855 research outputs found
Study of the decays B->D_s1(2536)+ anti-D(*)
We report a study of the decays B -> D_s1(2536)+ anti-D(*), where anti-D(*)
is anti-D0, D- or D*-, using a sample of 657 x 10^6 B anti-B pairs collected at
the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy
e+e- collider. The branching fractions of the decays B+ -> D_s1(2536)+ anti-D0,
B0 -> D_s1(2536)+ D- and B0 -> D_s1(2536)+ D*- multiplied by that of
D_s1(2536)+ -> (D*0K+ + D*+K0) are found to be (3.97+-0.85+-0.56) x 10^-4,
(2.75+-0.62+-0.36) x 10^-4 and (5.01+-1.21+-0.70) x 10^-4, respectively.Comment: 6 pages, 2 figues, submitted to PRD (RC
Lower facial remodeling with botulinum toxin type A for the treatment of masseter hypertrophy
Prevention and Therapy of Hepatocellular Carcinoma by Vaccination with TM4SF5 Epitope-CpG-DNA-Liposome Complex without Carriers
Although peptide vaccines have been actively studied in various animal models, their efficacy in treatment is limited. To improve the efficacy of peptide vaccines, we previously formulated an efficacious peptide vaccine without carriers using the natural phosphodiester bond CpG-DNA and a special liposome complex (Lipoplex(O)). Here, we show that immunization of mice with a complex consisting of peptide and Lipoplex(O) without carriers significantly induces peptide-specific IgG2a production in a CD4+ cells- and Th1 differentiation-dependent manner. The transmembrane 4 superfamily member 5 protein (TM4SF5) has gained attention as a target for hepatocellular carcinoma (HCC) therapy because it induces uncontrolled growth of human HCC cells via the loss of contact inhibition. Monoclonal antibodies specific to an epitope of human TM4SF5 (hTM4SF5R2-3) can recognize native mouse TM4SF5 and induce functional effects on mouse cancer cells. Pre-immunization with a complex of the hTM4SF5R2-3 epitope and Lipoplex(O) had prophylactic effects against tumor formation by HCC cells implanted in an mouse tumor model. Furthermore, therapeutic effects were revealed regarding the growth of HCC when the vaccine was injected into mice after tumor formation. These results suggest that our improved peptide vaccine technology provides a novel prophylaxis measure as well as therapy for HCC patients with TM4SF5-positive tumors
Studies of the Decay B+- -> D_CP K+-
We report studies of the decay B+- -> D_CP K+-, where D_CP denotes neutral D
mesons that decay to CP eigenstates. The analysis is based on a 29.1/fb data
sample of collected at the \Upsilon(4S) resonance with the Belle detector at
the KEKB asymmetric e+ e- storage ring. Ratios of branching fractions of
Cabibbo-suppressed to Cabibbo-favored processes involving D_CP are determined
to be B(B- -> D_1 K-)/B(B- -> D_1 pi-)=0.125 +- 0.036 +- 0.010 and B(B- -> D_2
K-)/B(B- -> D_2 pi-)=0.119 +- 0.028 +- 0.006, where indices 1 and 2 represent
the CP=+1 and CP=-1 eigenstates of the D0 - anti D0 system, respectively. We
also extract the partial rate asymmetries for B+- -> D_CP K+-, finding A_1 =
0.29 +- 0.26 +- 0.05 and A_2 = -0.22 +- 0.24 +- 0.04.Comment: 10 pages, 2 figures, submitted to Physical Review Letter
Acinetobacter baumannii Secretes Cytotoxic Outer Membrane Protein A via Outer Membrane Vesicles
Acinetobacter baumannii is an important nosocomial pathogen that causes a high morbidity and mortality rate in infected patients, but pathogenic mechanisms of this microorganism regarding the secretion and delivery of virulence factors to host cells have not been characterized. Gram-negative bacteria naturally secrete outer membrane vesicles (OMVs) that play a role in the delivery of virulence factors to host cells. A. baumannii has been shown to secrete OMVs when cultured in vitro, but the role of OMVs in A. baumannii pathogenesis is not well elucidated. In the present study, we evaluated the secretion and delivery of virulence factors of A. baumannii to host cells via the OMVs and assessed the cytotoxic activity of outer membrane protein A (AbOmpA) packaged in the OMVs. A. baumannii ATCC 19606T secreted OMVs during in vivo infection as well as in vitro cultures. Potential virulence factors, including AbOmpA and tissue-degrading enzymes, were associated with A. baumannii OMVs. A. baumannii OMVs interacted with lipid rafts in the plasma membranes and then delivered virulence factors to host cells. The OMVs from A. baumannii ATCC 19606T induced apoptosis of host cells, whereas this effect was not detected in the OMVs from the ΔompA mutant, thereby reflecting AbOmpA-dependent host cell death. The N-terminal region of AbOmpA22-170 was responsible for host cell death. In conclusion, the OMV-mediated delivery of virulence factors to host cells may well contribute to pathogenesis during A. baumannii infection
Improved Measurements of Partial Rate Asymmetry in B -> h h Decays
We report improved measurements of the partial rate asymmetry (Acp) in B -> h
h decays with 140fb^-1 of data collected with the Belle detector at the KEKB
e+e- collider. Here h stands for a charged or neutral pion or kaon and in total
five decay modes are included: K-+ pi+-, K0s pi-+, K-+ pi0, pi-+ pi0 and K0s
pi0. The flavor of the last decay mode is determined from the accompanying B
meson. Using a data sample 4.7 times larger than that of our previous
measurement, we find Acp(K-+ pi+-) -0.088+-0.035+-0.013, 2.4 sigma from zero.
