Biomedical subjects

K Abe

Publications and source records attributed to K Abe.

At least 163 records · Page 9Linked to original sources

PubMed2003

Glutamate enhances caspase-3 immunoreactivity in cultured spinal cord neurons of newborn rats.

The role of glutamate in the mechanism of spinal neuron death is not fully understood. With addition of glutamate to primary culture of 11-day-old rat spinal cord, the number of caspase-3 positive small neurons of the dorsal horn greatly increased at 6-24 h in contrast to the case with vehicle. The addition of glutamate made caspase-3 immunoreactivity stronger in the cytoplasm of large motor neurons in the ventral horn. The present results show that excessive amount of glutamate enhances apoptotic pathway through caspase-3 in cultured spinal neurons of newborn rat.

Animals↗

PubMed2003

Protection against ischemic brain damage by GDNF affecting cell survival and death signals.

Neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on cell survival and death signals were investigated after 90 min of transient middle cerebral artery occlusion (MCAO) in rats. Immunoreactivities of phosphorylated Akt (p-Akt), cleaved caspase-9 (c-cas9), and -3 (c-cas3) increased after the reperfusion in the penumbra in vehicle group with peaks at 3 h, 8 h, and 1 day, respectively. Topical application of GDNF (6.8 micrograms/9 microliters) on brain surface potentiated and prolonged p-Akt activation, but suppressed activation of the caspases, and reduced the number of terminal deoxynucleotidyl transferase-mediated dUDP-biotin in situ nick labeling (TUNEL) positive cells. These results suggest that GDNF plays a protective role against ischemic injury by controlling the balance between Akt pathway and caspase cascades.

Administration, Topical↗

PubMed2003

Targeting of post-ischemic cerebral endothelium in rat by liposomes bearing polyethylene glycol-coupled transferrin.

To achieve an efficient delivery targeting to post-ischemic cerebral vascular endothelium, PEG-liposome conjugated with transferrin (Tf) (Tf-PEG-liposome) was intravenously administered to the rats after 90 min of transient middle cerebral occlusion. The expression of Tf receptor (TfR) in the cerebral endothelium increased with a peak at 1 day after the reperfusion and returned to the control level by 6 days. The Tf-PEG fluorescence was marginally detectable in sham control brain, but remarkably increased with a peak at 2 days, showing about 70% of TfR positive vascular endothelium double-labeled with Tf-PEG. These results indicate that the Tf-PEG-liposome could be utilized as an efficient drug delivery tool to the brain after stroke.

Animals↗

PubMed2003

Functional improvement by electro-acupuncture after transient middle cerebral artery occlusion in rats.

Functional recovery by the application of electro-acupuncture (EA) on different acupoints was investigated using a transient middle cerebral artery occlusion (MCAO) model in rat. Acupoints were Baihui (D20) plus Renzhong (D26) (MCAO + D group), and Hanyan (G4), Xuanlu (G5), Xuanli (G6), plus Qubin (G7) (MCAP + G group). Animals with EA treatment showed significant functional improvements from 12 days after the reperfusion against those without EA treatment. Among EA treated groups, MCAO + G showed a more significant recovery than MCAO + D. Infarct volume revealed the significant reduction in the EA treated groups especially in MCAO + G at 30 days. Immunohistochemical study showed a remarkable induction of vascular endothelial growth factor (VEGF) in astrocytes of the peri-infarct area at 30 days, more in EA treated groups than in groups treated with MCAO alone. These results suggest that the acupoints applied in this study are effective for the functional recovery, and an enhanced expression of VEGF may play a certain role in recovery process after stroke.

Animals↗

PubMed2003

[Ruptured bronchial artery aneurysm; report of a case].

A 74-year-old man who went into shock following an acute hemomediastinum and left hemothorax was operated on. Postoperative angiographies revealed a saccular aneurysm of the left bronchial artery of 2.0 cm in diameter. Sixty days after the initial operation, the aneurysm was resected under F-F bypass. A saccular aneurysm was found at the root of the left bronchial artery, which had a very short segment between the aneurysm and the aorta. Pathological study of aneurysm revealed thinning of the wall and lack of tunica media.

Aged↗

PubMed2002

Measurements of branching fractions and CP-violating asymmetries in B0-->pi+pi-, K+pi-, K+K- decays.

