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S L Olsen

Publications and source records attributed to S L Olsen.

At least 37 records · Page 2Linked to original sources
PubMed2004

Observation of B+-->LambdaLambdaK+.

We report the first observation of the charmless hyperonic B decay, B+-->LambdaLambdaK+, using a 140 fb(-1) data sample recorded at the Upsilon(4S) resonance with the Belle detector at the KEKB (e+)(e-) collider. The measured branching fraction is B(B+-->LambdaLambdaK+) = (2.91(+0.90)(-0.70) +/- 0.38) x 10(-6). We also perform a search for the related decay mode B+-->LambdaLambdapi+, but do not find a significant signal. We set a 90% confidence-level upper limit of B(B+-->LambdaLambdapi+) < 2.8 x 10(-6).

Journal Article↗
PubMed2004

Evidence for B+-->omegal+nu.

We have searched for the decay B+-->omegal(+)nu (l=e or mu) in 78 fb(-1) of Upsilon(4S) data (85x10(6)BB events) accumulated with the Belle detector. The final state is fully reconstructed using the omega decay into pi(+)pi(-)pi(0), combined with detector hermeticity to estimate the neutrino momentum. A signal of 414+/-125 events is found in the data, corresponding to a branching fraction of (1.3+/-0.4+/-0.2+/-0.3)x10(-4), where the first two errors are statistical and systematic, respectively. The third error reflects the estimated form-factor uncertainty.

Journal Article↗
PubMed2004

Observation of a threshold enhancement in the plambda invariant-mass spectrum.

An enhancement near the m(p)+M(Lambda) mass threshold is observed in the combined pLambda and pLambda invariant-mass spectrum from J/psi-->pK(-)Lambda;+c.c. decays. It can be fit with an S-wave Breit-Wigner resonance with a mass m=2075+/-12(stat)+/-5(syst) MeV and a width of Gamma=90+/-35(stat)+/-9(syst) MeV; it can also be fit with a P-wave Breit-Wigner resonance. Evidence for a similar enhancement is also observed in psi(')-->pK(-)Lambda;+c.c. decays. The analysis is based on samples of 5.8x10(7)J/psi and 1.4x10(7)psi(') decays accumulated in the BES II detector at the Beijing Electron-Positron Collider.

Journal Article↗
PubMed2004

Search for the lepton-flavor-violating decay tau- -->micro-eta at Belle.

We have searched for the lepton flavor violating decay tau(-)-->micro(-)eta using a data sample of 84.3 fb(-1) accumulated with the Belle detector at KEK. The eta meson was detected through the decay modes: eta-->gammagamma and pi(+)pi(-)pi(0). No signal candidates are found, and we obtain an upper limit for the branching fraction B(tau(-)-->micro(-)eta)<3.4 x 10(-7) at the 90% confidence level.

Journal Article↗
PubMed2004

Observation of B+-->psi(3770)K+.

We report the first observation of the decay B+-->psi(3770)K+ where the psi(3770) is reconstructed in the D0(-)D(0) and D+D- decay channels. The obtained branching fraction is B(B+-->psi(3770)K+)=(0.48+/-0.11+/-0.07)x10(-3). We have measured the branching fraction for the decay B+-->D0(-)D0K+ to be (1.17+/-0.21+/-0.15)x10(-3) and set a 90% confidence level upper limit of 0.90 x 10(-3) for the decay B+-->D+D-K+. We also present the results of a search for possible decays to D(-)D and D0(-)D(0)pi(0) of the recently observed X(3872) particle. The analysis is based on 88 fb(-1) of data collected at the Upsilon(4S) resonance by the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider.

Journal Article↗
PubMed2004

Observation of B(+)-->pppi+, B0-->ppK0, and B(+)-->ppK(*+).

