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Biomedical subjects

K Abe

Publications and source records attributed to K Abe.

At least 109 records · Page 6Linked to original sources

Observation of B0-->omega K0, B+-->eta pi+, and B+-->eta K+ and study of related decays.

We present measurements of branching fractions and charge asymmetries for seven B-meson decays with an eta, eta', or omega meson in the final state. The data sample corresponds to 89x10(6) BB pairs produced from e(+)e(-) annihilation at the Upsilon(4S) resonance. We measure the following branching fractions in units of 10(-6): B(B+-->eta pi(+))=5.3+/-1.0+/-0.3, B(B+-->eta K+)=3.4+/-0.8+/-0.2, B(B0-->eta K0)=2.9+/-1.0+/-0.2 (<5.2, 90% C.L.), B(B+-->eta(')pi(+))=2.7+/-1.2+/-0.3 (<4.5, 90% C.L.), B(B+-->omega pi(+))=5.5+/-0.9+/-0.5, B(B+-->omega K+)=4.8+/-0.8+/-0.4, and B(B0-->omega K0)=5.9(+1.6)(-1.3)+/-0.5. The charge asymmetries are A(ch)(B+-->eta pi(+))=-0.44+/-0.18+/-0.01, A(ch)(B+-->eta K+)=-0.52+/-0.24+/-0.01, A(ch)(B+-->omega pi(+))=0.03+/-0.16+/-0.01, and A(ch)(B+-->omega K+)=-0.09+/-0.17+/-0.01.

Journal Article↗

Observation of radiative B-->phi K gamma decays.

The radiative decay B-->phi K gamma is observed for the first time. The branching fraction for the charged B--->phi K- gamma decay mode is measured to be B(B--->phi K- gamma)=(3.4+/-0.9+/-0.4)x10(-6). The photon energy distribution for the B--->phi K- gamma decay is presented. The signal for the neutral B(0)-->phi K(0)gamma decay mode is not statistically significant and an upper limit, B(B(0)-->phi K(0)gamma)<8.3x10(-6) at 90% C.L., is set. The analysis is based on a data set of 90 fb(-1) collected by the Belle experiment at the e(+)e(-) asymmetric collider KEKB.

Journal Article↗

Measurements of the D(sJ) resonance properties.

We report measurements of the properties of the D(+)(sJ)(2317) and D(+)(sJ)(2457) resonances produced in continuum e(+)e(-) annihilation near sqrt[s]=10.6 GeV. The analysis is based on an 86.9 fb(-1) data sample collected with the Belle detector at KEKB. We determine the masses to be M(D(+)(sJ)(2317))=2317.2+/-0.5(stat)+/-0.9(syst) MeV/c(2) and M(D(+)(sJ)(2457))=2456.5+/-1.3(stat)+/-1.3(syst) MeV/c(2). We observe the radiative decay mode D(+)(sJ)(2457)-->D(+)(s)gamma and the dipion decay mode D(+)(sJ)(2457)-->D(+)(s)pi(+)pi(-) and determine their branching fractions. No corresponding decays are observed for the D(sJ)(2317) state. These results are consistent with the spin-parity assignments of 0(+) for the D(sJ)(2317) and 1(+) for the D(sJ)(2457).

Journal Article↗

GABAA receptor-mediated inhibition by ethanol of long-term potentiation in the basolateral amygdala-dentate gyrus pathway in vivo.

Although ethanol has been reported to inhibit the induction of long-term potentiation in hippocampal CA1 and dentate gyrus synapses of rats, very little is known about the effect of ethanol on synaptic plasticity in other brain regions. Therefore, in the present study, we investigated the effect of ethanol on long-term potentiation in synaptic pathway from the basolateral amygdala to the dentate gyrus by using anesthetized rats in vivo. I.v. (20-40% x 2 ml/kg) or i.c.v. (30-40% x 5 microl) administration of ethanol did not affect the basal amplitude of dentate gyrus field potential evoked by basolateral amygdala stimulation, but significantly inhibited the induction of long-term potentiation following application of tetanic stimulation. Since long-term potentiation in this pathway was independent of N-methyl-d-aspartate receptors, the inhibitory effect of ethanol is unlikely to be caused by suppression of N-methyl-d-aspartate receptor function. Alternatively, long-term potentiation in this pathway was significantly suppressed by the benzodiazepine agonist diazepam (2 mg/kg, i.p.), and the inhibitory effect of ethanol was abolished by the GABAA receptor channel blocker picrotoxin (1 mg/kg, i.p.). The present study demonstrates that ethanol inhibits the induction of long-term potentiation in the basolateral amygdala-dentate gyrus pathway by enhancing GABAA receptor-mediated neurotransmission.

Amygdala↗

cDNA of canine heat shock protein 70 (HSP70).

