エジプト紅海沿岸のマングローブ林の林分構造

Established mangrove forests along the coastal area of the Arabian Peninsula and African side of the Red Sea are uniquely different from mangrove forests in other parts of the world because of their low biodiversity and harsh habitat of arid and highly saline conditions. Therefore mangrove forests in this area appear in patchy and scattered patterns at mouths of wadi or in sheltered lagoons with rare and irregular flooding. Most of them are pure forests of Avicennia marina, occasionally mixed with Rhizophora mucronata in the southern part of the Red Sea. In this study, we analyze the forest structure of A. marina and discuss the regeneration strategy and the forest dynamics of this unique mangrove species. Three experimental plots of 1000 to 2000 trees/ha were selected from north to south along the Red Sea coast. The highest tree size (6.8m) suggested severe effects of the high salinity of the Red Sea (3.2 to 4.9%) on tree growth. Dense mantle vegetation had developed at the forest edge facing the open sea to protect the forest interior against strong waves and wind. Tree growth was also prevented by severe drought on the landside edge of the forest. All the forests had a dense seedling bank throughout the forest floor, with a very high rate of turnover and regeneration, which seldom occurred in other forests

Influence of chronic hepatic failure on disposition kinetics of valproate excretion through a phase II reaction in rats treated with carbon tetrachloride

The influence of chronic hepatic failure on the disposition kinetics of valproate (VPA) excretion via a phase II reaction was examined in rats treated with carbon tetrachloride (1.0 mg/kg, s.c., 3 times a week) for 2 or 3 months. There was no significant difference in the plasma concentration-time courses of VPA among the control and two treated groups up to 120 min after i.v. administration of VPA (75 mg/kg), but subsequently the plasma concentrations of the treated groups declined significantly below the control levels. Expression of Mrp2 mRNA in the liver of the treated groups was significantly lower than in the control group; conversely that in the kidney was significantly higher. The enzyme activity of UGTs in the liver of the treated groups decreased significantly, but UGT1A8 mRNA expression in the duodenum was increased about 3-fold. Cumulative excretion of VPA glucuronide (VPA-G) in bile of the treated groups was reduced significantly, while that in urine was markedly increased. In conclusion, the area under the VPA plasma concentration-time curve was decreased significantly in rats with chronic hepatic failure owing to increased excretion of VPA-G via the kidney as a result of induction of Mrp2, and inhibition of enterohepatic circulation of VPA-G. Copyright © 2007 John Wiley & Sons, Ltd

Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Modulates Experimental Autoimmune Encephalomyelitis via an iNKT Cell-Dependent Mechanism

Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1) is a CEA family member that has been reported to have an important role in the regulation of Th1-mediated colitis. In this study, we examined the role of CEACAM1 in an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). Treatment of C57BL/6J mice with CEACAM1-Fc fusion protein, a homophilic ligand of CEACAM1, inhibited the severity of EAE and reduced myelin oligodendrocyte glycoprotein-derived peptide (MOG35–55)-reactive interferon-γ and interleukin-17 production. In contrast, treatment of these animals with AgB10, an anti-mouse CEACAM1 blocking monoclonal antibody, generated increased severity of EAE in association with increased MOG35–55-specific induction of both interferon-γ and interleukin-17. These results indicated that the signal elicited through CEACAM1 ameliorated EAE disease severity. Furthermore, we found that there was both a rapid and enhanced expression of CEACAM1 on invariant natural killer T cells after activation. The effect of CEACAM1-Fc fusion protein and anti-CEACAM1 mAb on both EAE and MOG35–55-reactive cytokine responses were abolished in invariant natural killer T cell–deficient Jα18−/− mice. Taken together, the ligation of CEACAM1 negatively regulates the severity of EAE by reducing MOG35–55-specific induction of both interferon-γ and interleukin-17 via invariant natural killer T cell-dependent mechanisms