640 research outputs found

    Self-Similar Collapse of Scalar Field with Plane Symmetry

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    Plane symmetric self-similar solutions to Einstein's four-dimensional theory of gravity are studied and all such solutions are given analytically in closed form. The local and global properties of these solutions are investigated and it is shown that some of the solutions can be interpreted as representing gravitational collapse of the scalar field. During the collapse, trapped surfaces are never developed. As a result, no black hole is formed. Although the collapse always ends with spacetime singularities, it is found that these singularities are spacelike and not naked.Comment: latex, two figure

    Amphiphysin I and regulation of synaptic vesicle endocytosis

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    Amphiphysin I, known as a major dynamin-binding partner localized on the collars of nascent vesicles, plays a key role in clathrin-mediated endocytosis (CME) of synaptic vesicles. Amphiphysin I mediates the invagination and fission steps of synaptic vesicles by sensing or facilitating membrane curvature and stimulating the GTPase activity of dynamin. Amphiphysin I may form a homodimer by itself or a heterodimer with amphiphysin II in vivo. Both amphiphysin I and II function as multilinker proteins in the clathrin-coated complex. Under normal physiological conditions, the functions of amphiphysin I and some other endocytic proteins are known to be regulated by phosphorylation and dephosphorylation. During hyperexcited conditions, the most recent data showed that amphiphysin I is truncated by the ca2-dependent protease calpain. Overexpression of the truncated form of amphi-physin I inhibited transferrin uptake and synaptic vesicle endocytosis (SVE). This suggests that amphi-physin I may be an important regulator for SVE when massive amounts of Ca2 flow into presynaptic terminals, a phenomenon observed in neurodegenerative disorders such as ischemia/anoxia, epilepsy, stroke, trauma and Alzheimer's disease. This review describes current knowledge regarding the general properties and functions of amphiphysin I as well as the functional regulations such as phosphorylation and proteolysis in nerve terminals.</p

    多価不飽和脂肪酸の神経芽腫細胞(Neuro2a)におけるアポトーシス抑制効果

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    Neuronal apoptosis is involved in neurodegenerative diseases such as Alzheimer's disease and Parkinson.s disease. An efficient means of preventing it remains to be found. Some n-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, 22 : 6n-3) and eicosapentaenoic acid (EPA, 20 : 5n-3) have been reported to be protective against the neuronal apoptosis and neuronal degeneration seen after spinal cord injury (SCI) [1]. However, it is unclear which kinds of PUFAs have the most potent ability to inhibit neuronal apoptosis and whether the simultaneous treatment of PUFAs inhibits the apoptosis. In the present study, we compared the abilities of various n-3- and n-6- PUFAs to inhibit the apoptosis induced after the administration of different apoptotic inducers, etoposide, okadaic acid, and AraC, in mouse neuroblastoma cells (Neuro2a). Preincubation with DHA (22 : 6n-3), eicosapentaenoic acid (EPA, 20 : 5n-3), alpha-linolenic acid (alpha-LNA, 18 : 3n-3), linoleic acid (LA, 18 : 2n-6), arachidonic acid (AA, 20 : 4n-3), and gamma-linolenic acid (gamma-LNA, 18 : 3n-6) significantly inhibited caspase-3 activity and LDH leakage but simultaneous treatment with the PUFAs had no effect on the apoptosis of Neuro2a cells. There were no significant differences of the anti-apoptotic eff ect among the PUFAs. These results suggest that PUFAs may not be effective for inhibiting neuronal cell death after acute and chronic neurodegenerative disorders. However, dietary supplementation with PUFAs may be beneficial as a potential means to delay the onset of the diseases and/or their rate of progression

    Cosmology in nonrelativistic general covariant theory of gravity

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    Horava and Melby-Thompson recently proposed a new version of the Horava-Lifshitz theory of gravity, in which the spin-0 graviton is eliminated by introducing a Newtonian pre-potential ϕ\phi and a local U(1) gauge field AA. In this paper, we first derive the corresponding Hamiltonian, super-momentum constraints, the dynamical equations, and the equations for ϕ\phi and AA, in the presence of matter fields. Then, we apply the theory to cosmology, and obtain the modified Friedmann equation and the conservation law of energy, in addition to the equations for ϕ\phi and AA. When the spatial curvature is different from zero, terms behaving like dark radiation and stiff-fluid exist, from which, among other possibilities, bouncing universe can be constructed. We also study linear perturbations of the FRW universe with any given spatial curvature kk, and derive the most general formulas for scalar perturbations. The vector and tensor perturbations are the same as those recently given by one of the present authors [A. Wang, Phys. Rev. D{\bf 82}, 124063 (2010)] in the setup of Sotiriou, Visser and Weinfurtner. Applying these formulas to the Minkowski background, we have shown explicitly that the scalar and vector perturbations of the metric indeed vanish, and the only remaining modes are the massless spin-2 gravitons.Comment: Revtex4, no figures. Gauge freedom was clarified and typos were corrected. Version to appear in Physical Reviews

    Weak antilocalization and electron-electron interaction in coupled multiple-channel transport in a Bi2_2Se3_3 thin film

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    Electron transport properties of a topological insulator Bi2_2Se3_3 thin film are studied in Hall-bar geometry. The film with a thickness of 10 nm is grown by van der Waals epitaxy on fluorophlogopite mica and Hall-bar devices are fabricated from the as-grown film directly on the mica substrate. Weak antilocalization and electron-electron interaction effects are observed and analyzed at low temperatures. The phase-coherence length extracted from the measured weak antilocalization characteristics shows a strong power-law increase with decreasing temperature and the transport in the film is shown to occur via coupled multiple (topological surface and bulk states) channels. The conductivity of the film shows a logarithmically decrease with decreasing temperature and thus the electron-electron interaction plays a dominant role in quantum corrections to the conductivity of the film at low temperatures.Comment: 12 pages, 5 figure

    Inhibitory effect of polyunsaturated fatty acids on apoptosis induced by etoposide, okadaic acid and AraC in Neuro2a cells

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    Neuronal apoptosis is involved in neurodegenerative diseases such as Alzheimer's disease and Parkinson.s disease. An efficient means of preventing it remains to be found. Some n-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, 22 : 6n-3) and eicosapentaenoic acid (EPA, 20 : 5n-3) have been reported to be protective against the neuronal apoptosis and neuronal degeneration seen after spinal cord injury (SCI) [1]. However, it is unclear which kinds of PUFAs have the most potent ability to inhibit neuronal apoptosis and whether the simultaneous treatment of PUFAs inhibits the apoptosis. In the present study, we compared the abilities of various n-3- and n-6- PUFAs to inhibit the apoptosis induced after the administration of different apoptotic inducers, etoposide, okadaic acid, and AraC, in mouse neuroblastoma cells (Neuro2a). Preincubation with DHA (22 : 6n-3), eicosapentaenoic acid (EPA, 20 : 5n-3), alpha-linolenic acid (alpha-LNA, 18 : 3n-3), linoleic acid (LA, 18 : 2n-6), arachidonic acid (AA, 20 : 4n-3), and gamma-linolenic acid (gamma-LNA, 18 : 3n-6) significantly inhibited caspase-3 activity and LDH leakage but simultaneous treatment with the PUFAs had no effect on the apoptosis of Neuro2a cells. There were no significant differences of the anti-apoptotic eff ect among the PUFAs. These results suggest that PUFAs may not be effective for inhibiting neuronal cell death after acute and chronic neurodegenerative disorders. However, dietary supplementation with PUFAs may be beneficial as a potential means to delay the onset of the diseases and/or their rate of progression
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