A nucleonic NJL model for finite nuclei: dynamic mass generation and ground-state observables

We test the compatibility of chiral symmetry, dynamic mass generation of the nucleon due to spontaneous breaking of chiral symmetry, and the description of finite nuclear systems by employing an NJL model understood as a chiral invariant effective theory for nucleons. We apply the model to nuclear matter as well as to finite nuclei. In the latter case, the model is adjusted to nuclear ground-state observables. We treat the case of a pure chiral theory and the physically more realistic case where a portion of the nucleon mass (160 MeV) explicitly breaks chiral symmetry. The best version of this current model is found to deliver reasonably good results simultaneously for both finite nuclei and the nucleon mass, which supports our motivation of probing a link between low-momentum QCD and the nuclear many-body problem. However, the observables calculated for finite nuclei are not as good as those coming from existing relativistic mean field models without explicit chiral symmetry.Comment: 19 pages, 3 eps figures, accepted for publication in Nucl. Phys.

Criteria for nonlinear parameters of relativistic mean field models

Based on the properties of the critical and the actual effective masses of sigma and omega mesons, criteria to estimate the values of the isoscalar nonlinear terms of the standard relativistic mean field model that reproduce stable equations of state in respect to particle hole excitation at high densities are derived. The relation between nuclear matter stability and the symmetric nuclear matter properties are shown. The criteria are used to analyze in a more systematic way the high-density longitudinal and transverse instabilities of some parameter sets of relativistic mean field models. The critical role of the vector and vector-scalar nonlinear terms is also discussed quantitatively.Comment: 21 pages, 10 figures, 4 tables. Accepted for Publication in Physical review

Vacuum, matter, antimatter and the problem of cold compression

We discuss the possibility of producing a new kind of nuclear system by putting a few antibaryons inside ordinary nuclei. The structure of such systems is calculated within the relativistic mean-field model assuming that the nucleon and antinucleon potentials are related by the G-parity transformation. The presence of antinucleons leads to decreasing vector potential and increasing scalar potential for the nucleons. As a result, a strongly bound system of high density is formed. Due to the significant reduction of the available phase space the annihilation probability might be strongly suppressed in such systems

Collective modes of asymmetric nuclear matter in Quantum HadroDynamics

We discuss a fully relativistic Landau Fermi liquid theory based on the Quantum Hadro-Dynamics ($QHD$) effective field picture of Nuclear Matter ({\it NM}). From the linearized kinetic equations we get the dispersion relations of the propagating collective modes. We focus our attention on the dynamical effects of the interplay between scalar and vector channel contributions. A beautiful ``mirror'' structure in the form of the dynamical response in the isoscalar/isovector degree of freedom is revealed, with a complete parallelism in the role respectively played by the compressibility and the symmetry energy. All that strongly supports the introduction of an explicit coupling to the scalar-isovector channel of the nucleon-nucleon interaction. In particular we study the influence of this coupling (to a $\delta$-meson-like effective field) on the collective response of asymmetric nuclear matter ($ANM$). Interesting contributions are found on the propagation of isovector-like modes at normal density and on an expected smooth transition to isoscalar-like oscillations at high baryon density. Important ``chemical'' effects on the neutron-proton structure of the mode are shown. For dilute $ANM$ we have the isospin distillation mechanism of the unstable isoscalar-like oscillations, while at high baryon density we predict an almost pure neutron wave structure of the propagating sounds.Comment: 18 pages (LATEX), 8 Postscript figures, uses "epsfig

Effect of tensor couplings in a relativistic Hartree approach for finite nuclei

The relativistic Hartree approach describing the bound states of both nucleons and anti-nucleons in finite nuclei has been extended to include tensor couplings for the $\omega$- and $\rho$-meson. After readjusting the parameters of the model to the properties of spherical nuclei, the effect of tensor-coupling terms rises the spin-orbit force by a factor of 2, while a large effective nucleon mass $m^{*}/M_{N} \approx 0.8$ sustains. The overall nucleon spectra of shell-model states are improved evidently. The predicted anti-nucleon spectra in the vacuum are deepened about 20 -- 30 MeV.Comment: 31 pages, 4 postscript figures include

Alcohol drinking and risk of Parkinson's disease: a case-control study in Japan

<p>Abstract</p> <p>Background</p> <p>Although some epidemiologic studies found inverse associations between alcohol drinking and Parkinson's disease (PD), the majority of studies found no such significant associations. Additionally, there is only limited research into the possible interactions of alcohol intake with aldehyde dehydrogenase (ALDH) 2 activity with respect to PD risk. We examined the relationship between alcohol intake and PD among Japanese subjects using data from a case-control study.</p> <p>Methods</p> <p>From 214 cases within 6 years of PD onset and 327 controls without neurodegenerative disease, we collected information on "peak", as opposed to average, alcohol drinking frequency and peak drinking amounts during a subject's lifetime. Alcohol flushing status was evaluated via questions, as a means of detecting inactive ALHD2. The multivariate model included adjustments for sex, age, region of residence, smoking, years of education, body mass index, alcohol flushing status, presence of selected medication histories, and several dietary factors.</p> <p>Results</p> <p>Alcohol intake during peak drinking periods, regardless of frequency or amount, was not associated with PD. However, when we assessed daily ethanol intake separately for each type of alcohol, only Japanese sake (rice wine) was significantly associated with PD (adjusted odds ratio of ≥66.0 g ethanol per day: 3.39, 95% confidence interval: 1.10-11.0, <it>P </it>for trend = 0.001). There was no significant interaction of alcohol intake with flushing status in relation to PD risk.</p> <p>Conclusions</p> <p>We did not find significant associations between alcohol intake and PD, except for the daily amount of Japanese sake. Effect modifications by alcohol flushing status were not observed.</p

