134 research outputs found

    Rebound Vibration of Two-Plates Bonded Model for an Internal Mirror of SLR Camera

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    In this study, the rebound vibration characteristics of the internal mirror of an SLR camera are investigated using experimental models. The mechanism of the mirror rebound phenomena is tested by using the two-rectangular-metal-plates model, which has two plates bonded by double-sided tape. The mirror (plates) model is supported by fixing its longitudinal edge on a horizontal rotatable shaft. The bonded-mirror-model swings down freely around a horizontal axis and hits a stopper. A laser displacement meter is used to measures the amount of rebound and the mirror model vibration behavior. The rebound angle varies by the stopper position and the bonded position of the double-sided tape. In the case of a small rebound angle, the mirror part of the plate (upper side plate) vibrates with large amplitude, and its movement is measured by a 3-dimentional high-speed camera.13th International Conference on Motion and Vibration Control (MOVIC 2016) and the 12th International Conference on Recent Advances in Structural Dynamics (RASD 2016)4–6 July 2016, Southampton, U

    Association between hand-grip strength and depressive symptoms: Locomotive Syndrome and Health Outcomes in Aizu Cohort Study (LOHAS).

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    First published online: February 21, 2015no study has examined the longitudinal association between hand-grip strength and mental health, such as depressive symptoms

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

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    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

    Pilot study to estimate the safety and effectiveness of hydroxyurea and methotrexate recurrent langerhans cell histiocytosis (LCH-HU-pilot)

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    This study was a non-blinded, multicenter, single-arm study. Recurrent (relapsed) LCH is defined as the appearance of new lesions or the enlargement of preexisting lesions due to LCH. In this study, all patients received hydroxyurea, and if the treatment response was unsatisfactory, methotrexate was added. The duration of treatment was 48 weeks. The primary endpoint was the rate of non-active disease achievement, which was 24 weeks after initiating hydroxyurea administration. No active disease is defined as the resolution of all the signs and symptoms related to LCH

    Five isoforms of the phosphatidylinositol 3-kinase regulatory subunit exhibit different associations with receptor tyrosine kinases and their tyrosine phosphorylations

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    AbstractThere are five isoforms of the regulatory subunit for the heterodimeric type of phosphatidylinositol 3-kinase. These five regulatory subunit isoforms were overexpressed using an adenovirus transfection system, and their own tyrosine phosphorylations and associations with various tyrosine kinase receptors were investigated. When overexpressed in CHO-PDGFR cells, the associations of these regulatory subunit isoforms with the platelet-derived growth factor receptor were similar. However, when overexpressed in CHO-IR cells, p55γ exhibited a significantly lower ability to bind with IRS-1 upon insulin stimulation, as compared with other regulatory subunit isoforms. Furthermore, p55α and p55γ were found to be tyrosine-phosphorylated. Finally, interestingly, when overexpressed in CHO-EGFR cells or A431 cells and stimulated with epidermal growth factor (EGF), phosphorylated EGF receptor was detected in p85α, p85β and p50α immunoprecipitates, but not in p55α and p55γ immunoprecipitates. In addition, EGF-induced tyrosine phosphorylation was observed in p85α, p85β, p55α and p55γ, but not in p50α, immunoprecipitates. Thus, each regulatory subunit exhibits specific responses regarding both the association with tyrosine-phosphorylated substrates and its own tyrosine phosphorylation. These results suggest that each isoform possesses specific roles in signal transduction, based on its individual tyrosine kinase receptor

    Vasodilative effects of prostaglandin E1 derivate on arteries of nerve roots in a canine model of a chronically compressed cauda equina

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    <p>Abstract</p> <p>Background</p> <p>Reduction of blood flow is important in the induction of neurogenic intermittent claudication (NIC) in lumbar spinal canal stenosis. PGE<sub>1 </sub>improves the mean walking distance in patients with NIC type cauda equina compression. PGE<sub>1 </sub>derivate might be effective in dilating blood vessels and improving blood flow in nerve roots with chronically compressed cauda equina. The aim of this study was to assess whether PGE<sub>1 </sub>derivate has vasodilatory effects on both arteries and veins in a canine model of chronic cauda equina compression.</p> <p>Methods</p> <p>Fourteen dogs were used in this study. A plastic balloon inflated to 10 mmHg was placed under the lamina of the 7th lumbar vertebra for 1 week. OP-1206-cyclodextrin clathrate (OP-1206-CD: prostaglandin E<sub>1 </sub>derivate) was administered orally. The blood vessels of the second or third sacral nerve root were identified using a specially designed surgical microscope equipped with a video camera. The diameter of the blood vessels was measured on video-recordings every 15 minutes until 90 minutes after the administration of the PGE<sub>1 </sub>derivate.</p> <p>Results</p> <p>We observed seven arteries and seven veins. The diameter and blood flow of the arteries was significantly increased compared with the veins at both 60 and 75 minutes after administration of the PGE<sub>1 </sub>derivate (p < 0.05). Blood flow velocity did not change over 90 minutes in either the arteries or veins.</p> <p>Discussion</p> <p>The PGE<sub>1 </sub>derivate improved blood flow in the arteries but did not induce blood stasis in the veins. Our results suggest that the PGE<sub>1 </sub>derivate might be a potential therapeutic agent, as it improved blood flow in the nerve roots in a canine model of chronic cauda equina compression.</p

