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Biomedical subjects

J Kaneko

Publications and source records attributed to J Kaneko.

At least 37 records · Page 2Linked to original sources
PubMed2002

Observation of double cć production in e+e- annihilation at squareroot[s] approximately 10.6 GeV.

We report the observation of prompt J/psi via double cc; production from the e+e- continuum. In this process one cc; pair fragments into a J/psi meson while the remaining pair either produces a charmonium state or fragments into open charm. Both cases have been experimentally observed. We find cross sections of sigma[e+e- -->J/psieta(c)(gamma)]xB(eta(c)-->>or=4 charged)=(0.033(+0.007)(-0.006)+/-0.009) pb and sigma(e+e- -->J/psiD(*+)X)=(0.53(+0.19)(-0.15)+/-0.14) pb and infer sigma(e+e- -->J/psicc;)/sigma(e+e- -->J/psiX)=0.59(+0.15)(-0.13)+/-0.12. These results are obtained from a 46.2 fb(-1) data sample collected near the Upsilon(4S) resonance, with the Belle detector at the KEKB collider.

Journal Article↗
PubMed2002

Observation of the decay B(0)-->D(+/-)D(*-/+).

We report the first observation of the decay B(0)-->D(+/-)D(*-/+) with the Belle detector at the KEKB e(+)e(-) Collider operated at the Upsilon(4S) resonance. The sum of branching fractions B(B(0)-->D(+)D(*-))+B(B(0)-->D(-)D(*+)) is measured to be (1.17+/-0.26(+0.22)(-0.25))x10(-3) using the full reconstruction method where both charmed mesons from B0 decays are reconstructed. A consistent value [(1.48+/-0.38(+0.28)(-0.31))x10(-3)] is obtained using a partial reconstruction technique that uses only the slow pion from the D(*-)-->D(-0)pi(-) decay and a fully reconstructed D(+) to reconstruct the B(0).

Journal Article↗
PubMed2002

Early-onset ataxia with ocular motor apraxia and hypoalbuminemia: the aprataxin gene mutations.

BACKGROUND: Early-onset ataxia with hypoalbuminemia is regarded as a variant form of Friedreich ataxia in Japan. Early-onset ataxia with hypoalbuminemia and ataxia with ocular motor apraxia have been considered as the same clinical entity because of the recent identification of a common mutation in the aprataxin gene. A new clinical entity named early-onset ataxia with ocular motor apraxia and hypoalbuminemia (EAOH) has been proposed to explain these two diseases. OBJECTIVE: To disclose the clinical features of EAOH and to identify the mutations in the aprataxin gene in six patients in four Japanese families with EAOH. METHODS: The clinical features, laboratory findings, sural nerve biopsy results, and brain MRI or CT findings for these patients were evaluated, and molecular analysis was performed, which involved sequencing of the aprataxin gene directly or use of the subcloning method. RESULTS: Cerebellar ataxia and peripheral neuropathy were noted in all six patients. Ocular motor apraxia was observed in five patients; two of these patients had obvious head thrust. Choreiform movements of the limbs and mental deterioration were observed in five patients. Although foot deformity was noted in five patients, kyphoscoliosis was noted only in one patient. In all patients, hypoalbuminemia and hypercholesterolemia were evident, and brain MRI or CT showed marked cerebellar atrophy. Nerve biopsy revealed depletion of large myelinated fibers in three of the five patients examined. Molecular analysis of the aprataxin gene revealed an insertion mutation (insT at nt167) and two missense mutations (A-to-G transition at nt80 and C-to-T transition at nt95, the former being novel). CONCLUSION: We found clinical heterogeneity in the patients with EAOH in this study. With the disease course, the choreiform movements tended to reduce in degree, and hypoalbuminemia became evident. Molecular analysis identified one insertion and two missense mutations including a novel missense one, which was located at a highly conserved amino acid residue in the aprataxin gene product.

Adult↗
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↗
PubMed2002

Observation of the color-suppressed decay B( 0)-->D(0)pi(0).

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.

Journal Article↗
PubMed2002

Observation of B+ --> chi(c0)K+.

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.

Journal Article↗
PubMed2002

Correlation between optimal tacrolimus doses and the graft weight in living donor liver transplantation.

The optimal doses of tacrolimus (FK) needed to reach and maintain a target blood level vary among cases of living donor liver transplantation (LDLT). One hundred and twenty four LDLTs in 122 patients were included in this study. Tacrolimus was administered by continuous intravenous infusion at a rate of 2.5 microg/kg/h just after the operation. The time needed to reach the target blood level and the dose needed to maintain this level for 1 week (17-18 ng/mL) were defined as the initial duration (ID) and secondary dose (SD), respectively. In the first 100 LDLTs, the correlations between ID or SD and some clinical factors were examined and equations for predicting ID or SD were derived. In the latest 24 LDLTs, FK was administered using these equations and the actual and calculated ID and SD values were compared. A multiple regression analysis revealed that only the graft weight/recipient standard liver volume (GW/SLV) ratio (%) correlated with ID or SD. Stepwise regression analysis led to the equations ID (h) = 0.4 x GW/SLV ratio + 0.2; SD (microg/kg/h) = 0.02 x GW/SLV ratio - 0.4. Simple regression analysis revealed a significant correlation between the actual and calculated ID and SD values (p < 0.0001). Initial duration and SD can be estimated from equations using the GW/SLV ratio.