Full-length canine HSP70 cDNA was sequenced and the expression of HSP70 mRNA was investigated. The full-length cDNA sequence of the HSP70 gene (2322 bp) contained a single long open reading frame (1920 bp) coding a protein of 640 amino acids. The amino acid sequence of the canine HSP70 gene shared about 90-95% sequence similarity with bovine, human and mouse HSP70 proteins. Southern blot analysis with HSP70 probe gave three distinct bands of 9.4 kb, 5 kb and 4.4 kb in BamHI digests and two distinct bands of 19 kb and 4 kb in EcoRI digests. Canine HSP70 mRNA was detectable in canine peripheral blood mononuclear cells and stomach but not in liver, kidney, spleen, small intestine, large intestine and skin of dogs.

Amino Acid Sequence↗

The membrane attack complex, C5b-9, up regulates collagen gene expression in renal tubular epithelial cells.

Evidence suggesting a direct role for proteinuria in the pathogenesis of renal tubulointerstitial fibrosis is accumulating. However the mechanism by which proteinuria leads to injury is unknown. In proteinuric states complement proteins are filtered through the glomerulus and could contribute to the tubular damage. The aim of this study was to investigate the role of complement activation in the progression of interstitial fibrosis. To determine whether complement activation may be responsible for the pro-fibrotic response that occurs in the tubulointerstitial compartment we stimulated primary cultures of proximal tubular epithelial cells with membrane attack complex, C5b-9. This led to increased mRNA concentrations of both collagen type IV and its intracellular chaperone, Heat Shock Protein 47 (HSP47). To determine whether this occurred in vivo Adriamycin was used to induce proteinuria in female Balb/c mice. The expression of collagen type IV and HSP47 was increased in proteinuric mice compared to control mice. In proteinuric mouse kidney, C3 was deposited at sites of tubulointerstitial injury and there was a relationship between C3 deposition and immunochemical staining for collagen type IV and HSP47. In situ hybridization suggested that the renal tubular epithelium was actively expressing HSP47 mRNA and, by implication, excess collagen. These observations support the hypothesis that complement activation on tubular epithelial cells can directly increase the pro-fibrotic process associated with tubulointerstitial damage.

Albuminuria↗

Quantitative evaluation of changes in anterior segment biometry by peripheral laser iridotomy using newly developed scanning peripheral anterior chamber depth analyser.

AIM: Using the newly developed scanning peripheral anterior chamber depth analyser (SPAC), the effects of peripheral laser iridotomy (PLI) on peripheral anterior chamber depth (PACD) were determined quantitatively as was the association between PACD and chronic elevation of intraocular pressure (IOP) after PLI. METHODS: 16 eyes of 15 patients with acute primary angle closure glaucoma (PACG) attack, 14 eyes of 14 patients with narrow angle and PACG attack in their fellow eyes, and 13 eyes of seven patients with chronic angle closure glaucoma (CACG) were enrolled. The SPAC scanned the anterior ocular segment from the optical axis to the limbus and took 21 consecutive slit lamp images at 0.4 mm intervals. A computer installed program automatically evaluated the PACD and the averaged values of three measurements were employed for analysis. RESULTS: PLI significantly increased PACD and changed the iris contour from convex to flat or concave in all the enrolled eyes. The extent of the PLI induced PACD increase was enhanced with increasing distance from the optical axis. Comparing PACDs after PLI, eyes that received prophylactic PLI showed the greatest extent of PLI induced PACD increase, followed by eyes with CACG and eyes with PACG attack. The PACD of eyes with PACG attack was almost the same as that of the fellow eyes of PACG attack before prophylactic PLI. Eyes with PACG attack showed poorer IOP control after PLI than eyes with narrow angle and CACG with PLI. CONCLUSIONS: PLI significantly increases PACD and the small PLI induced opening of PACD may contribute to chronic IOP elevation after PLI.

Aged↗

Severity dependent up-regulations of LOX-1 and MCP-1 in early sclerotic changes of common carotid arteries in spontaneously hypertensive rats.

Lectin-like oxidized low-density lipoprotein receptor (LOX-1) and monocyte chemoattractant protein-1 (MCP-1) are molecules involving in the initiation and progression of atherosclerosis. In order to examine a possible difference in LOX-1 and MCP-1 expressions depending on the severity of early stage of atherosclerosis, we investigated atherosclerotic changes by exposure to hypertension and hyperlipidemia in common carotid arteries (CCAs) of stroke-prone spontaneously hypertensive rat (SHR-SP). Three rat model groups such as control [Wistar Kyoto rat (WKY) group], hypertension (SHR-SP group) and hypertension + hyperlipidemia [SHR-SP + high fat and cholesterol (HFC) group] were used. Body weights, brain weights, systolic blood pressures and serum levels of total cholesterol, low-density lipoprotein and triglyceride were measured at 0, 5, 10 and 15 days after appropriate diet. Immunohistochemistry showed that the positive area and the strength of LOX-1 and MCP-1 were larger in the SHR-SP + HFC group than in the SHR-SP group, while no immunoreactivities were found in the WKY group. Conventional RT-PCR and real-time PCR analyses showed that mRNAs of those in the SHR-SP group were higher with greater up-regulation in the SHR-SP + HFC group. LOX-1 and MCP-1 expressions were coordinately up-regulated at mRNA and protein levels in an early stage of sclerosis depending on the severity of atherosclerotic stress. Activations of LOX-1 and MCP-1 are collectively involved in the early stage of atherosclerosis.

