Biomedical subjects

H J Kim

Publications and source records attributed to H J Kim.

At least 73 records · Page 4Linked to original sources

PubMed2005

Studies of CP violation in B-->J/PsiK* decays.

CP violation in B-->J/PsiK* decays is studied using an angular analysis in a data sample of 253 fb(-1) recorded with the Belle detector at the KEKB e(+)e(-) collider. The flavor separated measurements of the decay amplitudes indicate no evidence for direct CP violation. T-odd CP violation is studied using the asymmetries in triple product correlations, and the results are consistent with the standard model null predictions. The time-dependent angular analysis gives the following values of CP-violating parameters: sin(2phi(1) = 0.24 +/- 0.31 +/- 0.05 and cos(2phi(1)=0.56 +/- 0.79 +/- 0.11.

Journal Article↗

PubMed2005

Observation of B+ --> plambdagamma.

We report the first observation of the radiative hyperonic B decay B+ --> plambdagamma, using a 140 fb(-1) data sample recorded on upsilom(4S) resonance with the Belle detector at the KEKB asymmetric energy e+e- collider. The measured branching fraction is [symbol: see text](B+ --> plambdagamma) = (2.16(+0.58)(-0.53) +/- 0.20) x 10(-6). We examine its M(plambda) distribution and observe a peak near threshold. This feature is expected by the short-distance b --> sgamma transition. A search for B+ --> pepsilon0gamma yields no significant signal, and we set a 90% confidence-level upper limit on the branching fraction of [symbol: see textB+ --> pepsilon0gamma <4.6 x 10(-6).

Journal Article↗

PubMed2005

Measurement of time-dependent CP-violating asymmetries in B0 --> K(s)0K(s)0K(s)0 decay.

We present a measurement of CP-violation parameters in the B0 --> K(s)0K(s)0K(s)0 decay based on a sample of 275 x 10(6) BB pairs collected at the upsilon(4S) resonance with the Belle detector at the KEKB energy-asymmetric e+e- collider. One neutral B meson is fully reconstructed in the decay B0 --> K(s)0K(s)0K(s)0, and the flavor of the accompanying B meson is identified from its decay products. CP-violation parameters are obtained from the asymmetry in the distributions of the proper-time interval between the two B decays: S = +1.26 +/- 0.68(stat) +/- 0.20(syst) and [symbol: see text] = +0.54 +/- 0.34(stat) +/- 0.09(syst).

Journal Article↗

PubMed2005

Evidence for B0 --> D+ D- and observation of B- --> D0D- and B- -->D0D*- decays.

We report evidence for B(0) --> D(0)D(-) and the first observation of the decay modes B(-) --> D(0)D(-) and B(-) --> D(0)D(*-) based on a sample of 152 x 10(6) BB events collected by the Belle detector at KEKB. The branching fractions for B(0) --> D(+) D(-), B--->D(0)D(-), and B--> D(0)D(*-) are found to be (1.91 +/- 0.51 +/- 0.30) x10(-4), (4.83 +/- 0.78 +/- 0.58) x 10(-4), and (4.57 +/- 0.71 +/- 0.56) x 10(-4), respectively. Charge asymmetries in the B---> D(0)D(-) and B(-) --> D(0)D(*-) channels are consistent with zero.

Journal Article↗

PubMed2005

Measurement of the time-dependent CP-violating asymmetry in B(0)-->K(0)(S)pi(0)gamma decays.

We present a new measurement of CP-violation parameters in B(0)-->K(0)(S)pi(0)gamma decay based on a sample of 275 x 10(6) BB pairs collected at the Gamma(4S) resonance with the Belle detector at the KEKB energy-asymmetric e(+)e(-) collider. One of the B mesons is fully reconstructed in the B(0)-->K(0)(S)pi(0)gamma decay. The flavor of the accompanying B meson is identified from its decay products. CP-violation parameters are obtained from the asymmetry in the distribution of the proper time intervals between the two B decays. We obtain SK(0)(S)(pi(0)gamma) = -0.58(+0.46)(-0.38)(stat) +/- 0.11(syst) and AK(0)(S)(pi(0)gamma) = +0.03 +/- 0.34(stat) +/- 0.11(syst), for the K(0)(S)pi(0) invariant mass covering the full range up to 1.8 GeV/c2. We also measure the CP-violation parameters for the case B(0)-->K(*0)(-->K(0)(S)pi(0))gamma and obtain S(K(*0)gamma) = -0.79(+0.63)(-0.50)(stat) +/- 0.10(syst) for A(K(*0)gamma) fixed at 0.

