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幸博, 高橋; 吉博, 藤村; 芳明, 大久保; 資司, 安居; 充彦, 杉本; 定昭, 三上; 弘, 福井

doi:10.3925/jjtc1958.29.340

Cited by 33 publications

(50 citation statements)

References 8 publications

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“…Thus, MTX clearly must act in a manner different from calcium ionophores. Previous data on calcium influx in liposomes indicated no ionophore activity for MTX [18].…”

Section: Discussionmentioning

confidence: 85%

“…A distinction between these two mechanisms, direct activation of phospholipase C or stimulation of a calcium uptake system closely associated with phospholipase C by MTX, cannot be made as yet. The very high potency of MTX (ECso 150 pM), the stimulation by MTX of phosphoinositide breakdown in cells in which calcium ionophores have marginal effects (see section 3) and the lack of calcium ionophore activity for MTX in liposomes [18], all indicate that MTX does not stimulate phospholipase C simply by acting as a calcium ionophore.…”

Section: Discussionmentioning

confidence: 99%

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Maitotoxin, a potent, general activator of phosphoinositide breakdown

1989

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Maitotoxin (MTX), a potent marine toxin, elicits a calcium-dependent activation of cells that can be inhibited by calcium channel blockers like nifedipine. MTX also stimulates phosphoinositide breakdown in smooth muscle cells, NCB-20 cells and PC 12 cells through a nifedipine-insensitive mechanism. We now report that MTX stimulates phosphoinositide breakdown in a wide variety of ceils, and appears to repesent the first general activator of this second messenger-generating system. MTX-induced stimulation of phosphoinositide breakdown is dependent in every cell line on the presence of extracellular calcium. In differentiated HL60 cells, in which a chemotactic peptide (fMLP) activates phosphoinositide breakdown via a pertussis toxin-sensitive mechanism, MTX-induced stimulation is not affected by pertussis toxin treatment. A phorbol ester has no effect on the response to MTX. Thus, MTX stimulates phosphoinositide breakdown through a calcium-dependent mechanism that at least in three cell lines (PC12, NCB20 and HL60) is not mediated by a pathway that involves a pertussis toxin-sensitive guanine nucleotide-binding protein.

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“…Thus, MTX clearly must act in a manner different from calcium ionophores. Previous data on calcium influx in liposomes indicated no ionophore activity for MTX [18].…”

Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Maitotoxin, a potent, general activator of phosphoinositide breakdown

1989

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“…keratohyalin granules: TGa~¢, tran561utamirinse; P.ey,=tatln a¢. phospho~lated ~statin ~; SDS-PAGE, sodium dod~yl ~u,fate-polyacrylamid¢ ll~l el~trophor~i~; ',' ~,,,,, ~.,.s .... lal antibody, rich in lysine residues (l 3.7%) [9] and. furthermore, ker-atinocyte=, contain a large amount of TGase.…”

Section: Introductionmentioning

confidence: 99%

Phosphorylated cystatin α is a natural substrate of epidermal transglutaminase for formation of skin cornified envelope

1992

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Both keratohyalin ~mnalt~ (KHG) and eornifl~ envelolxs ~r¢ stained hi~to~hcnzieaily in an indirect immunofluor~nt study by anti.pho~phorylated c~tatin a antibody, indicating that phosphorylated ¢ystatin ¢~ is a component of the ¢ornifled envelope proteins, When pho,tphorylated eystatin 0t (P.c~tatin ¢) was incubated with epidermal tmnsglutamina~ frGa~) and Ca"" ions. pol~mcrized protein was prodaced by formation of P(F-glutamyl)ly,,ine cross.linking pcptide bonds between lysine rvddu¢~ ofeystatin ¢~ and gh~tamine residu~ of suitable protein(s} in the enzyme preparation. However, phosphowlatcd and non.pho~phorylatcd cystatins were polymerlzed to similar extents by the TGa~t, [mmunofluore~cent and immunodcetron microscopic ob~rvation,~ revealed that P-¢ystatin a could I~ det~:t~l in vivo in the KHG and e..ornifled envclop~. "treatment of sphiagosin¢, a specific inhibitor of protein kinar~ C, markedly r, uppr¢~=~.d the incorporation ofeystatin =z into KHG. Thus phosphorylation of cystatin a by protein kinar~ C may play an important role in tarli~ting cystatin a into KHG.

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“…This heat treatment was found to lead to good balance of tensile properties, fracture toughness and fatigue properties in the previous study. [1][2][3][4][5][6][7][8] This heat treatment condition may give a similar matrix microstructure to that of casting alloy. From these heat-treated bars, tensile and fatigue specimens were machined for a comparison with casting ones as will be also mentioned below.…”

Section: Methodsmentioning

confidence: 99%

“…Fundamental studies of the fatigue properties in the relation with microstructure have so far been done about a dental drawn Ag-Pd-Cu-Au-Zn alloy by authors. [1][2][3][4][5][6][7][8] However, since there is an individual difference in teeth and the type of dental caries is also different individually, when using dental prosthetic products, such as inlay and crown, it is difficult to use ready-made products. Therefore, dental prosthetic products, such as inlay and crown, are mainly fabricated by casting after taking models of treating parts.…”

Section: Introductionmentioning

confidence: 99%

Fatigue Properties of Cast Ag-Pd-Cu-Au-Zn Alloy for Dental Applications in the Relation with Casting Defects

et al. 2002

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Ag-Pd-Cu-Au-Zn type alloys have been widely used as dental prosthetic materials. In general, the dental prosthetic products are fabricated by a dental casting method. The dental castings contain the casting defects such as micro shrinkages, pores, surface roughness, etc. Cyclic stress, that is, fatigue stress due to the mastification is applied to the dental prosthesis in the practical use. Therefore, the effects of the casting defects such as micro shrinkages, pores and surface roughness on the fatigue properties of the cast Ag-Pd-Cu-Au-Zn type alloy were investigated in the comparison with the fatigue properties of the drawn Ag-Pd-Cu-Au-Zn alloy in this study. Fatigue tests of Ag-Pd-Cu-AuZn alloy cast using a dental casting machine were carried out, and then the fatigue properties of the cast alloy were investigated in the relation with casting defects. The fatigue strength of the cast Ag-Pd-Cu-Au-Zn alloy is considerably smaller than that of the drawn Ag-Pd-Cu-Au-Zn alloy. The fatigue crack of the cast alloy initiates preferentially at the shrinkage near the specimen surface. The scatter of the fatigue strength of the cast alloy becomes to be small by relating the fatigue life with the maximum stress intensity factor calculated assuming the shrinkage that becomes to be a fatigue crack initiation site as a initial crack. This means that the size of the shrinkage affects the fatigue strength of this cast alloy strongly. The tolerant size of the shrinkage that satisfies the target value of the fatigue limit (230 MPa) of this cast alloy is calculated to be below 80 µm using the equation derived in this study, which describes the relationship between the maximum stress intensity factor and the number of the cycles to failure.

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Cited by 33 publications

References 8 publications

Maitotoxin, a potent, general activator of phosphoinositide breakdown

Maitotoxin, a potent, general activator of phosphoinositide breakdown

Phosphorylated cystatin α is a natural substrate of epidermal transglutaminase for formation of skin cornified envelope

Fatigue Properties of Cast Ag-Pd-Cu-Au-Zn Alloy for Dental Applications in the Relation with Casting Defects

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