We report the first observation of a b-->u type charmless baryonic B decay, B+-->pppi(+), as well as b-->s type B0-->ppK0 and B+-->ppK(*+) decays. The analysis is based on a 78 fb(-1) data sample recorded on the Upsilon(4S) resonance with the Belle detector at KEKB. We find B(B+-->pppi(+))=(3.06(+0.73)(-0.62)+/-0.37)x10(-6), B(B0-->ppK0)=(1.88(+0.77)(-0.60)+/-0.23)x10(-6), and B(B+-->ppK(*+))=(10.3(+3.6+1.3)(-2.8-1.7))x10(-6). We also update B(B+-->ppK+)=(5.66(+0.67)(-0.57)+/-0.62)x10(-6) and present an upper limit on B(B0-->ppK(*0)) at the 90% confidence level. A common feature of the observed decay modes is threshold peaking in baryon pair invariant mass.

Journal Article↗
PubMed2004

Observation of the radiative decay D0-->phigamma.

We report the observation of the decay D0-->phigamma with a statistical significance of 5.4sigma in 78.1 fb(-1) of data collected by the Belle experiment at the KEKB e+e- collider. This is the first observation of a flavor-changing radiative decay of a charmed meson. The Cabibbo- and color-suppressed decays D0-->phipi(0), phieta are also observed for the first time. We measure branching fractions B(D0-->phigamma)=[2.60(+0.70)(-0.61)(stat)+0.15-0.17(syst)] x 10(-5), B(D0-->phipi(0))=[8.01+/-0.26(stat)+/-0.47(syst)] x 10(-4), and B(D0-->phieta)=[1.48+/-0.47(stat)+/-0.09(syst)] x 10(-4).

Journal Article↗
PubMed2004

Measurement of /V(ub)/ using inclusive B-->X(u)lnu decays with a novel X(u)-reconstruction method.

We report the measurement of an inclusive partial branching fraction for charmless semileptonic B decay and the extraction of /V(ub)/. Candidates for B-->X(u)lnu are identified with a novel X(u) reconstruction method based on neutrino reconstruction via missing 4-momentum and a technique called "simulated annealing." Based on 86.9 fb(-1) of data taken with the Belle detector, we obtain DeltaB(B-->X(u)lnu;M(X)<1.7 GeV/c2,q2>8.0 GeV2/c2)=[7.37+/-0.89(stat)+/-1.12(syst)+/-0.55(b-->c)+/-0.24(b-->u)]x10(-4) and determine |V(ub)|=[4.66+/-0.28(stat)+/-0.35(syst)+/-0.17(b-->c)+/-0.08(b-->u)+/-0.58(theory)]x10(-3).

Journal Article↗
PubMed2004

Observation of the decay psi(2S)-->K0SK0L.

The decay psi(2S)-->K(0)(S)K(0)(L) is observed using psi(2S) data collected with the Beijing Spectrometer at the Beijing Electron-Positron Collider; the branching fraction is determined to be B(psi(2S)-->K(0)(S)K(0)(L))=(5.24+/-0.47+/-0.48)x10(-5). Compared with J/psi-->K(0)(S)K(0)(L), the psi(2S) branching fraction is enhanced relative to the prediction of the perturbative QCD "12%" rule. The result, together with the branching fractions of psi(2S) decays to other pseudoscalar meson pairs (pi(+)pi(-) and K+K-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.

Journal Article↗
PubMed2004

Observation of radiative B-->phi K gamma decays.

The radiative decay B-->phi K gamma is observed for the first time. The branching fraction for the charged B--->phi K- gamma decay mode is measured to be B(B--->phi K- gamma)=(3.4+/-0.9+/-0.4)x10(-6). The photon energy distribution for the B--->phi K- gamma decay is presented. The signal for the neutral B(0)-->phi K(0)gamma decay mode is not statistically significant and an upper limit, B(B(0)-->phi K(0)gamma)<8.3x10(-6) at 90% C.L., is set. The analysis is based on a data set of 90 fb(-1) collected by the Belle experiment at the e(+)e(-) asymmetric collider KEKB.

Journal Article↗
PubMed2003

Observation of a narrow charmoniumlike state in exclusive B+/--->K+/-pi+pi-J/psi decays.

We report the observation of a narrow charmoniumlike state produced in the exclusive decay process B+/--->K+/-pi(+)pi(-)J/psi. This state, which decays into pi(+)pi(-)J/psi, has a mass of 3872.0+/-0.6(stat)+/-0.5(syst) MeV, a value that is very near the M(D0)+M(D(*0)) mass threshold. The results are based on an analysis of 152M B-Bmacr; events collected at the Upsilon(4S) resonance in the Belle detector at the KEKB collider. The signal has a statistical significance that is in excess of 10sigma.

