Rydberg-State-Resolved Resonant Energy Transfer in Cold Electric-Field-Controlled Intrabeam Collisions of NH3 with Rydberg He Atoms

The resonant transfer of energy from the inversion sublevels in NH3 to He atoms in triplet Rydberg states with principal quantum number n = 38 has been controlled using electric fields below 15 V/cm in intrabeam collisions at translational temperatures of ∼1 K. The experiments were performed in pulsed supersonic beams of NH3 seeded in He at a ratio of 1:19. The He atoms were prepared in the metastable 1s2s 3S1 level in a pulsed electric discharge in the trailing part of the beams. The velocity slip between the heavy NH3 and the lighter metastable He was exploited to perform collision studies at center-of-mass collision speeds of ∼70 m/s. Resonant energy transfer in the atom–molecule collisions was identified by Rydberg-state-selective electric-field ionization. The experimental data have been compared to a theoretical model of the resonant dipole–dipole interactions between the collision partners based on the impact parameter method

Rydberg-state ionization dynamics and tunnel ionization rates in strong electric fields

Tunnel ionization rates of triplet Rydberg states in helium with principal quantum numbers close to 37 have been measured in electric fields at the classical ionization threshold of ∼ 197 V/cm. The measurements were performed in the time domain by combining high-resolution continuous-wave laser photoexcitation and pulsed electric field ionization. The observed tunnel ionization rates range from 10 5 to 10 7 s − 1 and have, together with the measured atomic energy-level structure in the corresponding electric fields, been compared to the results of calculations of the eigenvalues of the Hamiltonian matrix describing the atoms in the presence of the fields to which complex absorbing potentials have been introduced. The comparison of the measured tunnel ionization rates with the results of these, and additional calculations for hydrogenlike Rydberg states performed using semiempirical methods, have allowed the accuracy of these methods of calculation to be tested. For the particular eigenstates studied the measured ionization rates are ∼ 5 times larger than those obtained from semiempirical expression

Control of Gene Expression by the Retinoic Acid-Related Orphan Receptor Alpha in HepG2 Human Hepatoma Cells

Retinoic acid-related Orphan Receptor alpha (RORα; NR1F1) is a widely distributed nuclear receptor involved in several (patho)physiological functions including lipid metabolism, inflammation, angiogenesis, and circadian rhythm. To better understand the role of this nuclear receptor in liver, we aimed at displaying genes controlled by RORα in liver cells by generating HepG2 human hepatoma cells stably over-expressing RORα. Genes whose expression was altered in these cells versus control cells were displayed using micro-arrays followed by qRT-PCR analysis. Expression of these genes was also altered in cells in which RORα was transiently over-expressed after adenoviral infection. A number of the genes found were involved in known pathways controlled by RORα, for instance LPA, NR1D2 and ADIPOQ in lipid metabolism, ADIPOQ and PLG in inflammation, PLG in fibrinolysis and NR1D2 and NR1D1 in circadian rhythm. This study also revealed that genes such as G6PC, involved in glucose homeostasis, and AGRP, involved in the control of body weight, are also controlled by RORα. Lastly, SPARC, involved in cell growth and adhesion, and associated with liver carcinogenesis, was up-regulated by RORα. SPARC was found to be a new putative RORα target gene since it possesses, in its promoter, a functional RORE as evidenced by EMSAs and transfection experiments. Most of the other genes that we found regulated by RORα also contained putative ROREs in their regulatory regions. Chromatin immunoprecipitation (ChIP) confirmed that the ROREs present in the SPARC, PLG, G6PC, NR1D2 and AGRP genes were occupied by RORα in HepG2 cells. Therefore these genes must now be considered as direct RORα targets. Our results open new routes on the roles of RORα in glucose metabolism and carcinogenesis within cells of hepatic origin

Differential transcription of the orphan receptor ROR beta in nuclear extracts derived from Neuro2A and HeLa cells

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Differential binding and transcriptional behaviour of two highly related orphan receptors, ROR alpha(4) and ROR beta(1)

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