A new scheme of causal viscous hydrodynamics for relativistic heavy-ion collisions: A Riemann solver for quark-gluon plasma

In this article, we present a state-of-the-art algorithm for solving the relativistic viscous hydrodynamics equation with the QCD equation of state. The numerical method is based on the second-order Godunov method and has less numerical dissipation, which is crucial in describing of quark-gluon plasma in high-energy heavy-ion collisions. We apply the algorithm to several numerical test problems such as sound wave propagation, shock tube and blast wave problems. In sound wave propagation, the intrinsic numerical viscosity is measured and its explicit expression is shown, which is the second-order of spatial resolution both in the presence and absence of physical viscosity. The expression of the numerical viscosity can be used to determine the maximum cell size in order to accurately measure the effect of physical viscosity in the numerical simulation.Comment: 38pages, 31 figures; published versio

H2S Sensing Properties and Mechanism of Macroporous Semiconductor Sensors

Macroporous (mp-) In2O3-based films with and without 1 wt% CuO loading were fabricated by a modified sol-gel technique employing polymethylmethacrylate microspheres as a template and their sensor responses to H2S and the reaction behavior of H2S over the sensor materials were investigated. Introduction of macropores into an In2O3 film and simultaneous loading of CuO on the In2O3 surface were enormously effective in improving the H2S response. The large surface area of mp-In2O3 loaded with CuO, which increased the reactivity of CuO with H2S, is probably the most important factor to enhance the H2S response.214th ECS Meeting : Honolulu, HI, October 12 - October 17, 200

The effect of truncation on prion-like properties of α-synuclein

Increasing evidence suggests that α-synuclein (αS) aggregates in brains of individuals with Parkinson\u27s disease and dementia with Lewy bodies can spread in a prion-like manner. Although the initial αS nuclei are pivotal in determining αS fibril polymorphs and resulting phenotypes, it is not clear how the initial fibril seeds are generated. Previous studies have shown that αS truncation might have an important role in αS aggregation. However, little is known about how this truncation influences αS\u27s propagation properties. In the present study, we generated αS fibrils from a series of truncated human αS constructs, characterized their structures and conformational stabilities, and investigated their ability to convert the conformation of full-length αS in vitro, in cultured cells, and in WT mice. We show that both C- and N-terminal truncations of human αS induce fibril polymorphs and exhibit different cross-seeding activities. N-terminally 10- or 30-residue–truncated human αS fibrils induced more abundant αS pathologies than WT fibrils in mice, whereas other truncated fibrils induced less abundant pathologies. Biochemical analyses of these truncated fibrils revealed that N-terminal 10- or 30-residue truncations of human αS change the fibril conformation in a manner that increases their structural compatibility with WT mouse αS fibrils and reduces their stability. C-terminally 20-residue–truncated fibrils displayed enhanced seeding activity in vitro. Our findings imply that truncation of αS can influence its prion-like pathogenicity, resulting in phenotypic diversity of α-synucleinopathies

Revised Structure of Cercidinin A, a Novel Ellagitannin Having (R)-Hexahydroxydiphenoyl Esters at the 3, 4-Positions of Glucopyranose

The structue of cercidinin A, an ellagitannin isolated from the bark of Cercidiphyllum japonicum, was revised to 1, 2, 6-tri-O-galloyl-3, 4-(R)-hexahydroxydipenoyl-β-D-glucose by two-dimensional NMR spectral analysis. Cercidinin A represents the first ellagitannin possessing a hexahydroxydiphenoyl group at the 3, 4-positions of a modified 4C1-glucopyranose core

RIM1 confers sustained activity and neurotransmitter vesicle anchoring to presynaptic Ca2+ channels.

International audienceThe molecular organization of presynaptic active zones is important for the neurotransmitter release that is triggered by depolarization-induced Ca2+ influx. Here, we demonstrate a previously unknown interaction between two components of the presynaptic active zone, RIM1 and voltage-dependent Ca2+ channels (VDCCs), that controls neurotransmitter release in mammalian neurons. RIM1 associated with VDCC beta-subunits via its C terminus to markedly suppress voltage-dependent inactivation among different neuronal VDCCs. Consistently, in pheochromocytoma neuroendocrine PC12 cells, acetylcholine release was significantly potentiated by the full-length and C-terminal RIM1 constructs, but membrane docking of vesicles was enhanced only by the full-length RIM1. The beta construct beta-AID dominant negative, which disrupts the RIM1-beta association, accelerated the inactivation of native VDCC currents, suppressed vesicle docking and acetylcholine release in PC12 cells, and inhibited glutamate release in cultured cerebellar neurons. Thus, RIM1 association with beta in the presynaptic active zone supports release via two distinct mechanisms: sustaining Ca2+ influx through inhibition of channel inactivation, and anchoring neurotransmitter-containing vesicles in the vicinity of VDCCs

Parkinson’s disease-associated iPLA2-VIA/PLA2G6 regulates neuronal functions and α-synuclein stability through membrane remodeling

Mutations in the iPLA2-VIA/PLA2G6 gene are responsible for PARK14-linked Parkinson’s disease (PD) with α-synucleinopathy. However, it is unclear how iPLA2-VIA mutations lead to α-synuclein (α-Syn) aggregation and dopaminergic (DA) neurodegeneration. Here, we report that iPLA2-VIA–deficient Drosophila exhibits defects in neurotransmission during early developmental stages and progressive cell loss throughout the brain, including degeneration of the DA neurons. Lipid analysis of brain tissues reveals that the acyl-chain length of phospholipids is shortened by iPLA2-VIA loss, which causes endoplasmic reticulum (ER) stress through membrane lipid disequilibrium. The introduction of wild-type human iPLA2-VIA or the mitochondria–ER contact site-resident protein C19orf12 in iPLA2-VIA–deficient flies rescues the phenotypes associated with altered lipid composition, ER stress, and DA neurodegeneration, whereas the introduction of a disease-associated missense mutant, iPLA2-VIA A80T, fails to suppress these phenotypes. The acceleration of α-Syn aggregation by iPLA2-VIA loss is suppressed by the administration of linoleic acid, correcting the brain lipid composition. Our findings suggest that membrane remodeling by iPLA2-VIA is required for the survival of DA neurons and α-Syn stability