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Articles by J Nagata
Total Records ( 15 ) for J Nagata
  A Watanabe , M. A Sohail , D. A Gomes , A Hashmi , J Nagata , F. S Sutterwala , S Mahmood , M. N Jhandier , Y Shi , R. A Flavell and W. Z. Mehal

The inflammasome is a cytoplasmic multiprotein complex that has recently been identified in immune cells as an important sensor of signals released by cellular injury and death. Analogous to immune cells, hepatic stellate cells (HSC) also respond to cellular injury and death. Our aim was to establish whether inflammasome components were present in HSC and could regulate HSC functionality. Monosodium urate (MSU) crystals (100 µg/ml) were used to experimentally induce inflammasome activation in LX-2 and primary mouse HSC. Twenty-four hours later primary mouse HSC were stained with -smooth muscle actin and visualized by confocal microscopy, and TGF-β and collagen1 mRNA expression was quantified. LX-2 cells were further cultured with or without MSU crystals for 24 h in a transwell chemotaxis assay with PDGF as the chemoattractant. We also examined inhibition of calcium (Ca2+) signaling in LX-2 cells treated with or without MSU crystals using caged inositol 1,4,5-triphosphate (IP3). Finally, we confirmed an important role of the inflammasome in experimental liver fibrosis by the injection of carbon tetrachloride (CCl4) or thioacetamide (TAA) in wild-type mice and mice lacking components of the inflammasome. Components of the inflammasome are expressed in LX-2 cells and primary HSC. MSU crystals induced upregulation of TGF-β and collagen1 mRNA and actin reorganization in HSCs from wild-type mice but not mice lacking inflammasome components. MSU crystals inhibited the release of Ca2+ via IP3 in LX-2 cells and also inhibited PDGF-induced chemotaxis. Mice lacking the inflammasome-sensing and adaptor molecules, NLRP3 and apoptosis-associated speck-like protein containing CARD, had reduced CCl4 and TAA-induced liver fibrosis. We concluded that inflammasome components are present in HSC, can regulate a variety of HSC functions, and are required for the development of liver fibrosis.

  M Ogura , H Kamimura , A Al Kalaly , K Nagayama , K Taira , J Nagata and S. Miyawaki

The purpose of the present study was to determine whether a force of 20 cN can be biologically active for tooth movement and to examine the pain intensity during the application of light (20 cN) or heavy (200 cN) continuous forces for 7 days.

In the first experiment, a force of 20 cN was applied to eight canines in five volunteers. The mean tooth movement during 10 weeks was 2.4 mm. In the second experiment, two forces of 20 or 200 cN were applied to maxillary premolars in 12 male subjects (aged 24–31 years) to measure pain intensity for 7 days. Spontaneous and biting pain were recorded every 2–4 hours on a 100 mm visual analogue scale (VAS). Wilcoxon signed-rank test was used for statistical analysis.

Comparing the VAS score at force initiation with the other time points, there was no significant difference in spontaneous pain for either group, or in biting pain for the light-force group. However, biting pain in the heavy-force group during the time period from 6 to 156 hours was significantly (P < 0.05) greater than that at force initiation. Comparing the VAS scores between the light- and heavy-force group, VAS scores for biting pain in the heavy-force group during the time period from 8 to 100 hours was significantly (P < 0.05) greater than that in the light-force group.

A force of 20 cN can move teeth, but pain intensity while biting may be greater approximately 8 hours to 5 days following the application of heavy continuous force compared with light force.

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