Journal Article↗

PubMed2005

Observation of the D1(2420)-->Dpi + pi- decays.

We report on the first observation of D0/1(2420)-->D0pi- pi+ and D+/1(2420-->D+ pi- pi+ decays (where the contribution from the dominant known D1-->D*pi decay mode is excluded) in the B- -->D0/1pi-) and (-)B0-->D+/1pi- decays, respectively. The observation is based on 15.2 x 10(7) B(-)B events collected with the Belle detector at the KEKB collider. We also set 90% confidence level upper limits for the branching fractions of the four following decays: B- -->D0/1pi-, D01-->D(*0)pi- pi+, (-)B0-->D+/1pi-, D+/1-->D(*+) pi- pi+, B- -->D(*0)2(2460)pi-, D(*0)2 -->D(*0) pi- pi+, (-)B0-->D(*+)2(2460)pi-, D(*+)2-->D(*+)pi- pi+.

Journal Article↗

PubMed2005

Measurement of polarization and triple-product correlations in B-->phiK* decays.

We present measurements of decay amplitudes and triple-product correlations in B-->phiK* decays based on 253 fb(-1) of data recorded at the Upsilon(4S) resonance with the Belle detector at the KEKB e(+)e(-) storage ring. The decay amplitudes for the three different helicity states are determined from the angular distributions of final-state particles. The longitudinal polarization amplitudes are found to be 0.45 +/- 0.05 +/- 0.02 for B0-->phiK(*0) and 0.52 +/- 0.08 +/- 0.03 for B+ -->phiK(*+) decays. CP- and T-odd CP-violating triple-product asymmetries are measured to be consistent with zero.

Journal Article↗

PubMed2005

Expression of 14-3-3 zeta and interaction with protein kinase C in the rat retina in early diabetes.

AIMS/HYPOTHESIS: The present study aimed to investigate the expression levels of and the relationship between 14-3-3 zeta and protein kinase C (PKC) in the retina of early diabetes. METHODS: Changes in the expression levels of, and interaction between, 14-3-3 zeta and PKC were investigated by Northern and Western blot analyses, immunoprecipitation and double immunostaining in the retina of diabetic rats after 6 weeks of diabetes. PKC activity was examined using a PKC assay. RESULTS: In the diabetic retina, the molecular levels of 14-3-3 zeta were reduced, while those of PKC beta and zeta were increased. Direct interaction between 14-3-3 zeta and PKC was markedly decreased in the retina after 6 weeks of diabetes, while PKC activity was increased. CONCLUSIONS/INTERPRETATION: These findings show that a reduction in 14-3-3 zeta can induce PKC activation, suggesting that this is a main cause of visual dysfunction in the retina during diabetes.

14-3-3 Proteins↗

PubMed2005

Observation of B0-->pi0pi0.

We report the observation of the decay B0-->pi(0)pi(0), using a 253 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB e(+)e(-) collider. The measured branching fraction is B(B0-->pi(0)pi(0))=(2.3(+0.4+0.2)(-0.5-0.3))x10(-6), with a significance of 5.8 standard deviations including systematic uncertainties. We also make a measurement of the direct CP violating asymmetry in this mode.

Journal Article↗

PubMed2005

Observation of a near-threshold omegaJ/psi mass enhancement in exclusive B-->KomegaJ/psi decays.

We report the observation of a near-threshold enhancement in the omegaJ/psi invariant mass distribution for exclusive B-->KomegaJ/psi decays. The results are obtained from a 253 fb(-1) data sample that contains 275 x 10(6) BB pairs that were collected near the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric energy e(+)e(-) collider. The statistical significance of the omegaJ/psi mass enhancement is estimated to be greater than 8sigma.

Journal Article↗

PubMed2005

Inhibition of IL-10-induced STAT3 activation by 15-deoxy-Delta12,14-prostaglandin J2.

