77 research outputs found

    Manipulating ionization path in a Stark map: Stringent schemes for the selective field ionization in highly excited Rb Rydberg atoms

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    We have developed a quite stringent method in selectivity to ionize the low angular- momentum (\ell) states which lie below and above the adjacent manifold in highly excited Rb Rydberg atoms. The method fully exploits the pulsed field-ionization characteristics of the manifold states in high slew-rate regime: Specifically the low \ell state below (above) the adjacent manifold is firstly transferred to the lowest (highest) state in the manifold via the adiabatic transition at the first avoided crossing in low slew-rate regime, and then the atoms are driven to a high electric field for ionization in high slew-rate regime. These extreme states of the manifold are ionized at quite different fields due to the tunneling process, resulting in thus the stringent selectivity. Two manipulation schemes to realize this method actually are demonstrated here experimentally.Comment: 10 pages, 4 figure

    Systematic observation of tunneling field-ionization in highly excited Rb Rydberg atoms

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    Pulsed field ionization of high-nn (90 n\leq n \leq 150) manifold states in Rb Rydberg atoms has been investigated in high slew-rate regime. Two peaks in the field ionization spectra were systematically observed for the investigated nn region, where the field values at the lower peak do not almost depend on the excitation energy in the manifold, while those at the higher peak increase with increasing excitation energy. The fraction of the higher peak component to the total ionization signals increases with increasing nn, exceeding 80% at nn = 147. Characteristic behavior of the peak component and the comparison with theoretical predictions indicate that the higher peak component is due to the tunneling process. The obtained results show for the first time that the tunneling process plays increasingly the dominant role at such highly excited nonhydrogenic Rydberg atoms.Comment: 8 pages, 5 figure

    Neutron Resonance Spectroscopy of 104Pd, 105Pd, and 110Pd

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    We have measured neutron resonances in the palladium isotopes 104, 105, and 110 for neutron energies from 1 to 2100 eV. Many new p-wave resonances have been observed. Their neutron widths and, in several cases, the radiative widths were measured. The average level spacings and the s-wave and p-wave neutron strength functions were determined. The time-of-flight method was used for both neutron total cross section measurements and total (n,γ) reaction yield measurements at the pulsed spallation neutron source of Los Alamos Neutron Science Center. Well established resonance spectroscopy for these isotopes is essential for the analysis of parity violation data that were recently measured in palladium

    Neutron Resonance Spectroscopy of 117Sn from1 eV to 1.5 keV

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    Parity violation has been studied recently for neutron resonances in 117Sn. The neutron resonance spectroscopy is essential for the analysis of the parity violation data. We have measured neutron resonances in 117Sn for neutron energies from 1 to 1500 eV using the time-of-flight method and the (n,γ) reaction. The sample was enriched to 87.6% 117Sn. Neutron scattering and radiative widths were determined, and orbital angular momentum assignments were made with a Bayesian analysis. The s-wave and p-wave strength functions and average level spacings were determined

    Parity Violation in Neutron Resonances of 117 Sn

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    Parity nonconservation (PNC) has been studied in neutron p-wave resonances of 117Sn. The longitudinal asymmetries were measured for 29 p-wave resonances in the neutron energy range 0.8 eV to 1100 eV. Statistically significant PNC effects were observed for four resonances. A statistical analysis determined the rms weak mixing matrix element and the weak spreading width. A weak spreading width of Γw=(0.28-0.15+0.56)×10-7 eV was obtained for117Sn

    Observation of a large parity nonconserving analyzing power in Xe

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    A large parity nonconserving longitudinal analyzing power was discovered in polarized-neutron transmission through Xe. An analyzing power of 4.3±0.2% was observed in a p-wave resonance at En=3.2 eV. The measurement was performed with a liquid Xe target of natural isotopic abundance that was placed in the polarized epithermal neutron beam, flight path 2, at the Manuel Lujan Neutron Science Center. This apparatus was constructed by the TRIPLE Collaboration, and has been used for studies of parity symmetry in compound nuclear resonances. Part of the motivation of the experiment was to discover a nucleus appropriate for a sensitive test of time-reversal invariance in polarized-neutron transmission. The large analyzing power of the observed resonance may make it possible to design a test of time reversal invariance using a polarized-Xe target

