Expansion of Elaeagnus umbellata on a gravel bar in the Naka River, Shikoku, Japan

Abstract The present study seeks to identify the expansion process of the shrub Elaeagnus umbellata Thunb. (Elaeagnaceae) on a gravel bar in the Naka River, Shikoku, Japan, in relation to the hydrogeomorphologic regime of the habitat. The establishment pattern was determined by a series of aerial photographs, and the establishment years were confirmed by examining tree rings taken from five different areas within the population. The topographic change of the river cross-section was analyzed and it was found that the establishment occurred exactly when and where the riverbed began to stabilize. The three cohorts of 15-, 10- and 4-year-olds were recognized, the younger individuals being downstream. The episodic age pattern was significantly synchronized with large floods occurring during the autumn fruit-ripening season. These spatial and temporal occurrence patterns indicated the probability of hydrochory, which ultimately enhanced the dissemination of endozoochorous E. umbellata seeds into the newly created habitat on the downstream part of the gravel bar. Another cause of quick dominance was its vigorous sprouting ability, which enabled the established E. umbellata to withstand damage and sediment burial by strong floods. The erosion of the deepest part of the riverbed increased the relative elevation of the vegetated stand, which ultimately decreased the frequency and magnitude of disturbance during flood inundation after the 1980s. Consequently the hydrogeomorphic regime of the floods played an important role in habitat creation, seed dispersal, and in the survival of the established individuals, and it determined the population formation and expansion of E. umbellata on the riparian gravel bar.     

Molecular Characterization of LjABCG1, an ATP-Binding Cassette Protein in Lotus japonicus

LjABCG1, a full-size ABCG subfamily of ATP-binding cassette proteins of a model legume, Lotus japonicus, was reported as a gene highly expressed during the early stages of nodulation, but have not been characterized in detail. In this study we showed that the induction of LjABCG1 expression was remarkable by methyl jasmonate treatment, and reporter gene experiments indicated that LjABCG1 was strongly expressed in the nodule parenchyma and cell layers adjacent to the root vascular tissue toward the nodule. LjABCG1 was suggested to be localized at the plasma membrane based on the fractionation of microsomal membranes as well as separation via aqueous two-phase partitioning. The physiological functions of LjABCG1 in symbiosis and pathogenesis were analyzed in homologous and heterologous systems. LjABCG1 knock-down L. japonicus plants did not show clear phenotypic differences in nodule formation, and not in defense against Pseudomonas syringae, either. In contrast, when LjABCG1 was expressed in the Arabidopsis pdr8-1 mutant, the penetration frequency of Phytophthora infestans, a potato late blight pathogen, was significantly reduced in LjABCG1/pdr8-1 than in pdr8-1 plants. This finding indicated that LjABCG1, at least partially, complemented the phenotype of pdr8 in Arabidopsis, suggesting the multiple roles of this protein in plant-microbe interactions.     

Inhalation of hydrogen gas attenuates left ventricular remodeling induced by intermittent hypoxia in mice

Sleep apnea syndrome increases the risk of cardiovascular morbidity and mortality. We previously reported that intermittent hypoxia increases superoxide production in a manner dependent on nicotinamide adenine dinucleotide phosphate and accelerates adverse left ventricular (LV) remodeling. Recent studies have suggested that hydrogen (H(2)) may have an antioxidant effect by reducing hydroxyl radicals. In this study, we investigated the effects of H(2) gas inhalation on lipid metabolism and LV remodeling induced by intermittent hypoxia in mice. Male C57BL/6J mice (n = 62) were exposed to intermittent hypoxia (repetitive cycle of 1-min periods of 5 and 21% oxygen for 8 h during daytime) for 7 days. H(2) gas (1.3 vol/100 vol) was given either at the time of reoxygenation, during hypoxic conditions, or throughout the experimental period. Mice kept under normoxic conditions served as controls (n = 13). Intermittent hypoxia significantly increased plasma levels of low- and very low-density cholesterol and the amount of 4-hydroxy-2-nonenal-modified protein adducts in the LV myocardium. It also upregulated mRNA expression of tissue necrosis factor-α, interleukin-6, and brain natriuretic peptide, increased production of superoxide, and induced cardiomyocyte hypertrophy, nuclear deformity, mitochondrial degeneration, and interstitial fibrosis. H(2) gas inhalation significantly suppressed these changes induced by intermittent hypoxia. In particular, H(2) gas inhaled at the timing of reoxygenation or throughout the experiment was effective in preventing dyslipidemia and suppressing superoxide production in the LV myocardium. These results suggest that inhalation of H(2) gas was effective for reducing oxidative stress and preventing LV remodeling induced by intermittent hypoxia relevant to sleep apnea.     

