A one-dimensional ultracold medium of extreme optical depth

We report on the preparation of a one-dimensional ultracold medium in a hollow-core photonic crystal fiber, reaching an effective optical depth of 1000(150). We achieved this extreme optical depth by transferring atoms from a magneto-optical trap into a far-detuned optical dipole trap inside the hollow-core fiber, yielding up to 2.5(3)$\times$10$^5$ atoms inside the core with a loading efficiency of $2.5(6)~\%$. The preparation of an ultracold medium of such huge optical depth paves the way towards new applications in quantum optics and nonlinear optics

Astrophysical Reaction Rates From Statistical Model Calculations

Theoretical reaction rates in the temperature range 0.01*10^9<=T[K]<=10.*10^9 are calculated in the statistical model (Hauser-Feshbach formalism) for targets with 10<=Z<=83 (Ne to Bi) and for a mass range reaching the neutron and proton driplines. Reactions considered are (n,gamma), (n,p), (n,alpha), (p,gamma), (p,alpha),(alpha,gamma), and their inverse reactions. Reaction rates as a function of temperature for thermally populated targets are given by analytic seven parameter fits. To facilitate comparison with experimental rates, the stellar enhancement factors are also tabulated. Two complete sets of rates have been calculated, one of which includes a phenomenological treatment of shell quenching for neutron-rich nuclei. These extensive datasets are provided on-line as electronic files, while a selected subset from one calculation is given as printed tables. A summary of the theoretical inputs and advice on the use of the provided tabulations is included.Comment: 22 pages of text and 1 table; accepted by Atomic Data Nuclear Data Tables; a preprint is also available from http://quasar.physik.unibas.ch/~tommy/adndt.htm

Nuclear Spin Effects in Optical Lattice Clocks

We present a detailed experimental and theoretical study of the effect of nuclear spin on the performance of optical lattice clocks. With a state-mixing theory including spin-orbit and hyperfine interactions, we describe the origin of the $^1S_0$-$^3P_0$ clock transition and the differential g-factor between the two clock states for alkaline-earth(-like) atoms, using $^{87}$Sr as an example. Clock frequency shifts due to magnetic and optical fields are discussed with an emphasis on those relating to nuclear structure. An experimental determination of the differential g-factor in $^{87}$Sr is performed and is in good agreement with theory. The magnitude of the tensor light shift on the clock states is also explored experimentally. State specific measurements with controlled nuclear spin polarization are discussed as a method to reduce the nuclear spin-related systematic effects to below 10$^{-17}$ in lattice clocks.Comment: 13 pages, 12 figures, submitted to PR

About the stability of the dodecatoplet

A new investigation is done of the possibility of binding the "dodecatoplet", a system of six top quarks and six top antiquarks, using the Yukawa potential mediated by Higgs exchange. A simple variational method gives a upper bound close to that recently estimated in a mean-field calculation. It is supplemented by a lower bound provided by identities among the Hamiltonians describing the system and its subsystems.Comment: 5 pages, two figures merged, refs. added, typos correcte

Dipeptidylpeptidase IV (CD26) defines leukemic stem cells (LSC) in chronic myeloid leukemia

Chronic myeloid leukemia (CML) is a stem cell (SC) neoplasm characterized by the BCR/ABL1 oncogene. Although mechanisms of BCR/ABL1-induced transformation are well-defined, little is known about effector-molecules contributing to malignant expansion and the extramedullary spread of leukemic SC (LSC) in CML. We have identified the cytokine-targeting surface enzyme dipeptidylpeptidase-IV (DPPIV/CD26) as a novel, specific and pathogenetically relevant biomarker of CD34+/CD38─ CML LSC. In functional assays, CD26 was identified as target enzyme disrupting the SDF-1-CXCR4-axis by cleaving SDF-1, a chemotaxin recruiting CXCR4+ SC. CD26 was not detected on normal SC or LSC in other hematopoietic malignancies. Correspondingly, CD26+ LSC decreased to low or undetectable levels during successful treatment with imatinib. CD26+ CML LSC engrafted NOD-SCID-IL-2Rγ−/− (NSG) mice with BCR/ABL1+ cells, whereas CD26─ SC from the same patients produced multilineage BCR/ABL1– engraftment. Finally, targeting of CD26 by gliptins suppressed the expansion of BCR/ABL1+ cells. Together, CD26 is a new biomarker and target of CML LSC. CD26 expression may explain the abnormal extramedullary spread of CML LSC, and inhibition of CD26 may revert abnormal LSC function and support curative treatment approaches in this malignancy