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Biomedical subjects

H Ozaki

Publications and source records attributed to H Ozaki.

At least 19 recordsLinked to original sources

Observation of B+ --> Lambda c+ Lambda c- K+ and B0 --> Lambda c+ Lambda c- K0 decays.

We report the first measurements of the doubly charmed baryonic B decays B --> Lambda c+ Lambda c- K. The B+ --> Lambda c+ Lambda c- K+ decay is observed with a branching fraction of (6.5(-0.9)(+1.0)+/-1.1+/-3.4)x10(-4) and a statistical significance of 15.4sigma. The B0 --> Lambda c+ Lambda c- K0 decay is observed with a branching fraction of (7.9(-2.3)(+2.9)+/-1.2+/-4.1)x10(-4) and a statistical significance of 6.6sigma. The branching fraction errors are statistical, systematic, and the error resulting from the uncertainty of the Lambda c+ --> pK- pi+ decay branching fraction. The analysis is based on 357 fb(-1) of data accumulated at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e+ e- collider.

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Study of J/psi-->pp[over],LambdaLambda[over] and observation of eta(c)-->LambdaLambda[over] at Belle.

We study the baryonic charmonium decays of B mesons B+-->etacK+ and B+-->J/psiK+, where the etac and J/psi subsequently decay into a pp[over] or LambdaLambda[over] pair. We measure the J/psi-->pp[over] and LambdaLambda[over] anisotropy parameters alphaB=-0.60+/-0.13+/-0.14 (pp[over]), -0.44+/-0.51+/-0.31 (LambdaLambda[over ]) and compare to results from e;{+}e;{-}-->J/psi formation experiments. We also report the first observation of etac-->LambdaLambda[over]. The measured branching fraction is B(etac-->LambdaLambda[over ])=(0.87(+0.24)/(-0.21)(stat)(+0.09/-0.14) (syst)+/-0.27(PDG))x10-3. This study is based on a 357 fb-1 data sample recorded on the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e+ e- collider.

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Observation of a near-threshold D(0)D[over](0)pi(0) enhancement in B-->D(0)D[over](0)pi(0)Kappa decay.

We report the first observation of a near-threshold enhancement in the D(0)D[over](0)pi(0) system from B-->D(0)D[over](0)pi(0)Kappa decays using a 414 fb(-1) data sample collected at the Upsilon(4S) resonance. The enhancement peaks at a mass M=3875.2+/-0.7(+0.3)/(-1.6) +/-0.8 MeV/c2 and the branching fraction for events in the peak is B(B-->D(0)D[over](0)pi(0)Kappa)=(1.22+/-0.31(+0.23)/(-0.30))x10(-4). The data were collected with the Belle detector at the KEKB energy-asymmetric e+ e- collider.

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Measurement of the quark mixing parameter cos2phi1 using time-dependent Dalitz analysis of B0 -->D[KS(0)pi + pi-]h0.

We present a measurement of the angle phi1 of the Cabibbo-Kobayashi-Maskawa unitarity triangle using a time-dependent Dalitz analysis of D-->KS(0)pi + pi- decays produced in neutral B meson decay to a neutral D meson and a light meson (B0-->D*h0). The method allows a direct extraction of 2phi1 and, therefore, helps to resolve the ambiguity between 2phi1 and pi-2phi1 in the measurement of sin2phi1. We obtain sin2phi1= 0.78 +/- 0.44 +/- 0.22 and cos2varphi1 = 1.87(-0.53-0.32)(+0.40 + 0.22). The sign of cos2phi1 is determined to be positive at 98.3% C.L.

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Measurement of azimuthal asymmetries in inclusive production of hadron pairs in e(+)e(-) annihilation at Belle.

The Collins effect connects transverse quark spin with a measurable azimuthal dependence in the yield of hadronic fragments around the quark's momentum vector. Using two different reconstruction methods, we find evidence of statistically significant azimuthal asymmetries for charged pion pairs in e(+)e(-) annihilation at a center-of-mass energy of 10.52 GeV, which can be attributed to a transverse polarization of the primordial quarks. The measurement was performed using a sample of 79 x 10(6) hadronic events collected with the Belle detector.

