Isotopic difference in the heteronuclear loss rate in a two-species surface trap

We have realized a two-species mirror-magneto-optical trap containing a mixture of $^{87}$Rb ($^{85}$Rb) and $^{133}$Cs atoms. Using this trap, we have measured the heteronuclear collisional loss rate $\beta_{Rb-Cs}'$ due to intra-species cold collisions. We find a distinct difference in the magnitude and intensity dependence of $\beta_{Rb-Cs}'$ for the two isotopes $^{87}$Rb and $^{85}$Rb which we attribute to the different ground-state hyperfine splitting energies of the two isotopes.Comment: 4 pages, 2 figure

Lamp reliability studies for improved satellite rubidium frequency standard

In response to the premature failure of Rb lamps used in Rb atomic clocks onboard NAVSTAR GPS satellites experimental and theoretical investigations into their failure mechanism were initiated. The primary goal of these studies is the development of an accelerated life test for future GPS lamps. The primary failure mechanism was identified as consumption of the lamp's Rb charge via direct interaction between Rb and the lamp's glass surface. The most effective parameters to accelerate the interaction between the Rb and the glass are felt to be RF excitation power and lamp temperature. Differential scanning calorimetry is used to monitor the consumption of Rb within a lamp as a function of operation time. This technique yielded base line Rb consumption data for GPS lamps operating under normal conditions

RB loss contributes to aggressive tumor phenotypes in MYC-driven triple negative breast cancer

Triple negative breast cancer (TNBC) is characterized by multiple genetic events occurring in concert to drive pathogenic features of the disease. Here we interrogated the coordinate impact of p53, RB, and MYC in a genetic model of TNBC, in parallel with the analysis of clinical specimens. Primary mouse mammary epithelial cells (mMEC) with defined genetic features were used to delineate the combined action of RB and/or p53 in the genesis of TNBC. In this context, the deletion of either RB or p53 alone and in combination increased the proliferation of mMEC; however, the cells did not have the capacity to invade in matrigel. Gene expression profiling revealed that loss of each tumor suppressor has effects related to proliferation, but RB loss in particular leads to alterations in gene expression associated with the epithelial-to-mesenchymal transition. The overexpression of MYC in combination with p53 loss or combined RB/p53 loss drove rapid cell growth. While the effects of MYC overexpression had a dominant impact on gene expression, loss of RB further enhanced the deregulation of a gene expression signature associated with invasion. Specific RB loss lead to enhanced invasion in boyden chambers assays and gave rise to tumors with minimal epithelial characteristics relative to RB-proficient models. Therapeutic screening revealed that RB-deficient cells were particularly resistant to agents targeting PI3K and MEK pathway. Consistent with the aggressive behavior of the preclinical models of MYC overexpression and RB loss, human TNBC tumors that express high levels of MYC and are devoid of RB have a particularly poor outcome. Together these results underscore the potency of tumor suppressor pathways in specifying the biology of breast cancer. Further, they demonstrate that MYC overexpression in concert with RB can promote a particularly aggressive form of TNB

Cyclin D-Cdk4,6 Drives Cell-Cycle Progression via the Retinoblastoma Protein's C-Terminal Helix.

The cyclin-dependent kinases Cdk4 and Cdk6 form complexes with D-type cyclins to drive cell proliferation. A well-known target of cyclin D-Cdk4,6 is the retinoblastoma protein Rb, which inhibits cell-cycle progression until its inactivation by phosphorylation. However, the role of Rb phosphorylation by cyclin D-Cdk4,6 in cell-cycle progression is unclear because Rb can be phosphorylated by other cyclin-Cdks, and cyclin D-Cdk4,6 has other targets involved in cell division. Here, we show that cyclin D-Cdk4,6 docks one side of an alpha-helix in the Rb C terminus, which is not recognized by cyclins E, A, and B. This helix-based docking mechanism is shared by the p107 and p130 Rb-family members across metazoans. Mutation of the Rb C-terminal helix prevents its phosphorylation, promotes G1 arrest, and enhances Rb's tumor suppressive function. Our work conclusively demonstrates that the cyclin D-Rb interaction drives cell division and expands the diversity of known cyclin-based protein docking mechanisms

Rubidium and lead abundances in giant stars of the globular clusters M 13 and NGC 6752

