8 research outputs found
Survey of Period Variations of Superhumps in SU UMa-Type Dwarf Novae
We systematically surveyed period variations of superhumps in SU UMa-type
dwarf novae based on newly obtained data and past publications. In many
systems, the evolution of superhump period are found to be composed of three
distinct stages: early evolutionary stage with a longer superhump period,
middle stage with systematically varying periods, final stage with a shorter,
stable superhump period. During the middle stage, many systems with superhump
periods less than 0.08 d show positive period derivatives. Contrary to the
earlier claim, we found no clear evidence for variation of period derivatives
between superoutburst of the same object. We present an interpretation that the
lengthening of the superhump period is a result of outward propagation of the
eccentricity wave and is limited by the radius near the tidal truncation. We
interpret that late stage superhumps are rejuvenized excitation of 3:1
resonance when the superhumps in the outer disk is effectively quenched. Many
of WZ Sge-type dwarf novae showed long-enduring superhumps during the
post-superoutburst stage having periods longer than those during the main
superoutburst. The period derivatives in WZ Sge-type dwarf novae are found to
be strongly correlated with the fractional superhump excess, or consequently,
mass ratio. WZ Sge-type dwarf novae with a long-lasting rebrightening or with
multiple rebrightenings tend to have smaller period derivatives and are
excellent candidate for the systems around or after the period minimum of
evolution of cataclysmic variables (abridged).Comment: 239 pages, 225 figures, PASJ accepte
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Multiple agonist induced changes in eicosanoid metabolites correlated with gene expression in macrophages
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Multiple agonist induced changes in eicosanoid metabolites correlated with gene expression in macrophages
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Kdo2-Lipid A of Escherichia coli, a defined endotoxin that activates macrophages via TLR-4.
The LIPID MAPS Consortium (www.lipidmaps.org) is developing comprehensive procedures for identifying all lipids of the macrophage, following activation by endotoxin. The goal is to quantify temporal and spatial changes in lipids that occur with cellular metabolism and to develop bioinformatic approaches that establish dynamic lipid networks. To achieve these aims, an endotoxin of the highest possible analytical specification is crucial. We now report a large-scale preparation of 3-deoxy-D-manno-octulosonic acid (Kdo)(2)-Lipid A, a nearly homogeneous Re lipopolysaccharide (LPS) sub-structure with endotoxin activity equal to LPS. Kdo(2)-Lipid A was extracted from 2 kg cell paste of a heptose-deficient Escherichia coli mutant. It was purified by chromatography on silica, DEAE-cellulose, and C18 reverse-phase resin. Structure and purity were evaluated by electrospray ionization/mass spectrometry, liquid chromatography/mass spectrometry and (1)H-NMR. Its bioactivity was compared with LPS in RAW 264.7 cells and bone marrow macrophages from wild-type and toll-like receptor 4 (TLR-4)-deficient mice. Cytokine and eicosanoid production, in conjunction with gene expression profiling, were employed as readouts. Kdo(2)-Lipid A is comparable to LPS by these criteria. Its activity is reduced by >10(3) in cells from TLR-4-deficient mice. The purity of Kdo(2)-Lipid A should facilitate structural analysis of complexes with receptors like TLR-4/MD2
Kdo2-Lipid A of Escherichia coli, a defined endotoxin that activates macrophages via TLR-4.
The LIPID MAPS Consortium (www.lipidmaps.org) is developing comprehensive procedures for identifying all lipids of the macrophage, following activation by endotoxin. The goal is to quantify temporal and spatial changes in lipids that occur with cellular metabolism and to develop bioinformatic approaches that establish dynamic lipid networks. To achieve these aims, an endotoxin of the highest possible analytical specification is crucial. We now report a large-scale preparation of 3-deoxy-D-manno-octulosonic acid (Kdo)(2)-Lipid A, a nearly homogeneous Re lipopolysaccharide (LPS) sub-structure with endotoxin activity equal to LPS. Kdo(2)-Lipid A was extracted from 2 kg cell paste of a heptose-deficient Escherichia coli mutant. It was purified by chromatography on silica, DEAE-cellulose, and C18 reverse-phase resin. Structure and purity were evaluated by electrospray ionization/mass spectrometry, liquid chromatography/mass spectrometry and (1)H-NMR. Its bioactivity was compared with LPS in RAW 264.7 cells and bone marrow macrophages from wild-type and toll-like receptor 4 (TLR-4)-deficient mice. Cytokine and eicosanoid production, in conjunction with gene expression profiling, were employed as readouts. Kdo(2)-Lipid A is comparable to LPS by these criteria. Its activity is reduced by >10(3) in cells from TLR-4-deficient mice. The purity of Kdo(2)-Lipid A should facilitate structural analysis of complexes with receptors like TLR-4/MD2
Endocannabinoids produced upon action potential firing evoke a Cl− current via type-2 cannabinoid receptors in the medial prefrontal cortex
The functional presence of type-2 cannabinoid receptors (CB2Rs) in layer II/III pyramidal neurons of the rat medial prefrontal cortex (mPFC) was recently demonstrated. In the present study, we show that the application of the endocannabinoids (eCBs) 2-arachidonoylglycerol (2-AG) and methanandamide [a stable analog of the eCB anandamide (AEA)] can activate CB2Rs of mPFC layer II/III pyramidal neurons, which subsequently induces a Cl- current. In addition, we show that action potential (AP) firing evoked by 20-Hz current injections results in an eCB-mediated opening of Cl- channels via CB2R activation. This AP-evoked synthesis of eCBs is dependent on the Ca2+ influx through N-type voltage-gated calcium channels. Our results indicate that 2-AG is the main eCB involved in this process. Finally, we demonstrate that under physiologically relevant intracellular Cl- conditions, 20-Hz AP firing leads to a CB2R-dependent reduction in neuronal excitability. Altogether, our data indicate that eCBs released upon action potential firing can modulate, through CB2R activation, neuronal activity in the mPFC. We discuss how this may be a mechanism to prevent excessive neuronal firing