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Biomedical subjects

Y Asano

Publications and source records attributed to Y Asano.

At least 127 records · Page 7Linked to original sources
PubMed2002

Precise measurement of B meson lifetimes with hadronic decay final states.

The lifetimes of the B(0) and B- mesons are extracted from 29.1 fb(-1) of data collected with the Belle detector at the KEK B factory. A fit to the decay length differences of neutral and charged B meson pairs, measured in events where one of the B mesons is fully reconstructed in several hadronic modes, yields tau(B(0)) = 1.554+/-0.030(stat)+/-0.019(syst) ps, tau(B-) = 1.695+/-0.026(stat)+/-0.015(syst) ps, and tau(B-)/tau(B(0)) = 1.091+/-0.023(stat)+/-0.014(syst).

Journal Article↗
PubMed2002

Measurement of the lifetime difference in D0 meson decays.

We report a measurement of the D0-D macro(0) mixing parameter y(CP) using 23.4 fb(-1) of data collected near the Upsilon(4S) resonance with the Belle detector at KEKB. y(CP) is measured from the lifetime difference of D0 mesons decaying into the K(-)pi(+) state and the CP-even eigenstate K(-)K(+). We find y(CP) = (-0.5+/-1.0(+0.7)(-0.8))x10(-2), where the first error is statistical and the second is systematic, corresponding to a 95% confidence interval -0.030<y(CP)<0.020.

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

Production of prompt charmonia in e(+)e(-) annihilation at square root of s approximately equals 0.6 GeV.

The production of prompt J/psi, psi(2S), chi(c1), and chi(c2) is studied using a 32.4 fb(-1) data sample collected with the Belle detector at Upsilon(4S) and at 60 MeV below the resonance. The yield of prompt J/psi mesons in the Upsilon(4S) sample is compatible with that of continuum production; we set an upper limit B(Upsilon(4S)-->J/psiX) < 1.9 x 10(-4) at the 95% confidence level, and find sigma(e(+)e(-)-->J/psiX) = 1.47 plus/minus 0.10 plus/minus 0.13 pb. The cross sections for prompt psi(2S) and direct J/psi are measured. The J/psi momentum spectrum, production angle distribution, and polarization are studied.

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

Evaluation of mitogen-induced responses in marine mammal and human lymphocytes by in-vitro exposure of butyltins and non-ortho coplanar PCBs.

The effects of exposure to butyltin compounds (BTs: tributyltin; TBT, dibutyltin; DBT and monobutyltin; MBT) and non-ortho coplanar PCBs (IUPAC 77, 126 and 169) on marine mammals and human lymphocyte were evaluated. Peripheral blood mononuclear cells (PBMCs) isolated from Dall's porpoises (Phocoenoides dalli), bottlenose dolphins (Tursiops truncatus), a California sealion (Zalophus californianus), a larga seal (Phocoa largha) and humans (Homo sapiens) were exposed at varying concentrations of BTs and coplanar PCBs. Concanavalin A (Con A)-stimulated mitogenesis found significantly suppressed (P<0.01) when the cells were exposed at 300 nM (89 ng/ml) of TBT and 330 nM of DBT (77 ng/ml), while MBT showed little cytotoxicity at treatment levels of up to 3,600 nM (620 ng/ml). BTs concentrations in the liver of Dall's porpoises from Japanese coastal waters ranged between 81-450 ng/g for TBT and 200-1,100 ng/g (wet wt.) for DBTs, which is greater than the cytotoxic levels registered in this study. In contrast, non-ortho coplanar PCBs did not suppress cell proliferation at concentrations of up to 30 nM (10 ng/ml). The residue levels of coplanar PCBs in the blubber of Dall's porpoises were 0.12-1.3 ng/g, which were one order of lower than those levels that do cell proliferation. When cells were exposed to a mixture of TBT/DBTand coplanar PCBs, the proliferation was significantly reduced to 33 nM DBT plus 34 nM CB-77 and 33 nM DBT plus 28 nM CB-169 mixtures, respectively. The investigations relating the contaminant-induced immunosuppression in marine mammals have been focused on persistent organochlorines such as PCBs. pesticides and dioxin compounds. However, this study suggested the possibility of BTs could also pose a serious threat to the immune functions in free-ranging marine mammals and humans.

Animals↗
PubMed2002

Insights into enzyme evolution revealed by the structure of methylaspartate ammonia lyase.