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Motility disorder in experimentally obstructed intestine: relationship between muscularis inflammation and disruption of the ICC network.

We designed a model of small intestinal obstruction in rats to investigate changes in intestinal contractility associated with the immunologically activated components in the tunica muscularis. Although histochemical study did not reveal any typical inflammatory signs such as leucocyte infiltration in the distended intestinal regions of model rats 2-3 weeks after surgical induction of intestinal obstruction, the number of ED2-positive macrophages appeared to be increased in the tunica muscularis. Expression of tumour necrosis factor (TNF)-alpha mRNA was also significantly increased, and the level of CD14 was also increased significantly in the tunica muscularis. Functional studies of distended intestinal muscle segments showed a marked decrease in absolute force stimulated by a cholinergic agent. In addition, the number of spontaneous rhythmic contractions was also reduced in the distended intestinal regions of the obstructed intestine, and this decrease was associated with a reduction in the number of interstitial cells of Cajal (ICC), as revealed by Kit-like immunoreactivity. These results suggest that, under the pro-inflammatory conditions of the tunica muscularis associated with intestinal obstruction, the release of bioactive substances, possibly from activated resident macrophages, may affect smooth muscle contractility. Furthermore, under these conditions, both the number and the function of neighbouring ICC may also be affected.

Animals↗

Role of TNF-alpha in muscularis inflammation and motility disorder in a TNBS-induced colitis model: clues from TNF-alpha-deficient mice.

Macroscopic and histological analysis revealed that the colonic inflammation induced by 2,4,6-trinitrobenzenesulphonic acid (TNBS) was of lower grade in tumour necrosis factor-alpha (TNF-alpha)(-/-) mice than in wild-type mice. Myeloperoxidase activity, an indicator of neutrophilic infiltration, was also low in both the mucosal and smooth muscle layer of the TNF-alpha(-/-) mouse colon. After the induction of inflammation with TNBS, the levels of proinflammatory cytokines, such as TNF-alpha, interleukin-1beta and interleukin-6, were elevated both in the inflamed mucosa and muscle layers in the wild-type mice; however, the productions of these cytokines were greatly reduced in the TNF-alpha(-/-) mouse colon. The contractions of isolated colonic smooth muscle strips induced by several stimulatory agents were significantly decreased after treatment with TNBS in wild-type mice; however, these contractions were scarcely affected in TNF-alpha(-/-) mice. Finally, using the organ culture method, we found that TNF-alpha directly (independent of mucosal inflammation) disturbs the smooth muscle function. These results suggest that TNF-alpha plays an essential role not only in mucosal inflammation but also in muscularis inflammation in the colon of mice with TNBS-induced colitis, and that TNF-alpha directly induces motor dysfunctions by acting on the smooth muscle.

Animals↗

Different susceptibilities of spontaneous rhythmicity and myogenic contractility to intestinal muscularis inflammation in the hapten-induced colitis.

We examined the time-dependent changes in the immunoreactivity of the smooth muscle region and the accompanying motility disorder in a hapten-induced rat model of colitis. Histological analysis and myeloperoxidase (MPO) activity indicated that inflammatory cells infiltrated into the muscle layer at 2 days after 2,4,6-trinitrobenzenesulphonic acid (TNBS) treatment. The infiltrated immune cells then gradually decreased in number, but were still present at 14 days. The expression of proinflammatory cytokine mRNAs (TNF-alpha, IL-1beta and IL-6) and proteins in the muscle layer was increased at 2 days, then began to decrease, returning to control levels at 14 days. The frequency of spontaneous rhythmicity was suppressed at 2 and 7 days, and returned to control levels at 14 days. Consistent with these observations, the immunoreactivity of the interstitial cells of Cajal network was disrupted at 2 and 7 days, which then gradually reformed at 14 days. On the other hand, the myogenic contractions induced by high K(+) and carbachol were decreased at 2 days, and were still inhibited at 14 days. These results suggest that spontaneous rhythmicity dysfunction may improve more rapidly than myogenic contractility dysfunction in a hapten-induced rat model of colitis.