Journal Article↗
PubMed2003

Observation of a near-threshold enhancement in the pp mass spectrum from radiative J/psi-->gammapp decays.

We observe a narrow enhancement near 2m(p) in the invariant mass spectrum of pp pairs from radiative J/psi-->gammapp decays. No similar structure is seen in J/psi-->pi(0)pp decays. The results are based on an analysis of a 58 x 10(6) event sample of J/psi decays accumulated with the BESII detector at the Beijing electron-positron collider. The enhancement can be fit with either an S- or P-wave Breit-Wigner resonance function. In the case of the S-wave fit, the peak mass is below 2m(p) at M=1859(+3)(-10) (stat)+5-25(syst) MeV/c(2) and the total width is Gamma<30 MeV/c(2) at the 90% confidence level. These mass and width values are not consistent with the properties of any known particle.

Journal Article↗
PubMed2003

Observation of B0-->pLambda(pi)(-).

We report the first observation of the charmless hyperonic B decay, B0-->pLambda(pi)(-), using a 78 fb(-1) data sample recorded on the Upsilon(4S) resonance with the Belle detector at KEKB. The measured branching fraction is B(B0-->pLambda(pi)(-))=(3.97(+1.00)(-0.80)+/-0.56)x10(-6). Searches for B0-->pLambda(K)- and pSigma(0)pi(-) yield no significant signals and we set 90% confidence-level upper limits of B(B0-->pLambda(K)-)<8.2x10(-7) and B(B0-->pSigma(0)pi(-))<3.8x10(-6).

Journal Article↗
PubMed2002

Observation of the eta(c)(2S) in Exclusive B-->KK(S)K-pi(+) Decays.

We report the observation of a narrow peak in the K(S)K-pi(+) invariant mass distribution in a sample of exclusive B-->KK(S)K-pi(+) decays collected with the Belle detector at the KEKB asymmetric e(+)e(-) collider. The measured mass of the peak is M=3654+/-6(stat)+/-8(syst) MeV/c(2), and we place a 90% confidence level upper limit on the width of Gamma<55 MeV/c(2). The properties agree with heavy-quark potential model expectations for the eta(c)(2S) meson, the n=2 singlet S charmonium state.

Journal Article↗
PubMed2001

Transcriptional activation of the nuclear receptor corepressor RIP140 by retinoic acid: a potential negative-feedback regulatory mechanism.

Through the use of microarray analysis it was discovered that the nuclear receptor coregulator, receptor interacting protein 140 (RIP140), was induced early during all-trans retinoic acid (RA)-induced differentiation of human embryonal carcinoma cells. A rapid, fourfold induction of RIP140 mRNA was detected within 3 h of RA treatment in human embryonal carcinoma and MCF-7 human breast cancer cells. RIP140 protein levels were induced within 6 h of RA treatment. The RA induction of RIP140 mRNA did not require de novo protein synthesis, consistent with RIP140 being a direct transcriptional target of retinoid receptors. Promoter/enhancer elements directly upstream of the RIP140 coding region supported RA-induced transcription of a luciferase gene. In addition the ability of overexpressed RIP140 to repress ligand activated retinoid receptors was confirmed. The finding that RIP140 is a direct transcriptional target of RA is one of the first examples of acute transcriptional regulation of a nuclear receptor coactivator or corepressor. These data are consistent with a model by which RA induction of RIP140 supplies a negative feedback signal toward ligand-activated retinoid receptors.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Mutation of a single conserved tryptophan in multidrug resistance protein 1 (MRP1/ABCC1) results in loss of drug resistance and selective loss of organic anion transport.

