Methane emission from paddy soils as affected by wheat straw returning mode

To study influence of wheat straw returning mode on CH₄ emission from paddy soils, a field experiment was conducted at Jurong, Jiangsu Province, China in 2006. Five treatments, no wheat straw applied (CK), wheat straw evenly incorporated into the topsoil (WI), wheat straw buried in ditches (WD), wheat straw strip-mulched onto the field surface (WM) and wheat straw burned in-situ (WB), were laid out in a randomized block design. Results showed that seasonal CH₄ emissions ranged from 6.9 to 28.1 g CH₄ m^?2. Wheat straw incorporation significantly increased CH₄ emission. No significant difference was observed between Treatments WI and WD in total CH₄ emission. Compared with Treatment WI, Treatment WM reduced total CH₄ emission by 32% and Treatment WB by 42%. Treatment WM was about 27% higher than Treatment CK in grain yield. Based on the findings, the best management of wheat straw prior to rice cultivation is strip-mulching wheat straw onto the field surface, which largely reduced CH₄ emission from rice fields with no decrease in rice yield.     

Demonstration by light and ultrastructural immunoperoxidase study of alpha-fetoprotein-positive non-hepatoma cells and hepatoma cells during 3'-methyl-4-dimethylaminoazobenzene hepatocarcinogenesis

Immunoreaction of alpha-fetoprotein (AFP) has been described in cholangiolar "oval" cells in the early stage of 3'-methyl-4-dimethylaminoazobenzene hepatocarcinogenesis. The subcellular location of AFP in the oval cells was in the perinuclear space, rough endoplasmic reticulum and Golgi apparatus. In livers with hyperplastic nodules there were two different types of foci containing AFP-positive cells. One type had a normal nucleocytoplasmic ratio and was seen in well-preserved hepatic trabecular structures, and the other had less cytoplasm and occurred in trabecular structures in disarray. AFP-immunoreactivity in the former type was visible in the perinuclear space and rough endoplasmic reticulum but scarce in the Golgi apparatus, and in the latter type it was present in the proliferative smooth endoplasmic reticulum and in several parts of Golgi apparatus in the submembranous or pericanalicular areas. In livers with hepatocarcinoma, AFP immunoreaction was detected in well-differentiated hepatocellular carcinomas, and the subcellular location of AFP was in the perinuclear space, rough endoplasmic reticulum and many developed Golgi complexes. Therefore, AFP-positive cells in livers with hyperplastic nodules are a new cell population in hepatocarcinogenesis, and each type is morphologically different from the oval cell.     

Effect of tea catechins on mitochondrial DNA 4977-bp deletions in human leucocytes

The catechins in green tea have antioxidative and antimutagenic effects. We examined the effect of green tea enriched with catechins on the presence of mitochondrial DNA (mtDNA) with a common 4977-bp deletion mutation (mtDNA4977) in human leucocytes. Ten healthy females [aged 20.80 +/- 1.03 years] drank 350 ml of catechin-rich tea daily after supper for 5 weeks. Blood samples were collected twice before, and twice after 5 weeks of consuming the tea. Deletions in mtDNA were analyzed using the nested polymerase chain reaction (PCR). We identified a common mtDNA4977 deletion in nine participants before drinking the tea. However, this mtDNA4977 deletion was not evident in leucocytes from most of the participants 5 weeks after drinking the tea. Catechins found in tea might contribute to the maintenance of health status by reducing damage to mtDNA and by maintaining the capacity of mtDNA for oxidative phosphorylation.     

Induction of permanent mixed chimerism and skin allograft tolerance across fully MHC-mismatched barriers by the additional myelosuppressive treatments in mice primed with allogeneic spleen cells followed by cyclophosphamide

A pure method of drug (cyclophosphamide plus busulfan)-induced skin allograft tolerance in mice that can regularly overcome fully H-2-mismatched barriers in mice has been established. The components of the method are i.v. administration of 1 x 108 allogeneic spleen cells on day 0, i.p. injection of 200 mg/kg CP and 25 mg/kg busulfan on day 2, and i.v. injection of T cell-depleted 1 x 107 bone marrow cells from the same donor on day 3. Recipient B10 (H-2b; IE-) mice prepared with this conditioning developed donor-specific tolerance, and long-lasting survival of skin allografts was shown in almost of the recipient mice. In the tolerant B10 mice prepared with new conditioning, stable multilineage mixed chimerism was observed permanently, and IE-reactive Vbeta11+ T cells were reduced in periphery as seen in untreated B10.D2 (H-2d; IE+) mice. The specific tolerant state was confirmed by the specific abrogation against donor Ag in the assays of CTL activity and MLR and donor-specific acceptance in the second skin grafting. These results demonstrated that the limitation of standard protocol of cyclophosphamide-induced tolerance, which have been reported by us since 1984, can be overcome by the additional treatments with the myelosuppressive drug busulfan, followed by 1 x 107 T cell-depleted bone marrow cells. To our knowledge, this is the first report to induce allograft tolerance with a short course of the Ag plus immunosuppressive drug treatment without any kind of mAbs (pure drug-induced tolerance).     

