Biomedical subjects
Publications and source records attributed to Y Chao.
We report the first observation of chi(c2) production in B meson decays. We find an inclusive B-->chi(c2)X branching fraction of (1.80(+0.23)(-0.28)+/-0.26) x 10(-3). The data set, collected with the Belle detector at the KEKB e(+)e(-) collider, consists of 31.9 x 10(6) BB events. We also present branching fractions and momentum spectra for both chi(c1) and chi(c2) production.
We report the observation of the decay mode B(+/-) --> p(-)pK(+/-)based on an analysis of 29.4 fb(-1) of data collected by the Belle detector at KEKB. This is the first example of a b-->s transition with baryons in the final state. The p(-)p mass spectrum in this decay is inconsistent with phase space and is peaked at low mass. The branching fraction for this decay is measured to be B(B+/--->p(-)pK+/-) = [4.3(+1.1)(-0.9)(stat)+/-0.5(syst)]x 10(-6). We also report upper limits for the decays B(0)-->p(-)pK(S) and B(+/-)-->p(-)p pi(+/-).
The lifetimes of the B(0) and B- mesons are extracted from 29.1 fb(-1) of data collected with the Belle detector at the KEK B factory. A fit to the decay length differences of neutral and charged B meson pairs, measured in events where one of the B mesons is fully reconstructed in several hadronic modes, yields tau(B(0)) = 1.554+/-0.030(stat)+/-0.019(syst) ps, tau(B-) = 1.695+/-0.026(stat)+/-0.015(syst) ps, and tau(B-)/tau(B(0)) = 1.091+/-0.023(stat)+/-0.014(syst).
We report a measurement of the D0-D macro(0) mixing parameter y(CP) using 23.4 fb(-1) of data collected near the Upsilon(4S) resonance with the Belle detector at KEKB. y(CP) is measured from the lifetime difference of D0 mesons decaying into the K(-)pi(+) state and the CP-even eigenstate K(-)K(+). We find y(CP) = (-0.5+/-1.0(+0.7)(-0.8))x10(-2), where the first error is statistical and the second is systematic, corresponding to a 95% confidence interval -0.030<y(CP)<0.020.
We report the first observation of color-suppressed B( 0)-->D(0)pi(0), D(*0)pi(0), D0eta, and D0omega decays, and evidence for B( 0)-->D(*0)eta and D(*0)omega. The branching fractions are B(B( 0)-->D0pi(0)) = (3.1 +/- 0.4 +/- 0.5)x10(-4), B(B( 0) -->D(*0)pi(0)) = (2.7(+0.8+0.5)(-0.7-0.6))x10(-4), B(B( 0) --> D0eta) = (1.4(+0.5)(-0.4) +/- 0.3)x10(-4), B(B( 0) --> D0omega) = (1.8 +/- 0.5(+0.4)(-0.3))x10(-4), and we set 90% confidence level upper limits of B(B( 0) --> D(*0)eta)<4.6 x 10(-4) and B(B( 0)-->D(*0)omega)<7.9 x 10(-4). The analysis is based on a data sample of 21.3 fb(-1) collected at the Upsilon(4S) resonance by the Belle detector at the KEKB e(+)e(-) collider.
The production of prompt J/psi, psi(2S), chi(c1), and chi(c2) is studied using a 32.4 fb(-1) data sample collected with the Belle detector at Upsilon(4S) and at 60 MeV below the resonance. The yield of prompt J/psi mesons in the Upsilon(4S) sample is compatible with that of continuum production; we set an upper limit B(Upsilon(4S)-->J/psiX) < 1.9 x 10(-4) at the 95% confidence level, and find sigma(e(+)e(-)-->J/psiX) = 1.47 plus/minus 0.10 plus/minus 0.13 pb. The cross sections for prompt psi(2S) and direct J/psi are measured. The J/psi momentum spectrum, production angle distribution, and polarization are studied.
