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K Abe

Publications and source records attributed to K Abe.

At least 235 records · Page 13Linked to original sources
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

A novel SOD1 gene mutation in familial ALS with low penetrance in females.

We identified a novel missense mutation in the Cu/Zn superoxide dismutase gene in a family with amyotrophic lateral sclerosis (ALS). The mutation was a transition of T to C, resulting in a substitution of leucine 126 to serine in exon 5. The family had very unique clinical features of extremely mild severity only in the legs of two male patients with onset of 42 and 52 years old, and their mothers did not develop any symptom even after reaching the age of 80 and carrying the same mutation. The present study suggests that there are other factors that delay or prevent the disease.

Adult↗
PubMed2001

Periodic metastable structures in the discrete straight phi4 model.

For the discrete straight phi(4) model a class of metastable periodic solutions is given in the form of Fourier series. From the symmetry consideration, we eliminate the harmonics with zero amplitudes and thus, reduce the number of degrees of freedom. For the rest of harmonics we establish the hierarchy of their significance. For solutions with a small period we give the exact expression of energy density in terms of amplitudes of harmonics. Conditions of existence and stability of the solutions are discussed. For some limiting cases the approximate solutions of different kinds are given. The analytical results are compared with the results of numerical study. We also discuss a mechanism of transition from a metastable periodic structure into the ground state and apply the results to the lock-in transition in dielectric crystals supporting incommensurate phase.

Journal Article↗
PubMed2001

Observation of CP violation in the B(0) meson system.

We present an updated measurement of time-dependent CP-violating asymmetries in neutral B decays with the BABAR detector at the PEP-II asymmetric B Factory at SLAC. This result uses an additional sample of Upsilon(4S) decays collected in 2001, bringing the data available to 32 x 10(6) BB macro pairs. We select events in which one neutral B meson is fully reconstructed in a final state containing charmonium and the flavor of the other neutral B meson is determined from its decay products. The amplitude of the CP-violating asymmetry, which in the standard model is proportional to sin2 beta, is derived from the decay time distributions in such events. The result sin2 beta = 0.59+/-0.14(stat)+/-0.05(syst) establishes CP violation in the B(0) meson system. We also determine absolute value of lambda = 0.93+/-0.09(stat)+/-0.03(syst), consistent with no direct CP violation.

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

Impaired retrograde axonal transport of adenovirus-mediated E. coli LacZ gene in the mice carrying mutant SOD1 gene.

A replication-defective recombinant adenoviral vector containing E. coli lacZ gene was injected into the gastrocnemius muscles of transgenic mice carrying mutant Cu/Zn superoxide dismutase (SOD1) gene and non-transgenic wild-type mice at 40 weeks of age. After 60 and 90 h of the injection, lacZ staining was observed at the distal ends of the sciatic nerves in both mice groups, with the number and the distances greatly reduced in the transgenic mice. Mean velocities of retrograde transport for lacZ was estimated to be 2.1 and 0.05 mm/24 h in non-transgenic and transgenic mice, respectively. These results indicate that the retrograde axonal transport of foreign gene product is impaired in the mice model for familial amyotrophic lateral sclerosis.

Adenoviridae↗
PubMed2001

Domain II of m-calpain is a Ca(2+)-dependent cysteine protease.

Calpain, a Ca(2+)-dependent cytosolic cysteine protease, proteolytically modulates specific substrates involved in Ca(2+)-mediated intracellular events, such as signal transduction, cell cycle, differentiation, and apoptosis. The 3D structure of m-calpain, in the absence of Ca(2+), revealed that the two subdomains (domains IIa and IIb) of the protease domain (II) have an 'open' conformation, probably due to interactions with other domains. Although the presence of an EF-hand structure was once predicted in the protease domain, no explicit Ca(2+)-binding structure was identified in the 3D structure. Therefore, it is predicted that if the protease domain is excised from the calpain molecule, it will have a Ca(2+)-independent protease activity. In this study, we have characterized a truncated human m-calpain that consists of only the protease domain. Unexpectedly, the proteolytic activity was Ca(2+)-dependent, very weak, and not effectively inhibited by calpastatin, a calpain inhibitor. Ca(2+)-dependent modification of the protease domain by the cysteine protease inhibitor, E-64c, was clearly observed as a SDS-PAGE migration change, indicating that the conformational changes of this domain are a result of Ca(2+) binding. These results suggest that the Ca(2+) binding to domain II, as well as to domains III, IV, and VI, is critical in the process of complete activation of calpain.

Calcium↗
PubMed2001

Magnetization transfer measurements of the hippocampus in the early diagnosis of Alzheimer's disease.

