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The dispersion state and aggregate structure of carbon black in polystyrene composites prepared by solvent casting suspensions in different dispersion media, i.e., chloroform, tetrahydrofuran, and toluene, with different particle contents and their effects on the bulk rheological properties of the composites were investigated by transmission electron microscopy, ultrasmall-angle and small-angle X-ray scattering, and dynamic viscoelasticity measurements. The macroscopic dispersion state of carbon black in the solvent-cast films was largely affected by the dispersion medium, reflecting the stability of the suspension in the polystyrene solution. The mass fractal dimension of carbon black in the polymeric matrix, which was evaluated by X-ray scattering techniques with a resolution of nanometers, tended to exhibit a higher value for the dispersion media with less carbon black dispersibility. The surface fractal dimension of carbon black in the polymer was independent of the dispersion medium and exhibited a lower value than carbon black powder due to physical adsorption of the polymer on the particle surface. The viscoelastic moduli for the melt polymer composites below and above the percolation limit varied according to the dispersion media, reflecting the difference in the macroscopic dispersion state and aggregate structure of carbon black in polystyrene. The dispersion state and aggregate structure of carbon black in polystyrene composites prepared by solvent casting suspensions in different dispersion media with different particle contents and their effects on the bulk rheological properties of the composites were investigated by transmission electron microscopy, ultrasmall-angle and small-angle X-ray scattering, and dynamic viscoelasticity measurements. The viscoelastic moduli of the melt polymer composites below and above the percolation limit varied with the dispersion medium, reflecting the difference in the macroscopic dispersion state and aggregate structure of carbon black in polystyrene.

Spin-trapping electron spin resonance (ESR) and gel permeation chromatography (GPC) were applied to analyze the thermal degradation mechanisms of poly(vinyl alcohol) (PVA). The lifetime of the short-lived radical intermediate produced by thermal degradation at up to 200 °C was extended via the spin-trapping method for the purpose of investigating its molecular structure. Under the addition of the spin-trapping reagents dimethyl-1-pyrroline-N-oxide (DMPO) or 3,5-dibromo-4-nitrosobenzenesulfonate (DBNBS), into the PVA, the production of some radical intermediates, including hydroxyl (•OH) and some main chain radicals (–CH=CH–•CH– and •CH(OH)–CH2–), was confirmed via simulation analysis of the observed ESR spectra. The GPC measurement revealed that the cross-linking reaction occurred more often at temperatures above 100 °C and that the main chain scission also occurs significantly at around 200 °C. The elimination of •OH is therefore a key reaction in PVA degradation, and •CH(OH)–CH2– is produced by the β-scission from the main chain radical –CH2–•C(OH)–CH2–. This last radical was not observed in the present study; however, it should be produced through a hydrogen abstraction by •OH.

Anabaena sensory rhodopsin (ASR) is a microbial rhodopsin found in eubacteria and functions as a photosensor. The photoreaction of ASR is photochromic between all-trans, 15-anti (ASRAT), and 13-cis, 15-syn (ASR13C) isomers. To understand primary protein dynamics in the photoreaction starting in ASRAT and ASR13C, picosecond time-resolved ultraviolet resonance Raman spectra were obtained. In the intermediate state appearing in the picosecond temporal region, spectral changes of Trp bands were observed. For both ASRAT and ASR13C, the intensities of the Trp bands were bleached within the instrumental response time and recovered with a time constant of 30 ps. This suggests that the rates of structural changes in the Trp residue in the vicinity of the chromophore do not depend on the direction of the isomerization of retinal. A comparison between spectra of the wild-type and Trp mutants indicates that the structures of Trp76 and Trp46 change upon the primary photoreaction of retinal.

C57BL/KsJ mice carrying homozygous db/db mutation (db/db mice) are characterized by extreme obesity and early onset of hyperglycemia. In an attempt to rectify diabetes of these mice, a pancreatic beta cell line MIN6, which retains glucose-inducible insulin secretion, was transplanted subcutaneously into the back of the mice. Glucose and insulin levels of individual mice were examined biweekly and their weight gain weekly. All mice were sacrificed at 100 days after the transplantation of MIN6 cells. In db/db mice that had received MIN6 cells, blood insulin levels were restored and blood glucose levels were reduced to those of non-diabetic mice, although they remained obese. Glucose tolerance test suggested that transplanted MIN6 cells responded to loaded glucose as beta cells of non-diabetic mice. Immunohistochemical study showed that transplanted MIN6 cells produced insulin. Fatty liver associated with diabetes mellitus observed in db/db mice was not found in the MIN6 cell-transplanted mice. Implication of the results is discussed with reference to potential therapies for severe diabetes.

