A deep sleep in coal beds Deep below the ocean floor, microorganisms from forest soils continue to thrive. Inagaki et al. analyzed the microbial communities in several drill cores off the coast of Japan, some sampling more than 2 km below the seafloor (see the Perspective by Huber). Although cell counts decreased with depth, deep coal beds harbored active communities of methanogenic bacteria. These communities were more similar to those found in forest soils than in other deep marine sediments. Science , this issue p. 420 ; see also p. 376

Gastric cancer (GC) is one of the most common malignancies worldwide. Genes whose expression is down-regulated in GC may be tumour suppressor genes. In the present study, genes with decreased expression in GC were screened for by serial analysis of gene expression (SAGE) data analysis and reverse transcription (RT)-polymerase chain reaction (PCR), and CLDN18 (encoding claudin-18) was identified. Quantitative RT-PCR revealed that expression of CLDN18 was down-regulated in 13 (56.5%) of 23 GCs. Immunostaining showed that normal gastric mucosa and Paneth cells of the duodenum expressed claudin-18 on cell membranes. Expression of claudin-18 was reduced in several intestinal metaplasias of the stomach. Of 20 samples of gastric adenoma, 18 (90.0%) showed decreased claudin-18 expression. Down-regulation of claudin-18 was observed in 84 of 146 GCs (57.5%) and correlated with poor survival in 65 advanced GCs (p = 0.0346). In addition, expression of the gastric and intestinal phenotypes of GC was examined by immunostaining for MUC5AC, MUC6, MUC2, and CD10. Of 38 GCs showing only the intestinal phenotype, down-regulation of claudin-18 was observed in 28 (73.7%), whereas in the remaining 108 GC cases, down-regulation of claudin-18 was observed in 56 (51.9%) (p = 0.0224). These results indicate that claudin-18 is a good marker of poor survival in GC. Down-regulation of claudin-18 may be involved in GCs with an intestinal phenotype, and may be an early event in gastric carcinogenesis.

International audienceA 1.6 km riser borehole was drilled at site C0009 of the NanTroSEIZE, in the center of the Kumano forearc basin, as a landward extension of previous drilling in the southwest Japan Nankai subduction zone. We determined principal horizontal stress orientations from analyses of borehole breakouts and drilling-induced tensile fractures by using wireline logging formation microresistivity images and caliper data. The maximum horizontal stress orientation at C0009 is approximately parallel to the convergence vector between the Philippine Sea plate and Japan, showing a slight difference with the stress orientation which is perpendicular to the plate boundary at previous NanTroSEIZE sites C0001, C0004 and C0006 but orthogonal to the stress orientation at site C0002, which is also in the Kumano forearc basin. These data show that horizontal stress orientations are not uniform in the forearc basin within the surveyed depth range and suggest that oblique plate motion is being partitioned into strike-slip and thrusting. In addition, the stress orientations at site C0009 rotate clockwise from basin sediments into the underlying accretionary prism

The 2011 moment magnitude 9.0 Tohoku-Oki earthquake produced a maximum coseismic slip of more than 50 meters near the Japan trench, which could result in a completely reduced stress state in the region. We tested this hypothesis by determining the in situ stress state of the frontal prism from boreholes drilled by the Integrated Ocean Drilling Program approximately 1 year after the earthquake and by inferring the pre-earthquake stress state. On the basis of the horizontal stress orientations and magnitudes estimated from borehole breakouts and the increase in coseismic displacement during propagation of the rupture to the trench axis, in situ horizontal stress decreased during the earthquake. The stress change suggests an active slip of the frontal plate interface, which is consistent with coseismic fault weakening and a nearly total stress drop.

The location of the Integrated Ocean Drilling Program's (IODP) Nankai Trough Seismogenic Zone Experiment (NanTroSEIZE) was based on regional two-dimensional seismic reflection surveys carried out by the Japan Agency for Marine-Earth Science and Technology (JAMSTEC). Final site locations were chosen based on a three-dimensional (3-D) seismic reflection survey acquired across the seaward margin of Kumano Basin and the accretionary prism from the basin to the deformation front. This survey covered a region 12 km wide (approximately parallel to the regional structural strike) and 56 km long (approximately perpendicular to the regional strike) and provided detailed images of the structure and seismic stratigraphy of the drill sites. Sites were drilled in the frontal thrust zone at the toe of the accretionary prism, the frontal region of the megasplay fault zone, and the forearc basin. The 3-D seismic data volume images a main frontal thrust at the prism toe with the hanging wall thrust at least 7.5 km seaward over the trench. This configuration is different from that in other parts of the Nankai prism. At the shallow end of the megasplay, the data images a complex thrust system that truncates older structures in the underlying accretionary prism and shows that the hanging wall block has overridden more than 1250 m of young slope sediments. At the forearc basin site, we interpret landward-dipping forearc basin strata onlapping older slope sediments, which in turn overlie an older part of the accretionary prism.

Rapid regrowth or recurrent growth of occult cancer cells are often observed after esophagectomy or postoperative complications. In order to clarify the mechanism of such oncological circumstances, we focused on neutrophil elastase (NE), which degrades a broad spectrum of extracellular matrix and cell surface proteins. In the present study, we demonstrated that NE stimulated the growth of all of the five esophageal cell lines (TE-1, -7, -8, -12 and -13) by MTT assay and promoted cell invasion by cell migration assay. Protransforming growth factor-• (pro-TGF-•) from the cell membrane was released to the culture medium as a mature form after treatment with 5 μg/ml NE, and it reached the maximum level of 153% compared to the control values at 15 min of treatment in TE-13 cells. The phosphorylation of epidermal growth factor receptor (EGFR) rapidly occurs after treatment with NE and triggered the extracellular signalregulated kinases 1 and 2 (ERK) signaling pathway. Moreover, NE induced release of platelet-derived growth factor-AA (PDGF-AA), PDGF-BB and vascular endothelial growth factor (VEGF) to 141.9, 227.7, and 171.6% of the control values, respectively. A specific NE inhibitor, sivelestat, significantly inhibited the NE-induced cell proliferation, cell invasion and subsequently inhibited the signal transduction pathway. Furthermore, sivelestat significantly inhibited NE-induced release of TGF-•, PDGF-AA, PDGF-BB and VEGF in the medium in TE-13 esophageal carcinoma cells. These results strongly indicate that NE released from activated neutrophils stimulates the growth and progression of esophageal cancer cells by releasing the growth factors on the cell surface and that sivelestat, a specific NE inhibitor, blocks these processes. Furthermore, we postulate that postoperative administration of sivelestat might be useful as a new molecular-targeting cancer therapy as well as for the treatment of postoperative respiratory complications.

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