OBJECTIVES: 15-Deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) is a natural ligand that activates the peroxisome proliferator-activated receptor (PPAR)-gamma, a member of the nuclear receptor family implicated in the regulation of lipid metabolism and adipocyte differentiation. Recent data have shown that 15d-PGJ2 exerts anti-inflammatory action via inhibition of the interferon gamma (IFN-gamma)-induced Jak-STAT signalling pathway. The anti-inflammatory effect of IL-10 is mediated via activated STAT3 (signal transducer and activator of transcription 3). In this study, we investigated whether 15d-PGJ2 inhibit IL-10-induced STAT activation. METHODS: We used western blotting, flow cytometric analysis and a real-time polymerase chain reaction. RESULTS: 15d-PGJ2 blocked IL-10-induced STAT1 and STAT3 activation in primary human monocytes, macrophages and THP-1 cells. Inhibition was not specific for IL-10, as induction of STAT activation by IFN-gamma and IL-6 was also inhibited by 15d-PGJ2. Inhibition of IL-10 signalling was induced within 1 h after pretreatment of 15d-PGJ2. Other PPARgamma agonists, such as troglitazone, did not inhibit IL-10 signalling. Treatment with GW9662, a specific PPARgamma antagonist, had no effect on 15d-PGJ2-mediated inhibition of IL-10 signalling even at higher concentrations (50 microM), indicating that 15d-PGJ2 affects the IL-10-induced Jak-STAT signalling pathway via an PPARgamma-independent mechanism. Actinomycin D had no effect on 15d-PGJ2-mediated inhibition of IL-10 signalling, indicating that inhibition of IL-10 signalling occurs independently of de novo gene expression. Also, inhibitors of extracellular signal-regulated kinase (ERKs) (PD98059), p38 MAPK (mitogen-activated protein kinase) (SB203580) and protein kinase C (PKC) (GF109203X, calphostin C) had no effect on 15d-PGJ2-mediated inhibition of IL-10 signalling. These results show that MAPKs and PKC are not involved in the inhibition of IL-10 signalling. CONCLUSIONS: We showed that 15d-PGJ2 non-specifically inhibits STAT signalling of the anti-inflammatory cytokine IL-10 as well as the proinflammatory cytokine IFN-gamma. These findings indicate the possibility that 15d-PGJ2 can have adverse effects in the management of diseases in which IL-10 plays a critical role in the suppression of inflammation.

Blotting, Western↗

PubMed2005

Study of B0-->rho+/- pi-/+ time-dependent CP violation at Belle.

We present a time-dependent analysis of CP violation in B0-->rho(+/-)pi(-/+) decays based on a 140 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at KEKB. We obtain the charge asymmetry A(rhopi)(CP)=-0.16+/-0.10(stat)+/-0.02(syst). An unbinned maximum-likelihood fit to the Deltat distributions yields C(rhopi)=0.25+/-0.17(stat)+0.02-0.06(syst), DeltaC(rhopi)=0.38+/-0.18(stat)+0.02-0.04(syst), S(rhopi)=-0.28+/-0.23(stat)+0.10-0.08(syst), and DeltaS(rhopi)=-0.30+/-0.24(stat)+/-0.09(syst). The direct CP violation parameters for B-->rho(+)pi(-) and B-->rho(-)pi(+) decays are A(+-)(rhopi)=-0.02+/-0.16(stat)+0.05-0.02(syst) and A(-+)(rhopi)=-0.53+/-0.29(stat)+0.09-0.04(syst).

Journal Article↗

PubMed2005

Observation of an isotriplet of excited charmed baryons decaying to lambda+c pi.

We report the observation of an isotriplet of excited charmed baryons, decaying into Lambda(+)(c)pi(-), Lambda(+)(c)pi(0), and Lambda(+)(c)pi(+). We measure the mass differences M(Lambda(+)(c)pi)-M(Lambda(+)(c)) and widths to be 515.4(+3.2+2.1)(-3.1-6.0) MeV/c(2), 61(+18+22)(-13-13) MeV for the neutral state; 505.4(+5.8+12.4)(-4.6-2.0) MeV/c(2), 62(+37+52)(-23-38) MeV for the charged state; and 514.5(+3.4+2.8)(-3.1-4.9) MeV/c(2), 75(+18+12)(-13-11) MeV for the doubly charged state, where the uncertainties are statistical and systematic, respectively. These results are obtained from a 281 fb(-1) data sample collected with the Belle detector near the Upsilon(4S) resonance, at the KEKB asymmetric energy e(+)e(-) collider.

Journal Article↗

PubMed2005

Observation of B+-->K1(1270)+gamma.

