Biomedical subjects

Y Asano

Publications and source records attributed to Y Asano.

At least 37 records · Page 2Linked to original sources

PubMed2006

Complete remission of minimal-change nephrotic syndrome induced by apheresis monotherapy.

We report a case of a 17-year-old male with relapse of minimal-change nephrotic syndrome (MCNS), in whom apheresis monotherapy without steroids or immunosuppressants resulted in complete remission. The patient initially developed nephrotic syndrome in February 1998. The first renal biopsy confirmed the diagnosis of MCNS. The patient was also found to be a carrier of hepatitis B virus. Steroid therapy was started with oral prednisolone 60 mg/day. Complete remission was achieved in 3 months, and the steroid treatment was tapered off in May 2001. During the steroid tapering, temporal exacerbation of liver function was noted. In July 2002, the patient was admitted to our hospital again due to relapse of nephrotic syndrome. Second biopsy reconfirmed the diagnosis of MCNS. Since the serum titer of HBV was elevated, apheresis monotherapy was selected to avoid the risk of steroid-induced fulminant hepatitis. Four sessions of low-density lipoprotein apheresis (LDL-A) and 5 sessions of double-filtration plasmapheresis (DFPP) reduced the proteinuria from 9.2 g/day to 0.2 g/day over 38 days without any additional medication. Proteinuria remained suppressed below 0.2 g/day for more than 12 months and no exacerbation of liver function was observed up to the final follow-up in September 2003. The present case suggested the potential of apheresis monotherapy to induce and maintain complete remission of MCNS and an important role of circulating factors in the pathogenesis of MCNS.

Adolescent↗

PubMed2006

Fanconi's syndrome and distal (type 1) renal tubular acidosis in a patient with primary Sjögren's syndrome with monoclonal gammopathy of undetermined significance.

Tubulointerstitial nephritis is a well-recognized complication in primary Sjögrens syndrome. Fanconi's syndrome is a far less frequent complication compared with distal tubular dysfunction. We here describe a 49-year-old woman with primary Sjögren's syndrome. In 1997, she was diagnosed with primary Sjögren's syndrome with tubulointerstitial nephritis, and was then treated with oral prednisolone for the tubulointerstitial nephritis. In 2002, she was referred to our hospital because of progressive fatigue. At that time, biclonal spike on serum protein (IgG-kappa and IgA-kappa) and Bence-Jones protein in urine were found. Bone marrow aspiration showed 1.0% plasma cell infiltration. Thus, a diagnosis of monoclonal gammopathy of undetermined significance (MGUS) was made. In 2004, she was again admitted to our hospital because of mild renal dysfunction and hypokalemia. Laboratory evaluation showed inappropriate, alkaline urine in hyperchloremic metabolic acidosis and a positive urine anion gap, indicating the presence of distal (Type 1) renal tubular acidosis (RTA). The urine concentration defect was also found. Further studies revealed proximal tubular dysfunction, including renal glycosuria, generalized aminoaciduria, phosphaturia, uricosuria and proximal RTA. The kidney biopsy represented diffuse and severe tubulointerstitial nephritis with dense infiltrates of lymphocytes and IgA and K light chain-positive plasma cells. No findings of multiple myeloma or malignant lymphoma were observed. In conclusion, our patient had Sjögren's syndrome with MGUS and exhibited dysfunction of both proximal tubule (Fanconi's syndrome) and distal tubule, which may be attributed to diffuse tubulointerstitial nephritis.

Acidosis, Renal Tubular↗

PubMed2005

Determination of /Vub/ from measurements of the inclusive charmless semileptonic partial rates of B mesons using full reconstruction tags.

We present a measurement of the Cabibbo-Kobayashi-Maskawa matrix element /Vub/, based on 253 fb(-1) of data collected by the Belle detector at the KEKB e+ e- asymmetric collider. Events are tagged by fully reconstructing one of the B mesons, produced in pairs from Gamma(4S). The signal for b --> u semileptonic decay is distinguished from the b --> c background using the hadronic mass Mx, the leptonic invariant mass squared q2 and the variable P+ [triple bond] Ex - /px/. The results are obtained for events with p(l)* > or = 1 GeV/c, in three kinematic regions (1) Mx < 1.7 GeV/c2, (2) Mx < 1.7 GeV/c2 combined with q2 > 8 GeV2/c2, and by (3) P+ < 0.66 GeV/c. The matrix element /Vub/ is found to be (4.09 +/- 0.19 +/- 0.20(+0.14) -0.15 +/- 0.18) x 10(-3), where the errors are statistical, systematic including Monte Carlo modeling, theoretical, and from shape function parameter determination, respectively.

