Lattice QCD Matrix Elements for the B_{s}

Predicting the B_{s}^{0}-B[over ¯]_{s}^{0} width difference ΔΓ_{s} relies on the heavy quark expansion and on hadronic matrix elements of ΔB=2 operators. We present the first lattice QCD results for matrix elements of the dimension-7 operators R_{2,3} and linear combinations R[over ˜]_{2,3} using nonrelativistic QCD for the bottom quark and a highly improved staggered quark (HISQ) action for the strange quark. Computations use MILC Collaboration ensembles of gauge field configurations with 2+1+1 flavors of sea quarks with the HISQ discretization, including lattices with physically light up or down quark masses. We discuss features unique to calculating matrix elements of these operators and analyze uncertainties from series truncation, discretization, and quark mass dependence. Finally we report the first standard model determination of ΔΓ_{s} using lattice QCD results for all hadronic matrix elements through O(1/m_{b}). The main result of our calculations yields the 1/m_{b} contribution ΔΓ_{1/m_{b}}=-0.022(10) ps^{-1}. Adding this to the leading order contribution, the standard model prediction is ΔΓ_{s}=0.092(14) ps^{-1}.

Strong-Isospin-Breaking Correction to the Muon Anomalous Magnetic Moment from Lattice QCD at the Physical Point.

All lattice-QCD calculations of the hadronic-vacuum-polarization contribution to the muon's anomalous magnetic moment to date have been performed with degenerate up- and down-quark masses. Here we calculate directly the strong-isospin-breaking correction to a_{µ}^{HVP} for the first time with physical values of m_{u} and m_{d} and dynamical u, d, s, and c quarks, thereby removing this important source of systematic uncertainty. We obtain a relative shift to be applied to lattice-QCD results obtained with degenerate light-quark masses of δa_{µ}^{HVP,m_{u}≠m_{d}}=+1.5(7)%, in agreement with estimates from phenomenology.

-1 V bias 67 GHz bandwidth Si-contacted germanium waveguide p-i-n photodetector for optical links at 56 Gbps and beyond.

We demonstrate a 67 GHz bandwidth silicon-contacted germanium waveguide p-i-n photodetector operating at -1 V with 6.8 fF capacitance. The dark current is below 4 nA. The responsivity is 0.74 A/W at 1550 nm and 0.93 A/W at 1310 nm wavelength. 56 Gbps on-off-keying data reception is demonstrated with clear open eye diagrams in both the C-band and O-band.

III-V-on-silicon anti-colliding pulse-type mode-locked laser.

An anti-colliding pulse-type III-V-on-silicon passively mode-locked laser is presented for the first time based on a III-V-on-silicon distributed Bragg reflector as outcoupling mirror implemented partially underneath the III-V saturable absorber. Passive mode-locking at 4.83 GHz repetition rate generating 3 ps pulses is demonstrated. The generated fundamental RF tone shows a 1.7 kHz 3 dB linewidth. Over 9 mW waveguide coupled output power is demonstrated.

High sensitivity 10Gb/s Si photonic receiver based on a low-voltage waveguide-coupled Ge avalanche photodetector.

We demonstrate low-voltage germanium waveguide avalanche photodetectors (APDs) with a gain × bandwidth product above 100GHz. A photonic receiver based on such a Ge APD, including a 0.13µm SiGe BiCMOS low-noise trans-impedance amplifier and a limiting amplifier, is realized. A 5.8dB sensitivity improvement is demonstrated at -5.9V bias at an avalanche gain of 6 through bit error ratio measurements. The absolute sensitivity in avalanche mode is -23.4dBm and -24.4dBm at a bit error ratio of 1 × 10(-12) and 1 × 10(-9) respectively.

Narrow-linewidth short-pulse III-V-on-silicon mode-locked lasers based on a linear and ring cavity geometry.

Picosecond-pulse III-V-on-silicon mode-locked lasers based on linear and ring extended cavity geometries are presented. In passive mode-locked operation a 12 kHz -3dB linewidth of the fundamental RF tone at 4.7 GHz is obtained for the linear cavity geometry and 16 kHz for the ring cavity geometry. Stabilization of the repetition rate of these devices using hybrid mode-locking is also demonstrated.

