| 1. |
- Ablikim, M., et al.
(författare)
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Measurements of (XcJ)-> K+K-K+K- decays
- 2006
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Ingår i: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 642:3, s. 197-202
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Tidskriftsartikel (refereegranskat)abstract
- Using 14M psi(2S) events taken with the BESII detector, chi(cJ) -> 2(K+K-) decays are studied. For the four-kaon final state, the branching fractions are B(chi(c0,1,2) ->.2(K+K-)) = (3.48 +/- 0.23 +/- 0.47) x 10(-3), (0.70 +/- 0.13 +/- 0.10) x 10(-3), and (2.17 +/- 0.20 +/- 0.31) x 10(-3). For the phi K+K- final state, the branching fractions, which are measured for the first time, are B(chi(c0,1,2) -> phi K+K-) = (1.03 +/- 0.22 +/- 0.15) x 10(-3), (0.46 +/- 0.16 +/- 0.06) x 10(-3), and (1.67 +/- 0.26 +/- 0.24) x 10(-4). For the phi phi final state, B(chi(c0,2) -> phi phi) = (0.94 +/- 0.21 +/- 0.13) x 10(-3) and (1.70 +/- 0.30 +/- 0.25) x 10(-3).
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| 2. |
- Schael, S, et al.
(författare)
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Precision electroweak measurements on the Z resonance
- 2006
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Ingår i: Physics Reports. - : Elsevier BV. - 0370-1573 .- 1873-6270. ; 427:5-6, s. 257-454
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Forskningsöversikt (refereegranskat)abstract
- We report on the final electroweak measurements performed with data taken at the Z resonance by the experiments operating at the electron-positron colliders SLC and LEP. The data consist of 17 million Z decays accumulated by the ALEPH, DELPHI, L3 and OPAL experiments at LEP, and 600 thousand Z decays by the SLID experiment using a polarised beam at SLC. The measurements include cross-sections, forward-backward asymmetries and polarised asymmetries. The mass and width of the Z boson, m(Z) and Gamma(Z), and its couplings to fermions, for example the p parameter and the effective electroweak mixing angle for leptons, are precisely measured: m(Z) = 91.1875 +/- 0.0021 GeV, Gamma(Z) = 2.4952 +/- 0.0023 GeV, rho(l) = 1.0050 +/- 0.0010, sin(2)theta(eff)(lept) = 0.23153 +/- 0.00016. The number of light neutrino species is determined to be 2.9840 +/- 0.0082, in agreement with the three observed generations of fundamental fermions. The results are compared to the predictions of the Standard Model (SM). At the Z-pole, electroweak radiative corrections beyond the running of the QED and QCD coupling constants are observed with a significance of five standard deviations, and in agreement with the Standard Model. Of the many Z-pole measurements, the forward-backward asymmetry in b-quark production shows the largest difference with respect to its SM expectation, at the level of 2.8 standard deviations. Through radiative corrections evaluated in the framework of the Standard Model, the Z-pole data are also used to predict the mass of the top quark, m(t) = 173(+10)(+13) GeV, and the mass of the W boson, m(W) = 80.363 +/- 0.032 GeV. These indirect constraints are compared to the direct measurements, providing a stringent test of the SM. Using in addition the direct measurements of m(t) and m(W), the mass of the as yet unobserved SM Higgs boson is predicted with a relative uncertainty of about 50% and found to be less than 285 GeV at 95% confidence level. (c) 2006 Elsevier B.V. All rights reserved.
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| 3. |
- Cao, Yong-Xiao, et al.
(författare)
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Ligustilide induces vasodilatation via inhibiting voltage dependent calcium channel and receptor-mediated Ca(2+) influx and release.
