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We present a new measurement of the Λ4H hypernuclear lifetime using in-flight K− + 4He → Λ4H + π0 reaction at the J-PARC hadron facility. We demonstrate, for the first time, the effective selection of the hypernuclear bound state using only the γ-ray energy decayed from π0. This opens the possibility for a systematic study of isospin partner hypernuclei through comparison with data from (K−, π−) reaction. As the first application of this method, our result for the Λ4H lifetime, τ(HΛ4)=206±8(stat.)±12(syst.)ps, is one of the most precise measurements to date. We are also preparing to measure the lifetime of the hypertriton (Λ3H) using the same setup in the near future.

We measured a set of π±Σ∓, π0Σ0, and π−Σ0 invariant mass spectra below and above the K¯N mass threshold in K−-induced reactions on deuteron. The measured πΣ mass spectral shape is well reproduced via the two-step mechanism, i.e., a neutron knocked out at a forward angle from a deuteron by an incident K−, with the K¯ recoiled backward reacting with the residual nucleon to produce π and Σ. We deduced the S-wave K¯N→πΣ and K¯N→K¯N scattering amplitudes in the isospin 0 channel in the framework of a K¯N and πΣ coupled channel. We find that a resonance pole corresponding to Λ(1405) is located at 1417.7−7.4+6.0 (fitting errors)−1.0+1.1 (systematic errors) + [−26.1−7.9+6.0 (fitting errors)−2.0+1.7 (systematic errors)] i MeV/c2, closer to the K¯N mass threshold than the value determined by the Particle Data Group.

Abstract The NA60 experiment has studied low-mass muon pair production in proton–nucleus collisions with a system of Be, Cu, In, W, Pb and U targets, using a 400 GeV proton beam at the CERN SPS. The transverse momentum spectra of the $$\rho /\omega $$ ρ/ω and $$\phi $$ ϕ mesons are measured in the full $$p_{\mathrm {T}}$$ pT range accessible, from $$p_{\mathrm {T}}= 0$$ pT=0 up to $$2 \, {\hbox {GeV/c}}$$ 2GeV/c . The nuclear dependence of the production cross sections of the $$\eta $$ η , $$\omega $$ ω and $$\phi $$ ϕ mesons has been found to be consistent with the power law $$\sigma _{\mathrm {pA}} \propto {\mathrm {A}}^\alpha $$ σpA∝Aα , with the $$\alpha $$ α parameter increasing as a function of $$p_{\mathrm {T}}$$ pT for all the particles, and an approximate hierarchy $$\alpha _\eta \approx \alpha _\phi > \alpha _\omega $$ αη≈αϕ>αω . The cross section ratios $$\sigma _\eta /\sigma _\omega $$ ση/σω , $$\sigma _\rho /\sigma _\omega $$ σρ/σω and $$\sigma _\phi /\sigma _\omega $$ σϕ/σω have been studied as a function of the size A of the production target, and an increase of the $$\eta $$ η and $$\phi $$ ϕ yields relative to the $$\omega $$ ω is observed from p–Be to p–U collisions.

We observed a distinct peak in the Λp invariant mass spectrum of He3(K−,Λp)n, well below mK+2mp, i.e., the mass threshold of the K− to be bound to two protons. By selecting a relatively large momentum-transfer region q=350∼650 MeV/c, one can kinematically separate the peak from the quasi-free process, K‾N→K‾N followed by the non-resonant absorption by the two spectator-nucleons K‾NN→ΛN. We found that the simplest fit to the observed peak gives us a Breit–Wigner pole position at BKpp=47±3(stat.)−6+3(sys.) MeV having a width ΓKpp=115±7(stat.)−20+10(sys.) MeV, and the S-wave Gaussian reaction form-factor parameter QKpp=381±14(stat.)−0+57(sys.) MeV/c, as a new form of the nuclear bound system with strangeness – “K−pp”. Keywords: Kaon, Strangeness, Mesonic nuclear bound state

ΔFosB is a stable transcription factor which accumulates in the nucleus accumbens (NAc), a key part of the brain's reward circuitry, in response to chronic exposure to cocaine or other drugs of abuse. While ΔFosB is known to heterodimerize with a Jun family member to form an active transcription factor complex, there has not to date been an open-ended exploration of other possible binding partners for ΔFosB in the brain. Here, by use of yeast two-hybrid assays, we identify PSMC5-also known as SUG1, an ATPase-containing subunit of the 19S proteasomal complex-as a novel interacting protein with ΔFosB. We verify such interactions between endogenous ΔFosB and PSMC5 in the NAc and demonstrate that both proteins also form complexes with other chromatin regulatory proteins associated with gene activation. We go on to show that chronic cocaine increases nuclear, but not cytoplasmic, levels of PSMC5 in the NAc and that overexpression of PSMC5 in this brain region promotes the locomotor responses to cocaine. Together, these findings describe a novel mechanism that contributes to the actions of ΔFosB and, for the first time, implicates PSMC5 in cocaine-induced molecular and behavioral plasticity.

