| 1. |
- Aktas, A, et al.
(författare)
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Inclusive production of D+, D-0, D-s(+) and D*(+) mesons in deep inelastic scattering at HERA
- 2005
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Ingår i: European Physical Journal C. Particles and Fields. - : Springer Science and Business Media LLC. - 1434-6044. ; 38:4, s. 447-459
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Tidskriftsartikel (refereegranskat)abstract
- Inclusive production cross sections are measured in deep inelastic scattering at HERA for meson states composed of a charm quark and a light antiquark or the charge conjugate. The measurements cover the kinematic region of photon virtuality 2 < Q(2) < 100 GeV2, inelasticity 0.05 < y < 0.7, D meson transverse momenta p(t)( D) greater than or equal to 2.5 GeV and pseudorapidity |eta( D)| less than or equal to 1.5. The identification of the D-meson decays and the reduction of the combinatorial background profit from the reconstruction of displaced secondary vertices by means of the H1 silicon vertex detector. The production of charmed mesons containing the light quarks u, d and s is found to be compatible with a description in which the hard scattering is followed by a factorisable and universal hadronisation process.
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| 2. |
- Soriano, S, et al.
(författare)
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Rapid regulation of K(ATP) channel activity by 17{beta}-estradiol in pancreatic {beta}-cells involves the estrogen receptor {beta} and the atrial natriuretic peptide receptor
- 2009
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Ingår i: Molecular endocrinology (Baltimore, Md.). - : The Endocrine Society. - 1944-9917 .- 0888-8809. ; 23:12, s. 1973-1982
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Tidskriftsartikel (refereegranskat)abstract
- The ATP-sensitive potassium (KATP) channel is a key molecule involved in glucose-stimulated insulin secretion. The activity of this channel regulates β-cell membrane potential, glucose- induced [Ca2+]i signals, and insulin release. In this study, the rapid effect of physiological concentrations of 17β-estradiol (E2) on KATP channel activity was studied in intact β-cells by use of the patch-clamp technique. When cells from wild-type (WT) mice were used, 1 nm E2 rapidly reduced KATP channel activity by 60%. The action of E2 on KATP channel was not modified in β-cells from ERα−/− mice, yet it was significantly reduced in cells from ERβ−/− mice. The effect of E2 was mimicked by the ERβ agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN). Activation of ERβ by DPN enhanced glucose-induced Ca2+ signals and insulin release. Previous evidence indicated that the acute inhibitory effects of E2 on KATP channel activity involve cyclic GMP and cyclic GMP-dependent protein kinase. In this study, we used β-cells from mice with genetic ablation of the membrane guanylate cyclase A receptor for atrial natriuretic peptide (also called the atrial natriuretic peptide receptor) (GC-A KO mice) to demonstrate the involvement of this membrane receptor in the rapid E2 actions triggered in β-cells. E2 rapidly inhibited KATP channel activity and enhanced insulin release in islets from WT mice but not in islets from GC-A KO mice. In addition, DPN reduced KATP channel activity in β-cells from WT mice, but not in β-cells from GC-A KO mice. This work unveils a new role for ERβ as an insulinotropic molecule that may have important physiological and pharmacological implications.
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