134 research outputs found

    First Measurements of eta_c Decaying into K^+K^-2(pi^+pi^-) and 3(pi^+pi^-)

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    The decays of eta_c to K^+K^-2(pi^+pi^-) and 3(pi^+pi^-) are observed for the first time using a sample of 5.8X10^7 J/\psi events collected by the BESII detector. The product branching fractions are determined to be B(J/\psi-->gamma eta_c)*B(eta_c-->K^+K^-pi^+pi^-pi^+pi^-)=(1.21+-0.32+- 0.23)X10^{-4},B(J/Οˆβˆ’βˆ’>gammaetac)βˆ—B(etacβˆ’βˆ’>Kβˆ—0KΛ‰βˆ—0pi+piβˆ’)=(1.29+βˆ’0.43+βˆ’0.32)X10βˆ’4,B(J/\psi-->gamma eta_c)*B(eta_c-->K^{*0}\bar{K}^{*0}pi^+pi^-)= (1.29+-0.43+-0.32)X10^{-4}, and (J/\psi-->gamma eta_c)* B(eta_c-->pi^+pi^-pi^+pi^-pi^+pi^-)= (2.59+-0.32+-0.48)X10^{-4}. The upper limit for eta_c-->phi pi^+pi^-pi^+pi^- is also obtained as B(J/\psi-->gamma eta_c)*B(eta_c--> phi pi^+pi^-pi^+pi^-)< 6.03 X10^{-5} at the 90% confidence level.Comment: 11 pages, 4 figure

    Resonances in J/Οˆβ†’Ο•Ο€+Ο€βˆ’J/\psi \to \phi \pi ^+\pi ^- and Ο•K+Kβˆ’\phi K^+K^-

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    A partial wave analysis is presented of J/Οˆβ†’Ο•Ο€+Ο€βˆ’J/\psi \to \phi \pi ^+\pi ^- and Ο•K+Kβˆ’\phi K^+K^- from a sample of 58M J/ψJ/\psi events in the BES II detector. The f0(980)f_0(980) is observed clearly in both sets of data, and parameters of the Flatt\' e formula are determined accurately: M=965Β±8M = 965 \pm 8 (stat) Β±6\pm 6 (syst) MeV/c2^2, g1=165Β±10Β±15g_1 = 165 \pm 10 \pm 15 MeV/c2^2, g2/g1=4.21Β±0.25Β±0.21g_2/g_1 = 4.21 \pm 0.25 \pm 0.21. The ϕππ\phi \pi \pi data also exhibit a strong ππ\pi \pi peak centred at M=1335M = 1335 MeV/c2^2. It may be fitted with f2(1270)f_2(1270) and a dominant 0+0^+ signal made from f0(1370)f_0(1370) interfering with a smaller f0(1500)f_0(1500) component. There is evidence that the f0(1370)f_0(1370) signal is resonant, from interference with f2(1270)f_2(1270). There is also a state in ππ\pi \pi with M=1790βˆ’30+40M = 1790 ^{+40}_{-30} MeV/c2^2 and Ξ“=270βˆ’30+60\Gamma = 270 ^{+60}_{-30} MeV/c2^2; spin 0 is preferred over spin 2. This state, f0(1790)f_0(1790), is distinct from f0(1710)f_0(1710). The Ο•KKΛ‰\phi K\bar K data contain a strong peak due to f2β€²(1525)f_2'(1525). A shoulder on its upper side may be fitted by interference between f0(1500)f_0(1500) and f0(1710)f_0(1710).Comment: 17 pages, 6 figures, 1 table. Submitted to Phys. Lett.

    Simple Metals at High Pressure

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    In this lecture we review high-pressure phase transition sequences exhibited by simple elements, looking at the examples of the main group I, II, IV, V, and VI elements. General trends are established by analyzing the changes in coordination number on compression. Experimentally found phase transitions and crystal structures are discussed with a brief description of the present theoretical picture.Comment: 22 pages, 4 figures, lecture notes for the lecture given at the Erice course on High-Pressure Crystallography in June 2009, Sicily, Ital

    Wall-thickness-dependent strength of nanotubular ZnO

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    We fabricate nanotubular ZnO with wall thickness of 45, 92, 123 nm using nanoporous gold (np-Au) with ligament diameter at necks of 1.43 mu m as sacrificial template. Through micro-tensile and micro-compressive testing of nanotubular ZnO structures, we find that the exponent m in (sigma) over bar proportional to (rho) over bar (m), where (sigma) over bar is the relative strength and (rho) over bar is the relative density, for tension is 1.09 and for compression is 0.63. Both exponents are lower than the value of 1.5 in the Gibson-Ashby model that describes the relation between relative strength and relative density where the strength of constituent material is independent of external size, which indicates that strength of constituent ZnO increases as wall thickness decreases. We find, based on hole-nanoindentation and glazing incidence X-ray diffraction, that this wall-thickness-dependent strength of nanotubular ZnO is not caused by strengthening of constituent ZnO by size reduction at the nanoscale. Finite element analysis suggests that the wall-thickness-dependent strength of nanotubular ZnO originates from nanotubular structures formed on ligaments of np-Au

