[1] Real-time crustal deformation monitoring is extremely important for achieving rapid understanding of actual earthquake scales, because the measured permanent displacement directly gives the true earthquake size (seismic moment, M w ) information, which in turn, provides tsunami forecasting. We have developed an algorithm to detect/ estimate static ground displacements due to earthquake faulting from real-time kinematic GPS (RTK-GPS) time series. The new algorithm identifies permanent displacements by monitoring the difference of a short-term average (STA) to a long-term average (LTA) of the GPS time series. We assessed the noise property and precision of the RTK-GPS time series with various baseline length conditions and orbits and discerned that the real-time ephemerides based on the International GNSS Service (IGS) are sufficient for crustal deformation monitoring with long baselines up to $1,000 km. We applied the algorithm to data obtained in the 2011 off the Pacific coast of Tohoku earthquake (M w 9.0) to test the possibility of coseismic displacement detections, and further, we inverted the obtained displacement fields for a fault model; the inversion estimated a fault model with M w 8.7, which is close to the actual M w of 9.0, within five minutes from the origin time. Once the fault model is estimated, tsunami waveforms can be immediately synthesized using pre-computed tsunami Green's functions. The calculated waveforms showed good agreement with the actual tsunami observations both in arrival times and wave heights, suggesting that the RTK-GPS data by our algorithm can provide reliable rapid tsunami forecasting that can complement existing tsunami forecasting systems based on seismic observations. Citation: Ohta, Y., et al. (2012), Quasi real-time fault model estimation for near-field tsunami forecasting based on RTK-GPS analysis: Application to the 2011 Tohoku-Oki earthquake (M w 9.0),

Objective: To investigate the efficacy and safety of 14 days' orally administered tolvaptan as adjunctive treatment for hepatic oedema in Japanese liver cirrhosis patients with insufficient response to conventional diuretics, with the option to increase dose in those who did not respond initially. Methods: This multicentre, single-arm, phase 3 study allocated patients with liver cirrhosis and persistent ascites to 7-day treatment with 7.5 mg/day tolvaptan followed by an additional 7 days' treatment. Responders at day 7 (achieving !1 kg body-weight reduction) continued on 7.5 mg/day tolvaptan; nonresponders (<1 kg body-weight reduction) received 15 mg/day tolvaptan. Conventional diuretic treatment continued throughout. The primary endpoint was change in body weight from baseline, as a marker of ascites volume. Results: A total of 51 patients received 7.5 mg/day tolvaptan for 7 days, which caused a significant reduction in mean body weight (55% response rate). During the second 7-day treatment period, 30 patients received 7.5 mg/day tolvaptan and 13 patients received tolvaptan 15 mg/day: response rates were 43% and 23%, respectively. Two serious adverse events were observed. Serum sodium was within normal range.

The results indicate that the mechanism of T cell hyporesponsiveness to HBcAg includes activation of HBcAg-induced regulatory T cells in contrast to an increase in TH2-committed cells in response to HBsAg.

The function of HBcAg-specific T(reg) cells was enhanced by sHSP60 produced from HBV-infected hepatocytes. Entecavir treatment suppressed the frequency and function of T(reg) cells; this might contribute to the persistence of HBV infection.

In colorectal cancer (CRC) patients, metastasis to the regional lymph node (LN) is an important first step in the dissemination of cancers. To identify the genes possibly involved in LN metastasis of CRC, we analyzed LN metastases in an orthotopic implantation mouse model with 22 CRC cell lines using Matrigel, an extracellular matrix protein derived from mice sarcoma, and combined the data with gene expression profiles of cDNA microarray of those cell lines. With this implantation analysis, the incidence of LN metastasis was 60% in 228 orthotopically implanted mice and varied from 100% to 0% among the cell lines. KM12c and Clone A showed LN metastasis in all orthotopically implanted mice, but DLD-1, HCT-8, and SW948 did not show LN metastases at all. In contrast, the incidence of liver and lung metastasis in 22 CRC cell lines was 13% and 1%, respectively. Combining those data with cDNA microarray in vitro, we isolated 636 genes that were differentially expressed depending on the incidence of LN metastasis. T he incidence of CRC has been increasing in Japan. Approximately 94 000 CRC patients were diagnosed in 1999, (1) and approximately 40 000 patients died of CRC in 2004.(2) Metastasis to regional LN is an important first step in the dissemination of CRC, and LN metastasis and liver metastasis affect the prognoses of CRC patients. The recurrence rate of CRC is directly associated with the extent of LN metastasis. Therefore, elucidating the mechanism of LN metastasis of CRC is considered to be crucial for developing an eventual solution to this problem. It is important to establish a spontaneous LN metastasis model for analyzing the mechanisms of LN metastasis in CRC. An orthotopic animal tumor model for CRC is a complementary tool for the study of tumors in vivo.Matrigel basement membrane matrix (Becton Dickinson, Franklin Lakes, NJ, USA) is a solubilized basement membrane preparation extracted from Engelbreth-Holm-Swarm mouse sarcoma. Its major component is laminin, followed by collagen IV, heparan sulfate proteoglycans, entactin, and nidogen.(4-9) At room temperature, Matrigel polymerizes and forms a "basement membrane" gel. The usefulness of Matrigel has been reported as an orthotopic implantation animal model of various kinds of cancers.(5,10-13) Tsutsumi et al. advocated an experimental animal model of LN metastasis using an orthotopic implantation method by intrarectal injection of human cancer cell-Matrigel solution in nude mice, but liver metastasis did not occur. (14) Takahashi et al. proposed a mouse model of rectal cancer established by intrarectal instillation of colon cancer cells following short-term induction of colitis using an irritant agent, but the metastasis to other organs such as liver and lung was not induced at significant levels.(15) Although some of the experimental models for metastasis of CRC have been developed, there is no report that addresses the relation between the metastasis of CRC and the change of gene expressions involved in the metastasis.Molecular studies have so far been ...