Landscape ecology and urban biodiversity in tropical Indonesian cities

Indonesia has recently been faced with a number of great problems: poverty, natural disasters such as tsunami, earthquakes, flooding and typhoons, volcanic eruptions, loss of biodiversity, decreasing water quality and quantity, increased pollution, and aesthetic degradation of the landscape. These disturbances have been caused by rapid changes in land use and land cover, deforestation, the application of monoculture farming systems in commercial agriculture, urbanization, industrialization, and other types of infrastructure development. The government, urban communities and companies have promoted some programs to ameliorate the problem of environmental degradation. The government has ratified law no. 26/2007 as a commitment to sustainability; this law ensures that cities are obliged to provide green open spaces covering a minimum of 30% of urbanized areas. Many metropolitan cities have feverishly enacted policies to promote greening programs, such as those applied in Jakarta. However, a new town—Sentul City—has engaged in policies that aim to create a well-designed eco-city with urban greenery and ecological networks. This new policy is supposed to herald a better future for urban quality. It is expected that green spaces will provide environmental services: water resource management, biodiversity conservation, carbon sequestration, and landscape beauty.     

An HLA-A3-binding prostate acid phosphatase-derived peptide can induce CTLs restricted to HLA-A2 and -A24 alleles

We previously reported peptide vaccine candidates for HLA-A3 supertype (-A3, -A11, -A31, -A33)-positive cancer patients. In the present study, we examined whether those peptides can also induce cytotoxic T lymphocyte (CTL) activity restricted to HLA-A2, HLA-A24, and HLA-A26 alleles. Fourteen peptides were screened for their binding activity to HLA-A*0201, -A*0206, -A*0207, -A*2402, and -A*2601 molecules and then tested for their ability to induce CTL activity in peripheral blood mononuclear cells (PBMCs) from prostate cancer patients. Among these peptides, one from the prostate acid phosphatase protein exhibited binding activity to HLA-A*0201, -A*0206, and -A*2402 molecules. In addition, PBMCs stimulated with this peptide showed that HLA-A2 or HLA-A24 restricted CTL activity. Their cytotoxicity toward cancer cells was ascribed to peptide-specific and CD8⁺ T cells. These results suggest that this peptide could be widely applicable as a peptide vaccine for HLA-A3 supertype-, HLA-A2-, and -A24-positive cancer patients.     

Response of soil microbial communities to changes in a forest ecosystem brought about by pine wilt disease

Japan has suffered a lot from forestry losses due to pine wilt disease caused by pinewood nematode infestations. Studies were conducted regarding its causative agent and the effects of natural vegetation succession after pine wilt disease, but its effects on microorganisms were not given equal attention. This study determined the effects of pine wilt disease on light conditions, soil microbial biomass, litter decomposition, microbial abundance and the physical and chemical properties of the soil. Results showed that in a forest currently affected by pine wilt disease, there was higher light penetration, greater microbial biomass carbon, and a faster rate of litter decomposition. Microbial abundance was shown to be reduced in pine wilt affected areas. There were close correlations between the biological and physicochemical properties of the soil, but the reason for the decrease in microbial abundance is not yet well understood, and thus requires further study.     

Prostaglandin E2 enhances interleukin-8 production via EP4 receptor in human pulmonary microvascular endothelial cells

