158 research outputs found

    Light Higgs boson scenario in the SUSY seesaw model

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    It is demonstrated that the light Higgs boson scenario, which the lightest Higgs mass is less than the LEP bound, mh > 114.4 GeV, is consistent with the SUSY seesaw model. With the assumptions of the universal right-handed neutrino mass and the hierarchical mass spectrum of the ordinary neutrinos, the bounds for the right-handed neutrino mass is investigated in terms of lepton flavor violating charged lepton decays. We also discuss the effect of the modification of renormalization group equations by the right-handed neutrinos on the b to s gamma process and the relic abundance of dark matter in the light Higgs boson scenario.Comment: 17 pages, 5 figure

    Isolation of Nebulin from Rabbit Skeletal Muscle and Its Interaction with Actin

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    Nebulin is about 800 kDa filamentous protein that binds the entire thin filament of vertebrate skeletal muscle sarcomeres. Nebulin cannot be isolated from muscle except in a completely denatured form by direct solubilization of myofibrils with SDS because nebulin is hardly soluble under salt conditions. In the present study, nebulin was solubilized by a salt solution containing 1 M urea and purified by DEAE-Toyopearl column chromatography via 4 M urea elution. Rotary-shadowed images of nebulin showed entangled knit-like particles, about 20 nm in diameter. The purified nebulin bound to actin filaments to form loose bundles. Nebulin was confirmed to bind actin, α-actinin, β-actinin, and tropomodulin, but not troponin or tropomyosin. The data shows that full-length nebulin can be also obtained in a functional and presumably native form, verified by data from experiments using recombinant subfragments

    Suppression of cell migration by phospholipase C-related catalytically inactive protein-dependent modulation of PI3K signalling

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    The metabolic processes of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] into PI(3,4,5)P3 and the subsequent PI(3,4,5)P3 signalling are involved in cell migration. Dysfunctions in the control of this pathway can cause human cancer cell migration and metastatic growth. Here we investigated whether phospholipase C-related catalytically inactive protein (PRIP), a PI(4,5)P2-binding protein, regulates cancer cell migration. PRIP overexpression in MCF-7 and BT-549 human breast cancer cells inhibited cell migration in vitro and metastasis development in vivo. Overexpression of the PRIP pleckstrin homology domain, a PI(4,5)P2 binding motif, in MCF-7 cells caused significant suppression of cell migration. Consistent with these results, in comparison with wild-type cells, Prip-deficient mouse embryonic fibroblasts exhibited increased cell migration, and this was significantly attenuated upon transfection with a siRNA targeting p110α, a catalytic subunit of class I phosphoinositide 3-kinases (PI3Ks). PI(3,4,5)P3 production was decreased in Prip-overexpressing MCF-7 and BT-549 cells. PI3K binding to PI(4,5)P2 was significantly inhibited by recombinant PRIP in vitro, and thus the activity of PI3K was downregulated. Collectively, PRIP regulates the production of PI(3,4,5)P3 from PI(4,5)P2 by PI3K, and the suppressor activity of PRIP in PI(4,5)P2 metabolism regulates the tumour migration, suggesting PRIP as a promising target for protection against metastatic progression.This work was supported by grants from JSPS KAKENHI Grant Numbers JP15K20372, JP17K11644, JP16K11503

    Possible involvement of iron-induced oxidative insults in neurodegeneration.

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    Involvement of iron in the development of neurodegenerative disorders has long been suggested, and iron that cannot be stored properly is suggested to induce iron toxicity. To enhance iron uptake and suppress iron storage in neurons, we generated transgenic (Tg) mice expressing iron regulatory protein 2 (IRP2), a major regulator of iron metabolism, in a neuron-specific manner. Although very subtle, IRP2 was expressed in all regions of brain examined. In the Tg mice, mitochondrial oxidative insults were observed including generation of 4-hydroxynonenal modified proteins, which appeared to be removed by a mitochondrial quality control protein Parkin. Inter-crossing of the Tg mice to Parkin knockout mice perturbed the integrity of neurons in the substantia nigra and provoked motor symptoms. These results suggest that a subtle, but chronic increase in IRP2 induces mitochondrial oxidative insults and accelerates neurodegeneration in a mouse model of Parkinson's disease. Thus, the IRP2 Tg may be a useful tool to probe the roles of iron-induced mitochondrial damages in neurodegeraration research

    女性がんサバイバーの心理的適応

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    The purpose of this study is to explore the psychological adjustments female cancer survivors undergo with respect to their femininity. Semi-structured interviews were performed with 29 female cancer(breast or gynecologic cancer)survivors in their20s to50s. Qualitative descriptive study data was interpreted according to Krippendorff’s content analysis method. As a result, six categories were generated as psychological adjustments utilized by female cancer survivors from the viewpoint of femininity : “I like the way I am” ; “I am charming as a woman” ; “I live independently as a woman” ; “I am expanding my life as a woman” ; “I can feel connected with someone” ; and “I have graduated from pessimism.” These could be interpreted as psychological adaptations that reflect feminine emotions and reflect the strength and resilience of female cancer survivors. In order for female cancer survivors to adjust to living with cancer in a psychologically healthy way, it was suggested that nursing support was important to restore the feelings of the survivors from the perspective of these feminine characteristics
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