Standard model predictions for B→Kℓ(+)ℓ- with form factors from lattice QCD.

We calculate, for the first time using unquenched lattice QCD form factors, the standard model differential branching fractions dB/dq2(B→Kℓ(+)ℓ(-)) for ℓ=e, µ, τ and compare with experimental measurements by Belle, BABAR, CDF, and LHCb. We report on B(B→Kℓ(+)ℓ(-)) in q2 bins used by experiment and predict B(B→Kτ(+)τ(-))=(1.41±0.15)×10(-7). We also calculate the ratio of branching fractions R(e)(µ)=1.00029(69) and predict R(ℓ)(τ)=1.176(40), for ℓ=e, µ. Finally, we calculate the "flat term" in the angular distribution of the differential decay rate F(H)(e,µ,τ) in experimentally motivated q2 bins.

Demonstration of Silicon-on-insulator mid-infrared spectrometers operating at 3.8 µm.

The design and characterization of silicon-on-insulator mid-infrared spectrometers operating at 3.8 µm is reported. The devices are fabricated on 200 mm SOI wafers in a CMOS pilot line. Both arrayed waveguide grating structures and planar concave grating structures were designed and tested. Low insertion loss (1.5-2.5 dB) and good crosstalk characteristics (15-20 dB) are demonstrated, together with waveguide propagation losses in the range of 3 to 6 dB/cm.

High-efficiency fiber-to-chip grating couplers realized using an advanced CMOS-compatible silicon-on-insulator platform.

A new generation of Silicon-on-Insulator fiber-to-chip grating couplers which use a silicon overlay to enhance the directionality and thereby the coupling efficiency is presented. Devices are realized on a 200 mm wafer in a CMOS pilot line. The fabricated fiber couplers show a coupling efficiency of -1.6 dB and a 3 dB bandwidth of 80 nm.

Precise charm to strange mass ratio and light quark masses from full lattice QCD.

By using a single formalism to handle charm, strange, and light valence quarks in full lattice QCD for the first time, we are able to determine ratios of quark masses to 1%. For m(c)/m(s) we obtain 11.85(16), an order of magnitude more precise than the current PDG average. Combined with 1% determinations of the charm quark mass now possible this gives m(s)(2 GeV)=92.4(1.5) MeV. The MILC result for m(s)/m(l)=27.2(3) yields m(l)(2 GeV)=3.40(7) MeV for the average of u and d quark masses.

Prediction of the B{c}{*} mass in full lattice QCD.

By using the highly improved staggered quark formalism to handle charm, strange, and light valence quarks in full lattice QCD, and NRQCD to handle bottom valence quarks, we are able to determine accurately ratios of the B meson vector-pseudoscalar mass splittings, in particular, [m(B{c}{*})-m(B{c})]/[m(B{s}{*})-m(B{s})]. We find this ratio to be 1.15(15), showing the "light" quark mass dependence of this splitting to be very small. Hence we predict m(B{c}{*})=6.330(7)(2)(6) GeV, where the first two errors are from the lattice calculation and the third from existing experiment. This is the most accurate prediction of a gold-plated hadron mass from lattice QCD to date.

Orai1 contributes to the establishment of an apoptosis-resistant phenotype in prostate cancer cells.

The molecular nature of calcium (Ca(2+))-dependent mechanisms and the ion channels having a major role in the apoptosis of cancer cells remain a subject of debate. Here, we show that the recently identified Orai1 protein represents the major molecular component of endogenous store-operated Ca(2+) entry (SOCE) in human prostate cancer (PCa) cells, and constitutes the principal source of Ca(2+) influx used by the cell to trigger apoptosis. The downregulation of Orai1, and consequently SOCE, protects the cells from diverse apoptosis-inducing pathways, such as those induced by thapsigargin (Tg), tumor necrosis factor α, and cisplatin/oxaliplatin. The transfection of functional Orai1 mutants, such as R91W, a selectivity mutant, and L273S, a coiled-coil mutant, into the cells significantly decreased both SOCE and the rate of Tg-induced apoptosis. This suggests that the functional coupling of STIM1 to Orai1, as well as Orai1 Ca(2+)-selectivity as a channel, is required for its pro-apoptotic effects. We have also shown that the apoptosis resistance of androgen-independent PCa cells is associated with the downregulation of Orai1 expression as well as SOCE. Orai1 rescue, following Orai1 transfection of steroid-deprived cells, re-established the store-operated channel current and restored the normal rate of apoptosis. Thus, Orai1 has a pivotal role in the triggering of apoptosis, irrespective of apoptosis-inducing stimuli, and in the establishment of an apoptosis-resistant phenotype in PCa cells.

