Biomedical subjects

H-C Huang

Publications and source records attributed to H-C Huang.

At least 37 records · Page 2Linked to original sources

PubMed2003

Measurement of time-dependent CP-violating asymmetries in B0-->phiK(0)S, K+K-K0(S), and eta'K0(S) decays.

We present an improved measurement of CP-violation parameters in B0-->phiK(0)(S), K(+)K(-)K(0)(S), and eta(')K(0)(S) decays based on a 140 fb(-1) data sample 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 one of the specified decay channels, and the flavor of the accompanying B meson is identified from its decay products. CP-violation parameters for each of the three modes are obtained from the asymmetries in the distributions of the proper-time intervals between the two B decays. We find that the observed CP asymmetry in the B-->phiK(0)(S) decay differs from the standard model (SM) expectation by 3.5 standard deviations, while the other cases are consistent with the SM.

Journal Article↗

PubMed2003

Observation of the D(sJ)(2317) and D(sJ)(2457) in B decays.

We report the first observation of the B-->Dmacr;D(sJ)(2317) and B-->Dmacr;D(sJ)(2457) decays based on 123.8x10(6) BBmacr; events collected with the Belle detector at KEKB. We observe the D(sJ)(2317) decay to D(s)pi(0) and the D(sJ)(2457) decay to the D(*)(s)pi(0) and D(s)gamma final states. We also set 90% C.L. upper limits for the decays D(sJ)(2317)-->D(*)(s)gamma, D(sJ)(2457)-->D(*)(s)gamma, D(sJ)(2457)-->D(s)pi(0), and D(sJ)(2457)-->D(s)pi(+)pi(-).

Journal Article↗

PubMed2003

Observation of B-->K*l+l-.

We report the observation of the flavor-changing neutral current decay B-->K(*)l(+)l(-) and an im-proved measurement of the decay B-->Kl(+)l(-), where l represents an electron or a muon, with a data sample of 140 fb(-1) accumulated at the Upsilon(4S) resonance with the Belle detector at KEKB. The results for the branching fractions are B(B-->K(*)l(+)l(-))=(11.5(+2.6)(-2.4)+/-0.8+/-0.2)x10(-7) and B(B-->Kl(+)l(-))=(4.8(+1.0)(-0.9)+/-0.3+/-0.1)x10(-7), where the first error is statistical, the second is systematic and the third is from model dependence.

Journal Article↗

PubMed2003

Evidence for B0-->pi0pi0.

We report evidence for the decay B0-->pi(0)pi(0). The analysis is based on a data sample of 152x10(6) BBmacr; pairs collected at the Upsilon(4S) resonance with the Belle detector at the KEKB e(+)e(-) storage ring. We detect a signal for B0-->pi(0)pi(0) with a significance of 3.4 standard deviations, and measure the branching fraction to be [1.7+/-0.6(stat)+/-0.2(syst)]x10(-6).

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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.

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PubMed2003

Evidence for B-->phiphiK.

We report evidence for the decay mode B-->phiphiK based on an analysis of 78 fb(-1) of data collected with the Belle detector at KEKB. This is the first example of a b-->sssss transition. The branching fraction for this decay is measured to be B(B+/--->phiphiK+/-)=(2.6(+1.1)(-0.9)+/-0.3)x10(-6) for a phiphi invariant mass below 2.85 GeV/c(2). Results for other related charmonium decay modes are also reported.

Journal Article↗

PubMed2003

Observation of B-/+-->rho-/+rho0 decays.

We report the first observation of the charmless vector-vector decay process B-/+-->rho(-/+)rho(0). The measurement uses a 78 fb(-1) data sample collected with the Belle detector at the KEKB asymmetric e(+)e(-) collider operating at the Upsilon(4S) resonance. We obtain a branching fraction of B(B-/+-->rho(-/+)rho(0))=[31.7+/-7.1(stat)+3.8-6.7(syst)]x10(-6). An analysis of the rho helicity-angle distributions gives a longitudinal polarization fraction of Gamma(L)/Gamma=0.95+/-0.11(stat)+/-0.02(syst). We also measure the direct-CP-violating asymmetry A(CP)(B-/+-->rho(-/+)rho(0))=0.00+/-0.22(stat)+/-0.03(syst).

Journal Article↗

PubMed2003

Measurement of branching fractions and polarization in B-->phiK(*) decays.