Animals↗

Canine distemper virus induces apoptosis through caspase-3 and -8 activation in vero cells.

We investigated the signal-transduction pathway of canine distemper virus-Onderstepoort (CDV-Ond) vaccine strain-mediated apoptosis in Vero cells. Canine distemper virus-Onderstepoort at a multiplicity of infection (MOI) of 0.1 induced DNA fragmentation 48 h after infection. Immunofluorescence staining revealed that 57% +/- 4% of the CDV-N-protein-positive cells were terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive, and all TUNEL-positive cells were CDV-N-protein-positive, indicating that CDV-Ond induced apoptosis only in the infected cells. We also found that CDV-Ond infection induced activation of caspase-3 and caspase-8. In the semi-quantitative reverse transcription-polymerase chain reaction assay for apoptosis-related genes, the expression of mRNA of the death receptor, Fas, was also increased in CDV-Ond-infected cells. In contrast, the expressions of Bcl-2 and Bax, regulators for intrinsic apoptotic signaling through the mitochondria, did not change. These results suggest that CDV-Ond induced apoptosis by activating caspase-3, possibly through caspase-8 signaling rather than through p53/Bax-mediated, mitochondrial signaling in the infected cells.

Animals↗

Photocatalytic oxidation of low concentration 2,4-D solution with new TiO2 fiber catalyst in a continuous flow reactor.

Environmental pollution by low concentrations of 2,4-Dichlorophenoxyacetic acid (2,4-D) is a concern these days due to ever increasingly stringent regulations. Photocatalysis with immobilized TiO2 fiber is a promising oxidation method. Laboratory experiments on photocatalytic degradation of 0.045 mmol l(-1) 2,4-D with the world's first high-strength TiO2 fiber catalyst were carried out in a continuous flow reactor in which the degradations were, in general, similar to those with high 2,4-D concentrations investigated elsewhere. Degradation and mineralization of 2,4-D were significantly enhanced with no initial pH adjustments. The rate constants for total organic carbon (TOC) without pH adjustment were about two-fold bigger than the pH adjustment cases. CO2 gas measurement and carbon mass-balance were carried out for the first time, where about 34% organic carbon converted into CO2 gas during four-hour oxidation. 2,4-Dichlorophenol (2,4-DCP), phenol, benzyl alcohol and two unknowns (RT = 2.65 and 3.78 min.) were detected as aromatic intermediates while Phenol was the new aromatic in HPLC analysis. Dechlorination efficiencies were high (> 70%) in all the cases, and more than 90% efficiencies were observed in chloride mass balance. Bigger flow rates and solution temperature fixed at 20 degrees C without pH adjustment greatly enhanced 2,4-D mineralization. These results can be an important basis in applying the treatment method for dioxin-contaminated water and wastewater.

2,4-Dichlorophenoxyacetic Acid↗

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).

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Search for D0-D0 mixing in D0 --> K+ pi(-) decays and measurement of the doubly-Cabibbo-suppressed decay rate.

We have searched for mixing in the D(0)-D (0) system by measuring the decay-time distribution of D(0) --> K(+) pi(-) decays. The analysis uses 90 fb(-1) of data collected by the Belle detector at the KEKB e(+) e(-) collider. We fit the decay-time distribution for the mixing parameters x' and y' and also for the parameter R(D), which is the ratio of the rate for the doubly-Cabibbo-suppressed decay D(0)--> K+ pi(-) to that for the Cabibbo-favored decay D(0)--> K-pi(+). We do these fits both assuming CP conservation and allowing for CP violation. We use a frequentist method to obtain a 95% C.L. region in the x'(2) - y' plane. Assuming no mixing, we measure R(D) = (0.381 +/- 0.017(+0.008)(-0.016))%.