Prostaglandin E(2) (PGE(2)) is a bioactive prostanoid implicated in the inflammatory processes of acute lung injury/acute respiratory distress syndrome. This study investigated whether PGE(2) can induce production of interleukin (IL)-8, the major chemokine for neutrophil activation, from human pulmonary microvascular endothelial cells (HPMVECs). PGE(2) significantly enhanced IL-8 protein production with increases in IL-8 mRNA expression and intracellular cAMP levels. HPMVECs expressed only EP4 receptor mRNA. The PGE(2) effects were mimicked by a selective EP4 receptor agonist, ONO-AE1-329, and inhibited by a selective EP4 receptor antagonist, ONO-AE3-208, or a protein kinase A inhibitor, Rp-adenosine 3',5'-cyclic monophosphorothioate triethylamine salt. The specific agonist for EP1, EP2, or EP3 receptor did not induce IL-8 production. PGE(2)-induced IL-8 production was accompanied by p38 phosphorylation and was significantly inhibited by a p38 inhibitor, SB-203580, but not by an ERK1/2 inhibitor, U-0126, or a JNK inhibitor, SP-600125. Additionally, PGE(2) increased cyclooxygenase-2 expression with no change in constitutive cyclooxygenase-1 expression, suggesting possible involvement of an autocrine or paracrine manner. In conclusion, PGE(2) enhances IL-8 production via EP4 receptor coupled to G(s) protein in HPMVECs. Activation of the cAMP/protein kinase A pathway, followed by p38 activation, is essential for these mechanisms. Because neutrophils play a critical role in the inflammation of acute lung injury/acute respiratory distress syndrome, IL-8 released from the pulmonary microvasculature in response to PGE(2) may contribute to pathophysiology of this disease.     

Identification of a nicotine transporter in leaf vacuoles of Nicotiana tabacum

Alkaloids are, in some plant species, transported from the source organ after their biosynthesis and moved to sink organs via long distance transport. One representative is nicotine, which is biosynthesized in roots, then translocated to the leaves, and finally accumulated in the leaf vacuoles in Nicotiana species. Although the nicotine translocation was identified more than 10 years ago, no transport protein has been characterized concerning the inter-organ movement of this alkaloid.We characterized a novel multidrug and toxic compound extrusion (MATE)-type transporter, Nt-JAT1 (Nicotiana tabacum jasmonate-inducible alkaloid transporter 1). Nt-JAT1 was co-regulated with biosynthetic genes following methyl jasmonate treatment. This MATE gene was expressed in the leaves, stems, and roots in tobacco plants. Biochemical analyses suggested that Nt-JAT1 transported nicotine. The location of Nt-JAT1 was shown to be the tonoplast. These data suggested that Nt-JAT1 plays an important role in the nicotine translocation by acting as a transporter responsible for the unloading of nicotine in the aerial parts of the plant and its deposition in the vacuoles (Fig. 1). To our knowledge, this is the first identification of a vacuolar transporter for alkaloids in plant. A possible application of this transporter for the production of valuable alkaloids is also discussed.Open in a separate windowFigure 1A model of nicotine accumulation in leaf cells. Nt-JAT1 transports nicotine to the vacuole via the H⁺ gradient at tonoplast.Key words: Nicotiana tabacum, nicotine, alkaloid, MATE, transporter, leaf vacuole     

Solution structure of a tmRNA-binding protein,SmpB, from Thermus thermophilus

The molecular mechanisms that govern cell movement are the subject of intense study, as they impact biologically and medically important processes such as leukocyte chemotaxis and angiogenesis, among others. We demonstrate that leukocyte chemotaxis is prevented by the macrolide immunosuppressant rapamycin, a specific inhibitor of the mammalian target of rapamycin (mTOR)/ribosomal p70-S6 kinase (p70S6K) pathway. Both neutrophil chemotaxis and chemokinesis elicited by granulocyte-macrophage colony-stimulating factor (GM-CSF) were strongly inhibited by rapamycin with an IC₅₀ of 0.3 nM. Inhibition, although at a higher dose, was also observed when the chemoattractant was interleukin-8. As for the mechanism, rapamycin targeted the increase of phosphorylation of p70S6K due to GM-CSF treatment, as demonstrated with specific anti-p70S6K immunoprecipitation and subsequent immunoblotting with anti-T⁴²¹/S⁴²⁴ antibodies. Rapamycin also inhibited GM-CSF-induced actin polymerization, a hallmark of leukocyte migration. The specificity of the effect of rapamycin was confirmed by the use of the structural analog FK506, which did not have a significant effect on chemotaxis but effectively rescued rapamycin-induced p70S6K inhibition. This was expected from a competitive effect of both molecules on FK506-binding proteins (FKBP). Additionally, GM-CSF-induced chemotaxis was completely (>90%) blocked by a combination of rapamycin and the MAPK kinase (MEK) inhibitor PD-98059. In summary, the results presented here indicate for the first time that rapamycin, at sub-nanomolar concentrations, inhibits GM-CSF-induced chemotaxis and chemokinesis. This serves to underscore the relevance of the mTOR/S6K pathway in neutrophil migration.