Adolescent↗
PubMed2001

Observation of the decay B --> Kl+l-.

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).

Journal Article↗
PubMed2001

Observation of B --> J/psi K(1)(1270).

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.

Journal Article↗
PubMed2001

Observation of Cabibbo suppressed B --> D(*)K- decays at Belle.

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.

Journal Article↗
PubMed2001

Observation of large CP violation in the neutral B meson system.

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.

Journal Article↗
PubMed2001

Phage conversion of Panton-Valentine leukocidin in Staphylococcus aureus: molecular analysis of a PVL-converting phage, phiSLT.

Staphylococcal Panton-Valentine leukocidin (PVL) is an important virulence factor, which causes leukocytolysis and tissue necrosis. Our previous report on the existence of the PVL genes (lukS-PV and lukF-PV) on the genome of prophage phiPVL in the Staphylococcus aureus strain V8 suggested the horizontal transmission of PVL genes by temperate bacteriophage among S. aureus (Kaneko, et al., 1998. Gene 215, 57-67). Here, we demonstrated the phage conversion of S. aureus leading to the production of PVL by discovery of a novel PVL-carrying phage, phiSLT (Staphylococcal Leukocytolytic Toxin) from a clinical isolate of S. aureus. phiSLT was able to lysogenize several clinical isolates of PVL-negative S. aureus strains as well as strain RN4220 at the conserved 29-bp sequence (attB) and all the lysogenized S. aureus strains had the ability to produce PVL. phiSLT had an elongated head of about 100x50 nm and a flexible tail of 400 nm long, that was quite different from phiPVL which had an isometric hexagonal head of about 60 nm diameter. The linear double-stranded phiSLT genome comprised 42,942 bp with 29-bp attachment core sequences and contained 62 open reading frames. Only 6.4 kbp region containing lysis cassette, PVL genes, attP, integrase, and orf204 of phiSLT was identical to that of phiPVL, while other regions were different from those of phiPVL. Thus, it can be concluded that PVL genes are carried by different temperate phages, which have the same attachment site.

Amino Acid Sequence↗
PubMed2001

Measurement of B(0)(d)-B_(0)(d) mixing rate from the time evolution of dilepton events at the upsilon(4S).

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.

Journal Article↗
PubMed2001

Measurement of the CP violation parameter sin2 phi(1) in B(0)(d) meson decays.

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).

Journal Article↗
PubMed2001

DNA inversion in the tail fiber gene alters the host range specificity of carotovoricin Er, a phage-tail-like bacteriocin of phytopathogenic Erwinia carotovora subsp. carotovora Er.

Carotovoricin Er is a phage-tail-like bacteriocin produced by Erwinia carotovora subsp. carotovora strain Er, a causative agent for soft rot disease in plants. Here we studied binding and killing spectra of carotovoricin Er preparations for various strains of the bacterium (strains 645Ar, EC-2, N786, and P7) and found that the preparations contain two types of carotovoricin Er with different host specificities; carotovoricin Era possessing a tail fiber protein of 68 kDa killed strains 645Ar and EC-2, while carotovoricin Erb with a tail fiber protein of 76 kDa killed strains N786 and P7. The tail fiber proteins of 68 and 76 kDa had identical N-terminal amino acid sequences for at least 11 residues. A search of the carotovoricin Er region in the chromosome of strain Er indicated the occurrence of a DNA inversion system for the tail fiber protein consisting of (i) two 26-bp inverted repeats inside and downstream of the tail fiber gene that flank a 790-bp fragment and (ii) a putative DNA invertase gene with a 90-bp recombinational enhancer sequence. In fact, when a 1,400-bp region containing the 790-bp fragment was amplified by a PCR using the chromosomal DNA of strain Er as the template, both the forward and the reverse nucleotide sequences of the 790-bp fragment were detected. DNA inversion of the 790-bp fragment also occurred in Escherichia coli DH5alpha when two compatible plasmids carrying either the 790-bp fragment or the invertase gene were cotransformed into the bacterium. Furthermore, hybrid carotovoricin CGE possessing the tail fiber protein of 68 or 76 kDa exhibited a host range specificity corresponding to that of carotovoricin Era or Erb, respectively. Thus, a DNA inversion altered the C-terminal part of the tail fiber protein of carotovoricin Er, altering the host range specificity of the bacteriocin.

Bacteriocins↗