Measurement of the electron transmission rate of the gating foil for the TPC of the ILC experiment

We have developed a gating foil for the time projection chamber envisaged as a central tracker for the international linear collider experiment. It has a structure similar to the Gas Electron Multiplier (GEM) with a higher optical aperture ratio and functions as an ion gate without gas amplification. The transmission rate for electrons was measured in a counting mode for a wide range of the voltages applied across the foil using an $^{55}$Fe source and a laser in the absence of a magnetic field. The blocking power of the foil against positive ions was estimated from the electron transmissions.Comment: 25 pages containing 14 figures and 1 tabl

First-principles study of a tilt grain-boundary in rutile

[[abstract]]The atomic and electronic structure of a tilt grain boundary in rutile TiO2 has been calculated in an ab initio manner. The method employs a plane-wave basis set and optimized pseudopotentials and is carried out within the local-density approximation of density-functional theory. The study focuses on the structure and energy of the ∑=15 36.9° (210)[001] tilt boundary, which is relaxed to equilibrium using a conjugate gradients iterative minimization technique. The calculations confirm the stability of a proposed atomic model for the boundary and provide some insight into its electronic structure.[[incitationindex]]SCI[[booktype]]紙本[[booktype]]電子

Phytochemistry and in vitro Anti-sickling activity of Senna Occidentalis L. (Fabaceae)

Introduction Sickle cell disease is an inherited genetic disorder characterized by the presence of abnormal hemoglobin, leading to the deformation of red blood cells and serious complications. It is a major public health problem in many countries of inter-tropical Africa. In the Democratic Republic of the Congo, over a million people (2%) are affected by this hemoglobinopathy. Purpose This study aimed to scientifically validate the anti-sickle cell activity of aqueous extracts of S. occindentalis seeds and to identify the chemical constituents responsible for this activity. Methods In this study, we used S. occidentalis seeds harvested at Ilebo in Central Kasai Province, while the blood samples used were taken from sickle-cell patients. The phytochemical composition was determined according to the standard method described previously by Iteku et al. and Nkasa et al. The Emmel test was carried out according to the standard protocol described previously by Bongo et al. Results The results obtained in this study showed that the seeds of this plant are rich in secondary metabolites such as total polyphenols (flavonoids, anthocyanins, leuco-athocyanins, tannins, and saponins), di-terpenes, alkaloids, and bound quinones. However, these seeds do not contain triterpenoids and steroids. Total seed extracts from this plant showed significant anti-sickle cell activity. Conclusion This study identified a medicinal plant used by the sickle cell disease community

Phosphodiesterase-III Inhibitor Prevents Hemorrhagic Transformation Induced by Focal Cerebral Ischemia in Mice Treated with tPA

The purpose of the present study was to investigate whether cilostazol, a phosphodiesterase-III inhibitor and antiplatelet drug, would prevent tPA-associated hemorrhagic transformation. Mice subjected to 6-h middle cerebral artery occlusion were treated with delayed tPA alone at 6 h, with combined tPA plus cilostazol at 6 h, or with vehicle at 6 h. We used multiple imaging (electron microscopy, spectroscopy), histological and neurobehavioral measures to assess the effects of the treatment at 18 h and 7 days after the reperfusion. To further investigate the mechanism of cilostazol to beneficial effect, we also performed an in vitro study with tPA and a phosphodiesterase-III inhibitor in human brain microvascular endothelial cells, pericytes, and astrocytes. Combination therapy with tPA plus cilostazol prevented development of hemorrhagic transformation, reduced brain edema, prevented endothelial injury via reduction MMP-9 activity, and prevented the blood-brain barrier opening by inhibiting decreased claudin-5 expression. These changes significantly reduced the morbidity and mortality at 18 h and 7 days after the reperfusion. Also, the administration of both drugs prevented injury to brain human endothelial cells and human brain pericytes. The present study indicates that a phosphodiesterase-III inhibitor prevents the hemorrhagic transformation induced by focal cerebral ischemia in mice treated with tPA

Guaranteed optimal reachability control of reaction-diffusion equations using one-sided Lipschitz constants and model reduction

We show that, for any spatially discretized system of reaction-diffusion, the approximate solution given by the explicit Euler time-discretization scheme converges to the exact time-continuous solution, provided that diffusion coefficient be sufficiently large. By "sufficiently large", we mean that the diffusion coefficient value makes the one-sided Lipschitz constant of the reaction-diffusion system negative. We apply this result to solve a finite horizon control problem for a 1D reaction-diffusion example. We also explain how to perform model reduction in order to improve the efficiency of the method