- 2006
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Ingår i: Vascular Pharmacology. - : Elsevier BV. - 1537-1891. ; 45:3, s. 171-176
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of the present study was to investigate the effect of ligustilide on vasodilatation in rat mesenteric artery and the mechanisms responsible for it. Isometric tension of rat mesenteric artery rings was recorded by a sensitive myograph system in vitro. The results showed that ligustilide at concentrations more than 10 mu M relaxed potassium chloride (KCl)-preconstricted rat mesenteric artery in a con centration-dependent manner. The vasodilatation effect of ligustilide was not dependent on endothelium. Ligustilide rightwards shifted concentration-response curves induced by KCl, calcium chloride (CaCl2), noradrenaline (NA) or 5-hydroxytryptamine (5-HT) in a non-parallel manner. This suggests that the vasodilatation effects were most likely via voltage-dependent calcium channel (VDCC) and receptor-operated calcium channel (ROCC). Propranolol, glibenclamide, tetraethylammonium and barium chloride did not affect the vasodilation induced by ligustilide, showing that beta-adrenoceptor, ATP sensitive potassium channel, calcium-activated potassium channel and inwardly rectifying potassium channel were not involved in the vasodilatation. Ligustilide concentration-dependently inhibited the vasoconstriction induced by NA or CaCl2 in Ca2+-free medium, indicating that the vasodilatation relates to inhibition of extracellular Ca2+ influx through VDCC and ROCC, and intracellular Ca2+ release from Ca2+ store. Since caffeine-induced contraction was inhibited by ligustilide, inhibition of intracellular Ca2+ released by ligustilide occurred via the ryanodine receptors. Our results suggest that ligustilide induces vasodilatation in rat mesenteric artery by inhibiting the VDCC and ROCC, and receptor-mediated Ca2+ influx and release. (c) 2006 Elsevier Inc. All rights reserved.
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| 4. |
- He, X, et al.
(författare)
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Short-term administration of ACTH improves plasma lipid profile and renal function in kidney transplant patients
- 2006
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Ingår i: Transplantation Proceedings. - : Elsevier BV. - 0041-1345. ; 38:5, s. 1371-1374
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Tidskriftsartikel (refereegranskat)abstract
- The present study investigated effects of short-term administration of adrenocorticotrophic hormone (ACTH) on blood lipid profile and renal function in kidney transplant patients. Six patients who had kidney transplantations 2 to 10 years earlier received ACTH intramuscularly (1 mg/d) for 4 days. We analyzed serum levels of lipids, lipoproteins, apolipoproteins, blood creatinine, and other parameters. Short-term ACTH treatment significantly decreased serum apolipoprotein B and apolipoprotein AI, whereas it significantly increased plasma high-density lipoproteins (HDL). Interestingly, creatinine level moderately decreased and creatinine clearances moderately increased among five of six patients. Hepatic function and serum concentration of cyclosporine did not change. There were no serious side effects during ACTH treatment. It was concluded that ACTH treatment had beneficial effects on serum lipoprotein profile, potentially improving renal function in kidney transplant patients. Further observations are needed to confirm these effects.
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| 5. |
- Xu, X., et al.
(författare)
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Effects of Ischemia-Reperfusion Injury on Apolipoprotein M Expression in the Liver
- 2006
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Ingår i: Transplantation Proceedings. - : Elsevier BV. - 0041-1345. ; 38:9, s. 2769-2773
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Tidskriftsartikel (refereegranskat)abstract
- The present study investigated the expression pattern of apolipoprotein M (apoM) mRNA in a rat model of hepatic ischemia-reperfusion injury (IRI). Animals were ischemic for I hour followed by various reperfusion times. As expected, serum alanine aminotransferase levels were significantly increased under IRI, which indicated the severity of liver injury. Hepatic mRNA levels of HSP70, which is the most common characterized protein within the family of heat-shock proteins (HSP), were significantly increased after 0.5 to 3 hours of IRI. Plasma Greactive protein, high-density lipoprotein-cholesterol, and lipoprotein (a) levels were significantly increased after 1-hour ischemia followed by 0.5 to 3 hours of reperfusion. Interestingly, similar to HSP70, apoM mRNA levels in the liver were gradually increased after 0.5 to 3 hours of IRI, whereas it returned to a lower level after 6 or 24 hours of IRI, which indicated that hepatic apoM expression was significantly influenced by the acute phase of IRI. However, plasma apoM levels were not increased in parallel, even slightly decreasing after 0.5 or I hour of IRI. We concluded that apoM mRNA expression pattern, like HSP70, in the liver showed rapid, significant changes during hepatic local IRI.