Methylaspartate ammonia lyase (MAL) catalyzes the magnesium-dependent reversible alpha,beta-elimination of ammonia from L-threo-(2S,3S)-3-methylaspartic acid to mesaconic acid. The 1.3 A MAD crystal structure of the dimeric Citrobacter amalonaticus MAL shows that each subunit comprises two domains, one of which adopts the classical TIM barrel fold, with the active site at the C-terminal end of the barrel. Despite very low sequence similarity, the structure of MAL is closely related to those of representative members of the enolase superfamily, indicating that the mechanism of MAL involves the initial abstraction of a proton alpha to the 3-carboxyl of (2S,3S)-3-methylasparic acid to yield an enolic intermediate. This analysis resolves the conflict that had linked MAL to the histidine and phenylalanine ammonia lyase family of enzymes.

Amino Acid Sequence↗
PubMed2002

Changes in osteoprotegerin and markers of bone metabolism during glucocorticoid treatment in patients with chronic glomerulonephritis.

It is well known that long-term glucocorticoid treatment causes osteoporosis, but the precise mechanism remains unclear. Recently, osteoprotegerin (OPG) has been identified as a cytokine that inhibits osteoclast differentiation. We have previously demonstrated that serum OPG is suppressed by glucocorticoids. Therefore, the present study was carried out to clarify the interrelationships between OPG and other markers of bone metabolism during glucocorticoid treatment. Thirteen patients (7 men, 6 women; 44.1 +/- 5.9 years old) with chronic glomerulonephritis who were to be treated with glucocorticoids for the first time were chosen for this study. Markers of bone metabolism, including serum OPG, osteocalcin (OC), bone-specific alkaline phosphatase activity (bAP), parathyroid hormone (PTH), tartrate-resistant acid phosphatase (TRAP), and bone mineral density (BMD), were measured before and during the treatment period. Glucocorticoids significantly reduced BMD of the lumbar spine in the 6 month treatment period (p < 0.01). Serum OPG was decreased significantly by glucocorticoids within 2 weeks (p < 0.001), and serum TRAP, a marker of bone resorption, was markedly increased (p < 0.001). On the other hand, there were no remarkable changes in serum PTH. Serum OC and bAP, markers of bone formation, were transiently reduced during the treatment period (p < 0.01). Furthermore, only serum OPG was positively and independently correlated with percentage BMD of age-matched reference (%AMR). These findings imply that glucocorticoid-induced bone loss develops rapidly via enhanced bone resorption and suppressed bone formation. Moreover, the increased bone resorption caused by glucocorticoids may be, at least in part, mediated by inhibition of OPG, not increment of PTH.

Adult↗
PubMed2002

A case of linear scleroderma with muscle calcification.

We report a 21-year-old man with linear scleroderma with muscle calcification revealed by a computed tomographic (CT) scan. Levels of serum calcium and phosphorus were normal. This is the first report of localized scleroderma with muscle calcification. Muscle involvement may cause contracture or functional abnormalities of the extremities. Therefore, CT scans may be useful in evaluating muscle involvement in patients with localized scleroderma.

Biopsy↗
PubMed2002

Clinical significance of serum surfactant protein D (SP-D) in patients with polymyositis/dermatomyositis: correlation with interstitial lung disease.

OBJECTIVE: To determine the clinical significance of serum surfactant protein D (SP-D) levels in patients with polymyositis/dermatomyositis (PM/DM). METHODS: Serum SP-D levels were assayed using a sensitive enzyme-linked immunosorbent assay in 59 patients with PM/DM and in 29 healthy controls. RESULTS: The serum level of SP-D was significantly higher in patients with PM/DM than in healthy controls (mean+/-S.D. 61.7+/-122.6 vs 31.0+/-12.4 ng/ml, P < 0.01). The serum SP-D level in patients with interstitial lung disease (ILD) was significantly higher than in those without ILD (118.7+/-220.2 vs 38.7+/-21.0 ng/ml, P < 0.001). Serum level of SP-D was correlated with the presence of ILD. The incidences of decreased vital capacity (%VC) and of decreased diffusing capacity of carbon monoxidase (%DLCO) were also significantly greater in patients with an elevated SP-D level than in those with a normal level (64 vs 7%, P < 0.02; 73 vs 27%, P < 0.01). Moreover, the serum SP-D level was inversely correlated with %VC (r=-0.452, P < 0.01) and %DLCO (r=-0.349, P < 0.05). CONCLUSION: The serum SP-D level may be a useful marker for ILD in patients with PM/DM.

Adult↗
PubMed2002

Anti-U5 snRNP antibody as a possible serological marker for scleroderma-polymyositis overlap.

OBJECTIVE: To determine the prevalence of the anti-U5 small nuclear ribonucleoprotein (snRNP) antibody in patients with systemic sclerosis. METHODS: Sera from 281 patients with systemic sclerosis, including 10 patients with overlapping polymyositis, were assayed using RNA immunoprecipitation and protein immunoprecipitation. RESULTS: Only one serum sample showed precipitation of U5 snRNA with scarce precipitation of U2, U1, U4 and U6 snRNAs. In addition, the serum precipitated a 200 kDa protein. The serum was from a 35-yr-old Japanese male patient with overlapping systemic sclerosis and polymyositis accompanied by large-cell lung carcinoma. The clinical appearance was similar to that of a case reported previously. CONCLUSION: The presence of the anti-U5 snRNP antibody in serum may be specific for scleroderma-polymyositis overlap syndrome.