Modification of chemical properties of cell walls by silicon and its role in regulation of the cell wall extensibility in oat leaves

Effects of silicon on the mechanical and chemical properties of cell walls in the second leaf of oat (Avena sativa L.) seedlings were investigated. The cell wall extensibility in the basal region of the second leaf was considerably higher than that in the middle and subapical regions. Externally applied silicon increased the cell wall extensibility in the basal region, but it did not affect the extensibility in the middle and subapical regions. The amounts of cell wall polysaccharides and phenolic compounds, such as diferulic acid (DFA) and ferulic acid (FA), per unit length were lower in the basal region than in the middle and subapical regions of the leaf, and silicon altered these amounts in the basal region. In this region, silicon decreased the amounts of matrix polymers and cellulose per unit length and of DFA and FA, both per unit length and unit matrix polymer content. Silicon treatment also lowered the activity of phenylalanine ammonia-lyase (PAL, EC 4.3.1.5) in the basal region. In contrast, the amount of silicon in cell walls increased in response to silicon treatment in three regions. These results suggest that in the basal region, silicon reduces the net wall mass and the formation of phenolic acid-mediated cross-linkages between wall polysaccharides. Such modifications of wall architecture may be responsible for the silicon-induced increase in the cell wall extensibility in oat leaves.     

Bio-photosensor: Cyanobacterial photosystem I coupled with transistor via molecular wire

We report on the first successful output of electrons directly from photosystem I (PSI) of thermophilic cyanobacteria to the gate of a field-effect transistor (FET) by bypassing electron flow via a newly designed molecular wire, i.e., artificial vitamin K₁, and a gold nanoparticle; in short, this newly manufactured photosensor employs a bio-functional unit as the core of the device. Photo-electrons generated by the irradiation of molecular complexes composed of reconstituted PSI on the gate were found to control the FET. This PSI-bio-photosensor can be used to interpret gradation in images. This PSI-FET system is moreover sufficiently stable for use exceeding a period of 1 year.     

Stimulation of Macrophages with the β-Glucan Produced by Aureobasidium pullulans Promotes the Secretion of Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL)

A β-glucan produced by Aureobasidium pullulans (AP-PG) is consisting of a β-(1,3)-linked main chain with β-(1,6)-linked glucose side residues. Various β-glucans consisting of β-(1,3)-linked main chain including AP-PG are believed to exhibit anti-tumor activities, and actually, anti-tumor activities of AP-PG in mice have been demonstrated. In this study, we demonstrate that stimulation with AP-PG induces TRAIL expression in mouse and human macrophage-like cell lines. TRAIL is known to be a cytokine which specifically induces apoptosis in transformed cells, but not in untransformed cells. The expression of TRAIL mRNA after stimulation with AP-PG was increased in RAW264.7 cells, Mono Mac 6 cells, and macrophage-differentiated THP-1 cells. The mRNA expression of TNF-α and FasL is only weakly increased after stimulation with AP-PG. The induction activity of TRAIL by curdlan, a bacterial β-glucan, was very similar to that by AP-PG in RAW264.7 cells, but weaker in macrophage-differentiated THP-1 cells. Activation of caspases was found in HeLa cells after treatment with the supernatant of cultured medium from AP-PG-stimulated Mono Mac 6 cells, and was inhibited by the anti-TRAIL neutralizing antibody. These findings suggest that the stimulation with AP-PG effectively induces TRAIL in macrophages, and that it may be related to apoptosis induction of tumor cells.     

Infection with Porphyromonas gingivalis Exacerbates Endothelial Injury in Obese Mice

Background

A number of studies have revealed a link between chronic periodontitis and cardiovascular disease in obese patients. However, there is little information about the influence of periodontitis-associated bacteria, Porphyromonas gingivalis (Pg), on pathogenesis of atherosclerosis in obesity.

Methods

In vivo experiment: C57BL/6J mice were fed with a high-fat diet (HFD) or normal chow diet (CD), as a control. Pg was infected from the pulp chamber. At 6 weeks post-infection, histological and immunohistochemical analysis of aortal tissues was performed. In vitro experiment: hTERT-immortalized human umbilical vein endothelial cells (HuhT1) were used to assess the effect of Pg/Pg-LPS on free fatty acid (FFA) induced endothelial cells apoptosis and regulation of cytokine gene expression.

Results

Weaker staining of CD31 and increased numbers of TUNEL positive cells in aortal tissue of HFD mice indicated endothelial injury. Pg infection exacerbated the endothelial injury. Immunohistochemically, Pg was detected deep in the smooth muscle of the aorta, and the number of Pg cells in the aortal wall was higher in HFD mice than in CD mice. Moreover, in vitro, FFA treatment induced apoptosis in HuhT1 cells and exposure to Pg-LPS increased this effect. In addition, Pg and Pg-LPS both attenuated cytokine production in HuhT1 cells stimulated by palmitate.

Conclusions

Dental infection of Pg may contribute to pathogenesis of atherosclerosis by accelerating FFA-induced endothelial injury.