High-precision determination of the pi, K, D, and Ds decay constants from lattice QCD.

We determine D and D(s) decay constants from lattice QCD with 2% errors, 4 times better than experiment and previous theory: f(D(s))=241(3) MeV, f(D)=207(4) MeV, and fD(s))/f(D)=1.164(11). We also obtain f(K)/f(pi)=1.189(7) and (f(D(s))/f(D))/(f(K)/f(pi))=0.979(11). Combining with experiment gives V(us)=0.2262(14) and V(cs)/V(cd) of 4.43(41). We use a highly improved quark discretization on MILC gluon fields that include realistic sea quarks, fixing the u/d, s, and c masses from the pi, K, and eta(c) meson masses. This allows a stringent test against experiment for D and D(s) masses for the first time (to within 7 MeV).

Epidermal growth factor-induced neuroendocrine differentiation and apoptotic resistance of androgen-independent human prostate cancer cells.

Neuroendocrine differentiation (NED) has been implicated in prostate cancer progression and hormone-therapy failure. Neuroendocrine cells are non-proliferating and escape apoptotic cell death, although their origin and the causes of their apoptotic resistance have as yet been poorly elucidated. This study demonstrates a new mechanism involved in controlling NED. We report that epidermal growth factor (5-50 ng/ml) promotes neuroendocrine-like differentiation of androgen-independent DU145 prostate cancer cells. This differentiation is associated with an increase in the expression of Neuron Specific Enolase (NSE) and a reduction in cell proliferation and is blocked by inhibiting tyrosine kinase activity with genistein and with compound 56 (C56). An increase in the cAMP level, using dibutryl cAMP (db-cAMP) (1 mM) and isobutylmethylxanthine (100 microM), does not promote NED by itself, but does increase the effect of EGF on NED. In addition, EGF-induced NED protects cells from apoptosis induced with thapsigargin (1 microM) by reducing the thapsigargin-induced cytosolic calcium overload. In order to describe how EGF-induced NED protects cells against thapigargin-induced calcium overload we investigated the spatiotemporal calcium signalling linked to apoptosis. By using thapsigargin in various conditions on DU145 cells and using micro-fluorimetric calcium measurements, we show that depletion of intracellular calcium store induces apoptosis and that the amplitude and duration of the capacitive calcium entry are two apoptosis-modulating parameters. We show that protection against thapsigargin-induced apoptosis conferred by NED is achieved by reducing the amount and the speed of calcium that can be released from calcium pools, as well as modulating the amplitude of the subsequent calcium entry.

B-meson decay constant from unquenched lattice QCD.

We present determinations of the -meson decay constant f(B) and f(B)(s)/f(B) using the MILC Collaboration unquenched gauge configurations, which include three flavors of light sea quarks. The mass of one of the sea quarks is kept around the strange quark mass, and we explore a range in masses for the two lighter sea quarks down to m(s)/8. The heavy quark is simulated using nonrelativistic QCD, and both the valence and sea light quarks are represented by the highly improved (AsqTad) staggered quark action. The good chiral properties of the latter action allow for a more accurate chiral extrapolation to physical up and down quarks than has been possible in the past. We find f(B)=216(9)(19)(4)(6) MeV and f(B)(s)/f(B)=1.20(3)(1).

Accurate determinations of alpha(s) from realistic lattice QCD.