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| 6. |
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| 7. |
- Cao, YX, et al.
(författare)
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Induces vasodilatation of rat mesenteric artery in vitro mainly by inhibiting receptor-mediated Ca2+-influx and Ca2+-release
- 2005
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Ingår i: Archives of Pharmacal Research. - 1976-3786. ; 28:6, s. 709-715
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1 mu M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the alpha(1)-adrenoreceptor. The beta-adrenoreceptor and ATIP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and CaCl2 in Ca2+-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular Ca2+ influx through the receptor-operated calcium channels and intracellular Ca2+ release from the Ca (2+) store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular Ca2+ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated Ca2+-influx and Ca2+-release, and partly from the endothelium mediated by EDHF.
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| 8. |
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| 9. |
- Chen, Kang, et al.
(författare)
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Immunoglobulin D enhances immune surveillance by activating antimicrobial, proinflammatory and B cell-stimulating programs in basophils
- 2009
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Ingår i: Nature Immunology. - : Springer Science and Business Media LLC. - 1529-2908 .- 1529-2916. ; 10:8, s. 121-889
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Tidskriftsartikel (refereegranskat)abstract
- Immunoglobulin D (IgD) is an enigmatic antibody isotype that mature B cells express together with IgM through alternative RNA splicing. Here we report active T cell-dependent and T cell-independent IgM-to-IgD class switching in B cells of the human upper respiratory mucosa. This process required activation-induced cytidine deaminase (AID) and generated local and circulating IgD-producing plasmablasts reactive to respiratory bacteria. Circulating IgD bound to basophils through a calcium-mobilizing receptor that induced antimicrobial, opsonizing, inflammatory and B cell-stimulating factors, including cathelicidin, interleukin 1 (IL-1), IL-4 and B cell-activating factor (BAFF), after IgD crosslinking. By showing dysregulation of IgD class-switched B cells and 'IgD-armed' basophils in autoinflammatory syndromes with periodic fever, our data indicate that IgD orchestrates an ancestral surveillance system at the interface between immunity and inflammation.
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| 10. |
- Ding, Ling, et al.
(författare)
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Effects of brominated flame retardants and brominated dioxins on steroidogenesis in H295R human adrenocortical carcinoma cell line
- 2007
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Ingår i: Environmental Toxicology and Chemistry. - : Society of Environmental Toxicology and Chemistry (SETAC). - 0730-7268 .- 1552-8618. ; 26:4, s. 764-772
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Tidskriftsartikel (refereegranskat)abstract
- Brominated flame retardants (BFRs) and brominated dioxins are emerging persistent organic pollutants that are ubiquitous in the environment and can be accumulated by wildlife and humans. These chemicals can disturb endocrine function. Recent studies have demonstrated that one of the mechanisms of endocrine disruption by chemicals is modulation of steroidogenic gene expression or enzyme activities. In this study, an in vitro assay based on the H295R human adrenocortical carcinoma cell line, which possesses most key genes or enzymes involved in steroidogenesis, was used to examine the effects of five bromophenols, two polybrominated biphenyls (PBBs 77 and 169), 2,3,7,8-tetrabromodibenzo-p-dioxin, and 2,3,7,8-tetrabromodibenzofuran on the expression of 10 key steroidogenic genes. The H295R cells were exposed to various BFR concentrations for 48 h, and the expression of specific genes - cytochrome P450 (CYP11A, CYP11B2, CYP17, CYP19, and CYP21), 3β- hydroxysteroid dehydrogenase (3βHSD2), 17β-hydroxysteroid dehydrogenase (17βHSD1 and 17βHSD4), steroidogenic acute regulatory protein (StAR), and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) - was quantitatively measured using real-time polymerase chain reaction. Cell viability was not affected at the doses tested. Most of the genes were either up- or down-regulated, to some extent, by BFR exposure. Among the genes tested, 3βHSD2 was the most markedly up-regulated, with a range of magnitude from 1.6- to 20-fold. The results demonstrate that bromophenol, bromobiphenyls, and bromodibenzo-p-dioxin/furan are able to modulate steroidogenic gene expression, which may lead to endocrine disruption.
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