Multidrug resistance protein 1 (MRP1/ABCC1) belongs to the ATP-binding cassette transporter superfamily and is capable of conferring resistance to a broad range of chemotherapeutic agents and transporting structurally diverse conjugated organic anions. In this study, we found that substitution of a highly conserved tryptophan at position 1246 with cysteine (W1246C-MRP1) in the putative last transmembrane segment (TM17) of MRP1 eliminated 17beta-estradiol 17-(beta-d-glucuronide) (E(2)17betaG) transport by membrane vesicles prepared from transiently transfected human embryonic kidney cells while leaving the capacity for leukotriene C(4)- and verapamil-stimulated glutathione transport intact. In addition, in contrast to wild-type MRP1, leukotriene C(4) transport by the W1246C-MRP1 protein was no longer inhibitable by E(2)17betaG, indicating that the mutant protein had lost the ability to bind the glucuronide. A similar phenotype was observed when Trp(1246) was replaced with Ala, Phe, and Tyr. Confocal microscopy of cells expressing Trp(1246) mutant MRP1 molecules fused at the C terminus with green fluorescent protein showed that they were correctly routed to the plasma membrane. In addition to the loss of E(2)17betaG transport, HeLa cells stably transfected with W1246C-MRP1 cDNA were not resistant to the Vinca alkaloid vincristine and accumulated levels of [(3)H]vincristine comparable to those in vector control-transfected cells. Cells expressing W1246C-MRP1 were also not resistant to cationic anthracyclines (doxorubicin, daunorubicin) or the electroneutral epipodophyllotoxin VP-16. In contrast, resistance to sodium arsenite was only partially diminished, and resistance to potassium antimony tartrate remained comparable to that of cells expressing wild-type MRP1. This suggests that the structural determinants required for transport of heavy metal oxyanions differ from those for chemotherapeutic agents. Our results provide the first example of a tryptophan residue being so critically important for substrate specificity in a eukaryotic ATP-binding cassette transporter.

ATP-Binding Cassette Transporters↗
PubMed1997

PTHrP and cell division: expression and localization of PTHrP in a keratinocyte cell line (HaCaT) during the cell cycle.

Parathyroid hormone-related protein (PTHrP) is highly expressed in normal skin keratinocytes, and its involvement in growth and differentiation processes in these cells has been implicated by several lines of evidence which include the use of antisense PTHrP (Kaiser et al., 1994, Mol. Endocrinol., 8:139-147). In this study, we have investigated whether PTHrP expression and its subcellular localization is linked to cell cycle progression in a human keratinocyte cell line (HaCat), which constitutively expresses and secretes PTHrP. PTHrP mRNA and immunoreactive PTHrP were assessed in asynchronous dividing cells and in cells blocked at G1 or G2 + M phases of the cell cycle using several different protocols. The response of PTHrP mRNA expression was examined following readdition of serum in the continued presence of cycle blockers, and after release from cell cycle block, or from cell synchronization by serum deprivation. PTHrP expression was greatest in actively dividing cells when cells were in S and G2 + M phases of the cell cycle and were lowest in quiescent G1 cells. Most notable were the high levels of PTHrP mRNA and protein in cells at G2 + M phase of the cell cycle at division. Furthermore, PTHrP was localized to the nucleolus in quiescent cells, but redistributed to the cytoplasm when cells were actively dividing. Taken together, these results support a role for PTHrP in cell division in keratinocytes. In asynchronously growing cells, PTHrP expression fell as cells became confluent at a time when cell growth is inhibited and cells begin to differentiate. Mitogen stimulation of HaCaT cells resulted in a rapid increase in PTHrP mRNA expression, but was dependent upon cells being in the G1 phase of the cell cycle. Cells blocked in G1 responded to mitogen both in the continued presence of aphidicolin or when released from block. Cells blocked at G2 + M with colcemid expressed high levels of PTHrP mRNA and protein, and PTHrP mRNA did not respond further to mitogen in the continued presence of blocker. However, in cells released from block at G2 + M by addition of serum, an increase in PTHrP expression was seen coincident with the progression of cells into G1. In contrast, in a squamous cancer cell line (COLO16), basal PTHrP expression was high and was not altered during the cell cycle or by cell cycle block, consistent with association of its dysregulated expression in malignant cells. The results of this study suggest that PTHrP may have two roles in the cell cycle; one in G1 in response to mitogen, and a second at cell division when its expression is high and it is relocated from the nucleolus to the cytoplasm.

Aphidicolin↗