Journal Article↗

PubMed2005

Measurements of B decays to two kaons.

We report measurements of B meson decays to two kaons using 253 fb(-1) of data collected with the Belle detector at the KEKB energy-asymmetric e+ e- collider. We find evidence for signals in B+ --> K0 K+ and B0 --> K0 K0 with significances of 3.0sigma and 3.5sigma, respectively. (Charge-conjugate modes are included.) The corresponding branching fractions are measured to be [symbol: see text](B+ --> K0 K+) = (1.0 +/- 0.4 +/- 0.1) x 10(-6) and [symbol: see text](B0 --> K0 K0) = (0.8 +/- 0.3 +/- 0.1) x 10(-6). These decay modes are examples of hadronic bd transitions. No signal is observed in the decay B0 --> K+ K-, and we set an upper limit of 3.7 x 10(-7) at 90% confidence level.

Journal Article↗

PubMed2005

Constitutively phosphorylated Smad3 interacts with Sp1 and p300 in scleroderma fibroblasts.

OBJECTIVE: To elucidate the role of transforming growth factor-beta (TGF-beta)/Smad signalling in the increased expression of the collagen gene in systemic sclerosis (SSc) fibroblasts. METHODS: Dermal fibroblasts from seven patients with diffuse SSc of recent onset and from seven healthy individuals were studied. The expression levels of Smad2, Smad3 and Smad4 proteins were determined by immunoblotting. Smad3 phosphorylation and the interaction of Smad3 with Sp1 or p300 were analysed using immunoprecipitation. The effects of overexpression of Smad proteins or Sp1 on the human alpha2(I) collagen gene transcription were investigated with chloramphenicol acetyltransferase (CAT) assays using the -772 COL1A2/CAT construct. RESULTS: Constitutive increased Smad3 phosphorylation was detected in SSc fibroblasts compared with normal fibroblasts. Increased interaction of Smad3 with Sp1 as well as p300 was also detected in SSc fibroblasts. The overexpression of Smad3 caused an increase of up to 5-fold in COL1A2 promoter activity in normal fibroblasts, while Smad3 caused a small increase in COL1A2 promoter activity in SSc fibroblasts. However, neither Smad2 nor Smad4 caused significant effects in COL1A2 promoter activity in normal fibroblasts or SSc fibroblasts. The overexpression of Sp1 caused further increase in COL1A2 promoter activity stimulated by TGF-beta in normal fibroblasts, but did not change COL1A2 promoter activity in the presence of TGF-beta in SSc fibroblasts. The combined overexpression of Smad3 and Sp1 significantly enhanced TGF-beta response in normal fibroblasts, but less markedly in SSc fibroblasts. CONCLUSIONS: These results suggested that SSc fibroblasts are less sensitive to exogenous TGF-beta stimulation because they are already activated by the autocrine TGF-beta loop.

Cells, Cultured↗

PubMed2005

Measurement of the wrong-sign decays D0 --> K+ pi- pi0 and D0 --> K+ pi- pi+ pi-, and search for CP violation.

Using 281 fb-1 of data from the Belle experiment recorded at or near the (4S) resonance, we have measured the rates of the "wrong-sign" decays D0 --> K+ pi- pi0 and D0 --> K+ pi- pi+ pi- relative to those of the Cabibbo-favored decays D0 --> K- pi+ pi0 and D0 --> K- pi+ pi+ pi-. These wrong-sign decays proceed via a doubly Cabibbo-suppressed amplitude or via D0-D0 mixing; the latter has not yet been observed. We obtain R(WS)(K pi pi0) = [0.229 +/- 0.015(stat)(+0.013)(-0.009)(syst)]% and R(WS)(K3pi) = [0.320 +/- 0.018(stat)(+0.018)(0.013)(syst)]%. The CP asymmetries are measured to be -0.006 +/- 0.053 and -0.018 +/- 0.044 for the K+ pi- pi0 and K+ pi- pi+ pi- final states, respectively.

