Assimilation of liquid hydrocarbon by microorganisms. I. Mechanism of hydrocarbon uptake.

The uptake mechanism of liquid hydrocarbons of low solubility in water was investigated, using microorganisms with different affinities for liquid hydrocarbon. Microorganisms which could utilize hydrocarbon were much more adherent to hydrocarbon than those which could not. The adhesive force between Candida intermedia IFO 0761 and hydrocarbon was higher than that of Candida tropicalis ATCC 20336, though both could utilize hydrocarbon; The total hydrocarbon uptake from the drop and accommodation forms of hydrocarbons was much higher than that from dissolved hydrocarbon. The uptake rate of drop-form hydrocarbon was nearly equal to that of accommodation-form hydrocarbon for C. intermedia, but was lower for C. tropicalis which shows lower adhesion to hydrocarbon.     

Reconstruction of the Human Colon Epithelium In Vivo

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Changes in activities of enzymes in erythrocytes from ddY mice supplemented with dietary selenium.

Plasma and erythrocyte enzyme activities were measured in ddY mice supplemented with dietary selenium (Se) from baker's yeast (Saccharomyces serevisiae) or selenious acid at 0.3 ppm Se content. Glutathione peroxidase (GSHpx) activities increased significantly in erythrocytes from mice supplemented with dietary Se. It was concluded that addition of dietary Se as food additive is very effective for activation of GSHpx in mice.     

Antibacterial effect of Kampo herbal formulation Hochu-ekki-to (Bu-Zhong-Yi-Qi-Tang) on Helicobacter pylori infection in mice

Because Helicobacter pylori (H. pylori) infection is a major cause of gastroduodenal diseases in humans, the eradication of H. pylori using antibiotics is very effective for the treatment of gastroduodenal diseases. However, it has recently been reported that resistance to these antibiotics is developing. In the present study, the antibacterial effect of a Kampo (traditional Japanese medicine) herbal formulation, Hochu-ekki-to (RET; Formula repletionis animalis et supletionis medii), against H. pylori was examined in vitro and in vivo. HET inhibited the growth of antibiotic-resistant strains of H. pylori as well as antibiotic-sensitive strains at a dose of 2.5 mg/ml in vitro. When 1,000 mg/kg of HET was administered orally to C57BL/6 mice for 7 days before or after inoculation with H. pylori, H. pylori in the stomach was significantly reduced in the HET-pre-treatment group compared with the control group. Furthermore, HET in combination with antibiotics completely eradicated the bacteria in mice. The expression of interferon (IFN)-gamma was induced in the gastric mucosa of the mice pre-treated with HET. There were no significant differences between the colonization of H. pylori in the control and HET treatment groups in IFN-gamma gene-deficient mice. These results suggest that the antibacterial effect of HET may be partly due to IFN-gamma induction, and that HET may be clinically useful for treatment of H. pylori infection.     

Mitochondrial dysfunction and increased reactive oxygen species impair insulin secretion in sphingomyelin synthase 1-null mice

Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin. Here, we generated and analyzed SMS1-null mice. SMS1-null mice exhibited moderate neonatal lethality, reduced body weight, and loss of fat tissues mass, suggesting that they might have metabolic abnormality. Indeed, analysis on glucose metabolism revealed that they showed severe deficiencies in insulin secretion. Isolated mutant islets exhibited severely impaired ability to release insulin, dependent on glucose stimuli. Further analysis indicated that mitochondria in mutant islet cells cannot up-regulate ATP production in response to glucose. We also observed additional mitochondrial abnormalities, such as hyperpolarized membrane potential and increased levels of reactive oxygen species (ROS) in mutant islets. Finally, when SMS1-null mice were treated with the anti-oxidant N-acetyl cysteine, we observed partial recovery of insulin secretion, indicating that ROS overproduction underlies pancreatic β-cell dysfunction in SMS1-null mice. Altogether, our data suggest that SMS1 is important for controlling ROS generation, and that SMS1 is required for normal mitochondrial function and insulin secretion in pancreatic β-cells.