Quasi-SU(3) Coupling Induced Oblate-Prolate Shape Phase Transition in the Casten Triangle.

Shapes and shape evolution in the mass-130 region, including the Te, Xe, and Ba isotopes, have long been a focus of discussion in nuclear physics. This mass region consists of complex many-body systems that can behave in astonishingly simple and regular ways, as classified in the Casten symmetry triangle. By applying the shell model Hamiltonian proposed recently, we carry out calculations using the Hartree-Fock-Bogolyubov plus generator coordinate method, in the large model space containing the (1g_{9/2},1g_{7/2},2d_{5/2},2d_{3/2},3s_{1/2},1h_{11/2},2f_{7/2}) orbits. Based on good reproduction of the experimentally known energy levels, spectroscopic quadrupole moments, and E2 transition probabilities, we identify the quasi-SU(3) couplings across the N=50 and 82 shell gaps, which play a role in driving shape evolution and phase transition discussed in the extended Casten triangle. Specifically, we demonstrate that the quasi-SU(3) coupling mechanism in the proton partner orbits (1g_{9/2}, 2d_{5/2}) tends to drive the system to be more γ soft, and that in the neutron partner orbits (1h_{11/2}, 2f_{7/2}) are responsible for the oblate-to-prolate shape phase transition. With an emphasis on discussing spectroscopic quadrupole moments, our Letter uncovers hidden symmetries from the vast shell-model configurations and adds microscopical insights into the empirical symmetry triangle.

Study of the N=32 and N=34 Shell Gap for Ti and V by the First High-Precision Multireflection Time-of-Flight Mass Measurements at BigRIPS-SLOWRI.

The atomic masses of ^{55}Sc, ^{56,58}Ti, and ^{56-59}V have been determined using the high-precision multireflection time-of-flight technique. The radioisotopes have been produced at RIKEN's Radioactive Isotope Beam Factory (RIBF) and delivered to the novel designed gas cell and multireflection system, which has been recently commissioned downstream of the ZeroDegree spectrometer following the BigRIPS separator. For ^{56,58}Ti and ^{56-59}V, the mass uncertainties have been reduced down to the order of 10 keV, shedding new light on the N=34 shell effect in Ti and V isotopes by the first high-precision mass measurements of the critical species ^{58}Ti and ^{59}V. With the new precision achieved, we reveal the nonexistence of the N=34 empirical two-neutron shell gaps for Ti and V, and the enhanced energy gap above the occupied νp_{3/2} orbit is identified as a feature unique to Ca. We perform new Monte Carlo shell model calculations including the νd_{5/2} and νg_{9/2} orbits and compare the results with conventional shell model calculations, which exclude the νg_{9/2} and the νd_{5/2} orbits. The comparison indicates that the shell gap reduction in Ti is related to a partial occupation of the higher orbitals for the outer two valence neutrons at N=34.

Search for the Pair Production of Dark Particles X with K_{L}

We present the first search for the pair production of dark particles X via K_{L}^{0}→XX with X decaying into two photons using the data collected by the KOTO experiment. No signal was observed in the mass range of 40-110 MeV/c^{2} and 210-240 MeV/c^{2}. This sets upper limits on the branching fractions as B(K_{L}^{0}→XX)<(1-4)×10^{-7} and B(K_{L}^{0}→XX)<(1-2)×10^{-6} at the 90% confidence level for the two mass regions, respectively.

Electric Monopole Transition from the Superdeformed Band in

The electric monopole (E0) transition strength ρ^{2} for the transition connecting the third 0^{+} level, a "superdeformed" band head, to the "spherical" 0^{+} ground state in doubly magic ^{40}Ca is determined via e^{+}e^{-} pair-conversion spectroscopy. The measured value ρ^{2}(E0;0_{3}^{+}→0_{1}^{+})=2.3(5)×10^{-3} is the smallest ρ^{2}(E0;0^{+}→0^{+}) found in A<50 nuclei. In contrast, the E0 transition strength to the ground state observed from the second 0^{+} state, a band head of "normal" deformation, is an order of magnitude larger ρ^{2}(E0;0_{2}^{+}→0_{1}^{+})=25.9(16)×10^{-3}, which shows significant mixing between these two states. Large-scale shell-model (LSSM) calculations are performed to understand the microscopic structure of the excited states and the configuration mixing between them; experimental ρ^{2} values in ^{40}Ca and neighboring isotopes are well reproduced by the LSSM calculations. The unusually small ρ^{2}(E0;0_{3}^{+}→0_{1}^{+}) value is due to destructive interference in the mixing of shape-coexisting structures, which are based on several different multiparticle-multihole excitations. This observation goes beyond the usual treatment of E0 strengths, where two-state shape mixing cannot result in destructive interference.