Using a sample of 31.3x10(6) BB pairs collected with the Belle detector at the Upsilon(4S) resonance, we make the first observation of the charged B meson decay to chi(c0) and a charged kaon. The measured branching fraction is B(B+-->chi(c0)K+) = (6.0(+2.1)(-1.8)+/-1.1)x10(-4), where the first error is statistical, and the second is systematic.
We report a search for the flavor-changing neutral current decay B-->K(*)l+l- using a 29.1 fb(-1) data sample accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB e+e- storage ring. We observe the decay process B-->Kl+l-(l = e, mu), for the first time, with a branching fraction of B(B-->Kl+l-) = (0.75(+0.25)(-0.21)+/-0.09)x10(-6).
Fenofibrate is a potent hypolipidemic agent that lowers plasma lipid levels and may thus decrease the incidence of atherosclerosis. Here we investigated the molecular mechanism of fenofibrate's hypolipidemic action by characterizing its in vivo effects on the expression of mRNAs and the activities of pivotal enzymes in cholesterol and triglyceride metabolism in the hamster. Treatment of hamsters with fenofibrate led to a dose-dependent reduction in serum cholesterol concentrations. Studies on the incorporation of [(14)C]acetate and [(14)C]mevalonate into cholesterol suggested that this effect occurs primarily through inhibition of cholesterol biosynthesis at steps prior to mevalonate. Fenofibrate decreased levels of hepatic enzyme activities and mRNAs for 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) synthase and HMG CoA reductase. A potential mechanism for transcriptional regulation of these enzymes is via SREBP-2 that we found to be suppressed 2-fold by fenofibrate. Fenofibrate also lowered circulatory triglyceride levels. In keeping with the effect, we observed strong suppression of fatty acid synthase, acetyl-CoA carboxylase and apolipoprotein C-III mRNA and stimulation of lipoprotein lipase and acyl-CoA oxidase mRNA in the liver of fenofibrate-treated hamsters. These observations suggest that the effect of fenofibrate on triglyceride metabolism is likely to be a result of both decreased fatty acid synthesis and increased lipoprotein lipase and acyl-CoA oxidase gene expression in the liver. Surprisingly, alterations in lipoprotein lipase, acyl-CoA oxidase, acetyl-CoA carboxylase, and apolipoprotein C-III could not be observed in hamster hepatocytes incubated with fenofibric acid in vitro. These observations raise the possibility that changes in these genes may be secondary to the metabolic alterations occurring in animals but not in cultured cells and thus that the effect of fenofibrate on these genes may be indirect.
We report the first observation of the exclusive decay process B-->J/psi K(1)(1270) using a sample of 11.2M BB macro meson pairs collected in the Belle detector at the KEKB asymmetric energy e(+)e(-) collider. We measure branching fractions of B[B(0)-->J/psi K(0)(1)(1270)] = (1.30+/-0.34+/-0.32) x 10(-3) and B[B(+)-->J/psi K(+)(1)(1270)] = (1.80+/-0.34+/-0.39) x 10(-3), where the first error is statistical and the second is systematic. These modes constitute approximately 15% of the total number of B-->J/psi X decays. No evidence is seen for B-->J/psi K(1)(1400) and we set an upper limit for this branching fraction.
We report observations of the Cabibbo suppressed decays B-->D((*))K- using a 10.4 fb(-1) data sample accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB e(+)e(-) storage ring. We find that the ratios of Cabibbo suppressed to Cabibbo favored branching fractions are B(B--->D0K-)/B(B--->D0pi(-)) = 0.079+/-0.009+/-0.006, B(B(0)-->D+K-)/B(B(0)-->D+pi(-)) = 0.068+/-0.015+/-0.007, B(B--->D(*0)K-)/B(B--->D(*0)pi(-)) = 0.078+/-0.019+/-0.009, and B(B(0)-->D(*+)K-)/B(B(0)-->D(*+)pi(-)) = 0.074+/-0.015+/-0.006. These are the first observations of the B-->D+K-, D(*0)K-, and D(*+)K- decay processes.