The mass shift of the vector mesons in nuclei is known to be a powerful tool for investigating the mechanism of generating hadron mass from the QCD vacuum. The mechanism is known to be the spontaneous breaking of chiral symmetry. One of the approach to investigate spontaneous breaking of chiral symmetry in nuclear media is formation of meson nucleus bound state and measurring energy level of the state which will be a direct connection to the (...q) expectation value in nucleus. We propose the experiment to study in-medium mass modification of the φ meson using the formation of φ-meson bound state at J-PARC/Japan. We demonstrate that a clear missing-mass spectrum can be obtained efficiently by (..., φ) spectroscopy together with the Λ tagging, using the primary reaction channel ...p → φφ. A systematic study over several nuclear targets will yield a unique, definitive and precise determination of the in-medium mass modification of the vector meson φ(s...). This paper gives an overview of the physics motivation and the detector concept, and explains the direction of the initial research and development effort. [ABSTRACT FROM AUTHOR]

SHPS-1 is a transmembrane protein whose extracellular region interacts with CD47 and whose cytoplasmic region undergoes tyrosine phosphorylation and there by binds the protein tyrosine phosphatase SHP-2. Formation of this complex is implicated in regulation of cell migration by an unknown mechanism. A CD47-Fc fusion protein or antibodies to SHPS-1 inhibited migration of human melanoma cells or of CHO cells overexpressing SHPS-1. Overexpression of wild-type SHPS-1 promoted CHO cell migration, whereas expression of the SHPS-1-4F mutant, which lacks the phosphorylation sites required for SHP-2 binding, had no effect. Antibodies to SHPS-1 failed to inhibit migration of CHO cells expressing SHPS-1-4F. SHPS-1 ligands induced the dephosphorylation of SHPS-1 and dissociation of SHP-2. Antibodies to SHPS-1 also enhanced Rho activity and induced both formation of stress fibers and adoption of a less polarized morphology in melanoma cells. Our results suggest that engagement of SHPS-1 by CD47 prevents the positive regulation of cell migration by this protein. The CD47- SHPS-1 system and SHP-2 might thus contribute to the inhibition of cell migration by cell-cell contact. [ABSTRACT FROM AUTHOR]

Mammalian embryos are thought to cleave equally during early development. Therefore, the contents including organelles such as mitochondria (mt) in oocytes are supposed to be delivered symmetrically into each blastomere of the resulting embryo. However, a recent report showed higher oxygen consumption, ATP production, and mt distribution in trophectoderms from mouse blastocysts than that in inner cell masses (Houghton 2006 Differentiation 74, 11–18). We hypothesized that this phenomenon could be preceded by the asymmetrical mt distribution into blastomeres at earlier stages. Oocytes, 2-cell embryos, and 4-cell embryos from BDF1 were measured to determine volumes, ATP contents, and mtDNA copy numbers in the whole egg and individual blastomeres that had been separated in Ca/Mg-free KSOM with added 0.02% EDTA. The volumes of blastomeres were calculated by the sphere volume formula. The ATP contents were determined using a luminometer and commercial kits (BacTiter-Glo, Promega, Madison, WI, USA). The mtDNA copy numbers were quantified absolutely using real-time PCR. The data was analyzed by 1-way ANOVA followed by Fisher''s least significant difference test. We found about a 10% difference in volume between the largest and the smallest blastomeres from a 4-cell embryo. At the 4-cell stage, the largest blastomeres were significantly larger than the middle-sized and smallest blastomeres, and the next largest blastomeres were significantly larger than the smallest blastomeres (largest: 41 093 µm3, next largest: 39 671 µm3, middle-sized: 37 725 µm3, smallest: 36 518 µm3; n = 25). The procedure for separation of blastomeres did not significantly reduce theATP contents of embryos. We observed the same pattern of significant differences in theATP contents among the 4 blastomeres at the 4-cell stage (largest: 0.141 pmol, next largest: 0.124 pmol, middle-sized: 0.112 pmol, smallest: 0.098 pmol, n = 27). The largest blastomeres from 4-cell embryos contained about 1.4-fold higherATP than the smallest blastomeres. There was no significant difference in the mtDNA copy numbers in oocytes (n = 7), whole 2-cell embryos (n = 6), whole 4-cell embryos (n = 13), the sum of 2 blastomeres from the same 2-cell embryo (n = 6), and the sum of 4 blastomeres from the same 4-cell embryo (n = 6; 245 071 22 696, 267 567 30 989, 262 931 12 952, 239 717 16 813, 247 012 16 166, respectively; SEM). However, the larger blastomere of 2-cell embryo had a higher mtDNA copy number than the smaller blastomeres (largest: 137 100 11 493, smallest: 102 617 6205; P < 0.05). The largest blastomeres of 4-cell embryo had about 1.4 times (P < 0.05) higher mtDNA copy numbers than the smallest blastomeres (largest: 72 072 4112, next largest: 66 198 5767, middle-sized: 57 596 3922, smallest: 51 146 3081). We found differences in volumes, ATP contents, and mtDNA copy numbers among blastomeres from the same embryos at the 4-cell stage. These qualitative differences could be related to embryonic metabolism in mouse early development. [ABSTRACT FROM AUTHOR]