Study of the K_{L}→π

The rare decay K_{L}→π^{0}νν[over ¯] was studied with the dataset taken at the J-PARC KOTO experiment in 2016, 2017, and 2018. With a single event sensitivity of (7.20±0.05_{stat}±0.66_{syst})×10^{-10}, three candidate events were observed in the signal region. After unveiling them, contaminations from K^{±} and scattered K_{L} decays were studied, and the total number of background events was estimated to be 1.22±0.26. We conclude that the number of observed events is statistically consistent with the background expectation. For this dataset, we set an upper limit of 4.9×10^{-9} on the branching fraction of K_{L}→π^{0}νν[over ¯] at the 90% confidence level.

Sequential Nature of (p,3p) Two-Proton Knockout from Neutron-Rich Nuclei.

Twenty-one two-proton knockout (p,3p) cross sections were measured from neutron-rich nuclei at ∼250 MeV/nucleon in inverse kinematics. The angular distribution of the three emitted protons was determined for the first time, demonstrating that the (p,3p) kinematics are consistent with two sequential proton-proton collisions within the projectile nucleus. Ratios of (p,3p) over (p,2p) inclusive cross sections follow the trend of other many-nucleon removal reactions, further reinforcing the sequential nature of (p,3p) in neutron-rich nuclei.

Underlying Structure of Collective Bands and Self-Organization in Quantum Systems.

The underlying structure of low-lying collective bands of atomic nuclei is discussed from a novel perspective on the interplay between single-particle and collective degrees of freedom, by utilizing state-of-the-art configuration interaction calculations on heavy nuclei. Besides the multipole components of the nucleon-nucleon interaction that drive collective modes forming those bands, the monopole component is shown to control the resistance against such modes. The calculated structure of ^{154}Sm corresponds to the coexistence between prolate and triaxial shapes, while that of ^{166}Er exhibits a deformed shape with a strong triaxial instability. Both findings differ from traditional views based on ß/γ vibrations. The formation of collective bands is shown to be facilitated from a self-organization mechanism.

Are There Signatures of Harmonic Oscillator Shells Far from Stability? First Spectroscopy of

The first measurement of the low-lying states of the neutron-rich ^{110}Zr and ^{112}Mo was performed via in-beam γ-ray spectroscopy after one proton removal on hydrogen at ∼200 MeV/nucleon. The 2_{1}^{+} excitation energies were found at 185(11) keV in ^{110}Zr, and 235(7) keV in ^{112}Mo, while the R_{42}=E(4_{1}^{+})/E(2_{1}^{+}) ratios are 3.1(2), close to the rigid rotor value, and 2.7(1), respectively. These results are compared to modern energy density functional based configuration mixing models using Gogny and Skyrme effective interactions. We conclude that first levels of ^{110}Zr exhibit a rotational behavior, in agreement with previous observations of lighter zirconium isotopes as well as with the most advanced Monte Carlo shell model predictions. The data, therefore, do not support a harmonic oscillator shell stabilization scenario at Z=40 and N=70. The present data also invalidate predictions for a tetrahedral ground state symmetry in ^{110}Zr.

Large-Scale Shell-Model Analysis of the Neutrinoless ßß Decay of

We present the nuclear matrix element for the neutrinoless double-beta decay of ^{48}Ca based on large-scale shell-model calculations including two harmonic oscillator shells (sd and pf shells). The excitation spectra of ^{48}Ca and ^{48}Ti, and the two-neutrino double-beta decay of ^{48}Ca are reproduced in good agreement to the experimental data. We find that the neutrinoless double-beta decay nuclear matrix element is enhanced by about 30% compared to pf-shell calculations. This reduces the decay lifetime by almost a factor of 2. The matrix-element increase is mostly due to pairing correlations associated with cross-shell sd-pf excitations. We also investigate possible implications for heavier neutrinoless double-beta decay candidates.

Erratum: Large-Scale Shell-Model Analysis of the Neutrinoless ßß Decay of

This corrects the article DOI: 10.1103/PhysRevLett.116.112502.