We present the first measurement of decay amplitudes in B-->phiK* and measurements of branching fractions in B-->phiK(*) decays based on 78.1 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 different phiK*0 helicity states are measured from the angular distributions of final state particles in the transversity basis. The longitudinal and transverse complex amplitudes are |A0|2=0.43+/-0.09+/-0.04, |A(perpendicular)|2=0.41+/-0.10+/-0.04, arg((A(parallel))=-2.57+/-0.39+/-0.09, and arg((A(perpendicular))=0.48+/-0.32+/-0.06. The direct CP-violating asymmetries are found to be consistent with zero.

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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↗

PubMed2003

Observation of B0 -->D0K0 and B0 -->D0K*0 decays.

We report on a search for B(0)-->D(*0)K(*0) decays based on 85 x 10(6) BB events collected with the Belle detector at KEKB. The B(0)-->D0K(0) and B(0)-->D0K(*0) decays have been observed for the first time with the branching fractions B(B(0)-->D0K(0))=(5.0(+1.3)(-1.2)+/-0.6)x10(-5) and B(B(0)-->D0K(*0))=(4.8(+1.1)(-1.0)+/-0.5)x10(-5). No significant signal has been found for the B(0)-->D(*0)K*0) and B(0)-->D(*0)K(*0) decay modes, and upper limits at 90% C.L. are presented.

Journal Article↗

PubMed2003

Studies of the decay B+/- -->D(CP)K+/-.

We report studies of the Cabibbo-suppressed decay B+/--->D(CP)K+/-, where D(CP) denotes CP eigenstates of the D0-D0; system. The analysis is based on a 29.1 fb(-1) sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e(+)e(-) storage ring. We measure ratios of branching fractions, relative to Cabibbo-favored B+/--->D(CP)pi(+/-), of B(B--->D1K-)/B(B--->D1pi(-))=0.125+/-0.036+/-0.010 and B(B--->D2K-)/B(B--->D2pi(-))=0.119+/-0.028+/-0.006; the index 1 (2) denotes the CP=+1 (-1) eigenstate. We also extract the partial rate asymmetries for B+/--->D(CP)K+/-, finding A(1)=0.29+/-0.26+/-0.05 and A(2)=-0.22+/-0.24+/-0.04.

Journal Article↗

PubMed2003

Observation of the decay B0-->lambda+cp.

We report the measurement of the charmed baryonic decay B(0)-->Lambda(+)(c)p with a branching fraction of (2.19(+0.56)(-0.49)+/-0.32+/-0.57)x10(-5) and a statistical significance of 5.8 sigma. The errors are statistical, systematic, and the error of the Lambda(+)(c)-->pK(-)pi(+) decay branching fraction. This is the first observation of a two-body baryonic B decay. The analysis is based on 78.2 fb(-1) of data accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e(+)e(-) collider.

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PubMed2003

Measurement of branching fractions for B-->eta(c)K(*) decays.

We report measurements of branching fractions for charged and neutral B-->eta(c)K decays where the eta(c) meson is reconstructed in the K(0)(S)K+/-pi(-/+), K+K-pi(0), K(*0)K-pi(+), and pp; decay channels. The neutral B0 channel is a CP eigenstate and can be used to measure the CP violation parameter sin(2phi(1). We also report the first observation of the B0-->eta(c)K(*0) mode. The results are based on an analysis of 29.1 fb(-1) of data collected by the Belle detector at KEKB.

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PubMed2003

Measurement of the electroweak penguin process B-->X(s)l+l-.

We report the first measurement of the branching fraction for the inclusive decay B-->X(s)l(+)l(-), where l is either an electron or a muon, and X(s) is a hadronic recoil system that contains an s quark. We analyzed a data sample of 65.4 x 10(6) B meson pairs collected with the Belle detector at the KEKB e(+)e(-) asymmetric-energy collider. We find B(B-->X(s)l(+)l(-))=[6.1 +/-1.4(stat) +1.4-1.1(syst)] x 10(-6) for dilepton masses greater than 0.2 GeV/c(2).

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PubMed2003

Temporal and spatial expression of bone morphogenetic proteins in extracorporeal shock wave-promoted healing of segmental defect.