We present measurements of branching fractions and CP-violating asymmetries for two-body neutral B meson decays to charged pions and kaons based on a sample of about 88x10(6) Upsilon(4S)-->BB decays. From a time-independent fit we measure the charge-averaged branching fractions B(B0-->pi+pi-)=(4.7+/-0.6+/-0.2)x10(-6), B(B0-->K+pi-)=(17.9+/-0.9+/-0.7)x10(-6), and the direct CP-violating charge asymmetry A(Kpi)=-0.102+/-0.050+/-0.016 [-0.188,-0.016], where the ranges in square brackets indicate the 90% confidence intervals. From a time-dependent fit we measure the B0-->pi+pi- CP-violating parameters S(pipi)=0.02+/-0.34+/-0.05 [-0.54,+0.58] and C(pipi)=-0.30+/-0.25+/-0.04 [-0.72,+0.12].

Journal Article↗

PubMed2002

Activation of cell-survival signal Akt by GDNF in normal rat brain.

Glial cell line-derived neurotrophic factor (GDNF) activates protein kinase Akt/PKB by phosphorylation (p-Akt) which plays key roles in cell survival. In the current study, we investigated a temporal expression of p-Akt by immunohistochemical analysis after a topical application of GDNF to normal cerebral hemisphere of rats. Although p-Akt immunoreactivity was weakly present in the sham control neural cells, GDNF application greatly enhanced it at 3 h, which lasted until 1 day. These results indicate that p-Akt is expressed in neuronal cells under physiological conditions, and that topical application of GDNF greatly enhanced the phosphorylation of Akt in normal rat brain.

Animals↗

PubMed2002

Measurement of the B(0)-B(0) mixing parameter Deltam(d) using semileptonic B0 decays.

We present a measurement of the B0-Bmacr;(0) mixing parameter Deltam(d) using neutral B meson pairs in 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. We exclusively reconstruct one neutral B meson in the semileptonic B0-->D(*-)l(+)nu decay mode and identify the flavor of the accompanying B meson from its decay products. From the distribution of the time intervals between the two flavor-tagged B meson decay points, we obtain Deltam(d)=(0.494+/-0.012+/-0.015) ps(-1), where the first error is statistical and the second error is systematic.

Journal Article↗

PubMed2002

Observation of D+(s)K- and evidence for D+(s)pi- final states in neutral B decays.

We report the first observation of a B meson decay that is not accessible by a direct spectator process. The channel B(0)-->D(+)(s)K- is found in a sample of 85 x 10(6) BB; events, collected with the Belle detector at KEKB, with a branching fraction B(B(0)-->D(+)(s)K-)=(4.6(+1.2)(-1.1)+/-1.3) x 10(-5). We also obtain evidence for the B0-->D(+)(s)pi(-) decay with branching fraction B(B0-->D(+)(s)pi(-))=(2.4(+1.0)(-0.8)+/-0.7) x 10(-5). This value may be used to extract a model-dependent value of |V(ub)|.

Journal Article↗

PubMed2002

Radiative B meson decays into kpigamma and kpipigamma final states.

We report observations of radiative B meson decays into the K+pi(-)gamma and K+pi(-)pi(+)gamma final states. In the B0-->K+pi(-)gamma channel, we present evidence for decays via an intermediate tensor meson state with a branching fraction of B(B0-->K(*)(2)(1430)(0)gamma)=[1.3+/-0.5(stat)+/-0.1(syst)]x10(-5). We measure the branching fraction B(B+-->K+pi(-)pi(+)gamma)=[2.4+/-0.5(stat) +0.4-0.2(syst)]x10(-5), in which the B+-->K(*0)pi(+)gamma and B+-->K+rho(0)gamma channels dominate. The analysis is based on a data set of 29.4 fb(-1) recorded by the Belle experiment at the KEKB collider.

Journal Article↗

PubMed2002

Enhanced phosphorylation of PTEN in rat brain after transient middle cerebral artery occlusion.

