[Bis(3,5‐diisopropylpyrazol‐1‐yl‐κ N 2 )dihydroborato](triphenylphosphane‐κ P )copper(I)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/102235/1/S0108270113015965.pd

Room-Temperature Electron Spin Transport in a Highly Doped Si Channel

We report on the first demonstration of generating a spin current and spin transport in a highly doped Si channel at room temperature (RT) using a four-terminal lateral device with a spin injector and a detector consisting of an Fe/MgO tunnel barrier. Spin current was generated using a nonlocal technique, and spin injection signals and Hanle-type spin precession were successfully detected at 300 K, thus proving spin injection with the elimination of spurious signals. The spin diffusion length and its lifetime at RT were estimated to be 0.6 \"im and 1.3 ns by the Hanle-type spin precession, respectively.Comment: 14 pages, 4 Figure

Keishibukuryogan, a Traditional Japanese Medicine, Inhibits Platelet Aggregation in Guinea Pig Whole Blood

Effects of keishibukuryogan (KBG) on platelet aggregation were investigated. To ensure the specificity of KBG, tokishakuyakusan (TSS) and kamisyoyosan (KSS), which are known to have platelet aggregation-inhibiting effects, and rikkunshito (RKT) and shakuyakukanzoto (SKT), which are considered to be devoid of such effects, were used for comparison. The platelet aggregation of each test drug was measured by the screen filtration pressure method using whole blood of guinea pigs and expressed as a collagen-induced pressure rate (%) or a collagen concentration required for 50% increase in the pressure rate (PATI value). KBG suppressed the collagen-induced whole blood pressure rate increase and increased the PATI value, like TSS and KSS. Neither RKT nor SKT showed these effects. The Moutan cortex and Cinnamomi cortex, the constituent crude drugs of KBG, showed KBG-like pressure rate suppression and PATI-increasing effects. Furthermore, paeonol, a representative component of Moutan cortex, and aspirin which is known to have platelet aggregation-inhibiting activity (COX-1 inhibitor) also showed similar effects. These results suggest that the platelet aggregation-inhibiting activity of the constituent crude drugs Moutan cortex and Cinnamomi cortex is involved in the improving effects of KBG on impaired microcirculation and that paeonol plays a role in these effects

SGLT2阻害薬であるイプラグリフロジンは2型糖尿病自然発症モデルであるOLETFラットにおいて肝線維化進展を抑制する。

BACKGROUND: It is widely understood that insulin resistance (IR) critically correlates with the development of liver fibrosis in several types of chronic liver injuries. Several experiments have proved that anti-IR treatment can alleviate liver fibrosis. Sodium-glucose cotransporter 2 (SGLT2) inhibitors comprise a new class of antidiabetic agents that inhibit glucose reabsorption in the renal proximal tubules, improving IR. The aim of this study was to elucidate the effect of an SGLT2 inhibitor on the development of liver fibrosis using obese diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats and their littermate nondiabetic Long-Evans Tokushima Otsuka (LETO) rats. METHODS: Male OLETF and LETO rats were intraperitoneally injected with porcine serum twice a week for 12 weeks to augment liver fibrogenesis. Different concentrations of ipragliflozin (3 and 6 mg/kg) were orally administered during the experimental period. Serological and histological data were examined at the end of the experimental period. The direct effect of ipragliflozin on the proliferation of a human hepatic stellate cell (HSC) line, LX-2, was also evaluated in vitro. RESULTS: OLETF rats, but not LETO rats, received 12 weeks of porcine serum injection to induce severe fibrosis. Treatment with ipragliflozin markedly attenuated the development of liver fibrosis and expression of hepatic fibrosis markers, such as alpha smooth muscle actin, collagen 1A1, and transforming growth factor beta (TGF-β), and improved IR in a dose-dependent manner in OLETF rats. In contrast, the proliferation of LX-2 in vitro was not affected, suggesting that ipragliflozin had no significant direct effect on the proliferation of HSCs. CONCLUSION: In conclusion, our dataset suggests that an SGLT2 inhibitor could alleviate the development of liver fibrosis by improving IR in naturally diabetic rats. This may provide the basis for creating new therapeutic strategies for chronic liver injuries with IR.博士（医学）・甲第665号・平成29年3月15日© Japanese Society of Gastroenterology 2016The final publication is available at Springer via http://dx.doi.org/10.1007/s00535-016-1200-6