    Evolution of Plant Nucleotide-Sugar Interconversion Enzymes

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    Nucleotide-diphospho-sugars (NDP-sugars) are the building blocks of diverse polysaccharides and glycoconjugates in all organisms. In plants, 11 families of NDP-sugar interconversion enzymes (NSEs) have been identified, each of which interconverts one NDP-sugar to another. While the functions of these enzyme families have been characterized in various plants, very little is known about their evolution and origin. Our phylogenetic analyses indicate that all the 11 plant NSE families are distantly related and most of them originated from different progenitor genes, which have already diverged in ancient prokaryotes. For instance, all NSE families are found in the lower land plant mosses and most of them are also found in aquatic algae, implicating that they have already evolved to be capable of synthesizing all the 11 different NDP-sugars. Particularly interesting is that the evolution of RHM (UDP-L-rhamnose synthase) manifests the fusion of genes of three enzymatic activities in early eukaryotes in a rather intriguing manner. The plant NRS/ER (nucleotide-rhamnose synthase/epimerase-reductase), on the other hand, evolved much later from the ancient plant RHMs through losing the N-terminal domain. Based on these findings, an evolutionary model is proposed to explain the origin and evolution of different NSE families. For instance, the UGlcAE (UDP-D-glucuronic acid 4-epimerase) family is suggested to have evolved from some chlamydial bacteria. Our data also show considerably higher sequence diversity among NSE-like genes in modern prokaryotes, consistent with the higher sugar diversity found in prokaryotes. All the NSE families are widely found in plants and algae containing carbohydrate-rich cell walls, while sporadically found in animals, fungi and other eukaryotes, which do not have or have cell walls with distinct compositions. Results of this study were shown to be highly useful for identifying unknown genes for further experimental characterization to determine their functions in the synthesis of diverse glycosylated molecules

    General Anesthetics Inhibit Erythropoietin Induction under Hypoxic Conditions in the Mouse Brain

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    Background: Erythropoietin (EPO), originally identified as a hematopoietic growth factor produced in the kidney and fetal liver, is also endogenously expressed in the central nervous system (CNS). EPO in the CNS, mainly produced in astrocytes, is induced under hypoxic conditions in a hypoxia-inducible factor (HIF)-dependent manner and plays a dominant role in neuroprotection and neurogenesis. We investigated the effect of general anesthetics on EPO expression in the mouse brain and primary cultured astrocytes. Methodology/Principal Findings: BALB/c mice were exposed to 10 % oxygen with isoflurane at various concentrations (0.10–1.0%). Expression of EPO mRNA in the brain was studied, and the effects of sevoflurane, halothane, nitrous oxide, pentobarbital, ketamine, and propofol were investigated. In addition, expression of HIF-2a protein was studied by immunoblotting. Hypoxia-induced EPO mRNA expression in the brain was significantly suppressed by isoflurane in a concentration-dependent manner. A similar effect was confirmed for all other general anesthetics. Hypoxia-inducible expression of HIF-2a protein was also significantly suppressed with isoflurane. In the experiments using primary cultured astrocytes, isoflurane, pentobarbital, and ketamine suppressed hypoxia-inducible expression of HIF-2a protein and EPO mRNA. Conclusions/Significance: Taken together, our results indicate that general anesthetics suppress activation of HIF-2 an

    Obervation of \chi_{cJ}--> omega omega decays

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    Decays of \chi_{c0,2}\ar\ww are observed for the first time using a sample of 14.0Γ—10614.0\times 10^6 ψ(2S)\psi(2S) events collected with the BESII detector. The branching ratios are determined to be {\cal B}(\chi_{c0}\ar \ww)=(2.29\pm 0.58\pm 0.41)\times 10^{-3} and {\cal B}(\chi_{c2}\ar\ww)=(1.77\pm 0.47\pm 0.36)\times 10^{-3}, where the first errors are statistical and the second systematic. The significances of the two signals are 4.4Οƒ4.4\sigma and 4.7Οƒ4.7\sigma, respectively.Comment: 6 pages, 6 figure

    Pressure-induced amorphous-to-amorphous configuration change in Ca-Al metallic glasses

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    Pressure-induced amorphous-to-amorphous configuration changes in Ca-Al metallic glasses (MGs) were studied by performing in-situ room-temperature high-pressure x-ray diffraction up to about 40β€…GPa. Changes in compressibility at about 18β€…GPa, 15.5β€…GPa and 7.5β€…GPa during compression are detected in Ca80Al20, Ca72.7Al27.3, and Ca66.4Al33.6 MGs, respectively, whereas no clear change has been detected in the Ca50Al50 MG. The transfer of s electrons into d orbitals under pressure, reported for the pressure-induced phase transformations in pure polycrystalline Ca, is suggested to explain the observation of an amorphous-to-amorphous configuration change in this Ca-Al MG system. Results presented here show that the pressure induced amorphous-to-amorphous configuration is not limited to f electron-containing MGs

    The prevalence of hyperuricemia in China: a meta-analysis

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    <p>Abstract</p> <p>Background</p> <p>The prevalence of hyperuricemia varied in different populations and it appeared to be increasing in the past decades. Recent studies suggest that hyperuricemia is an independent risk factor for cardiovascular disease. However, there has not yet been a systematic analysis of the prevalence of hyperuricemia in China.</p> <p>Methods</p> <p>Epidemiological investigations on hyperuricemia in China published in journals were identified manually and on-line by using CBMDISC, Chongqing VIP database and CNKI database. Those Reported in English journals were identified using MEDLINE database. Selected studies had to describe an original study defined by strict screening and diagnostic criteria. The fixed effects model or random effects model was employed according to statistical test for homogeneity.</p> <p>Results</p> <p>Fifty-nine studies were selected, the statistical information of which was collected for systematic analysis. The results showed that the pooled prevalence of hyperuricemia in male was 21.6% (95%CI: 18.9%-24.6%), but it was only 8.6% (95%CI: 8.2%-10.2%) in female. It was found that thirty years was the risk point age in male and it was fifty years in female.</p> <p>Conclusions</p> <p>The prevalence of hyperuricemia is different as the period of age and it increases after 30 years in male and 50 in female. Interventions are necessary to change the risk factors before the key age which is 30 years in male and 50 in female.</p
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