A phosphatase PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a tumor suppressor gene that suppresses cell growth, inhibits cell migration, and induces apoptosis. Phosphorylated form of PTEN (p-PTEN) is a key survival factor relating PI3K-Akt pathway and their downstream effectors. A spatiotemporal profiles of PTEN and p-PTEN expression were immunohistochemically examined after 90 min of transient middle cerebral artery occlusion in rats. In the ischemic core, PTEN progressively decreased by 3 days, whereas a rapid but transient increase of p-PTEN was found with a peak at 1 h after the reperfusion. In contrast, in the ischemic penumbra, PTEN showed a minor change and a gradual but sustained p-PTEN expression was observed in the ischemic penumbra with a peak at 12 h. In addition, the balance of population among strongly, moderately, and weakly stained cells was different between the ischemic core and penumbra at their peak time points. These results suggest an important role of p-PTEN for cell survival after ischemia as an upstream regulator for PI3K-Akt.

Animals↗

PubMed2002

Measurement of the CP asymmetry amplitude sin2beta with B0 mesons.

We present results on time-dependent CP asymmetries in neutral B decays to several CP eigenstates. The measurements use a data sample of about 88 x 10(6) Upsilon(4S)-->B(-)B decays collected between 1999 and 2002 with the BABAR detector at the PEP-II asymmetric-energy B factory at SLAC. We study events in which one neutral B meson is fully reconstructed in a final state containing a charmonium meson and the other B meson is determined to be either a B(0) or B(-0) from its decay products. The amplitude of the CP asymmetry, which in the standard model is proportional to sin2beta, is derived from the decay-time distributions in such events. We measure sin2beta=0.741+/-0.067(stat)+/-0.034(syst) and |lambda|=0.948+/-0.051(stat)+/-0.030(syst). The magnitude of lambda is consistent with unity, in agreement with the standard model expectation of no direct CP violation in these modes.

Journal Article↗

PubMed2002

Observation of B+/- -->omegaK+/- decay.

We report the first observation of the charmless two-body mode B+/--->omegaK+/- decay, and a new measurement of the branching fraction for the B+/--->omegapi(+/-) decay. The measured branching fractions are B(B+/--->omegaK+/-)=(9.2(+2.6)(-2.3)+/-1.0)x10(-6) and B(B+/--->omegapi(+/-))=(4.2(+2.0)(-1.8)+/-0.5)x10(-6). We also measure the partial rate asymmetry of B+/--->omegaK+/- decays and obtain A(CP)=-0.21+/-0.28+/-0.03. The results are based on a data sample of 29.4 fb(-1) collected on the Upsilon(4S) resonance by the Belle detector at the KEKB e(+)e(-) collider.

Journal Article↗

PubMed2002

Observation of B(0)-->D((*)0)pp.

The B meson decay modes B-->Dpp; and B-->D(*)pp; have been studied using 29.4 fb(-1) of data collected with the Belle detector at KEKB. The B;(0)-->D(0)pp; and B;(0)-->D(*0)pp; decays have been observed for the first time with branching fractions B(B;(0)-->D(0)pp;)=(1.18+/-0.15+/-0.16)x10(-4) and B(B;(0)-->D(*0)pp;)=(1.20(+0.33)(-0.29)+/-0.21)x10(-4). No signal has been found for the B+-->D(+)pp; and B+-->D(*+)pp; decay modes, and the corresponding upper limits at 90% C.L. are presented.

Journal Article↗

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

Therapeutic time window of adenovirus-mediated GDNF gene transfer after transient middle cerebral artery occlusion in rat.

The time dependent influence of adenovirus-mediated glial cell line-derived neurotrophic factor (GDNF) gene (Ad-GDNF) was examined after 90 min of transient middle cerebral artery occlusion (MCAO) in rats. Treatment with Ad-GDNF significantly reduced the infarct volume when immediately administered after the reperfusion, but became insignificant when administered at 1 h after the reperfusion as were the cases treated with vehicle- and adenoviral vector containing the E. coli lacZ gene (Ad-LacZ)-treated groups. The protective effect of GDNF was related to the significant reduction of the number of TUNEL positive cells as well as immunohistochemical positive cells for active caspase-3 but not -9. These results showed that exogenous GDNF gene transfer successfully reduced the infarct size in a time-dependant manner by suppressing active caspase-3 but not active caspase-9. However, the therapeutic time window was shorter than the effect of GDNF protein itself previously reported.

Adenoviridae↗

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↗