First Measurement of Collectivity of Coexisting Shapes Based on Type II Shell Evolution: The Case of

BACKGROUND: Type II shell evolution has recently been identified as a microscopic cause for nuclear shape coexistence. PURPOSE: Establish a low-lying rotational band in ^{96}Zr. METHODS: High-resolution inelastic electron scattering and a relative analysis of transition strengths are used. RESULTS: The B(E2;0_{1}^{+}→2_{2}^{+}) value is measured and electromagnetic decay strengths of the 2_{2}^{+} state are deduced. CONCLUSIONS: Shape coexistence is established for ^{96}Zr. Type II shell evolution provides a systematic and quantitative mechanism to understand deformation at low excitation energies.

Successful treatment of cytomegalovirus enteritis after unrelated allogeneic stem cell transplantation by the infusion of ex vivo-expanded CD4+ lymphocytes derived from the recipient's peripheral blood donor cells.

Adoptive immunotherapies have been developed for antiviral agent-refractory cytomegalovirus (CMV) disease after stem cell transplantation (SCT). However, the application of such strategies is limited, particularly in terms of need for donor cooperation regarding blood sampling and inaccessibility in the setting of cord blood transplantation. Herein, we describe the first successful treatment of antiviral agent-refractory CMV enteritis after allogeneic SCT by the infusion of ex vivo-expanded donor-derived CD4(+) lymphocytes obtained from the recipient's peripheral blood.

Low-Lying Structure of (50)Ar and the N=32 Subshell Closure.

The low-lying structure of the neutron-rich nucleus (50)Ar has been investigated at the Radioactive Isotope Beam Factory using in-beam γ-ray spectroscopy with (9)Be((54)Ca,(50)Ar+γ)X, (9)Be((55)Sc,(50)Ar+γ)X, and (9)Be((56)Ti,(50)Ar+γ)X multinucleon removal reactions at ∼220 MeV/u. A γ-ray peak at 1178(18) keV is reported and assigned as the transition from the first 2(+) state to the 0(+) ground state. A weaker, tentative line at 1582(38) keV is suggested as the 4(1)(+)→2(1)(+) transition. The experimental results are compared to large-scale shell-model calculations performed in the sdpf model space using the SDPF-MU effective interaction with modifications based on recent experimental data for exotic calcium and potassium isotopes. The modified Hamiltonian provides a satisfactory description of the new experimental results for (50)Ar and, more generally, reproduces the energy systematics of low-lying states in neutron-rich Ar isotopes rather well. The shell-model calculations indicate that the N=32 subshell gap in (50)Ar is similar in magnitude to those in (52)Ca and (54)Ti and, notably, predict an N=34 subshell closure in (52)Ar that is larger than the one recently reported in (54)Ca.

Severe hyponatremia caused by syndrome of inappropriate secretion of antidiuretic hormone developed as initial manifestation of human herpesvirus-6-associated acute limbic encephalitis after unrelated bone marrow transplantation.

Severe hyponatremia is a critical electrolyte abnormality in allogeneic stem cell transplantation (allo-SCT) recipients and >50% of cases of severe hyponatremia are caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Here, we present a patient with rapidly progressive severe hyponatremia as an initial sign and symptom of human herpesvirus-6-associated post-transplantation acute limbic encephalitis (HHV-6 PALE) after allo-SCT. A 45-year-old woman with acute lymphoblastic leukemia received unrelated bone marrow transplantation from a one locus-mismatched donor at the DR locus. On day 21, she developed a generalized seizure and loss of consciousness with severe hyponatremia, elevated serum antidiuretic hormone (ADH), and decreased serum osmolality. A high titer of HHV-6 DNA was detected in cerebrospinal fluid. Treatment with foscarnet sodium and hypertonic saline was started with improvement of neurological condition within several days. Although an elevated serum ADH, low serum osmolality, and high urinary osmolality persisted for 2 months, she had no other recurrent symptoms of encephalitis. Our experience suggests that hyponatremia accompanied by SIADH should be recognized as a prodromal or concomitant manifestation of HHV-6 PALE, and close monitoring of serum sodium levels in high-risk patients for HHV-6 PALE is necessary for immediate diagnosis and treatment initiation.

Selective capture of acentric fragments by micronuclei provides a rapid method for purifying extrachromosomally amplified DNA.

The amplification and overexpression of a number of oncogenes is strongly associated with the progression of a variety of different cancers. We now present a strategy to purify amplified DNA on double minute chromosomes (DMs) to enable analysis of their prevalence and contribution to tumourigenesis. Using cell lines derived from four different tumour types, we have developed a general and rapid method to purify micronuclei that are known to entrap extrachromosomal elements. The isolated DNA is highly enriched in DM sequences and can be used to prepare probes to localize the progenitor single copy chromosomal regions. The capture of DMs by micronuclei appears to be dependent on their lack of a centromere rather than their small size.