We present measurements of the neutron-capture elements Rb and Pb in five giant stars of the globular cluster NGC 6752 and Pb measurements in four giants of the globular cluster M 13. The abundances were derived by comparing synthetic spectra with high resolution, high signal-to-noise ratio spectra obtained using HDS on the Subaru telescope and MIKE on the Magellan telescope. The program stars span the range of the O-Al abundance variation. In NGC 6752, the mean abundances are [Rb/Fe] = -0.17 +/- 0.06 (sigma = 0.14), [Rb/Zr] = -0.12 +/- 0.06 (sigma = 0.13), and [Pb/Fe] = -0.17 +/- 0.04 (sigma = 0.08). In M 13 the mean abundance is [Pb/Fe] = -0.28 +/- 0.03 (sigma = 0.06). Within the measurement uncertainties, we find no evidence for a star-to-star variation for either Rb or Pb within these clusters. None of the abundance ratios [Rb/Fe], [Rb/Zr], or [Pb/Fe] are correlated with the Al abundance. NGC 6752 may have slightly lower abundances of [Rb/Fe] and [Rb/Zr] compared to the small sample of field stars at the same metallicity. For M 13 and NGC 6752 the Pb abundances are in accord with predictions from a Galactic chemical evolution model. If metal-poor intermediate-mass asymptotic giant branch stars did produce the globular cluster abundance anomalies, then such stars do not synthesize significant quantities of Rb or Pb. Alternatively, if such stars do synthesize large amounts of Rb or Pb, then they are not responsible for the abundance anomalies seen in globular clusters.Comment: Accepted for publication in Ap

Rubidium and lead abundances in giant stars of the globular clusters M4 and M5

We present measurements of the neutron-capture elements Rb and Pb for bright giants in the globular clusters M4 and M5. The clusters are of similar metallicity ([Fe/H] = -1.2) but M4 is decidedly s-process enriched relative to M5: [Ba/Fe] = +0.6 for M4 but 0.0 for M5. The Rb and Pb abundances were derived by comparing synthetic spectra with high-resolution, high signal-to-noise ratio spectra obtained with MIKE on the Magellan telescope. Abundances of Y, Zr, La, and Eu were also obtained. In M4, the mean abundances from 12 giants are [Rb/Fe] = 0.39 +/- 0.02 (sigma = 0.07), [Rb/Zr] = 0.17 +/- 0.03 (sigma = 0.08), and [Pb/Fe] = 0.30 +/- 0.02 (sigma = 0.07). In M5, the mean abundances from two giants are [Rb/Fe] = 0.00 +/- 0.05 (sigma = 0.06), [Rb/Zr] = 0.08 +/- 0.08 (sigma = 0.11), and [Pb/Fe] = -0.35 +/- 0.02 (sigma = 0.04). Within the measurement uncertainties, the abundance ratios [Rb/Fe], [Pb/Fe] and [Rb/X] for X = Y, Zr, La are constant from star-to-star in each cluster and none of these ratios are correlated with O or Na abundances. While M4 has a higher Rb abundance than M5, the ratios [Rb/X] are similar in both clusters indicating that the nature of the s-products are very similar for each cluster but the gas from which M4's stars formed had a higher concentration of these products.Comment: Accepted for publication in Ap

Guanylyl cyclase activation reverses resistive breathing–induced lung injury and inflammation

Inspiratory resistive breathing (RB), encountered in obstructive lung diseases, induces lung injury. The soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP) pathway is down-regulated in chronic and acute animal models of RB, such as asthma, chronic obstructive pulmonary disease, and in endotoxin-induced acute lung injury. Our objectives were to: (1) characterize the effects of increased concurrent inspiratory and expiratory resistance in mice via tracheal banding; and (2) investigate the contribution of the sGC/cGMP pathway in RB-induced lung injury. Anesthetized C57BL/6 mice underwent RB achieved by restricting tracheal surface area to 50% (tracheal banding). RB for 24 hours resulted in increased bronchoalveolar lavage fluid cellularity and protein content, marked leukocyte infiltration in the lungs, and perturbed respiratory mechanics (increased tissue resistance and elasticity, shifted static pressure–volume curve right and downwards, decreased static compliance), consistent with the presence of acute lung injury. RB down-regulated sGC expression in the lung. All manifestations of lung injury caused by RB were exacerbated by the administration of the sGC inhibitor, 1H-[1,2,4]oxodiazolo[4,3-]quinoxalin-l-one, or when RB was performed using sGCα1 knockout mice. Conversely, restoration of sGC signaling by prior administration of the sGC activator BAY 58-2667 (Bayer, Leverkusen, Germany) prevented RB-induced lung injury. Strikingly, direct pharmacological activation of sGC with BAY 58-2667 24 hours after RB reversed, within 6 hours, the established lung injury. These findings raise the possibility that pharmacological targeting of the sGC–cGMP axis could be used to ameliorate lung dysfunction in obstructive lung diseases