Oxidative stress markers and phosphorus magnetic resonance spectroscopy in a patient with GLUT1 deficiency treated with modified Atkins diet.

Glucose transporter type 1 deficiency syndrome is an inborn error of glucose transport across blood-tissue barriers, and the modified Atkins diet is an effective and well-tolerated treatment. To investigate the effects of the modified Atkins diet, we examined the cerebrospinal fluid markers and performed phosphorus magnetic resonance spectroscopy in a patient with glucose transporter type 1 deficiency syndrome before and after the modified Atkins diet. Cerebrospinal fluid levels of the oxidative stress markers, 8-hydroxy-2'-deoxyguanosine and hexanoyl-lysine adduct, were markedly increased above the cutoff index and were normalized 18 months after the modified Atkins diet.

Surface charge controlled magnetic nanoparticles with grafting of poly(4-vinylpyridine).

Poly(4-vinylpyridine)-grafted magnetic nanoparticles were prepared by the "graft to" method. Surface-modified magnetic particles are covered with a hydrophobic layer because it can be dispersed in organic solvents such as methanol, toluene, benzene, and chloroform, but not in water. Surface charge control with magnetic nanoparticles of various isoelectric point was achieved by quaternization of pyridyl groups, and the positively charged particles can be dispersed in water within a wide range of pH.

Role of endogenous nitric oxide and prostaglandin in duodenal bicarbonate response induced by mucosal acidification in rats.

Duodenal HCO3- secretion increases in response to mucosal acidification by luminal acid. Although this process is known to be mediated by endogenous prostaglandins (PGs), the role of nitric oxide (NO) in this response has been little studied. We examined the effects of indomethacin and N(G)-nitro-L-arginine methyl ester (L-NAME) on the acid-induced HCO3- secretion in the rat duodenum, together with those on PGE2 generation as well as luminal release of NO metabolites (NOx).