Evaluation of pulse sequences used for magnetic resonance sialography.

OBJECTIVES: To determine the most appropriate sequences for the visualization of small parotid ducts in MR sialography. METHODS: MR images of a phantom consisting of distilled water in polyethylene tubes were obtained with turbo-spin echo (TSE), single-shot turbo-spin echo (SSTSE), half-fourier acquisition, single-shot turbo-spin echo (HASTE) and turbo gradient-spin echo (TGSE) pulse sequences and compared visually and quantitatively. MR sialograms obtained from healthy volunteers and patients with Sjögren's syndrome (SS) were obtained using the same four sequences. RESULTS: In the phantom, TSE images were best and the contrast-noise ratio (CNR) highest. In the volunteers, the main ducts were especially clearly visualized with TSE and in SSTSE; however, the majority of secondary and/or tertiary parotid ducts were not depicted by any of the sequences used. In SS patients, images of small main ducts and small pseudocysts were clearer using TSE. However, TSE could not depict the narrow main ducts or peripheral ducts or very small pseudocysts. CONCLUSIONS: TSE is considered the most suitable MR sequence for assessing small parotid gland ducts. However, further improvement is needed since it does not always visualize them sufficiently.

Changes of hepatic lipid and fatty acid profiles in rats administered iron-deficient diet and ethanol.

This investigation was undertaken to elucidate the effects of iron deficiency and/or ethanol ingestion on lipid metabolism of female rat liver. 40 Wistar rats (about 40 g weight) were fed a normal diet (Fe: 40 ppm) or an iron-deficient diet (Fe: 5 ppm) for 8 wk. Half of the rats in each group were given 10% ethanol in the drinking water for the last 4 wk. In rats fed the iron-deficient diet (D), the content of total hepatic lipid was higher than that in the rats given the normal diet (N). From the gas chromatography analyses of the fatty acids in total lipids, only the proportion of 18:2n-6 was increased, whereas those of 16:1n-7 and 20:4n-6 decreased. In rats given ethanol and an iron-sufficient diet (NE), the contents of all lipids with the exception of phospholipid were significantly higher than those in the N group. The percentages of fatty acids 12:0, 14:0, 16:0, 18:1 and 20:1 in the total hepatic lipid were increased, whereas those fatty acids of 18:0, 20:4, 22:6 and 24:0 were decreased. In the rats given ethanol and an iron-deficient diet (DE), the contents of all hepatic lipid components did not differ significantly from those in the D group. The percentages of fatty acids 12:0, 14:0 and 16:1 in the total hepatic lipid were increased. These data suggest that ethanol ingestion by iron-deficient rats does not induce the same changes in their hepatic lipid components and fatty acid patterns as those seen in fatty degeneration of the liver.

Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets.

Rats (Wistar, female, 4 weeks old) were fed iron-deficient (Fe-; 2.2 micrograms Fe/g) or manganese- and copper-deficient (Mn.Cu-; 0.3 microgram Mn/g, 0.4 microgram Cu/g) diets for 8 weeks to determine the oxidative damage of DNA by element deficiency. After feeding of the diets, 2-nitropropane (2-NP, 80 mg/kg body weight) was administered i.p. as an inducer of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) to the element-deficient rats. The hemoglobin concentration of rats in the Fe- group showed an induction of severe anemia (8.4 g/100 ml whole blood). In the Mn.Cu- group, Mn-superoxide dismutase (SOD) activities of plasma and Cu.Zn-SOD activities were significantly lower than that of the normal diet group. However, total SOD activities of plasma were not depressed severely in contrast to that of the liver in the Mn.Cu- group. Background (spontaneous) levels of 8-OH-dG in normal diet group were 0.96 +/- 0.37/10(5) deoxyguanosine (dG), however, significantly higher levels were detected in the Fe- group (1.56 +/- 0.19, P < 0.01). Conversely, a lower (but not significant) level of 8-OH-dG than the normal diet group were detected in the Mn.Cu- group (0.78 +/- 0.08). Six hours after 2-NP treatment, 8-OH-dG levels in liver DNA were significantly induced to 1.44 +/- 0.24 in the normal diet fed group 1.89 +/- 0.22 in the Fe- and 1.08 +/- 0.12 in the Mn.Cu- groups. Compared to the normal diet group, these induced levels of 8-OH-dG in the Fe- group were significantly higher (P < 0.05), and that in Mn.Cu- group were significantly lower (P < 0.05). The high level of 8-OH-dG in severe iron deficiency might be the results of: (i) an increase of hydroxyl radical generation by accumulated copper in hepatocytes; or (ii), a depression of enzymatic activity for removing 8-hydroxy-2'-deoxyguanosine in DNA, which is dependent on divalent cations. On the other hand, the low level of 8-OH-dG in manganese and copper deficiency might be the result of a decrease of lipid peroxidation which has been suggested to be an intermediator from active oxygen species to hydroxyl radical.