2O3

The PI3K/Akt and MAPK-ERK1/2 pathways are altered in STZ induced diabetic rat placentas

Diabetic pregnancy is associated with complications such as early and late embryonic death, fetal growth disorders, placental abnormalities, and embryonal-placental metabolic disorders. Excessive apoptosis and/or changes of proliferation mechanisms are seen as a major event in the pathogenesis of diabetesinduced embryonic death, placental weight and structural anomalies. Akt and ERK1/2 proteins are important for placental and fetal development associated with cellular proliferation and differentiation mechanisms. The mechanism underlying the placental growth regulatory effects of hyperglycemia have not been elucidated. Moreover, it is still not determined how Akt and ERK1/2 proteins related proliferation and apoptosis mechanisms are influenced by Streptozotocin (STZ) induced diabetic rat placental development. The aim of this study was to investigate the expression levels and spatio-temporal immunolocalizations of Akt, p-Akt, ERK1/2 and p-ERK1/2 proteins in normal and STZ-treated diabetic rat placental development. In order to compose the diabetic group, pregnant females were injected with a single dose of 40mg/kg STZ intraperitonally seven days before their sacrifice at 12th, 14th, 16th, 18th and 20th day of their gestation. We found that maternal diabetic environment led to a decrease in ERK1/2 and Akt phosphorylation during rat placental development. It could be said that MAPK ERK1/2 and PI3K/Akt cell signaling pathways are affected from hyperglycemic conditions in rat placentas. In conclusion, hyperglycemia-induced placental and embryonal developmental abnormalities could be associated with reduction of Akt and ERK1/2 phosphorylation