Journal Article↗

PubMed2005

Clinical significance of serum levels of matrix metalloproteinase-13 in patients with systemic sclerosis.

OBJECTIVES: To investigate the clinical significance of serum matrix metalloproteinase-13 (MMP-13) levels in patients with systemic sclerosis (SSc). METHODS: Serum MMP-13 levels were determined by using a peptide substrate cleavage assay in 20 patients with diffuse cutaneous SSc (dcSSc), 20 with limited cutaneous SSc (lcSSc) and 10 normal controls. RESULTS: The serum MMP-13 levels in patients with dcSSc or lcSSc were significantly lower than those in normal controls (53.4 +/- 14.1 vs 73.2 +/- 11.5 ng/ml, P < 0.0005; 59.4 +/- 14.8 vs 73.2 +/- 11.5 ng/ml, P < 0.005, respectively), but there was no significant difference in the serum MMP-13 levels between patients with dcSSc and those with lcSSc. Disease duration prior to the diagnosis was significantly shorter in SSc patients with decreased serum MMP-13 levels than in those with normal levels (3.0 +/- 2.2 vs 8.6 +/- 7.6 yr, P < 0.0005). In addition, serum MMP-13 levels were moderately correlated with the duration of the disease (r = 0.451, P < 0.05). Though there was no significant difference in the frequencies of pulmonary fibrosis or reduced %DLco (diffusing capacity of lung for carbon monoxide), the frequency of reduced %VC (vital capacity) was significantly greater in patients with decreased serum MMP-13 levels than in those with normal levels (73 vs 24%, P < 0.05). CONCLUSIONS: Matrix metalloproteinase-13 may be involved in the fibrotic process of SSc, especially in the initiation of fibrosis. The serum MMP-13 levels may serve as a useful marker for the severity of pulmonary fibrosis in patients with SSc.

Adult↗

PubMed2005

Near-threshold diffractive psi-meson photoproduction from the proton.

Photoproduction of a phi meson on protons was studied by means of linearly polarized photons at forward angles in the low-energy region from threshold to Egamma = 2.37 GeV. The differential cross sections at t = -|t|min do not increase smoothly as Egamma increases but show a local maximum at around 2.0 GeV. The angular distributions demonstrate that phi mesons are photoproduced predominantly by helicity-conserving processes, and the local maximum is not likely due to unnatural-parity processes.

Journal Article↗

PubMed2005

Measurements of the branching fraction and polarization in B+ --> rho+ K*0 decays.

We present the results of a study of the charmless vector-vector decay B+ --> rho+ K*0, based on 253 fb(-1) of data collected with the Belle detector at the KEKB asymmetric-energy e+ e- collider. We obtain the branching fraction B(B+ --> rho+ K*0) = [8.9 +/- 1.7(stat) +/- 1.2(syst)] x 10(-6). We also perform a helicity analysis of the rho and K* vector mesons, and obtain the longitudinal polarization fraction f(L)(B+ --> rho+ K*0) = 0.43 +/- 0.11(stat)(-0.02)(+0.05) (syst).

Journal Article↗

PubMed2005

Improved evidence for direct CP violation in B0-->pi+pi- decays and model-independent constraints on phi2.

We present a new measurement of the time-dependent CP-violating parameters in B(0)--> pi(+)pi(-) decays with 275 x 10(6) BB pairs collected with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider operating at the Gamma(4S) resonance. We find 666 +/- 43 B(0) --> pi(+)pi(-) events and measure the CP-violating parameters: S(pipi) = -0.67 +/- 0.16(stat) +/- 0.06(syst) and A(pipi) = +0.56 +/- 0.12(stat) +/- 0.06(syst). We find evidence for large direct CP violation with a significance greater than 4 standard deviations for any S(pipi) value. Using isospin relations, we obtain 95.4% confidence intervals for the Cabibbo-Kobayashi-Maskawa quark-mixing matrix angle phi(2) of 0 degree < phiv(2) < 19 degrees and 71 degrees < phi(2) < 180 degrees.

Journal Article↗

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

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↗