Effect of dissolved oxygen on methane production from bottom sediment in a eutrophic stratified lake.

Clarifying the role of sulfate and dissolved oxygen (DO) in methane production may allow for precise and accurate modeling of methane emissions in eutrophic lakes. We conducted field observations of sulfate, methane, and DO concentrations in Lake Abashiri, a typical brackish and eutrophic lake in a cold region, to develop a DO-based method for quantitively estimating methane production in a eutrophic lake and analyzed the results. We found that sulfate concentrations decreased rapidly from 900.0 mg/L in water overlying the sediments to nearly 0.0 mg/L in the bottom sediment. Methane production was almost uniform across sediment depths of 0.05 to 0.25 m, ranging from 1400 to 1800 µmol/m2/day. Also, methane production was found to be a function of DO concentrations in water overlying the bottom and could be modeled by a logistic function: constant production at 1,400 µmol/m2/day for DO concentrations of 0.0 to 3.0 mg/L, rapidly decreasing to 0 µmol/m2/day for DO concentrations of 3.0 to 6.0 mg/L. This methane model was verified using a simple one-dimensional numerical model that showed good agreement with field observations. Our results thus suggest that the proposed methane model reduces uncertainty in estimating methane production in a eutrophic lake.

Diffusive methane burst during a blue tide, wind-driven event in a meromictic lake.

Strong stratification has formed in Lake Abashiri, a typical meromictic lake in Hokkaido, in the subarctic zone in Japan. When the anoxic water of the lower layer is upwelled to the surface by a strong wind, fish and corbicula clams die due to a lack of dissolved oxygen. This event is called as blue tide. It was observed that the dissolved methane in the lake decreased more than 100 t after the blue tide which occurred in 2008. This is the discovery of the phenomenon that a large quantity of methane diffuses to the atmosphere caused by upwelling of anoxic water which contains dissolved methane. We named the event as "methane burst". It is also the first report that the wind-driven upwelling is reproduced using a numerical analysis code and the methane burst is analyzed. During this blue tide, the methane flux was approximately 170 times greater than usual.

[Reduction method of patients' radiation dose considering the size of field of view with a digital cine X-ray system loading a flat-panel detector].

Angiographic equipment has tended toward using flat-panel detector (FPD). However, the radiation dose varies depending on the size of field of view (FOV) in the FPD. Although we were using 7 inch FOV in cardiac procedures, we examined a way to reduce the patients' radiation dose by using 8 inch FOV utilizing a digital zoom processing. We measured the absorbed dose rates at an interventional reference point (IRP) with 20 cm acrylic board to compare 8 inch FOV using a digital zoom processing with 7 inch FOV. Additionally we visually evaluated these phantom images. Result of comparison of absorbed dose rates at IRP, 8 inch FOV using a digital zoom processing was reduced more than 7 inch FOV (fluoroscopic 29.0% and digital cine 37.5%). These phantom images were of equivalent quality. The method to use 8 inch FOV utilizing a digital zoom processing technique in cardiac procedures is one of the effective radiation exposure reduction methods.

The apoptotic protease-activating factor 1-mediated pathway of apoptosis is dispensable for negative selection of thymocytes.

Negative selection is a process to delete potentially autoreactive clones in developing thymocytes. Programmed cell death or apoptosis is thought to play an important role in this selection process. In this study, we investigated the role of apoptotic protease-activating factor 1 (Apaf1), a mammalian homologue of CED-4, in programmed cell death during the negative selection in thymus. There was no developmental abnormality in thymocytes from newborn Apaf1(-/-) mice in terms of CD4 and CD8 expression pattern and thymocyte number. Clonal deletion by endogenous male H-Y Ag of Apaf1-deficient thymocytes with transgenic expression of H-Y Ag-specific TCRs (H-Y Tg/Apaf1(-/-) thymocytes) was normally observed in lethally irradiated wild-type mice reconstituted with fetal liver-derived hemopoietic stem cells. Clonal deletion induced in vitro by a bacterial superantigen was also normal in fetal thymic organ culture. Thus, Apaf1-mediated pathway of apoptosis is dispensable for the negative selection of thymocytes. However, H-Y Tg/Apaf1(-/-) thymocytes showed partial resistance to H-Y peptide-induced deletion in vitro as compared with H-Y Tg/Apaf1(+/-) thymocytes, implicating the Apaf1-mediated apoptotic pathway in the negative selection in a certain situation. In addition, the peptide-induced deletion was still observed in H-Y Tg/Apaf1(-/-) thymocytes in the presence of a broad spectrum caspase inhibitor, z-VAD-fmk, suggesting the presence of caspase-independent cell death pathway playing roles during the negative selection. We assume that mechanisms for the negative selection are composed of several cell death pathways to avoid failure of elimination of autoreactive clones.

Calcineurin-dependent mitochondrial disturbances in calcium-induced apoptosis of human immunodeficiency virus gp160-expressing CD4+ cells.

In CD4+ UE160 cells with inducible expression of gp160, mechanisms of apoptosis induced by human immunodeficiency virus (HIV) Env protein were analyzed. Induction of gp160 caused intracellular calcium increase followed by the release of cytochrome c from mitochondria, which was inhibited by calcineurin inhibitors. Association of BAD with Bcl-xL was observed, and a portion of BAD was dephosphorylated after induction of gp160. These data suggested that calcineurin plays a role in the HIV Env-induced apoptosis in a mitochondrion-dependent way.

Role of internalization in the pathogenicity of Shiga toxin-producing Escherichia coli infection in a gnotobiotic murine model.

We investigated the role of bacterial internalization in the killing caused by Shiga toxin-producing Escherichia coli (STEC) infection using a gnotobiotic murine model. A high number of internalized STEC was found in the colonic epithelial cells of STEC-infected mice by both an ex vivo assay and transmission electron microscopy. Most of these mice were killed within 10 days after infection. However, the implantation of lactic acid bacteria in such mice before infection markedly decreased the number of internalized STECs and also completely protected these hosts from killing by a STEC infection. The inhibition of such internalization by immunoglobulin also prevented the hosts from being killed. The Shiga toxin levels in these hosts indicated an inhibition of the penetration of Shiga toxins produced in the colon to the underlying tissue. These results suggested that the internalization plays an important role in the pathogenicity caused by STEC infection in a gnotobiotic murine model.