We measured magnetization transfer ratios (MTRs) of the hippocampus in 38 patients with Alzheimer's disease (AD), including very mild (Clinical Dementia Rating [CDR] 0.5, n=12), mild (CDR 1, n=14), and moderate stages (CDR 2, n=12), and in 21 healthy elderly control subjects. Medial temporal lobe atrophy was graded subjectively on a five-point scale by two observers blinded to clinical data. Compared with the controls, each of the AD groups, including the very mild group, had significant atrophy of the medial temporal lobe and a decrease in MTRs of the hippocampus. Logistic regression analysis revealed that the overall discrimination rate with MTR measurement and visual analysis of the atrophy was 85% and 73% between the control group and the CDR 0.5 group, 89% and 80% between the control group and the CDR 1 group, and 100% and 91% between the control group and the CDR 2 group, respectively. MTR measurements may provide additional information in detecting structural damage of the hippocampus of AD and be helpful in providing improved diagnosis and early detection of AD.

Aged↗
PubMed2001

Expression of polysialylated neural cell adhesion molecule in rat brain after transient middle cerebral artery occlusion.

The highly polysialylated form of neural cell adhesion molecule (PSA-NCAM) is important for neurite outgrowth. With this molecule as a marker of plastic change in neurons, we investigated its temporal expression in rat brain after transient middle cerebral artery (MCA) occlusion. In sham-control brain, only subependymal neurons showed a positive immunoreactivity for PSA-NCAM. After 90 min of transient MCA occlusion, neurons in the piriform cortex began to be positively stained at 1 h, while neurons in the cortex and caudate of the MCA territory became positive after 8 h. The stainings persisted for 1 and 3 days after reperfusion. The present results indicate that neurons in the cerebral cortex and caudate have the capability of plastic change in the adult brain, and that those in the piriform cortex rapidly undergo plastic change probably in response to transneuronal injury.

Animals↗
PubMed2001

Biochemical and pathological study of endogenous 1-benzyl-1,2,3,4-tetrahydroisoquinoline-induced parkinsonism in the mouse.

We administered 1-benzyl-1,2,3,4-tetrahydroisoquinoline (1-BnTIQ; 80 mg/kg, i.p.), an endogenous neurotoxin known to cause bradykinesia, the Parkinson's disease-like symptom, in order to obtain biochemical and pathological evidence of behavioral abnormalities. Immunohistochemical analysis demonstrated that 1-BnTIQ did not decrease the number of tyrosine hydroxylase-positive cells in the substantia nigra. Biochemical analysis demonstrated significantly increased striatal dopamine (DA) content, while DA metabolites in the striatum remained at control levels. We concluded that the 1-BnTIQ-induced bradykinesia has a different mechanism of action than that underlying the MPTP-induced depletion of striatal DA neurons.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2001

Increases in mRNA levels for Talpha1-tubulin in the rat kindling model of epilepsy.

The expression of mRNA for Talpha1-tubulin, a cytoskeletal protein, was studied in the rat kindling model of epilepsy. The Talpha1-tubulin mRNA level increased significantly in the dentate gyrus (DG) and CA3 of hippocampus ipsilateral to stimulation from 8 h to 4 weeks after amygdaloid kindled seizures. The peak increase was observed at 1 week after the last seizures both in the DG and CA3. These results suggest that the microtubule formation contributes to synaptic remodeling and reorganization of neural networks, which may be based on the kindling-inducing epileptogenesity.

Animals↗
PubMed2001

The YXXQ motif in gp 130 is crucial for STAT3 phosphorylation at Ser727 through an H7-sensitive kinase pathway.

The signal transducer and activator of transcription (STAT) 3 is essential for mediating signals from the receptors for a variety of cytokines and growth factors, including IL-6 and EGF, and from cytoplasmic tyrosine kinases. Upon stimulation, STAT3 is phosphorylated at Ser727 and Tyr705. However, the role of phosphorylation at Ser727, and the kinase pathways responsible for this phosphorylation in IL-6 signaling remain obscure. Here we show that IL-6 activates at least two distinct STAT3 serine kinase pathways and that an H7-sensitive pathway is dominant over a PD98059-sensitive one in HepG2 cells stimulated with a low concentration of IL-6. The analysis, using a series of chimeric receptors containing the extracellular domain of the G-CSF receptor, the truncated form of gp 130, and additional short peptides at the gp 130 carboxy-terminus, showed that the YXXQ motif of gp 130 was sufficient for the H7-sensitive STAT3 Ser727 phosphorylation. This YXXQ-mediated pathway does not involve Erk, p38, JNK, or PKCdelta, and requires a site in the region from 533 to 711 of STAT3 for phosphorylation in vivo. Moreover, we show that Ser727 is required for full transcriptional activity of STAT3 for two different response elements. Thus, the YXXQ motif regulates STAT3 activities in two ways in response to even a low concentration of IL-6: it recruits STAT3 to the receptor for tyrosine phosphorylation, and activates an unidentified H7-sensitive pathway leading to the serine phosphorylation of STAT3.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2001

Time dependent amelioration against ischemic brain damage by glial cell line-derived neurotrophic factor after transient middle cerebral artery occlusion in rat.

