Our previous study has shown that an extremely low-frequency magnetic field (ELF-MF) induces nitric oxide (NO) synthesis by Ca(2+) -dependent NO synthase (NOS) in rat brain. The present study was designed to confirm that ELF-MF affects neuronal NOS (nNOS) in several brain regions and to investigate the correlation between NO and nNOS activation. The exposure of rats to a 2 mT, 60 Hz ELF-MF for 5 days resulted in increases of NO levels in parallel with cGMP elevations in the cerebral cortex, striatum, and hippocampus. Cresyl violet staining and electron microscopic evaluation revealed that there were no significant differences in the morphology and number of neurons in the cerebral cortex, striatum, and hippocampus. Differently, the numbers of nNOS-immunoreactive (IR) neurons were significantly increased in those cerebral areas in ELF-MF-exposed rats. These data suggest that the increase in NO could be due to the increased expression and activation of nNOS in cells. Based on NO signaling in physiological and pathological states, ELF-MF created by electric power systems may induce various physiological changes in modern life.

We have investigated whether extremely low frequency magnetic field (ELF-MF) induces lipid peroxidation and reactive oxygen species in mouse cerebellum. After exposure to 60 Hz ELF-MF at 2.3 mT intensity for 3 hours, there was a significant increase in malondialdehyde level and hydroxyl radical. ELF-MF significantly induced concomitant increase in superoxide dismutase without alteration in glutathione peroxidase activity. While glutathione contents were not altered, ascorbic acid levels were significantly decreased by ELF-MF exposure. These results indicate that ELF-MF may induce oxidative stress in mouse cerebellum. However, the mechanism remains further to be characterized.

A Gram-stain-positive, rod-shaped, endospore-forming bacterium, strain CAU 9038 T , was isolated from a tidal-flat sediment of DaeYiJac Island, Republic of Korea, and its taxonomic position was investigated using a polyphasic approach. The cell-wall peptidoglycan contained meso-diaminopimelic acid. The major polar lipids were diphosphatidylglycerol and phosphatidylglycerol, the major isoprenoid quinone was MK-7 and the dominant cellular fatty acid was anteiso-C 15 : 0 . The DNA G+C content was 51.6 mol%. 16S rRNA gene sequence analysis showed that the strain belonged to the genus Paenibacillus, with ,96.1 % sequence similarity to type strains of Paenibacillus species with validly published names. The most closely related type strains to CAU 9038 T were Paenibacillus thailandensis S3-4A T (96.1 % similarity) and

Lysolipids such as LPA, S1P and SPC have diverse biological activities including cell proliferation, differentiation, and migration. We investigated signaling pathways of LPA-induced contraction in feline esophageal smooth muscle cells. We used freshly isolated smooth muscle cells and permeabilized cells from cat esophagus to measure the length of cells. Maximal contraction occurred at 10-6 M and the response peaked at 30s. To identify LPA receptor subtypes in cells, western blot analysis was performed with antibodies to LPA receptor subtypes. LPA1 and LPA3 receptor were detected at 50 kDa and 44 kDa. LPA-induced contraction was almost completely blocked by LPA receptor (1/3) antagonist KI16425. Pertussis toxin (PTX) inhibited the contraction induced by LPA, suggesting that the contraction is mediated by a PTX-sensitive G protein. Phospholipase C (PLC) inhibitors U73122 and neomycin, and protein kinase C (PKC) inhibitor GF109203X also reduced the contraction. The PKC-mediated contraction may be isozyme-specific since only PKCε antibody inhibited the contraction. MEK inhibitor PD98059 and JNK inhibitor SP600125 blocked the contraction. However, there is no synergistic effect of PKC and MAPK on the LPA-induced contraction. In addition, RhoA inhibitor C3 exoenzyme and ROCK inhibitor Y27632 significantly, but not completely, reduced the contraction. The present study demonstrated that LPA-induced contraction seems to be mediated by LPA receptors (1/3), coupled to PTX-sensitive G protein, resulting in activation of PLC, PKC-ε pathway, which subsequently mediates activation of ERK and JNK. The data also suggest that RhoA/ROCK are involved in the LPA-induced contraction.

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