Adult↗
PubMed2002

Effect of ticlopidine hydrochloride on erythropoietin-induced rise in blood pressure in patients on maintenance hemodialysis.

BACKGROUND/AIMS: A recent observation that antiplatelet-aggregation drugs, including ticlopidine hydrochloride, may prevent erythropoietin (EPO)-induced rise in blood pressure in hemodialysis (HD) patients remains a subject of particular interest. The aim of the present study was to determine the effect of ticlopidine hydrochloride on EPO-induced rise in blood pressure of HD patients with special reference to blood levels of vasoactive substances. METHODS: HD patients who showed hypertension or aggravation of preceding hypertension with EPO treatment were selected for this study. Ticlopidine hydrochloride was administered at a dose of 200 mg daily for 4 weeks. Blood pressure and serum levels of nitric oxide (NO), atrial natriuretic peptide (ANP) and endothelin (ET) were determined before and after drug administration. Patients were divided into two groups, one of which showed a drop in mean blood pressure (MBP) of >10 mm Hg (group I) and one which did not (group II), and a comparison was made between them with respect to the blood parameters. RESULTS: Five of 15 patients showed a drop of MBP of >10 mm Hg (group I), and 10 patients did not show any change in MBP (group II). In group I, there was a significant increase in blood NO levels compared to the concentrations before ticlopidine administration, while there was no change in group II. With respect to ANP and ET, there was no significant change in either of the groups. CONCLUSION: The findings suggest that the preventive effect of ticlopidine hydrochloride on EPO-induced rise in blood pressure may partly be related to the enhancement of NO production in patients on maintenance HD.

Adult↗
PubMed2002

Cellular component of vascular calcification. Fibroblasts are essential for calcium deposition in cultured cells.

It has been reported that calcium deposition and calcium content in cultured human aortic smooth muscle cells (SMC) increased when the cells are incubated in a medium with a high phosphate concentration (2 mM). To determine the cellular components or soluble factors contributing to the deposition, we cultured commercially available SMC, fibroblasts (Fb) and endothelial cells (Ed). These cells and their mixtures were incubated for 10 days in normal or high-phosphate media. Calcium crystals were stained by the von-Kossa staining and counted in the defined area. Calcium content was measured by a colorimetric assay. SMC were incubated in high-phosphate media (up to 2 mM) or beta-glycerophosphate (beta-GP) media, resulting in no obvious deposition of calcium crystals, irrespective of the coating of type I collagen on the dish. Next, various combinations of cells were cultured, and a significant number of depositions were observed only when Fb were included in the combination. The calcium content was significantly higher in cultures of SMC and Fb. The calcium deposition on single or mixture of the cells did not increase compared with control when cells were incubated in a high concentration of phosphate, cultured in the existence of beta-GP or uremic serum. We therefore conclude that Fb, rather than SMC or Ed, are essential for calcium deposition and calcium accumulation in culture. Phosphate concentration in the medium and uremic serum did not influence the deposition of calcium.

Calcification, Physiologic↗
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

Crystallization and preliminary X-ray analysis of Citrobacter amalonaticus methylaspartate ammonia lyase.

Methylaspartate ammonia lyase (MAL) catalyses the reversible alpha,beta-elimination of ammonia from L-threo-(2S,3S)-3-methylaspartic acid to give mesaconic acid. Crystals of Citrobacter amalonaticus MAL have been obtained by the hanging-drop method of vapour diffusion using ammonium sulfate as the precipitant. Three crystal forms were obtained from identical crystallization conditions, two of which (forms A and B) diffract to high resolution, whilst the third form diffracted poorly. Crystals of form A diffract to beyond 2.1 A and have been characterized as belonging to one of the enantiomorphic space groups P4(1)22 or P4(3)22, with unit-cell parameters a = b = 66.0, c = 233.1 A, alpha = beta = gamma = 90 degrees and a monomer in the asymmetric unit. Crystals of form B diffract to beyond 1.5 A and belong to space group C222, with unit-cell parameters a = 128.3, b = 237.4, c = 65.8 A, alpha = beta = gamma = 90 degrees and a dimer in the asymmetric unit. Determination of the structure of MAL will be an important step in resolving current conflicts concerning the enzyme mechanism which differ between one which places MAL as a member of the superfamily of ammonia lyases whose catalytic activity requires a cofactor formed by post-translational modification of the enzyme and another which links MAL to the enolase superfamily.

Ammonia-Lyases↗