Results for other decay modes are also presented.Comment: 9 pages, 1 figur
Search for CP violation in the decay B0->D*+-D-+
We report a search for CP-violating asymmetry in B0 -> D*+- D-+ decays. The
analysis employs two methods of B0 reconstruction: full and partial. In the
full reconstruction method all daughter particles of the B0 are required to be
detected; the partial reconstruction technique requires a fully reconstructed
D- and only a slow pion from the D*+ -> D0 pi_slow+ decay. From a fit to the
distribution of the time interval corresponding to the distance between two B
meson decay points we calculate the CP-violating parameters and find the
significance of nonzero CP asymmetry to be 2.7 standard deviations.Comment: 4 pages, 3 figure
Production of phi mesons at mid-rapidity in sqrt(s_NN) = 200 GeV Au+Au collisions at RHIC
We present the first results of meson production in the K^+K^- decay channel
from Au+Au collisions at sqrt(s_NN) = 200 GeV as measured at mid-rapidity by
the PHENIX detector at RHIC. Precision resonance centroid and width values are
extracted as a function of collision centrality. No significant variation from
the PDG accepted values is observed. The transverse mass spectra are fitted
with a linear exponential function for which the derived inverse slope
parameter is seen to be constant as a function of centrality. These data are
also fitted by a hydrodynamic model with the result that the freeze-out
temperature and the expansion velocity values are consistent with the values
previously derived from fitting single hadron inclusive data. As a function of
transverse momentum the collisions scaled peripheral.to.central yield ratio RCP
for the is comparable to that of pions rather than that of protons. This result
lends support to theoretical models which distinguish between baryons and
mesons instead of particle mass for explaining the anomalous proton yield.Comment: 326 authors, 24 pages text, 23 figures, 6 tables, RevTeX 4. To be
submitted to Physical Review C as a regular article. Plain text data tables
for the points plotted in figures for this and previous PHENIX publications
are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm
Disproportionate Alterations in the Anterior and Posterior Insular Cortices in Obsessive–Compulsive Disorder
Recent studies have reported that the insular cortex is involved in the pathophysiology of obsessive–compulsive disorder (OCD). However, specific morphometric abnormalities of the insular subregions remain unclear. In this study, we examined insular cortical volume to determine whether the volume of the anterior and posterior insular cortices of unmedicated OCD patients differed according to different symptom dimensions.Using magnetic resonance imaging, we measured the gray matter volumes of the insular cortex and its subregions (anterior and posterior divisions) in 41 patients with OCD (31 drug-naïve and 10 non-medicated) and 53 healthy controls. Volumetric measures of the insular cortex were compared according to different OC symptoms. Enlarged anterior and reduced posterior insular cortices were observed in OCD patients. The insular volumetric alterations were more significant in OCD patients with predominant checking rather than cleaning symptoms when compared with healthy controls.Our results suggest the presence of unbalanced anterior and posterior insular volumetric abnormalities in unmedicated OCD patients and emphasize the distinct role of the insular cortex in different OC symptoms. We propose that the insular morphometric alterations may influence the modulation of interoceptive processing, the insular functional role, in OCD patients with different symptoms
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