Time dependent influence of glial cell line-derived neurotrophic factor (GDNF) was examined after 90 min of transient middle cerebral artery occlusion (MCAO) in rats. Treatment with GDNF significantly reduced the infarct volume stained with 2,3,5-triphenyltetrazolium chloride (TTC) when GDNF was topically applied at 0 and 1 h of reperfusion, but became insignificant at 3 h as compared to vehicle group. The protective effect of GDNF was closely related to the significant reduction of the number of terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) positive cells as well as immunofluorescently positive cells for active forms of caspases, especially active caspase-3 but not -9. Thus, the present study showed that topical application of GDNF significantly reduced infarct size in a time-dependent manner, while the therapeutic time window was shorter than other chemical compounds such as an NMDA receptor antagonist (MK-801) and a free radical scavenger (alpha-phenyl-tert-butyl-nitrone, PBN). The effect of GDNF was stronger in suppressing active caspase-3 than active caspase-9.

Animals↗
PubMed2001

Efficient radical trapping at the surface and inside the phospholipid membrane is responsible for highly potent antiperoxidative activity of the carotenoid astaxanthin.

The effects of the carotenoids beta-carotene and astaxanthin on the peroxidation of liposomes induced by ADP and Fe(2+) were examined. Both compounds inhibited production of lipid peroxides, astaxanthin being about 2-fold more effective than beta-carotene. The difference in the modes of destruction of the conjugated polyene chain between beta-carotene and astaxanthin suggested that the conjugated polyene moiety and terminal ring moieties of the more potent astaxanthin trapped radicals in the membrane and both at the membrane surface and in the membrane, respectively, whereas only the conjugated polyene chain of beta-carotene was responsible for radical trapping near the membrane surface and in the interior of the membrane. The efficient antioxidant activity of astaxanthin is suggested to be due to the unique structure of the terminal ring moiety.

Adenosine Diphosphate↗
PubMed2001

Induction of highly polysialylated neural cell adhesion molecule (PSA-NCAM) in postischemic gerbil hippocampus mainly dissociated with neural stem cell proliferation.

We investigated a possible expression of highly polysialylated neural cell adhesion molecule (PSA-NCAM) in gerbil hippocampus after 5 min of transient global ischemia in association to the proliferation of neural stem cell labeled with bromodeoxyuridine (BrdU). The number of PSA-NCAM positive cells increased in the granule cell layer (GCL) of dentate gyrus (DG) by 1.9 to 2.7-fold at 10 and 20 days after the reperfusion. The number of BrdU-labeled cells increased mainly in the subgranular zone of DG by 7.2 to 8.0-fold at 5 and 10 days after the reperfusion. Immunofluorescence for PSA-NCAM and BrdU showed that the majority of DG cells were not double labeled, while one or two cells per section were double labeled in the deepest portion of the GCL only at 10 days after the reperfusion. These results suggest different predominant spatial distribution and chronological change of PSA-NCAM positive and BrdU-labeled cells in DG after transient ischemia.

Animals↗
PubMed2001

EAAT1 and EAAT2 immunoreactivity in transgenic mice with a G93A mutant SOD1 gene.

Immunocytochemical and quantitative analyses were used to correlate the localisation of excitatory amino acid transporter proteins EAAT1, EAAT2 with time in spinal motoneurones of presymptomatic and symptomatic mice with the G93A mutant SOD1 gene. Specimens from age-matched non-transgenic wild-type mice served as controls. EAAT1 and EAAT2 immunoreactivity was well-preserved in the gray matter in both controls and transgenic mice at all ages, and there was no difference in the expression of EAAT1 and EAAT2 immunoreactivity between controls and transgenic mice. These findings suggest that EAAT1 and EAAT2 may not play a pivotal role in the degeneration of motoneurons in this animal model.

ATP-Binding Cassette Transporters↗
PubMed2001

Impairment of mammary lobular development induced by expression of TGFbeta1 under the control of WAP promoter does not suppress tumorigenesis in MMTV-infected transgenic mice.

It has previously been shown that transgenic female mice expressing TGFbeta1 under control of regulatory elements of the whey-acidic protein (WAP) gene were unable to lactate. This was due to the increased apoptosis of the cells committed to the lobular-lactogenic phenotype. Our goal was to determine whether the expression of WAP-TGFbeta1 transgene could inhibit MMTV (mouse mammary tumor virus) tumorigenic activity in the mammary gland. It is well known that the infection with this virus produces focal hyperplastic secretory nodules (HANs) and, some variants can also induce ductal pregnancy-dependent lesions (plaques). In either case, MMTV infection leads ultimately to the appearance of malignant mammary tumors. The results shown herein demonstrate that TGFbeta1 expression in the secretory mammary epithelium does not suppress mammary tumorigenesis in MMTV infected mice. Although MMTV infected WAP-TGFbeta1 transgenic females displayed a strong impairment of lobule-alveolar development, carcinogenesis induced by any of the four MMTV variants used herein proceeded unabated. WAP-TGFbeta1 tumors that showed a strong expression at the WAP promoter, appeared later and grew more slowly than their wild-type counterparts. Transgenic females also had a lower incidence of HANs and plaques. Our study suggests that the epithelial target cells for tumorigenic mutations are probably progenitor cells that are not susceptible to the apoptotic effect of TGFbeta1. Alternatively, their daughters cells that display the secretory phenotype and could be more involved in the formation of premalignant lesions continue to die due to the expression of the transgene.

Animals↗