ショウカドウ ノ イショウ ゲンジョウ ブンセキ ト ソウケン トウジ ノ スガタ ニ カンスル コウサツ

Shokado hermitage (Shokado hereafter), which was designed and built in 1637 by Shokado Shojo (1584-1639), one of the distinguished artists in the Edo period, has a unique function combined with flexible flow lines both as Hojo (chief priest’s living space) and Chashitu (tea ceremony room), and it was controlled by the creative planning and introduction of spatial elements. Shokado has been moved from the original location and reconstructed several times while its components fortunately escaped destruction due to Haibutsu kishaku (anti-Buddhist movement at the beginning of the Meiji era), and now stands in the garden of Shokado Museum. Rsearch shows its photos in the 19th century but no reliable material has been found to prove its original condition. This paper aims to depict the original state of Shokado basing on its previous studies and our own documentary search and fieldwork. The actual subjects are; Shokado’s location, accompanying gardens, entrances, earthen-floor room, wooden-floor rooms, narrow verandah, kamado kitchen stove and decorative ceiling which we were able to conduct on-site investigation. At present the workable method to achieve this aim is to combine previous and new pieces of information in a creative and skillful way.学術論

Pluto’s ocean is capped by gas hydrates

Many icy solar system bodies possess subsurface oceans. At Pluto, Sputnik Planitia’s location near the equator suggests the presence of a subsurface ocean and a locally thinned ice shell. To maintain an ocean, Pluto needs to retain heat inside. On the other hand, to maintain large variations in ice shell thickness, Pluto’s ice shell needs to be cold. Achieving such an interior structure is problematic. Here we show that the presence of a thin layer of clathrate hydrates (gas hydrates) at the base of the ice shell can explain both the long-term survival of the ocean and the maintenance of shell thickness contrasts. Clathrate hydrates act as a thermal insulator, preventing the ocean from complete freezing while keeping the ice shell cold and immobile. The most likely clathrate guest gas is methane either contained in precursor bodies and/or produced by cracking of organic materials in the hot rocky core. Nitrogen molecules initially contained and/or produced later in the core would likely not be trapped as clathrate hydrates, instead supplying the nitrogen-rich surface and atmosphere. The formation of a thin clathrate hydrate layer capping a subsurface ocean may be an important generic mechanism maintaining long-lived subsurface oceans in relatively large but minimally-heated icy satellites and Kuiper Belt Objects

Cleavage of host cytokeratin-6 by lysine-specific gingipain induces gingival inflammation in periodontitis patients

Background/Purpose. Lysine-specific gingipain (Kgp) is a virulence factor secreted from Porphyromonas gingivalis (P. gingivalis), a major etiological bacterium of periodontal disease. Keratin intermediate filaments maintain the structural integrity of gingival epithelial cells, but are targeted by Kgp to produce a novel cytokeratin 6 fragment (K6F). We investigated the release of K6F and its induction of cytokine secretion. Methods. K6F present in the gingival crevicular fluid of periodontal disease patients and in gingipain-treated rat gingival epithelial cell culture supernatants was measured by matrix-assisted laser desorption/ionization time-of-flight mass spectrometer-based rapid quantitative peptide analysis using BLOTCHIP. K6F in gingival tissues was immunostained, and cytokeratin 6 protein was analyzed by immunofluorescence staining and flow cytometry. Activation of MAPK in gingival epithelial cells was evaluated by immunoblotting. ELISA was used to measure K6F and the cytokines release induced by K6F. Human gingival fibroblast migration was assessed using a Matrigel invasion chamber assay. Results. We identified K6F, corresponding to the C-terminus region of human cytokeratin 6 (amino acids 359–378), in the gingival crevicular fluid of periodontal disease patients and in the supernatant from gingival epithelial cells cultured with Kgp. K6F antigen was distributed from the basal to the spinous epithelial layers in gingivae from periodontal disease patients. Cytokeratin 6 on gingival epithelial cells was degraded by Kgp, but not by Arg-gingipain, P. gingivalis lipopolysaccharide or Actinobacillus actinomycetemcomitans lipopolysaccharide. K6F, but not a scrambled K6F peptide, induced human gingival fibroblast migration and secretion of interleukin (IL)-6, IL-8 and monocyte chemoattractant protein-1. These effects of K6F were mediated by activation of p38 MAPK and Jun N-terminal kinase, but not p42/44 MAPK or p-Akt. Conclusion. Kgp degrades gingival epithelial cell cytokeratin 6 to K6F that, on release, induces invasion and cytokine secretion by human gingival fibroblasts. Thus, Kgp may contribute to the development of periodontal disease