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Transfection of antisense core 2 beta1,6-N-acetylglucosaminyltransferase-1 cDNA suppresses selectin ligand expression and tissue infiltration of B-cell precursor leukemia cells.

B-cell precursor (BCP) leukemia cells infiltrate into peripheral organs and the disease often relapses. Inhibition of tissue infiltration may improve the treatment outcome of BCP-leukemia patients. Selectin ligand has been suggested to play an important role in the infiltration of leukemia cells. However, the regulation mechanisms and involvement in tissue infiltration of selectin ligand expression in BCP-leukemia cells are not fully understood. In this study, we report that BCP-leukemia cells express selectin ligand on O-sialoglycoproteins. Core 2 beta1,6-N-acetylglucosaminyltransferase-1 (C2GnT-1) is mainly expressed in BCP-leukemia cells. Transfection of the antisense C2GnT-1 cDNA resulted in a significant reduction of either selectin ligand expression or selectin-dependent cell adhesion in BCP-leukemia cell line KM3 cells. Migration ability into mouse peripheral organs was reduced significantly in the antisense transfectant. These findings suggest that C2GnT-1 regulates selectin ligand expression. Downregulation of the selectin ligand expression level inhibits tissue infiltration of BCP-leukemia cells. C2GnT-1 may be a candidate of therapeutic target for the inhibition of infiltration of leukemia cells.

Cell Movement↗

Clearance rates of cerivastatin metabolites in a patient with cerivastatin-induced rhabdomyolysis.

We report on a patient who developed acute rhabdomyolysis after taking cerivastatin. A 74-year-old hypercholestrerolaemic woman taking cerivastatin (0.15 mg/day) for 22 days complained of general muscle weakness and muscle pain. Her serum creatinine phosphokinase level was 19,190 IU/L. Serum myoglobin was over 3000 ng/mL. Serum concentration of cerivastatin at 6 h after taking the last dose (0.15 mg) was 8062.5 ng/L, which was almost 5.7 times higher than that of normal persons. The serum concentration of cerivastatin showed that the half-life of cerivastatin in this patient was 22.4 h, compared with 2.4 h for normal controls. Cerivastatin is catabolized by cytochrome P450, 3A4 and 2C8 to M-1, and by 2C8 to M-23. The ratio of M-23 to M-1 in her serum was much lower than that of control persons (0.64 vs. 2.08). She had previously taken simvastatin which is metabolized by CYP3A4, without any sign and symptoms of rhabdomyolysis. These results suggest that the slowed clearance of cerivastatin in this patient might have been compounded by cytochrome P450, 2C8 dysfunction.

Acute Disease↗

Quantification of dioxin in the sieved fraction of river sediment.

Dioxin pollution of aquatic sediments has been one of the important environmental problems in Japan. Grain size distribution and organic constituents may play important roles in dioxins contents in sediments, which have not been well investigated. This paper aims to quantify dioxins (PCDDs/Fs and co-PCBs) in sieved surface sediment fractions obtained from Kizu and Sumiyoshi Rivers in Osaka, Japan. The samples were prepared and analyzed following the 'Manual of the Survey and Measurement of Dioxins in Sediment' (Environment Agency of Japan, 2000). The results showed that TEQ concentrations of dioxins increased with decreasing grain size in sediment fractions. Sediment fractions with less than 20 microm grain size showed the highest dioxin contents. Dioxins with five and six chlorine atoms dominated other congeners in less than 20 microm fractions. The dioxin TEQ concentrations increased with total organic carbon (TOC), total carbon (TC), ignition loss (IL), total sulphur and nitrogen contents in the sediment fractions. Thus, reporting dioxin contents in sediments without considering grain size distribution may be erroneous, and conventional sedimentation and separation techniques might not be useful for treating contaminated sediments. This information can be useful for effective remediation of dioxin-contaminated sediments.

Dioxins↗

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).

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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.

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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.

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