Rasd1 Modulates the Coactivator Function of NonO in the Cyclic AMP Pathway

All living organisms exhibit autonomous daily physiological and behavioural rhythms to help them synchronize with the environment. Entrainment of circadian rhythm is achieved via activation of cyclic AMP (cAMP) and mitogen-activated protein kinase signaling pathways. NonO (p54nrb) is a multifunctional protein involved in transcriptional activation of the cAMP pathway and is involved in circadian rhythm control. Rasd1 is a monomeric G protein implicated to play a pivotal role in potentiating both photic and nonphotic responses of the circadian rhythm. In this study, we have identified and validated NonO as an interacting partner of Rasd1 via affinity pulldown, co-immunoprecipitation and indirect immunofluorescence studies. The GTP-hydrolysis activity of Rasd1 is required for the functional interaction. Functional interaction of Rasd1-NonO in the cAMP pathway was investigated via reporter gene assays, chromatin immunoprecipitation and gene knockdown. We showed that Rasd1 and NonO interact at the CRE-site of specific target genes. These findings reveal a novel mechanism by which the coregulator activity of NonO can be modulated

A Genome-Wide Linkage Scan for Distinct Subsets of Schizophrenia Characterized by Age at Onset and Neurocognitive Deficits

As schizophrenia is genetically and phenotypically heterogeneous, targeting genetically informative phenotypes may help identify greater linkage signals. The aim of the study is to evaluate the genetic linkage evidence for schizophrenia in subsets of families with earlier age at onset or greater neurocognitive deficits.Patients with schizophrenia (n  =  1,207) and their first-degree relatives (n  =  1,035) from 557 families with schizophrenia were recruited from six data collection field research centers throughout Taiwan. Subjects completed a face-to-face semi-structured interview, the Continuous Performance Test (CPT), the Wisconsin Card Sorting Test, and were genotyped with 386 microsatellite markers across the genome.A maximum nonparametric logarithm of odds (LOD) score of 4.17 at 2q22.1 was found in 295 families ranked by increasing age at onset, which had significant increases in the maximum LOD score compared with those obtained in initial linkage analyses using all available families. Based on this subset, a further subsetting by false alarm rate on the undegraded and degraded CPT obtained further increase in the nested subset-based LOD on 2q22.1, with a score of 7.36 in 228 families and 7.71 in 243 families, respectively.We found possible evidence of linkage on chromosome 2q22.1 in families of schizophrenia patients with more CPT false alarm rates nested within the families with younger age at onset. These results highlight the importance of incorporating genetically informative phenotypes in unraveling the complex genetics of schizophrenia

Convergent functional genomics of anxiety disorders: translational identification of genes, biomarkers, pathways and mechanisms

Anxiety disorders are prevalent and disabling yet understudied from a genetic standpoint, compared with other major psychiatric disorders such as bipolar disorder and schizophrenia. The fact that they are more common, diverse and perceived as embedded in normal life may explain this relative oversight. In addition, as for other psychiatric disorders, there are technical challenges related to the identification and validation of candidate genes and peripheral biomarkers. Human studies, particularly genetic ones, are susceptible to the issue of being underpowered, because of genetic heterogeneity, the effect of variable environmental exposure on gene expression, and difficulty of accrual of large, well phenotyped cohorts. Animal model gene expression studies, in a genetically homogeneous and experimentally tractable setting, can avoid artifacts and provide sensitivity of detection. Subsequent translational integration of the animal model datasets with human genetic and gene expression datasets can ensure cross-validatory power and specificity for illness. We have used a pharmacogenomic mouse model (involving treatments with an anxiogenic drug—yohimbine, and an anti-anxiety drug—diazepam) as a discovery engine for identification of anxiety candidate genes as well as potential blood biomarkers. Gene expression changes in key brain regions for anxiety (prefrontal cortex, amygdala and hippocampus) and blood were analyzed using a convergent functional genomics (CFG) approach, which integrates our new data with published human and animal model data, as a translational strategy of cross-matching and prioritizing findings. Our work identifies top candidate genes (such as FOS, GABBR1, NR4A2, DRD1, ADORA2A, QKI, RGS2, PTGDS, HSPA1B, DYNLL2, CCKBR and DBP), brain–blood biomarkers (such as FOS, QKI and HSPA1B), pathways (such as cAMP signaling) and mechanisms for anxiety disorders—notably signal transduction and reactivity to environment, with a prominent role for the hippocampus. Overall, this work complements our previous similar work (on bipolar mood disorders and schizophrenia) conducted over the last decade. It concludes our programmatic first pass mapping of the genomic landscape of the triad of major psychiatric disorder domains using CFG, and permitted us to uncover the significant genetic overlap between anxiety and these other major psychiatric disorders, notably the under-appreciated overlap with schizophrenia. PDE10A, TAC1 and other genes uncovered by our work provide a molecular basis for the frequently observed clinical co-morbidity and interdependence between anxiety and other major psychiatric disorders, and suggest schizo-anxiety as a possible new nosological domain