Extracorporeal shock wave (ESW) is a noninvasive acoustic wave, which has recently been demonstrated to promote bone repair. The actual healing mechanism triggered by ESW has not yet been identified. Bone morphogenetic proteins (BMP) have been implicated as playing an important role in bone development and fracture healing. In this study, we aimed to examine the involvement of BMP-2, BMP-3, BMP-4, and BMP-7 expression in ESW promotion of fracture healing. Rats with a 5-mm segmental femoral defect were given ESW treatment using 500 impulses at 0.16 mJ/mm(2). Femurs and calluses were subjected to immunohistochemistry and RT-PCR assay 1, 2, 4, and 8 weeks after treatment. Histological observation demonstrated that fractured femurs received ESW treatment underwent intensive mesenchymal cell aggregation, hypertrophic chondrogenesis, and endochondral/intramembrane ossification, resulting in the healing of segmental defect. Aggregated mesenchymal cells at the defect, chondrocytes at the hypertrophic cartilage, and osteoblasts adjunct to newly formed woven bone showed intensive proliferating cell nuclear antigen expression. ESW treatment significantly promoted BMP-2, BMP-3, BMP-4, and BMP-7 mRNA expression of callus as determined by RT-PCR, and BMP immunoreactivity appeared throughout the bone regeneration period. Mesenchymal cells and immature chondrocytes showed intensive BMP-2, BMP-3, and BMP-4 immunoreactivity. BMP-7 expression was evident on osteoblasts located at endochondral ossification junction. Our findings suggest that BMP play an important role in signaling ESW-activated cell proliferation and bone regeneration of segmental defect.

Animals↗

PubMed2003

Cyclooxygenase expression in splanchnic hyposensitivity to glypressin of bleeding portal hypertensive rats.

BACKGROUND: Prostacyclin mediates, at least partly, the splanchnic vascular hyporesponsiveness to glypressin in bleeding portal hypertensive rats. This study investigated the relative contribution of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in the splanchnic hyposensitivity to glypressin in rats with portal hypertension induced by partial portal vein ligation (PVL). METHODS: Fourteen days after the operation, the rats were divided into without- and with-bleeding groups. Three series of PVL rats were used to investigate (i). the haemodynamic effects of glypressin (0.07 mg x kg(-1) intravenously), (ii). COX-1/COX-2 mRNA expression over abdominal aorta and superior mesenteric artery and (iii). plasma levels of 6-keto-prostaglandin-F1alpha. In rats with a hypotensive haemorrhage, 4.5 mL of blood was withdrawn and 50% of the withdrawn blood was re-infused before blood and vessel sampling or the administration of glypressin. RESULTS: Splanchnic hyposensitivity to glypressin was demonstrated in the haemorrhage-transfused PVL rats with enhanced COX-1 expression of superior mesenteric artery and increased plasma levels of 6-keto-prostaglandin-F1alpha. There were no differences in the COX-2 expression of superior mesenteric artery and COX-1 and COX-2 expressions of abdominal aorta between without- and with-bleeding groups. CONCLUSION: In portal hypertensive rats with acute haemorrhage, COX-1 over-expression in the superior mesenteric artery plays a role in mediating the splanchnic hyposensitivity to glypressin.

Animals↗

PubMed2002

Measurement of the B(0)-B(0) mixing parameter Deltam(d) using semileptonic B0 decays.

We present a measurement of the B0-Bmacr;(0) mixing parameter Deltam(d) using neutral B meson pairs in 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. We exclusively reconstruct one neutral B meson in the semileptonic B0-->D(*-)l(+)nu decay mode and identify the flavor of the accompanying B meson from its decay products. From the distribution of the time intervals between the two flavor-tagged B meson decay points, we obtain Deltam(d)=(0.494+/-0.012+/-0.015) ps(-1), where the first error is statistical and the second error is systematic.

Journal Article↗

PubMed2002

Increased protein stability as a mechanism that enhances Nrf2-mediated transcriptional activation of the antioxidant response element. Degradation of Nrf2 by the 26 S proteasome.

Nrf2 (NF-E2-related factor 2) is a central transcription factor involved in the transcriptional activation of many genes encoding phase II drug-metabolizing enzymes via the antioxidant response element. Nrf2 has previously been found to undergo nuclear translocation by a phosphorylation-dependent mechanism mediated by protein kinase C in HepG2 cells treated with tert-butylhydroquinone, beta-naphthoflavone, or 12-O-tetradecanoylphorbol-13-acetate. In the present report, we have found that the levels of Nrf2 were increased in cells treated with tert-butylhydroquinone or beta-naphthoflavone by a post-transcriptional mechanism. Treatment of HepG2 cells with cycloheximide resulted in the loss of Nrf2 within 30 min. By contrast, treatment with the proteasome inhibitors (lactacystin or MG-132) caused an accumulation of Nrf2 as well as an induction of reporter gene activity in cells transfected with the GSTA2 antioxidant response element-chloramphenicol acetyl transferase construct. Similarly, the protein phosphatase inhibitor okadaic acid also caused an accumulation of Nrf2, whereas the reverse effects were observed with PD 98059 and U 0126, two compounds that block the activation of the MAPK/ERK signaling cascade. These data suggest that Nrf2 is degraded by the ubiquitin-dependent pathway and that phosphorylation of Nrf2 leads to an increase in its stability and subsequent transactivation activity.

Antioxidants↗