Suppression and Regression of Choroidal Neovascularization in Mice by a Novel CCR2 Antagonist, INCB3344

PURPOSE: To investigate the effect of an intravitreally administered CCR2 antagonist, INCB3344, on a mouse model of choroidal neovascularization (CNV). METHODS: CNV was induced by laser photocoagulation on Day 0 in wild type mice. INCB3344 or vehicle was administered intravitreally immediately after laser application. On Day 14, CNV areas were measured on retinal pigment epithelium (RPE)-choroid flat mounts and histopathologic examination was performed on 7 µm-thick sections. Macrophage infiltration was evaluated by immunohistochemistry on RPE-choroid flat mounts and quantified by flow cytometry on Day 3. Expression of vascular endothelial growth factor (VEGF) protein in RPE-choroid tissue was examined by immunohistochemistry and ELISA, VEGF mRNA in sorted macrophages in RPE-choroid tissue was examine by real-time PCR and expression of phosphorylated extracellular signal-regulated kinase (p-ERK 1/2) in RPE-choroid tissue was measured by Western blot analysis on Day 3. We also evaluated the efficacy of intravitreal INCB3344 to spontaneous CNV detected in Cu, Zn-superoxide dismutase (SOD1) deficient mice. Changes in CNV size were assessed between pre- and 1week post-INCB3344 or vehicle administration in fundus photography and fluorescence angiography (FA). RESULTS: The mean CNV area in INCB3344-treated mice decreased by 42.4% compared with the vehicle-treated control mice (p<0.001). INCB3344 treatment significantly inhibited macrophage infiltration into the laser-irradiated area (p<0.001), and suppressed the expression of VEGF protein (p = 0.012), VEGF mRNA in infiltrating macrophages (p<0.001) and the phosphorylation of ERK1/2 (p<0.001). The area of spontaneous CNV in Sod1⁻/⁻ mice regressed by 70.35% in INCB3344-treated animals while no change was detected in vehicle-treated control mice (p<0.001). CONCLUSIONS: INCB3344 both inhibits newly forming CNV and regresses established CNV. Controlling inflammation by suppressing macrophage infiltration and angiogenic ability via the CCR-2/MCP-1 signal may be a useful therapeutic strategy for treating CNV associated with age-related macular degeneration

Morphological and Functional Changes in the Retina after Chronic Oxygen-Induced Retinopathy

The mouse model of oxygen-induced retinopathy (OIR) has been widely used for studies of retinopathy of prematurity (ROP). This disorder, characterized by abnormal vascularization of the retina, tends to occur in low birth weight neonates after exposure to high supplemental oxygen. Currently, the incidence of ROP is increasing because of increased survival of these infants due to medical progress. However, little is known about changes in the chronic phase after ROP. Therefore, in this study, we examined morphological and functional changes in the retina using a chronic OIR model. Both the a- and b-waves in the OIR model recovered in a time-dependent manner at 4 weeks (w), 6 w, and 8 w, but the oscillatory potential (OP) amplitudes remained depressed following a return to normoxic conditions. Furthermore, decrease in the thicknesses of the inner plexiform layer (IPL) and inner nuclear layer (INL) at postnatal day (P) 17, 4 w, and 8 w and hyperpermeability of blood vessels were observed in conjunction with the decrease in the expression of claudin-5 and occludin at 8 w. The chronic OIR model revealed the following: (1) a decrease in OP amplitudes, (2) morphological abnormalities in the retinal cells (limited to the IPL and INL) and blood vessels, and (3) an increase in retinal vascular permeability via the impairment of the tight junction proteins. These findings suggest that the experimental animal model used in this study is suitable for elucidating the pathogenesis of ROP and may lead to the development of potential therapeutic agents for ROP treatment

Prevention of Apoptosis by Mitochondrial Phosphatase PGAM5 in the Mushroom Body Is Crucial for Heat Shock Resistance in Drosophila melanogaster

The heat shock (HS) response is essential for survival of all organisms. Although the machinery of the HS response has been extensively investigated at the cellular level, it is poorly understood at the level of the organism. Here, we show the crucial role of the mushroom body (MB) in the HS response in Drosophila. Null mutants of the mitochondrial phosphatase Drosophila PGAM5 (dPGAM5) exhibited increased vulnerability to HS, which was reversed by MB-specific expression of the caspase inhibitor p35, and similar vulnerability was induced in wild-type flies by knockdown of MB dPGAM5. Elimination of the MB did not affect the HS response of wild-type flies, but did increase the resistance of dPGAM5-deficient flies to HS. Thus, the MB may possess an apoptosis-dependent toxic function, the suppression of which by dPGAM5 appears to be crucial for HS resistance