We report in this paper on obvious fibrotic lesions in the liver of mice undergoing specified graft-versus-host reaction (GVHR). B6 CD8+ splenocytes were transferred into (bm 12 × bm 1)F1 mice to induce GVHR. Recipient mice had been thymectomized and administrated with anti-CD8 monoclonal antibody (mAb) to deplete CD8+ cells from the hosts. Two weeks after the mAb administration, recipient mice were injected with B6 CD8+ cells and sacrificed further two or four weeks later for analyzing hepatic lesions histopathologically. Light microscopic analyses revealed the presence of concentric fibrosis around both small and large duct levels and the infiltration of mononuclear cells into portal areas. Focal necrrosis of hepatocytes was also detected electron-microscopically. These findings suggest that CD8+ T lymphocytes might play an important role in the induction of fibrotic lesions in the liver.

We aimed to examine the safety and antitumor effects of a combination of S-1 and paclitaxel in patients with unresectable or recurrent gastric cancer in a phase I/II setting.The study was designed as a phase I/II clinical trial. In phase I portion, the dose of paclitaxel was escalated to estimate the maximum-tolerated dose (MTD) and recommended dose (RD) of paclitaxel with fixed dose of S-1. S-1 (daily dose, 80 mg/m(2)) was given orally on days 1-21 every 35-day cycle (rest on days 22-35). Paclitaxel was administered intravenously on days 1, 8 and 15, at an initial dose of 40 mg/m(2), stepping up to 70 mg/m(2) in 10-mg/m(2) increment. Dose-limiting toxicity (DLT) was defined as grade 4 hematological toxicity, grade 3 or higher nonhematological toxicity, and treatment discontinuation due to adverse reactions during the first course of treatment. In phase II portion, the efficacy and toxicity at the RD of paclitaxel with S-1 were assessed.The MTD of paclitaxel was estimated to be 60 mg/m(2), because33.3% of patients (2/3) developed DLTs. DLT included postponement of treatment due to grade 2 neutropenia, and grade 3 stomatitis, anorexia, and nausea. Therefore, the RD of paclitaxel was estimated to be 50 mg/m(2). In the phase II portion, 22 patients were evaluated with 50 mg/m(2) paclitaxel and 80 mg/m(2) S-1 in a 35-day cycle. The response rate was 54.5% (95% CI, 32.2-75.6%). The median survival time was 283 days (95% CI, 218-508 days). The median number of treatment courses was 4 (range 1-10), indicating that this regimen could be given repeatedly.This phase I/II trial of combination therapy with S-1 and paclitaxel in patients with unresectable or recurrent gastric cancer showed that this regimen has substantial antitumor activity and can be given safely.

In this paper, we examined the induction of autoimmune-like histologic changes in the liver and other organs of mice undergoing graft-versus-host reaction (GVHR) with MHC class I disparity by the administration of bacterial lipopolysaccharide (LPS), on the assumption that stimulation with LPS could be an exacerbating factor. Spleen cells of C57BL 6 (B6) mice were injected twice into (B6 × bml) F1 recipient mice at an interval of 7 days to induce MHC class I GVHR and then challenged with 1 μg of LPS intravenously on the next day of the cell transfer. The hepatic lesions of the group of MHC class I GVHR mice challenged with LPS showed marked cellular infiltration at the portal area and focal necrosis was observed in the hepatic lobule. The major infiltrating cells were CD8 + , and others including CD4 + cells being of minor populations. In addition, ductal lesions in extrahepatic organs, including the pancreas and salivary glands also showed marked cellular infiltration. Thus, we have demonstrated that LPS induced ductal lesions in mice with MHC class I disparity. CD8 + cells were detected at the destructive hepatic lesions, which might be effector cells. These findings indicate that LPS might be one of the potential factors which augment autoimmune-like lesions.