We obtain a new value for the QCD coupling constant by combining lattice QCD simulations with experimental data for hadron masses. Our lattice analysis is the first to (1) include vacuum polarization effects from all three light-quark flavors (using MILC configurations), (2) include third-order terms in perturbation theory, (3) systematically estimate fourth and higher-order terms, (4) use an unambiguous lattice spacing, and (5) use an [symbol: see text](a2)-accurate QCD action. We use 28 different (but related) short-distance quantities to obtain alpha((5)/(MS))(M(Z)) = 0.1170(12).

Alterations in the regulatory volume decrease (RVD) and swelling-activated Cl- current associated with neuroendocrine differentiation of prostate cancer epithelial cells.

Neuroendocrine (NE) differentiation of prostate epithelial/basal cells is a hallmark of advanced, androgen-independent prostate cancer, for which there is no successful therapy. Here we report for the first time on alterations in regulatory volume decrease (RVD) and its key determinant, swelling-activated Cl- current (I(Cl,swell)), associated with NE differentiation of androgen-dependent LNCaP prostate cancer epithelial cells. NE-differentiating regimens, namely, chronic cAMP elevation or androgen deprivation, resulted in generally augmented I(Cl,swell) and enhanced RVD. This occurred as a result of both the increased endogenous expression of ClC-3, which is a volume-sensitive Cl- channel involved, as we show, in I(Cl,swell) in LNCaP (lymph-node carcinoma of the prostate) cells and the weaker negative I(Cl,swell) control from Ca2+ entering via store-dependent pathways. The changes in the RVD of NE-differentiated cells generally mimicked those reported for Bcl-2-conferred apoptotic resistance. Our results suggest that strengthening the mechanism that helps to maintain volume constancy may contribute to better survival rates of apoptosis-resistant NE cells.

Bs and Ds decay constants in three-flavor lattice QCD.

Capitalizing on recent advances in lattice QCD, we present a calculation of the leptonic decay constants f(B(s)) and f(D(s)) that includes effects of one strange sea quark and two light sea quarks via an improved staggered action. By shedding the quenched approximation and the associated lattice scale uncertainty, lattice QCD greatly increases its predictive power. Nonrelativistic QCD is used to simulate heavy quarks with masses between 1.5m(c) and m(b). We arrive at the following results: f(B(s))=260+/-7+/-26+/-8+/-5 and f(D(s))=290+/-20+/-29+/-29+/-6 MeV. The first quoted error is the statistical uncertainty, and the rest estimate the sizes of higher order terms neglected in this calculation. All of these uncertainties are systematically improvable by including another order in the weak coupling expansion, the nonrelativistic expansion, or the Symanzik improvement program.

High-precision lattice QCD confronts experiment.

The recently developed Symanzik-improved staggered-quark discretization allows unquenched lattice-QCD simulations with much smaller (and more realistic) quark masses than previously possible. To test this formalism, we compare experiment with a variety of nonperturbative calculations in QCD drawn from a restricted set of "gold-plated" quantities. We find agreement to within statistical and systematic errors of 3% or less. We discuss the implications for phenomenology and, in particular, for heavy-quark physics.

Ca2+ homeostasis and apoptotic resistance of neuroendocrine-differentiated prostate cancer cells.

Neuroendocrine (NE) differentiation is a hallmark of advanced, androgen-independent prostate cancer, for which there is no successful therapy. NE tumor cells are nonproliferating and escape apoptotic cell death; therefore, an understanding of the apoptotic status of the NE phenotype is imperative for the development of new therapies for prostate cancer. Here, we report for the first time on alterations in intracellular Ca(2+) homeostasis, which is a key factor in apoptosis, caused by NE differentiation of androgen-dependent prostate cancer epithelial cells. NE-differentiating regimens, either cAMP elevation or androgen deprivation, resulted in a reduced endoplasmic reticulum Ca(2+)-store content due to both SERCA 2b Ca(2+) ATPase and luminal Ca(2+) binding/storage chaperone calreticulin underexpression, and to a downregulated store-operated Ca(2+) current. NE-differentiated cells showed enhanced resistance to thapsigargin- and TNF-alpha-induced apoptosis, unrelated to antiapoptotic Bcl-2 protein overexpression. Our results suggest that targeting the key players determining Ca(2+) homeostasis in an attempt to enhance the proapoptotic potential of malignant cells may prove to be a useful strategy in the treatment of advanced prostate cancer.