Thermal Restoration of Chiral Symmetry in Supersymmetric Nambu-Jona-Lasinio Model with Soft SUSY Breaking

The supersymmetric version of the Nambu-Jona-Lasinio model is investigated in connection with the chiral symmetry breaking induced by a soft SUSY breaking term. It is found that the broken chiral symmetry due to the soft breaking term is restored at suitably high temperature and the symmetry restoration occurs as first-order phase transitions. The critical temperature at which the chiral symmetry is restored is determined as a function of the strength of the soft breaking term and the field coupling constant. The dynamical fermion mass is calculated at finite temperature. Some possible applications to the breaking scenario of unified field theories are discussed.Comment: 9 pages, 2 figure

Pattern of Chiral Symmetry Restoration at Finite Temperature in A Supersymmetric Composite Model

The structure of chiral symmetry restorations at finite temperature is thoroughly investigated in the supersymmetric Nambu-Jona-Lasinio model with a soft supersymmetry breaking term. It is found that the broken chiral symmetry at vanishing temperature is restored at sufficiently high temperature in two patterns, i. e., the first order and second order phase transition depending on the choice of the coupling constant $G$ and the supersymmetry breaking parameter $\Delta$. The critical curves expressing the phase boundaries in the $G-\Delta$ plane are completely determined and the dynamically generated fermion mass is calculated as a function of temperature.Comment: 12 pages, 4 figures, REVTe

The high-lying 6^6Li levels at excitation energy around 21 MeV

The $^3$H+$^3$He cluster structure in $^6$Li was investigated by the $^3$H($\alpha$,$^3$H $^3$He)n kinematically complete experiment at the incident energy $E_\alpha$ = 67.2 MeV. We have observed two resonances at $E_x^*$ = 21.30 and 21.90 MeV which are consistent with the $^3$He($^3$H, $\gamma$)$^6$Li analysis in the Ajzenberg-Selove compilation. Our data are compared with the previous experimental data and the RGM and CSRGM calculations.Comment: 12 pages, 6 figures. Accepted for publication in J. Phys. Soc. Jp

A Model of Curvature-Induced Phase Transitions in Inflationary Universe

Chiral phase transitions driven by space-time curvature effects are investigated in de Sitter space in the supersymmetric Nambu-Jona-Lasinio model with soft supersymmetry breaking. The model is considered to be suitable for the analysis of possible phase transitions in inflationary universe. It is found that a restoration of the broken chiral symmetry takes place in two patterns for increasing curvature : the first order and second order phase transition respectively depending on initial settings of the four-body interaction parameter and the soft supersymmetry breaking parameter. The critical curves expressing the phase boundaries in these parameters are obtained. Cosmological implications of the result are discussed in connection with bubble formations and the creation of cosmic strings during the inflationary era.Comment: 12 pages, 3 figures, REVTe

Curvature-induced phase transitions in the inflationary universe - Supersymmetric Nambu-Jona-Lasinio Model in de Sitter spacetime -

The phase structure associated with the chiral symmetry is thoroughly investigated in de Sitter spacetime in the supersymmetric Nambu-Jona-Lasinio model with supersymmetry breaking terms. The argument is given in the three and four space-time dimensions in the leading order of the 1/N expansion and it is shown that the phase characteristics of the chiral symmetry is determined by the curvature of de Sitter spacetime. It is found that the symmetry breaking takes place as the first order as well as second order phase transition depending on the choice of the coupling constant and the parameter associated with the supersymmetry breaking term. The critical curves expressing the phase boundary are obtained. We also discuss the model in the context of the chaotic inflation scenario where topological defects (cosmic strings) develop during the inflation.Comment: 29 pages, 6 figures, REVTe

Assisted evolution enables HIV-1 to overcome a high trim5α-imposed genetic barrier to rhesus macaque tropism

Diversification of antiretroviral factors during host evolution has erected formidable barriers to cross-species retrovirus transmission. This phenomenon likely protects humans from infection by many modern retroviruses, but it has also impaired the development of primate models of HIV-1 infection. Indeed, rhesus macaques are resistant to HIV-1, in part due to restriction imposed by the TRIM5α protein (rhTRIM5α). Initially, we attempted to derive rhTRIM5α-resistant HIV-1 strains using two strategies. First, HIV-1 was passaged in engineered human cells expressing rhTRIM5α. Second, a library of randomly mutagenized capsid protein (CA) sequences was screened for mutations that reduced rhTRIM5α sensitivity. Both approaches identified several individual mutations in CA that reduced rhTRIM5α sensitivity. However, neither approach yielded mutants that were fully resistant, perhaps because the locations of the mutations suggested that TRIM5α recognizes multiple determinants on the capsid surface. Moreover, even though additive effects of various CA mutations on HIV-1 resistance to rhTRIM5α were observed, combinations that gave full resistance were highly detrimental to fitness. Therefore, we employed an 'assisted evolution' approach in which individual CA mutations that reduced rhTRIM5α sensitivity without fitness penalties were randomly assorted in a library of viral clones containing synthetic CA sequences. Subsequent passage of the viral library in rhTRIM5α-expressing cells resulted in the selection of individual viral species that were fully fit and resistant to rhTRIM5α. These viruses encoded combinations of five mutations in CA that conferred complete or near complete resistance to the disruptive effects of rhTRIM5α on incoming viral cores, by abolishing recognition of the viral capsid. Importantly, HIV-1 variants encoding these CA substitutions and SIVmac239 Vif replicated efficiently in primary rhesus macaque lymphocytes. These findings demonstrate that rhTRIM5α is difficult to but not impossible to evade, and doing so should facilitate the development of primate models of HIV-1 infection

CD28 between tolerance and autoimmunity: The side effects of animal models [version 1; referees: 2 approved]

Regulation of immune responses is critical for ensuring pathogen clearance and for preventing reaction against self-antigens. Failure or breakdown of immunological tolerance results in autoimmunity. CD28 is an important co-stimulatory receptor expressed on T cells that, upon specific ligand binding, delivers signals essential for full T-cell activation and for the development and homeostasis of suppressive regulatory T cells. Many in vivo mouse models have been used for understanding the role of CD28 in the maintenance of immune homeostasis, thus leading to the development of CD28 signaling modulators that have been approved for the treatment of some autoimmune diseases. Despite all of this progress, a deeper understanding of the differences between the mouse and human receptor is required to allow a safe translation of pre-clinical studies in efficient therapies. In this review, we discuss the role of CD28 in tolerance and autoimmunity and the clinical efficacy of drugs that block or enhance CD28 signaling, by highlighting the success and failure of pre-clinical studies, when translated to humans