We report the observation of the radiative decay B+-->K1(1270)(+) gamma using a data sample of 140 fb(-1) taken at the Upsilon(4S) resonance with the Belle detector at the KEKB e+e- collider. We find the branching fraction to be B(B+-->K1(1270)(+)gamma)=(4.3+/-0.9(stat.)+/-0.9(syst.))x10(-5) with a significance of 7.3sigma. We find no significant signal for B+-->K1(1400)(+)gamma and set an upper limit B(B+-->K1(1400)(+)gamma)<1.5 x 10(-5) at the 90% confidence level. We also measure inclusive branching fractions for B+-->K+pi+pi-gamma and B0-->K0pi+pi-gamma in the mass range 1 GeV/c(2)<M(K+(0)pi+pi-)<2 GeV/c(2).

Journal Article↗

PubMed2005

Study of the suppressed decays B- -->[K+pi-](D)K- and B- -->[K+pi-]Dpi-.

We report a study of the suppressed decays B--->[K(+)pi(-)](D)K- and B--->[K(+)pi(-)](D)pi(-), where [K(+)pi(-)](D) indicates that the K+pi(-) pair originates from a neutral D meson. These decay modes are sensitive to the unitarity triangle angle varphi(3). We use a data sample containing 275 x 10(6) BB pairs recorded at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e(+)e(-) storage ring. The signal for B--->[K(+)pi(-)](D)K- is not statistically significant, and we set a limit r(B)<0.27 at 90% confidence level, where r(B) is the magnitude of the ratio of amplitudes |A(B--->D 0K-)/A(B--->D0K-)|. We observe a signal with 6.4sigma statistical significance in the related mode, B--->[K(+)pi(-)](D)pi(-).

Journal Article↗

PubMed2005

Observation of B0-->D*sJ(2317)+K- decay.

The decays B0-->D+sJK- and B0-->D-sJpi+ are studied for the first time. A significant signal is observed in the B0-->D*sJ(2317)+K- decay channel with B(B0-->D*sJ(2317)+K-) x B(D*sJ(2317)+-->D+spi0)=(5.3(+1.5)(-1.3)+/-0.7+/-1.4) x 10(-5). No signals are observed in the B0-->D*sJ(2317)-pi+, B0-->DsJ(2460)+K-, and B 0-->DsJ(2460)-pi+ decay modes, and upper limits are obtained. The analysis is based on a data set of 140 fb(-1) collected by the Belle experiment at the asymmetric e+e- collider KEKB.

Journal Article↗

PubMed2005

Measurement of the branching fraction and CP asymmetry in B+ --> rho+pi0.

We report a measurement of the branching fraction for the decay B+ --> rho(+) pi(0) based on a 140 fb(-1) data sample collected with the Belle detector at the KEKB asymmetric e(+)e(-) collider. We measure the branching fraction B(B(+) --> rho(+)pi(0)) = (13.2 +/- 2.3(stat)(+1.4)(-1.9)(syst)) x 10(-6), and the CP-violating asymmetry A(CP)(B-/+ -->rho(-/+)pi(0))=0.06 +/- 0.17(stat)(+0.04)(-0.05)(syst).

Journal Article↗

PubMed2005

Phorbol ester up-regulates aldose reductase expression in A549 cells: a potential role for aldose reductase in cell cycle modulation.

Over-expression of aldose reductase (AR) has been observed in many cancer cells. To clarify the role of AR in tumor cells, we investigated the pathways mediating expression of the AR gene induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), a potent tumor promoter. In A549 human lung adenocarcinoma cells, TPA elicited a dose- and time-dependent increase in AR mRNA level with an elevated enzyme activity. The TPA-induced increase in mRNA level and promoter activity of the AR gene was significantly attenuated in the presence of an inhibitor of protein kinase C, tyrosine kinase, or nuclear factor kappaB (NF-kappaB). TPA augmented the NF-kappaB-dependent gene transcription, indicating the involvement of NF-kappaB in this regulation. Accumulation of TPA-treated cells in S phase was almost completely abolished in the presence of ethyl 1-benzyl-3-hydroxy-2(5H)-oxopyrrole-4-carboxylate, an AR inhibitor. Taken together, TPA augmented the promoter activity of the AR gene via the activation of protein kinase and NF-kappaB. The inhibition of AR may assist in the chemotherapy of malignant tumors by suppressing the rapid growth of cancer cells.

Aldehyde Reductase↗