    Enhanced Nogo-P3 amplitudes of mothers compared with non-mother women during an emotional Go/Nogo task

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    Background: It is known that emotion regulatory responses of humans are changed by the experiences they have, but in particular, they are changed by becoming a mother. A recent study has found how a woman&apos;s emotion regulatory response to a child&apos;s crying changes after becoming a mother. However, mothers&apos; emotion regulatory responses other than those to children and the association between emotion regulatory response and parental stress are still unknown. Methods: Eighteen healthy Japanese females (nine mothers and nine non-mothers) participated in the experiment. They performed an emotional Go/Nogo task, with facial expressions of others (angry, happy, and neutral faces) used as emotional stimuli. The percentage of correct responses, response time, and event-related potentials (ERPs) during the task was measured. Results: This comparison revealed that the mother group had a larger P3 (Nogo-P3) amplitude than the non-mother group when Nogo trials were held. This indicates that in mothers, there was greater activation of the behavioral inhibition-related brain areas than in non-mother women when they inhibited inappropriate behavior following recognition of facial expressions of others. In addition, in the mother group, there was a negative correlation between parental stress levels and Nogo-P3 amplitudes evoked by angry faces. This suggests that there is a relation between the level of parental stress of mothers and their emotion regulatory responses to angry faces. Conclusions: Our results demonstrate that mothers&apos; emotion regulatory processes may differ from those of non-mothers in response, not only to a child&apos;s crying but also to expressions of emotions by others, and also suggest that the inhibitory recognition activity of mothers can be affected by parental stres

    Porphyromonas gingivalis SOD における活性中心近傍に局在するアミノ酸残基の金属特異的活性における関与:Leu ₇2 Trp およびLeu ₇6 Phe の2残基変異による検討

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    The role of superoxide dismutase (SOD) as a radical scavenger in Porphyromonas gingivalis is well documented. P. gingivalis SOD (Pg SOD), which is characterized by a metal–tolerant activity, can use either iron or manganese as a cofactor. Leu ₇2 and Leu ₇6, located near the active–site metal, are characteristic amino acid sequences of Pg SOD proteins, although they are substituted to Trp in the ₇2 position and Phe in the ₇6 position in most iron–containing SOD (Fe–SOD) proteins. In the present study, we constructed a mutant of the enzyme with changes from Leu ₇2 to Trp and Leu ₇6 to Phe. This mutant SOD was examined with respect to its metal–dependent activity and structural characterization. We herein conclude the integrity of Leu ₇2 and Leu ₇6 is a necessary requisite for the metal–tolerant activity of Pg SOD

    Altered expression of a putative progenitor cell marker DCAMKL1 in the rat gastric mucosa in regeneration, metaplasia and dysplasia

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    <p>Abstract</p> <p>Background</p> <p>Doublecortin and calcium/calmodulin-dependent protein kinase-like-1 (DCAMKL1) is a candidate marker for progenitor cells in the gastrointestinal mucosa. Lineage cells in the gastric mucosa are derived from progenitor cells, but this process can be altered after injury. Therefore, we explored DCAMKL1 expression under pathological conditions.</p> <p>Methods</p> <p>An immunohistochemical analysis was performed in rat stomach with acute superficial injury, chronic ulcer, intestinal metaplasia and dysplasia.</p> <p>Results</p> <p>DCAMKL1 was exclusively expressed in immature quiescent cells in the isthmus of normal fundic glands, where putative progenitor cells are thought to reside. DCAMKL1-positive cells and proliferating cells shed into the lumen after superficial injury and re-appeared during the regenerative process, mainly in the superficial mucosa. In the marginal mucosa around the active ulcer, parietal and chief cells diminished, foveolar hyperplasia was evident, and trefoil factor family 2 (TFF2)/spasmolytic polypeptide-expressing metaplasia (SPEM) emerged at the gland base. DCAMKL1 cells re-emerged in the deep mucosa juxtaposed with SPEM and proliferating cells. In the healing ulcer, the TFF2 cell population expanded and seemed to redifferentiate to chief cells, while proliferating cells and DCAMKL1 cells appeared above and below the TFF2 cells to promote healing. SPEM appeared and PCNA cells increased in the intestinalized mucosa, and DCAMKL1 was expressed in the proximity of the PCNA cells in the deep mucosa. DCAMKL1, PCNA and TFF2 were expressed in different dysplastic cells lining dilated glands near SPEM.</p> <p>Conclusion</p> <p>The ultrastructural appearance of DCAMKL1-positive cells and the expression patterns of DCAMKL1 in normal and pathological states indicate that the cells belong to a progenitor cell population. DCAMKL1 expression is closely associated with TFF2/SPEM cells after injury. DCAMKL1 cells repopulate close to proliferating, hyperplastic, metaplastic and dysplastic cells, and the progenitor zone shifts according to the pathological circumstances.</p
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