A mutation in the ceruloplasmin gene is associated with systemic hemosiderosis in humans.

We identified a mutation in the ceruloplasmin (Cp) gene in a Japanese family with aceruloplasminemia, some of whose members showed extrapyramidal disorders, cerebellar ataxia, and diabetes mellitus. A post-mortem study of the proband revealed excessive iron deposition mainly in the brain, liver and pancreas. The G to A transition at the splice acceptor site introduces a premature termination codon at the amino acid position 991 by defective splicing, thereby truncating the carboxyl terminus of Cp in affected individuals. We conclude that the mutation in the Cp gene is associated with systemic hemosiderosis in humans.

Charcot-Marie-Tooth neuropathy type 1B is associated with mutations of the myelin P0 gene.

P0, a major structural protein of peripheral myelin, is a homophilic adhesion molecule and maps to chromosome 1q22-q23, in the region of the locus for Charcot-Marie-Tooth neuropathy type 1B (CMT1B). We have investigated P0 as a candidate gene in two pedigrees with CMT1B and found point mutations which are completely linked with the disease (Z = 5.5, theta = 0). The mutations, glutamate substitution for lysine 96 or aspartate 90, are located in the extracellular domain, which plays a significant role in myelin membrane adhesion. Individuals with CMT1B are heterozygous for the normal allele and the mutant allele. Our results indicate that P0 is a gene responsible for CMT1B.

Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase.

Autosomal recessive juvenile parkinsonism (AR-JP), one of the most common familial forms of Parkinson disease, is characterized by selective dopaminergic neural cell death and the absence of the Lewy body, a cytoplasmic inclusion body consisting of aggregates of abnormally accumulated proteins. We previously cloned PARK2, mutations of which cause AR-JP (ref. 2), but the function of the gene product, parkin, remains unknown. We report here that parkin is involved in protein degradation as a ubiquitin-protein ligase collaborating with the ubiquitin-conjugating enzyme UbcH7, and that mutant parkins from AR-JP patients show loss of the ubiquitin-protein ligase activity. Our findings indicate that accumulation of proteins that have yet to be identified causes a selective neural cell death without formation of Lewy bodies. Our findings should enhance the exploration of the molecular mechanisms of neurodegeneration in Parkinson disease as well as in other neurodegenerative diseases that are characterized by involvement of abnormal protein ubiquitination, including Alzheimer disease, other tauopathies, CAG triplet repeat disorders and amyotrophic lateral sclerosis.

Positional cloning of the APECED gene.

Autoimmune polyglandular syndrome type I (APS 1, also called APECED) is an autosomal-recessive disorder that maps to human chromosome 21q22.3 between markers D21S49 and D21S171 by linkage studies. We have isolated a novel gene from this region, AIRE (autoimmune regulator), which encodes a protein containing motifs suggestive of a transcription factor including two zinc-finger (PHD-finger) motifs, a proline-rich region and three LXXLL motifs. Two mutations, a C-->T substitution that changes the Arg 257 (CGA) to a stop codon (TGA) and an A-->G substitution that changes the Lys 83 (AAG) to a Glu codon (GAG), were found in this novel gene in Swiss and Finnish APECED patients. The Arg257stop (R257X) is the predominant mutation in Finnish APECED patients, accounting for 10/12 alleles studied. These results indicate that this gene is responsible for the pathogenesis of APECED. The identification of the gene defective in APECED should facilitate the genetic diagnosis and potential treatment of the disease and further enhance our general understanding of the mechanisms underlying autoimmune diseases.

Insertion of beta-satellite repeats identifies a transmembrane protease causing both congenital and childhood onset autosomal recessive deafness.

Approximately 50% of childhood deafness is caused by mutations in specific genes. Autosomal recessive loci account for approximately 80% of nonsyndromic genetic deafness. Here we report the identification of a new transmembrane serine protease (TMPRSS3; also known as ECHOS1) expressed in many tissues, including fetal cochlea, which is mutated in the families used to describe both the DFNB10 and DFNB8 loci. An 8-bp deletion and insertion of 18 monomeric (approximately 68-bp) beta-satellite repeat units, normally present in tandem arrays of up to several hundred kilobases on the short arms of acrocentric chromosomes, causes congenital deafness (DFNB10). A mutation in a splice-acceptor site, resulting in a 4-bp insertion in the mRNA and a frameshift, was detected in childhood onset deafness (DFNB8). This is the first description of beta-satellite insertion into an active gene resulting in a pathogenic state, and the first description of a protease involved in hearing loss.