Animals↗

Pirfenidone attenuates expression of HSP47 in murine bleomycin-induced pulmonary fibrosis.

Heat shock protein (HSP) 47, a collagen-specific molecular chaperone, is involved in the processing and/or secretion of procollagen. The present study was undertaken to investigate whether treatment with the antifibrotic drug pirfenidone attenuates the bleomycin (BL)-induced overexpression of HSP47 in the lungs. Male ICR mice were intravenously injected with BL or saline (SA). Pirfenidone or control drug (CD) was administered 14 days after commencement of BL or SA, and continued throughout the course of the experiment. The mice were randomly divided into three experimental groups: 1) SA-treated with CD (SA group); 2) BL-treated with CD (BL group); and 3) BL-treated with pirfenidone (pirfenidone group). Lungs of the pirfenidone group showed a marked reduction of fibrotic lesions compared with the corresponding BL group. Immunohistochemical studies showed that BL treatment significantly increased the number of macrophages, myofibroblasts, HSP47-positive type II pneumocytes and HSP47-positive interstitial spindle-shaped cells. Treatment with pirfenidone significantly reduced the number of these cells compared with the corresponding BL group. Furthermore, treatment with pirfenidone significantly suppressed the BL-induced increase of the positive ratio of HSP47 and alpha-smooth muscle actin to interstitial spindle-shaped cells. The present study results showed that pirfenidone inhibited heat shock protein 47-positive cells and myofibroblasts, the principal cells responsible for the accumulation and deposition of extracellular matrix seen in pulmonary fibrosis.

Analysis of Variance↗

Expression and activity analyses of CTLA4 in peripheral blood lymphocytes in systemic lupus erythematosus patients.

The objective of this study was to determine the expression and activity of CTLA4 in T-cells of systemic lupus erythematosus (SLE) patients. Expression of CTLA4 on freshly isolated peripheral blood T-cells was evaluated in 33 SLE patients and 25 controls using flow cytometry. The T-cells from 19 SLE patients and 22 controls were stimulated and cultured with Chinese hamster ovary cells expressing CD80 (CHO-CD80) or with CHO cells. T-cell proliferation was determined with [3H] thymidine incorporation (CPM), and the inhibitory effect of CTLA4 on T-cell proliferation was evaluated by the ratio of CPM for T-cells with CHO-CD80 cells to that of T-cells with CHO cells (the CHO-CD80/CHO ratio). Intracellular CTLA4 expression in freshly isolated peripheral blood T-cells was significantly higher in SLE patients than the controls (P < 0.05), but there was no correlation with clinical features or disease activity. The CHO-CD80/CHO ratio of SLE patients was significantly higher than that of the controls (P < 0.05). Among SLE patients, the CHO-CD80/CHO ratio of patients with lupus nephritis was significantly higher than that of patients without lupus nephritis (P < 0.05). In conclusion, our data suggest that CTLA4 expression is not impaired in SLE patients, but there is a possibility of decreased inhibitory effect of CTLA4 involved in the pathogenesis of SLE.

Adolescent↗

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↗

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↗

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↗

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).

Journal Article↗

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.

Journal Article↗

Comparison of conventional and diffusion-weighted MRI and proton MR spectroscopy in patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like events.

The mechanism of neurological disturbances in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is controversial. We studied 12 patients with MELAS using conventional and diffusion weighted MRI (DWI) and MR spectroscopy (MRS), to look at the physiopathology of the stroke-like events. Although conventional MRI showed lesions in all patients, DWI was more sensitive. One patient did not show high signal on DWI 48 h after a from stroke-like episode, but MRS demonstrated a lactate peak in left occipital lobe; 2 weeks after the attack, high signal was demonstrated on the right frontal lobe where MRS had shown a lactate peak. Our findings suggest a possible predictive ability of (1)H-MRS, in showing early MELAS lesions and supports the hypothesis that mitochondrial metabolic dysfunction may precedes abnormalities on DWI.

Adolescent↗

Observation of a significant excess of pi0pi0 events in B meson decays.

We present a study of the decay B0-->pi(0)pi(0) based on a sample of 124 x 10(6) BB pairs recorded by the BABAR detector at the PEP-II asymmetric-energy B Factory at SLAC. We observe 46+/-13+/-3 events, where the first error is statistical and the second is systematic, corresponding to a significance of 4.2 standard deviations including systematic uncertainties. We measure the branching fraction B(B0-->pi(0)pi(0))=(2.1+/-0.6+/-0.3)x10(-6), averaged over B0 and B(0) decays.

Journal Article↗