    Negative Autoregulation by Fas Stabilizes Adult Erythropoiesis and Accelerates Its Stress Response

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    Erythropoiesis maintains a stable hematocrit and tissue oxygenation in the basal state, while mounting a stress response that accelerates red cell production in anemia, blood loss or high altitude. Thus, tissue hypoxia increases secretion of the hormone erythropoietin (Epo), stimulating an increase in erythroid progenitors and erythropoietic rate. Several cell divisions must elapse, however, before Epo-responsive progenitors mature into red cells. This inherent delay is expected to reduce the stability of erythropoiesis and to slow its response to stress. Here we identify a mechanism that helps to offset these effects. We recently showed that splenic early erythroblasts, ‘EryA’, negatively regulate their own survival by co-expressing the death receptor Fas, and its ligand, FasL. Here we studied mice mutant for either Fas or FasL, bred onto an immune-deficient background, in order to avoid an autoimmune syndrome associated with Fas deficiency. Mutant mice had a higher hematocrit, lower serum Epo, and an increased number of splenic erythroid progenitors, suggesting that Fas negatively regulates erythropoiesis at the level of the whole animal. In addition, Fas-mediated autoregulation stabilizes the size of the splenic early erythroblast pool, since mutant mice had a significantly more variable EryA pool than matched control mice. Unexpectedly, in spite of the loss of a negative regulator, the expansion of EryA and ProE progenitors in response to high Epo in vivo, as well as the increase in erythropoietic rate in mice injected with Epo or placed in a hypoxic environment, lagged significantly in the mutant mice. This suggests that Fas-mediated autoregulation accelerates the erythropoietic response to stress. Therefore, Fas-mediated negative autoregulation within splenic erythropoietic tissue optimizes key dynamic features in the operation of the erythropoietic network as a whole, helping to maintain erythroid homeostasis in the basal state, while accelerating the stress response

    JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny

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    Background: It has been reported that the phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway regulates erythropoietin (EPO)-induced survival, proliferation, and maturation of early erythroid progenitors. Erythroid cell proliferation and survival have also been related to activation of the JAK-STAT pathway. The goal of this study was to observe the function of EPO activation of JAK-STAT and PI3K/AKT pathways in the development of erythroid progenitors from hematopoietic CD34(+) progenitor cells, as well as to distinguish early EPO target genes in human erythroid progenitors during ontogeny. Methods: Hematopoietic CD34(+) progenitor cells, isolated from fetal and adult hematopoietic tissues, were differentiated into erythroid progenitor cells. We have used microarray analysis to examine JAK-STAT and PI3K/AKT related genes, as well as broad gene expression modulation in these human erythroid progenitor cells. Results: In microarray studies, a total of 1755 genes were expressed in fetal liver, 3844 in cord blood, 1770 in adult bone marrow, and 1325 genes in peripheral blood-derived erythroid progenitor cells. The erythroid progenitor cells shared 1011 common genes. Using the Ingenuity Pathways Analysis software, we evaluated the network pathways of genes linked to hematological system development, cellular growth and proliferation. The KITLG, EPO, GATA1, PIM1 and STAT3 genes represent the major connection points in the hematological system development linked genes. Some JAK-STAT signaling pathway-linked genes were steadily upregulated throughout ontogeny (PIM1, SOCS2, MYC, PTPN11), while others were downregulated (PTPN6, PIAS, SPRED2). In addition, some JAK-STAT pathway related genes are differentially expressed only in some stages of ontogeny (STATs, GRB2, CREBB). Beside the continuously upregulated (AKT1, PPP2CA, CHUK, NFKB1) and downregulated (FOXO1, PDPK1, PIK3CG) genes in the PI3K-AKT signaling pathway, we also observed intermittently regulated gene expression (NFKBIA, YWHAH). Conclusions: This broad overview of gene expression in erythropoiesis revealed transcription factors differentially expressed in some stages of ontogenesis. Finally, our results show that EPO-mediated proliferation and survival of erythroid progenitors occurs mainly through modulation of JAK-STAT pathway associated STATs, GRB2 and PIK3 genes, as well as AKT pathway-coupled NFKBIA and YWHAH genes
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