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We present a measurement of the standard model CP violation parameter sin2 phi(1) based on a 29.1 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. One neutral B meson is fully reconstructed as a J/psi K(S), psi(2S)K(S), chi(c1)K(S), eta(c)K(S), J/psi K(L), or J/psi K(*0) decay and the flavor of the accompanying B meson is identified from its decay products. From the asymmetry in the distribution of the time intervals between the two B meson decay points, we determine sin2 phi(1) = 0.99+/-0.14(stat)+/-0.06(syst). We conclude that we have observed CP violation in the neutral B meson system.
We report a determination of the B(0)(d)-&B_(0)(d) mixing parameter Deltam(d) based on the time evolution of dilepton yields in Upsilon(4S) decays. The measurement is based on a 5.9 fb(-1) data sample collected by the Belle detector at KEKB. The proper-time difference distributions for same-sign and opposite-sign dilepton events are simultaneously fitted to an expression containing Deltam(d) as a free parameter. Using both muons and electrons, we obtain Deltam(d) = 0.463+/-0.008 (stat)+/-0.016 (syst) ps(-1). This is the first determination of Deltam(d) from time evolution measurements at the Upsilon(4S). We also place limits on possible CPT violations.
We present a measurement of the standard model CP violation parameter sin2 phi(1) (also known as sin2beta) based on a 10.5 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e(+)e(-) collider. One neutral B meson is reconstructed in the J/psiK(S), psi(2S)K(S), chi(c1)K(S), eta(c)K(S), J/psiK(L), or J/psipi(0) CP-eigenstate decay channel and the flavor of the accompanying B meson is identified from its charged particle decay products. From the asymmetry in the distribution of the time interval between the two B-meson decay points, we determine sin2 phi(1) = 0.58(+0.32)(-0.34)(stat)+0.09-0.10(syst).
Bacterial cellulose (BC) production by Acetobacter xylinum subsp. sucrofermentans BPR2001 was carried out in a 50-1 internal-loop airlift reactor in air at an initial fructose concentration of 40 g/l. The BC production rate was 0.059 g/l per h. When oxygen-enriched air was supplied instead of air, the BC production rate increased to 0.093 g/l per h, and the BC yield was enhanced from 11% in air to 18%. When the initial fructose concentrations were varied from 30 to 70 g/l, the highest BC yield (35%) the highest production rate (0.22 g/l x per h), and the highest concentration of BC produced (10.4 g/l) were observed at 60-70 g/l fructose. From the carbon mass balance calculated at the final stage of cultivation, it was observed that enhanced BC production was reflected as a decrease in both CO2 evolution and the concentration of other unknown substances, suggesting the efficient utilization of energy for BC synthesis despite O2 limitation.
Combination of selecting agents that act on different cellular mechanisms is a common strategy in cancer chemotherapy. GL331 is a new potent topoisomerase II (Topo II) poison; distinctly, paclitaxel is a microtubule-interfering cancer chemotherapeutic agent. In this study, we intended to evaluate the efficacy of combining GL331 with paclitaxel in cell killing and apoptotic induction in nasopharyngeal carcinoma NPC-TW01 cells. By MTT and internucleosomal DNA cleavage assays, we found that pretreatment or simultaneous treatment of NPC-TW01 cells with GL331 could significantly interfere with paclitaxel's cell killing and apoptosis-inducing activity. When the administration schedule was reversed, the cytotoxicity of GL331 was attenuated by paclitaxel pretreatment. The anti-cancer activity produced by combining GL331 with paclitaxel was obviously lower than the addition of the activities of two individual agents. NPC-TW01 cells were treated with GL331 and 3H-labeled paclitaxel simultaneously or with GL331 before 3H-labeled paclitaxel. In both conditions, GL331 did not reduce the [3H]paclitaxel level in the cells, suggesting that GL331's interference with paclitaxel's cell-killing and apoptosis-inducing efficacy did not result from any inhibition of cellular uptake or retention of paclitaxel. In addition, we found that GL331-induced perturbation of cell cycle progression dramatically over-rode the patterns of mitotic arrest induced by paclitaxel, and the mechanism could be the inhibition of cyclin B1/CDC2 kinase and MAD2 checkprotein activities.
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