Synthesis of Vanadium Carbide by Mechanical Activation Assisted Carbothermic Reduction.

Vanadium carbide is known, for its hardness and other unique properties, as a refractory material. The synthesis of vanadium carbide is always associated with the utilization of expensive active metals, such as aluminum, calcium and magnesium, as a reducing agent to extract the vanadium metal from its corresponding oxide, followed by carbidization. The carbidization of reduced vanadium requires a complicated process and elevated temperature. Mechanical activation to synthesize vanadium carbide from its corresponding oxide and carbon source represents a promising, straightforward and less energy-intensive route. In the present study, vanadium carbide is synthesized by the carbothermic reduction of a mechanically activated mixture of V2O5 and carbon black as reducing agents without any additives. The reduction process is monitored by means of thermogravimetric analysis. The reduction products are characterized by X-ray diffraction and field emission scanning electron microscope. It is found that V8C7 with an average crystallite size of 88 nm can be synthesized from a V2O5-C mixture after milling for 15 h and further heating at 1050 °C for 1 h in an inert atmosphere.

A moderately high fat diet promotes salt-sensitive hypertension in obese zucker rats by impairing nitric oxide production.

The objective of this research was to examine the contribution of a moderately high fat (MHF) diet to the development of salt-sensitive hypertension in obese Zucker rats. Lean and obese Zucker rats were fed either a MHF diet or a diet of standard rat chow (control diet) for 10 weeks. From week 4 through week 10, the drinking water was supplemented with 1% NaCl. Blood pressure was measured weekly, and urinary excretion of nitric oxide metabolites (NO(x)) was determined at weeks 4 and 10. At week 10, renal nitric oxide synthase (NOS) activity was assessed in kidney homogenates. Blood pressures of obese, but not lean, rats on the MHF fat diet were significantly increased by salt-supplementation, whereas blood pressures of rats on the control diet were not appreciably affected. NO(x) excretion was increased in response to salt-supplementation in rats on the control diet, with the effect being particularly dramatic in obese rats. After salt-supplementation, NO(x) excretion by rats on the MHF diet was lower than rats on the control diet. In obese rats on the MHF diet, this decrease in NO production was accompanied by a reduction in renal NOS activity. These results indicate that obese rats are more inclined than lean rats to develop diet-induced hypertension in response to a moderately high fat, salt-supplemented diet. Furthermore, they suggest that MHF diet-induced defects in NO production may promote the salt-sensitivity of blood pressure in obese Zucker rats, which appear to require more NO to maintain blood pressure during a salt challenge.